Jungtinės Valstijos - anglų - NLM (National Library of Medicine)

remedyrepack inc. - clonazepam (unii: 5pe9fde8gb) (clonazepam - unii:5pe9fde8gb) - seizure disorders: clonazepam tablets are useful alone or as an adjunct in the treatment of the lennox- gastaut syndrome (petit mal variant), akinetic and myoclonic seizures. in patients with absence seizures (petit mal) who have failed to respond to succinimides, clonazepam tablets may be useful. some loss of effect may occur during the course of clonazepam treatment (see precautions: loss of effect). panic disorder: clonazepam tablets are indicated for the treatment of panic disorder, with or without agoraphobia, as defined in dsm-v. panic disorder is characterized by the occurrence of unexpected panic attacks and associated concern about having additional attacks, worry about the implications or consequences of the attacks, and/or a significant change in behavior related to the attacks. the efficacy of clonazepam tablets was established in two 6- to 9-week trials  in panic disorder patients whose diagnoses corresponded to the dsm-lilr category of panic disorder (see clinical pharmacology: clinical trials). panic disorder (dsm-v) is characterized by recurrent unexpected panic attacks, i.e., a discrete  period of intense fear or discomfort in which four (or more) of the following symptoms develop abruptly and reach a peak within 10 minutes: (1) palpitations, pounding heart or accelerated heart rate; (2) sweating; (3) trembling or shaking; (4) sensations of shortness of breath or smothering; (5) feeling of choking; (6) chest pain or discomfort; (7) nausea or abdominal distress; (8) feeling dizzy, unsteady, lightheaded or faint; (9) derealization (feelings of unreality) or depersonalization (being detached from oneself); (10) fear of losing control; (11) fear of dying; (12) paresthesias (numbness  or tingling  sensations); (13) chills or hot flushes. the effectiveness of clonazepam tablets in long-term use, that is, for more than 9 weeks, has not been systematically studied in controlled clinical trials. the physician who elects to use clonazepam tablets for extended periods should periodically reevaluate the long- term usefulness of the drug for the individual patient (see dosage and administration). clonazepam tablets are contraindicated in patients with the following conditions: - history of sensitivity to benzodiazepines - clinical or biochemical evidence of significant liver disease - acute narrow angle glaucoma (it may be used in patients with open angle glaucoma who are receiving appropriate therapy). controlled substance class: clonazepam tablets contain clonazepam, a schedule iv controlled substance. abuse: clonazepam tablet is a benzodiazepine and a cns depressant with a potential for abuse and addiction. abuse is the intentional, non-therapeutic use of a drug, even once, for its desirable psychological or physiological effects. misuse is the intentional use, for therapeutic purposes, of a drug by an individual in a way other than prescribed by a health care provider or for whom it was not prescribed. drug addiction is a cluster of behavioral, cognitive, and physiological phenomena that may include a strong desire to take the drug, difficulties in controlling drug use (e.g., continuing drug use despite harmful consequences, giving a higher priority to  drug  use  than other  activities  and obligations), and possible tolerance or physical dependence. even taking benzodiazepines as prescribed may put patients at risk for abuse and misuse of their medication. abuse and misuse  may  lead to addiction. abuse and misuse of benzodiazepines often (but not always) involve the use of doses greater than the maximum recommended dosage and commonly involve concomitant use of other medications, alcohol, and/or illicit substances, which is associated with an increased frequency of serious adverse outcomes, including respiratory depression, overdose, or death. benzodiazepines are often sought by individuals who abuse drugs and other substances, and by individuals with addictive disorders (see warnings: abuse, misuse, and addiction ). the following adverse reactions have occurred with benzodiazepine abuse  and/or  misuse: abdominal pain, amnesia, anorexia, anxiety, aggression, ataxia, blurred vision, confusion, depression, disinhibition, disorientation, dizziness, euphoria, impaired concentration and memory, indigestion, irritability, muscle pain, slurred speech, tremors, and vertigo. the following severe adverse reactions have occurred with benzodiazepine abuse and/or  misuse: delirium, paranoia, suicidal ideation and behavior, seizures, coma, breathing  difficulty, and  death. death is more often associated with polysubstance use  (especially benzodiazepines  with other  cns depressants such as opioids and alcohol) . dependence: physical dependence clonazepam tablets may produce physical dependence from continued therapy. physical dependence is a state that develops as a result of physiological adaptation in response to repeated drug use, manifested by withdrawal signs and symptoms after abrupt discontinuation or a significant dose reduction of a drug. abrupt discontinuation or rapid dosage reduction of benzodiazepines or administration of flumazenil, a benzodiazepine antagonist, may precipitate acute withdrawal reactions, including seizures, which can be life-threatening. patients at an increased risk of withdrawal adverse reactions after benzodiazepine discontinuation or  rapid dosage reduction include those who take higher dosages (i.e., higher and/or more frequent doses) and those who have had longer durations of use (see warnings: dependence and withdrawal reactions) to reduce the risk of withdrawal reactions, use a gradual taper to discontinue clonazepam tablets or reduce the dosage (see dosage and administration: discontinuation or dosage reduction of clonazepam tablets and warnings: dependence and withdrawal reactions). acute withdrawal signs and symptoms acute withdrawal signs and symptoms associated with benzodiazepines have included abnormal involuntary movements, anxiety, blurred vision, depersonalization, depression, derealization, dizziness, fatigue, gastrointestinal adverse reactions (e.g., nausea, vomiting, diarrhea, weight loss, decreased appetite), headache, hyperacusis, hypertension, irritability, insomnia, memory impairment, muscle  pain and stiffness, panic attacks, photophobia, restlessness, tachycardia, and tremor. more severe acute withdrawal signs and symptoms, including life-threatening reactions, have  included catatonia, convulsions, delirium tremens, depression, hallucinations, mania, psychosis, seizures and suicidality. protracted withdrawal syndrome protracted withdrawal syndrome associated with benzodiazepines is characterized by anxiety, cognitive impairment, depression, insomnia, formication, motor symptoms (e.g.,  weakness,  tremor,  muscle twitches), paresthesia, and tinnitus that persists beyond 4 to  6  weeks after initial benzodiazepine withdrawal. protracted withdrawal symptoms may last weeks to more  than 12 months . as  a result, there may be difficulty in differentiating withdrawal symptoms from potential re-emergence or continuation of symptoms for which the benzodiazepine was being used. tolerance tolerance to clonazepam tablets  may  develop  from continued  therapy.  tolerance is a physiological state characterized by a reduced response to  a drug  after repeated administration (i.e., a higher dose of a drug is required to produce the same effect that was once obtained at a lower dose). tolerance to the therapeutic effect of clonazepam tablets may  develop; however, little tolerance develops to the amnestic reactions and other cognitive impairments caused by benzodiazepines. following the short-term treatment of patients with panic disorder in studies 1 and 2 (see clinical pharmacology: clinical trials) , patients were gradually withdrawn during a 7-week downward- titration (discontinuance) period. overall, the discontinuance period was associated with good tolerability and a very modest clinical deterioration, without evidence of a significant rebound phenomenon. however, there are not sufficient data from adequate and well-controlled long-term clonazepam studies in patients with panic disorder to accurately estimate the risks of withdrawal symptoms and dependence that may be associated with such use. what is the most important information i should know about clonazepam tablets? - clonazepam tablet is a benzodiazepine medicine. taking benzodiazepines with opioid medicines, alcohol, or other central nervous system (cns) depressants (including street drugs) can cause severe drowsiness, breathing problems (respiratory depression), coma, and death. get emergency help right away if any of the following happens: - shallow or slowed breathing - breathing stops (which may lead to the heart stopping) - excessive sleepiness (sedation) do not drive or operate heavy machinery until you know how taking clonazepam tablets with opioids affects you. - risk of abuse, misuse, and addiction . there is a risk of abuse, misuse, and addiction with benzodiazepines, including clonazepam tablet which can lead to overdose and serious side effects including coma and death. - serious side effects including coma and death have happened in people who have abused or misused benzodiazepines, including clonazepam tablets. these serious side effects may also include delirium, paranoia, suicidal thoughts or actions, seizures, and difficulty breathing. call your healthcare provider or go to the nearest hospital emergency room right away if you get any of these serious side effects. - you can develop an addiction even if you take clonazepam tablets as prescribed by your healthcare provider. - take clonazepam tablets exactly as your healthcare provider prescribed. - do not share your clonazepam tablets with other people. - keep clonazepam tablets in a safe place and away from children. - physical dependence and withdrawal reactions. clonazepam tablets can cause physical dependence and withdrawal reactions. do not suddenly stop taking clonazepam tablets . stopping clonazepam tablets suddenly can cause serious and life-threatening side effects, including, unusual movements, responses, or expressions, seizures, sudden and severe mental or nervous system changes, depression, seeing or hearing things that others do not see or hear, an extreme increase in activity or talking, losing touch with reality, and suicidal thoughts or actions. call your healthcare provider or go to the nearest hospital emergency room right away if you get any of these symptoms. some people who suddenly stop benzodiazepines have symptoms that can last for several weeks to more than 12 months, including, anxiety, trouble remembering, learning, or concentrating, depression, problems sleeping, feeling like insects are crawling under your skin, weakness, shaking, muscle twitching, burning or prickling feeling in your hands, arms, legs or feet, and ringing in your ears. physical dependence is not the same as drug addiction. your healthcare provider can tell you more about the differences between physical dependence and drug addiction. do not take more clonazepam tablets than prescribed or take clonazepam tablets for longer than prescribed. - do not suddenly stop taking clonazepam tablets . stopping clonazepam tablets suddenly can cause serious and life-threatening side effects, including, unusual movements, responses, or expressions, seizures, sudden and severe mental or nervous system changes, depression, seeing or hearing things that others do not see or hear, an extreme increase in activity or talking, losing touch with reality, and suicidal thoughts or actions. call your healthcare provider or go to the nearest hospital emergency room right away if you get any of these symptoms. - some people who suddenly stop benzodiazepines have symptoms that can last for several weeks to more than 12 months, including, anxiety, trouble remembering, learning, or concentrating, depression, problems sleeping, feeling like insects are crawling under your skin, weakness, shaking, muscle twitching, burning or prickling feeling in your hands, arms, legs or feet, and ringing in your ears. - physical dependence is not the same as drug addiction. your healthcare provider can tell you more about the differences between physical dependence and drug addiction. - do not take more clonazepam tablets than prescribed or take clonazepam tablets for longer than prescribed. - clonazepam tablets can make you sleepy or dizzy and can slow your thinking and motor skills. this may get better over time. do not drive, operate heavy machinery, or do other dangerous activities until you know how clonazepam tablets affects you. clonazepam tablets may cause problems with your coordination, especially when you are walking or picking things up. - do not drive, operate heavy machinery, or do other dangerous activities until you know how clonazepam tablets affects you. - clonazepam tablets may cause problems with your coordination, especially when you are walking or picking things up. - do not drink alcohol or take other drugs that may make you sleepy or dizzy while taking clonazepam tablets until you talk to your healthcare provider. when taken with alcohol or drugs that cause sleepiness or dizziness, clonazepam tablets may make your sleepiness or dizziness worse. - like other antiepileptic drugs, clonazepam tablets may cause suicidal thoughts or actions in a very small number of people, about 1 in 500. call your healthcare provider right away if you have any of these symptoms, especially if they are new, worse, or worry you: - thoughts about suicide or dying ◦ attempt to commit suicide ◦ new or worse depression - new or worse anxiety ◦ feeling agitated or restless ◦ panic attacks - trouble sleeping (insomnia) ◦ new or worse irritability ◦ acting aggressive, being angry, or violent - acting on dangerous impulses ◦ an extreme increase in activity and talking (mania) ◦ other unusual changes in behavior or mood how can i watch for early symptoms of suicidal thoughts and actions? - pay attention to any changes, especially sudden changes, in mood, behaviors, thoughts, or feelings. - keep all follow-up visits with your healthcare provider as scheduled. call your healthcare provider between visits as needed, especially if you are worried about symptoms. suicidal thoughts or actions can be caused by things other than medicines. if you have suicidal thoughts or actions, your healthcare provider may check for other causes. do not stop clonazepam tablets without first talking to a healthcare provider. - stopping clonazepam tablets suddenly can cause serious problems. stopping clonazepam tablets - suddenly can cause seizures that will not stop (status epilepticus). what are clonazepam tablets? - clonazepam tablets are prescription medicine used alone or with other medicines to treat: certain types of seizure disorders (epilepsy) in adults and children panic disorder with or without fear of open spaces (agoraphobia) in adults - certain types of seizure disorders (epilepsy) in adults and children - panic disorder with or without fear of open spaces (agoraphobia) in adults clonazepam tablet is a federally controlled substance (c-iv) because it contains clonazepam that can be abused or lead to dependence. keep clonazepam tablets in a safe place to prevent misuse and abuse. selling or giving away clonazepam tablets may harm others, and is against the law. tell your healthcare provider if you have ever abused or been dependent on alcohol, prescription medicines, or street drugs. it is not known if clonazepam tablets are safe or effective in treating panic disorder in children younger than 18 years old. who should not take clonazepam tablets? do not take clonazepam tablets if you: - are allergic to benzodiazepines - have significant liver disease - have an eye disease called acute narrow angle glaucoma ask your healthcare provider if you are not sure if you have any of the problems listed above. before you take clonazepam tablets, tell your healthcare provider if you: - have liver or kidney problems - have lung problems (respiratory disease) - have or have had depression, mood problems, or suicidal thoughts or behavior - have any other medical problems - are pregnant or plan to become pregnant. it is not known if clonazepam tablets can harm your unborn baby. tell your healthcare provider right away if you become pregnant while taking clonazepam tablets. you and your healthcare provider will decide if you should take clonazepam tablets while you are pregnant. - studies in pregnant animals have shown harmful effects of benzodiazepine medications (including the active ingredient in clonazepam tablets) on the developing fetus. - children born to mothers receiving benzodiazepine medications (including clonazepam tablets) late in pregnancy may be at some risk of experiencing breathing problems, feeding problems, hypothermia, and withdrawal symptoms. - if you become pregnant while taking clonazepam tablets, talk to your healthcare provider about registering with the north american antiepileptic drug pregnancy registry. you can register by calling 1-888-233-2334. the purpose of this registry is to collect information about the safety of antiepileptic drugs during pregnancy - are breastfeeding or plan to breastfeed. clonazepam can pass into breast milk. you and your healthcare provider should decide how you will feed your baby while you take clonazepam tablets. tell your healthcare provider about all the medicines you take, including prescription and over-the-counter medicines, vitamins, and herbal supplements. taking clonazepam tablets with certain other medicines can cause side effects or affect how well clonazepam tablets or the other medicines work. do not start or stop other medicines without talking to your healthcare provider. how should i take clonazepam tablets? - take clonazepam tablets exactly as your healthcare provider tells you. if you take clonazepam tablets for seizures, your healthcare provider may change the dose until you are taking the right amount of medicine to control your symptoms. - clonazepam is available as a tablet. - do not stop taking clonazepam tablets without first talking to your healthcare provider. stopping clonazepam tablets suddenly can cause serious problems. - clonazepam tablets should be taken with water and swallowed whole. - if you take too much clonazepam tablets, call your healthcare provider or local poison control center right away. what should i avoid while taking clonazepam tablets? - clonazepam tablets can slow your thinking and motor skills. do not drive, operate heavy machinery, or do other dangerous activities until you know how clonazepam tablets affects you. - do not drink alcohol or take other medicines that may make you sleepy or dizzy while taking clonazepam tablets until you talk to your healthcare provider. when taken with alcohol or medicines that cause sleepiness or dizziness, clonazepam tablets may make your sleepiness or dizziness much worse. what are the possible side effects of clonazepam tablets? see “what is the most important information i should know about clonazepam tablets?” clonazepam tablets can also make your seizures happen more often or make them worse. call your healthcare provider right away if your seizures get worse while taking clonazepam tablets. the most common side effects of clonazepam tablets include: - drowsiness • dizziness • fatigue - problems with walking and coordination • depression • problems with memory these are not all the possible side effects of clonazepam tablets. call your doctor for medical advice about side effects. you may report side effects to fda at 1-800-fda-1088 or contact advagen pharma ltd, at 866-488-0312. how should i store clonazepam tablets? - store clonazepam tablets at 20°c to 25°c (68°f -77°f) [see usp controlled room temperature]. - keep clonazepam tablets and all medicines out of the reach of children. general information about the safe and effective use of clonazepam tablets. medicines are sometimes prescribed for purposes other than those listed in a medication guide. do not use clonazepam tablets for a condition for which it was not prescribed. do not give clonazepam tablets to other people, even if they have the same symptoms that you have. it may harm them. you can ask your pharmacist or healthcare provider for information about clonazepam tablets that is written for health professionals. for more information, contact advagen pharma ltd, at 866-488-0312. what are the ingredients in clonazepam tablets? active ingredient: clonazepam inactive ingredients: - 0.5 mg tablets contain lactose monohydrate, polyethylene glycol, microcrystalline cellulose, croscarmellose sodium, magnesium stearate, fd & c yellow 6 al lake, d & c yellow 10 al lake - 1 mg tablets contain lactose monohydrate, polyethylene glycol, microcrystalline cellulose, croscarmellose sodium, magnesium stearate, fd & c blue 1 al lake and fd & c blue 2 al lake - 2 mg tablets contain lactose monohydrate, polyethylene glycol, microcrystalline cellulose, croscarmellose sodium and magnesium stearate this medication guide has been approved by the u.s. food and drug administration. repackaged by / distributed by: remedyrepack inc. 625 kolter drive, indiana, pa 15701 (724) 465-8762

Jungtinės Valstijos - anglų - NLM (National Library of Medicine)

remedyrepack inc. - clonazepam (unii: 5pe9fde8gb) (clonazepam - unii:5pe9fde8gb) - seizure disorders: clonazepam tablets are useful alone or as an adjunct in the treatment of the lennox- gastaut syndrome (petit mal variant), akinetic and myoclonic seizures. in patients with absence seizures (petit mal) who have failed to respond to succinimides, clonazepam tablets may be useful. some loss of effect may occur during the course of clonazepam treatment (see precautions: loss of effect). panic disorder: clonazepam tablets are indicated for the treatment of panic disorder, with or without agoraphobia, as defined in dsm-v. panic disorder is characterized by the occurrence of unexpected panic attacks and associated concern about having additional attacks, worry about the implications or consequences of the attacks, and/or a significant change in behavior related to the attacks. the efficacy of clonazepam tablets was established in two 6- to 9-week trials  in panic disorder patients whose diagnoses corresponded to the dsm-lilr category of panic disorder (see clinical pharmacology: clinical trials). panic disorder (dsm-v) is characterized by recurrent unexpected panic attacks, i.e., a discrete  period of intense fear or discomfort in which four (or more) of the following symptoms develop abruptly and reach a peak within 10 minutes: (1) palpitations, pounding heart or accelerated heart rate; (2) sweating; (3) trembling or shaking; (4) sensations of shortness of breath or smothering; (5) feeling of choking; (6) chest pain or discomfort; (7) nausea or abdominal distress; (8) feeling dizzy, unsteady, lightheaded or faint; (9) derealization (feelings of unreality) or depersonalization (being detached from oneself); (10) fear of losing control; (11) fear of dying; (12) paresthesias (numbness  or tingling  sensations); (13) chills or hot flushes. the effectiveness of clonazepam tablets in long-term use, that is, for more than 9 weeks, has not been systematically studied in controlled clinical trials. the physician who elects to use clonazepam tablets for extended periods should periodically reevaluate the long- term usefulness of the drug for the individual patient (see dosage and administration). clonazepam tablets are contraindicated in patients with the following conditions: - history of sensitivity to benzodiazepines - clinical or biochemical evidence of significant liver disease - acute narrow angle glaucoma (it may be used in patients with open angle glaucoma who are receiving appropriate therapy). controlled substance class: clonazepam tablets contain clonazepam, a schedule iv controlled substance. abuse: clonazepam tablet is a benzodiazepine and a cns depressant with a potential for abuse and addiction. abuse is the intentional, non-therapeutic use of a drug, even once, for its desirable psychological or physiological effects. misuse is the intentional use, for therapeutic purposes, of a drug by an individual in a way other than prescribed by a health care provider or for whom it was not prescribed. drug addiction is a cluster of behavioral, cognitive, and physiological phenomena that may include a strong desire to take the drug, difficulties in controlling drug use (e.g., continuing drug use despite harmful consequences, giving a higher priority to  drug  use  than other  activities  and obligations), and possible tolerance or physical dependence. even taking benzodiazepines as prescribed may put patients at risk for abuse and misuse of their medication. abuse and misuse  may  lead to addiction. abuse and misuse of benzodiazepines often (but not always) involve the use of doses greater than the maximum recommended dosage and commonly involve concomitant use of other medications, alcohol, and/or illicit substances, which is associated with an increased frequency of serious adverse outcomes, including respiratory depression, overdose, or death. benzodiazepines are often sought by individuals who abuse drugs and other substances, and by individuals with addictive disorders (see warnings: abuse, misuse, and addiction ). the following adverse reactions have occurred with benzodiazepine abuse  and/or  misuse: abdominal pain, amnesia, anorexia, anxiety, aggression, ataxia, blurred vision, confusion, depression, disinhibition, disorientation, dizziness, euphoria, impaired concentration and memory, indigestion, irritability, muscle pain, slurred speech, tremors, and vertigo. the following severe adverse reactions have occurred with benzodiazepine abuse and/or  misuse: delirium, paranoia, suicidal ideation and behavior, seizures, coma, breathing  difficulty, and  death. death is more often associated with polysubstance use  (especially benzodiazepines  with other  cns depressants such as opioids and alcohol) . dependence: physical dependence clonazepam tablets may produce physical dependence from continued therapy. physical dependence is a state that develops as a result of physiological adaptation in response to repeated drug use, manifested by withdrawal signs and symptoms after abrupt discontinuation or a significant dose reduction of a drug. abrupt discontinuation or rapid dosage reduction of benzodiazepines or administration of flumazenil, a benzodiazepine antagonist, may precipitate acute withdrawal reactions, including seizures, which can be life-threatening. patients at an increased risk of withdrawal adverse reactions after benzodiazepine discontinuation or  rapid dosage reduction include those who take higher dosages (i.e., higher and/or more frequent doses) and those who have had longer durations of use (see warnings: dependence and withdrawal reactions) to reduce the risk of withdrawal reactions, use a gradual taper to discontinue clonazepam tablets or reduce the dosage (see dosage and administration: discontinuation or dosage reduction of clonazepam tablets and warnings: dependence and withdrawal reactions). acute withdrawal signs and symptoms acute withdrawal signs and symptoms associated with benzodiazepines have included abnormal involuntary movements, anxiety, blurred vision, depersonalization, depression, derealization, dizziness, fatigue, gastrointestinal adverse reactions (e.g., nausea, vomiting, diarrhea, weight loss, decreased appetite), headache, hyperacusis, hypertension, irritability, insomnia, memory impairment, muscle  pain and stiffness, panic attacks, photophobia, restlessness, tachycardia, and tremor. more severe acute withdrawal signs and symptoms, including life-threatening reactions, have  included catatonia, convulsions, delirium tremens, depression, hallucinations, mania, psychosis, seizures and suicidality. protracted withdrawal syndrome protracted withdrawal syndrome associated with benzodiazepines is characterized by anxiety, cognitive impairment, depression, insomnia, formication, motor symptoms (e.g.,  weakness,  tremor,  muscle twitches), paresthesia, and tinnitus that persists beyond 4 to  6  weeks after initial benzodiazepine withdrawal. protracted withdrawal symptoms may last weeks to more  than 12 months . as  a result, there may be difficulty in differentiating withdrawal symptoms from potential re-emergence or continuation of symptoms for which the benzodiazepine was being used. tolerance tolerance to clonazepam tablets  may  develop  from continued  therapy.  tolerance is a physiological state characterized by a reduced response to  a drug  after repeated administration (i.e., a higher dose of a drug is required to produce the same effect that was once obtained at a lower dose). tolerance to the therapeutic effect of clonazepam tablets may  develop; however, little tolerance develops to the amnestic reactions and other cognitive impairments caused by benzodiazepines. following the short-term treatment of patients with panic disorder in studies 1 and 2 (see clinical pharmacology: clinical trials) , patients were gradually withdrawn during a 7-week downward- titration (discontinuance) period. overall, the discontinuance period was associated with good tolerability and a very modest clinical deterioration, without evidence of a significant rebound phenomenon. however, there are not sufficient data from adequate and well-controlled long-term clonazepam studies in patients with panic disorder to accurately estimate the risks of withdrawal symptoms and dependence that may be associated with such use. what is the most important information i should know about clonazepam tablets? - clonazepam tablet is a benzodiazepine medicine. taking benzodiazepines with opioid medicines, alcohol, or other central nervous system (cns) depressants (including street drugs) can cause severe drowsiness, breathing problems (respiratory depression), coma, and death. get emergency help right away if any of the following happens: - shallow or slowed breathing - breathing stops (which may lead to the heart stopping) - excessive sleepiness (sedation) do not drive or operate heavy machinery until you know how taking clonazepam tablets with opioids affects you. - risk of abuse, misuse, and addiction . there is a risk of abuse, misuse, and addiction with benzodiazepines, including clonazepam tablet which can lead to overdose and serious side effects including coma and death. - serious side effects including coma and death have happened in people who have abused or misused benzodiazepines, including clonazepam tablets. these serious side effects may also include delirium, paranoia, suicidal thoughts or actions, seizures, and difficulty breathing. call your healthcare provider or go to the nearest hospital emergency room right away if you get any of these serious side effects. - you can develop an addiction even if you take clonazepam tablets as prescribed by your healthcare provider. - take clonazepam tablets exactly as your healthcare provider prescribed. - do not share your clonazepam tablets with other people. - keep clonazepam tablets in a safe place and away from children. - physical dependence and withdrawal reactions. clonazepam tablets can cause physical dependence and withdrawal reactions. do not suddenly stop taking clonazepam tablets . stopping clonazepam tablets suddenly can cause serious and life-threatening side effects, including, unusual movements, responses, or expressions, seizures, sudden and severe mental or nervous system changes, depression, seeing or hearing things that others do not see or hear, an extreme increase in activity or talking, losing touch with reality, and suicidal thoughts or actions. call your healthcare provider or go to the nearest hospital emergency room right away if you get any of these symptoms. some people who suddenly stop benzodiazepines have symptoms that can last for several weeks to more than 12 months, including, anxiety, trouble remembering, learning, or concentrating, depression, problems sleeping, feeling like insects are crawling under your skin, weakness, shaking, muscle twitching, burning or prickling feeling in your hands, arms, legs or feet, and ringing in your ears. physical dependence is not the same as drug addiction. your healthcare provider can tell you more about the differences between physical dependence and drug addiction. do not take more clonazepam tablets than prescribed or take clonazepam tablets for longer than prescribed. - do not suddenly stop taking clonazepam tablets . stopping clonazepam tablets suddenly can cause serious and life-threatening side effects, including, unusual movements, responses, or expressions, seizures, sudden and severe mental or nervous system changes, depression, seeing or hearing things that others do not see or hear, an extreme increase in activity or talking, losing touch with reality, and suicidal thoughts or actions. call your healthcare provider or go to the nearest hospital emergency room right away if you get any of these symptoms. - some people who suddenly stop benzodiazepines have symptoms that can last for several weeks to more than 12 months, including, anxiety, trouble remembering, learning, or concentrating, depression, problems sleeping, feeling like insects are crawling under your skin, weakness, shaking, muscle twitching, burning or prickling feeling in your hands, arms, legs or feet, and ringing in your ears. - physical dependence is not the same as drug addiction. your healthcare provider can tell you more about the differences between physical dependence and drug addiction. - do not take more clonazepam tablets than prescribed or take clonazepam tablets for longer than prescribed. - clonazepam tablets can make you sleepy or dizzy and can slow your thinking and motor skills. this may get better over time. do not drive, operate heavy machinery, or do other dangerous activities until you know how clonazepam tablets affects you. clonazepam tablets may cause problems with your coordination, especially when you are walking or picking things up. - do not drive, operate heavy machinery, or do other dangerous activities until you know how clonazepam tablets affects you. - clonazepam tablets may cause problems with your coordination, especially when you are walking or picking things up. - do not drink alcohol or take other drugs that may make you sleepy or dizzy while taking clonazepam tablets until you talk to your healthcare provider. when taken with alcohol or drugs that cause sleepiness or dizziness, clonazepam tablets may make your sleepiness or dizziness worse. - like other antiepileptic drugs, clonazepam tablets may cause suicidal thoughts or actions in a very small number of people, about 1 in 500. call your healthcare provider right away if you have any of these symptoms, especially if they are new, worse, or worry you: - thoughts about suicide or dying ◦ attempt to commit suicide ◦ new or worse depression - new or worse anxiety ◦ feeling agitated or restless ◦ panic attacks - trouble sleeping (insomnia) ◦ new or worse irritability ◦ acting aggressive, being angry, or violent - acting on dangerous impulses ◦ an extreme increase in activity and talking (mania) ◦ other unusual changes in behavior or mood how can i watch for early symptoms of suicidal thoughts and actions? - pay attention to any changes, especially sudden changes, in mood, behaviors, thoughts, or feelings. - keep all follow-up visits with your healthcare provider as scheduled. call your healthcare provider between visits as needed, especially if you are worried about symptoms. suicidal thoughts or actions can be caused by things other than medicines. if you have suicidal thoughts or actions, your healthcare provider may check for other causes. do not stop clonazepam tablets without first talking to a healthcare provider. - stopping clonazepam tablets suddenly can cause serious problems. stopping clonazepam tablets - suddenly can cause seizures that will not stop (status epilepticus). what are clonazepam tablets? - clonazepam tablets are prescription medicine used alone or with other medicines to treat: certain types of seizure disorders (epilepsy) in adults and children panic disorder with or without fear of open spaces (agoraphobia) in adults - certain types of seizure disorders (epilepsy) in adults and children - panic disorder with or without fear of open spaces (agoraphobia) in adults clonazepam tablet is a federally controlled substance (c-iv) because it contains clonazepam that can be abused or lead to dependence. keep clonazepam tablets in a safe place to prevent misuse and abuse. selling or giving away clonazepam tablets may harm others, and is against the law. tell your healthcare provider if you have ever abused or been dependent on alcohol, prescription medicines, or street drugs. it is not known if clonazepam tablets are safe or effective in treating panic disorder in children younger than 18 years old. who should not take clonazepam tablets? do not take clonazepam tablets if you: - are allergic to benzodiazepines - have significant liver disease - have an eye disease called acute narrow angle glaucoma ask your healthcare provider if you are not sure if you have any of the problems listed above. before you take clonazepam tablets, tell your healthcare provider if you: - have liver or kidney problems - have lung problems (respiratory disease) - have or have had depression, mood problems, or suicidal thoughts or behavior - have any other medical problems - are pregnant or plan to become pregnant. it is not known if clonazepam tablets can harm your unborn baby. tell your healthcare provider right away if you become pregnant while taking clonazepam tablets. you and your healthcare provider will decide if you should take clonazepam tablets while you are pregnant. - studies in pregnant animals have shown harmful effects of benzodiazepine medications (including the active ingredient in clonazepam tablets) on the developing fetus. - children born to mothers receiving benzodiazepine medications (including clonazepam tablets) late in pregnancy may be at some risk of experiencing breathing problems, feeding problems, hypothermia, and withdrawal symptoms. - if you become pregnant while taking clonazepam tablets, talk to your healthcare provider about registering with the north american antiepileptic drug pregnancy registry. you can register by calling 1-888-233-2334. the purpose of this registry is to collect information about the safety of antiepileptic drugs during pregnancy - are breastfeeding or plan to breastfeed. clonazepam can pass into breast milk. you and your healthcare provider should decide how you will feed your baby while you take clonazepam tablets. tell your healthcare provider about all the medicines you take, including prescription and over-the-counter medicines, vitamins, and herbal supplements. taking clonazepam tablets with certain other medicines can cause side effects or affect how well clonazepam tablets or the other medicines work. do not start or stop other medicines without talking to your healthcare provider. how should i take clonazepam tablets? - take clonazepam tablets exactly as your healthcare provider tells you. if you take clonazepam tablets for seizures, your healthcare provider may change the dose until you are taking the right amount of medicine to control your symptoms. - clonazepam is available as a tablet. - do not stop taking clonazepam tablets without first talking to your healthcare provider. stopping clonazepam tablets suddenly can cause serious problems. - clonazepam tablets should be taken with water and swallowed whole. - if you take too much clonazepam tablets, call your healthcare provider or local poison control center right away. what should i avoid while taking clonazepam tablets? - clonazepam tablets can slow your thinking and motor skills. do not drive, operate heavy machinery, or do other dangerous activities until you know how clonazepam tablets affects you. - do not drink alcohol or take other medicines that may make you sleepy or dizzy while taking clonazepam tablets until you talk to your healthcare provider. when taken with alcohol or medicines that cause sleepiness or dizziness, clonazepam tablets may make your sleepiness or dizziness much worse. what are the possible side effects of clonazepam tablets? see “what is the most important information i should know about clonazepam tablets?” clonazepam tablets can also make your seizures happen more often or make them worse. call your healthcare provider right away if your seizures get worse while taking clonazepam tablets. the most common side effects of clonazepam tablets include: - drowsiness • dizziness • fatigue - problems with walking and coordination • depression • problems with memory these are not all the possible side effects of clonazepam tablets. call your doctor for medical advice about side effects. you may report side effects to fda at 1-800-fda-1088 or contact advagen pharma ltd, at 866-488-0312. how should i store clonazepam tablets? - store clonazepam tablets at 20°c to 25°c (68°f -77°f) [see usp controlled room temperature]. - keep clonazepam tablets and all medicines out of the reach of children. general information about the safe and effective use of clonazepam tablets. medicines are sometimes prescribed for purposes other than those listed in a medication guide. do not use clonazepam tablets for a condition for which it was not prescribed. do not give clonazepam tablets to other people, even if they have the same symptoms that you have. it may harm them. you can ask your pharmacist or healthcare provider for information about clonazepam tablets that is written for health professionals. for more information, contact advagen pharma ltd, at 866-488-0312. what are the ingredients in clonazepam tablets? active ingredient: clonazepam inactive ingredients: - 0.5 mg tablets contain lactose monohydrate, polyethylene glycol, microcrystalline cellulose, croscarmellose sodium, magnesium stearate, fd & c yellow 6 al lake, d & c yellow 10 al lake - 1 mg tablets contain lactose monohydrate, polyethylene glycol, microcrystalline cellulose, croscarmellose sodium, magnesium stearate, fd & c blue 1 al lake and fd & c blue 2 al lake - 2 mg tablets contain lactose monohydrate, polyethylene glycol, microcrystalline cellulose, croscarmellose sodium and magnesium stearate this medication guide has been approved by the u.s. food and drug administration. repackaged by / distributed by: remedyrepack inc. 625 kolter drive, indiana, pa 15701 (724) 465-8762

Jungtinės Valstijos - anglų - NLM (National Library of Medicine)

remedyrepack inc. - diclofenac sodium (unii: qtg126297q) (diclofenac - unii:144o8ql0l1) - diclofenac sodium topical gel is indicated for the relief of the pain of osteoarthritis of joints amenable to topical treatment, such as the knees and those of the hands. - diclofenac sodium topical gel has not been evaluated for use on the spine, hip, or shoulder. diclofenac sodium topical gel is contraindicated in the following patients: - known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to diclofenac or any components of the drug product [see warnings and precautions( 5.7, 5.9)] - history of asthma, urticaria, or other allergic-type reactions after taking aspirin or other nsaids. severe, sometimes fatal, anaphylactic reactions to nsaids have been reported in such patients [see warnings and precautions( 5.7, 5.8)] - in the setting of coronary artery bypass graft (cabg) surgery [see warnings and precautions (5.1)] pregnancy category c prior to 30 weeks gestation; category d starting 30 weeks gestation  risk summary use of nsaids, including diclofenac sodium topical gel, during the third trimester of pregnancy increases the risk of premature closure of the fetal ductus arteriosus. avoid use of nsaids, including diclofenac sodium topical gel, in pregnant women starting at 30 weeks of gestation (third trimester). there are no adequate and well-controlled studies of diclofenac sodium topical gel in pregnant women. human and animal studies indicate that diclofenac crosses the placenta.  data from observational studies regarding potential embryofetal risks of nsaid use in women in the first or second trimesters of pregnancy are inconclusive. in the general u.s. population, all clinically recognized pregnancies, regardless of drug exposure, have a background rate of 2-4% for major malformations, and 15-20% for pregnancy loss. in animal reproduction studies, no evidence of teratogenicity was observed in mice, rats, or rabbits given diclofenac during the period of organogenesis at doses up to approximately 5, 5, and 10 times, respectively, the maximum recommended topical dose of diclofenac sodium topical gel, despite the presence of maternal and fetal toxicity at these doses [see data] . based on animal data, prostaglandins have been shown to have an important role in endometrial vascular permeability, blastocyst implantation, and decidualization. in animal studies, administration of prostaglandin synthesis inhibitors such as diclofenac, resulted in increased pre- and post-implantation loss. clinical considerations labor or delivery there are no studies on the effects of diclofenac sodium topical gel during labor or delivery. in animal studies, nsaids, including diclofenac, inhibit prostaglandin synthesis, cause delayed parturition, and increase the incidence of stillbirth. data animal data reproductive and developmental studies in animals demonstrated that diclofenac sodium administration during organogenesis did not produce teratogenicity despite the induction of maternal toxicity and fetal toxicity in mice at oral doses up to 20 mg/kg/day (approximately 5 times the maximum recommended human dose (mrhd) of diclofenac sodium topical gel based on bioavailability and body surface area (bsa) comparison), and in rats and rabbits at oral doses up to 10 mg/kg/day (approximately 5 and 10 times the mrhd based on bioavailability and bsa comparison).  in a study in which pregnant rats were orally administered 2 or 4 mg/kg diclofenac (approximately 1 and 2 times the mrhd based on bioavailability and bsa comparison) from gestation day 15 through lactation day 21, significant maternal toxicity (peritonitis, mortality) was noted.  these maternally toxic doses were associated with dystocia, prolonged gestation, reduced fetal weights and growth, and reduced fetal survival. risk summary based on available data, diclofenac may be present in human milk. the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for cataflam and any potential adverse effects on the breastfed infant from the cataflam or from the underlying maternal condition.          data one woman treated orally with a diclofenac salt, 150 mg/day, had a milk diclofenac level of 100 mcg/l, equivalent to an infant dose of about 0.03 mg/kg/day.  diclofenac was not detectable in breast milk in 12 women using diclofenac (after either 100 mg/day orally for 7 days or a single 50 mg intramuscular dose administered in the immediate postpartum period). infertility females based on the mechanism of action, the use of prostaglandin-mediated nsaids, including diclofenac sodium topical gel, may delay or prevent rupture of ovarian follicles, which has been associated with reversible infertility in some women. published animal studies have shown that administration of prostaglandin synthesis inhibitors has the potential to disrupt prostaglandin- mediated follicular rupture required for ovulation. small studies in women treated with nsaids have also shown a reversible delay in ovulation. consider withdrawal of nsaids, including diclofenac sodium topical gel, in women who have difficulties conceiving or who are undergoing investigation of infertility. safety and effectiveness in pediatric patients have not been established. elderly patients, compared to younger patients, are at greater risk for nsaid-associated serious cardiovascular, gastrointestinal, and/or renal adverse reactions. if the anticipated benefit for the elderly patient outweighs these potential risks, start dosing at the low end of the dosing range, and monitor patients for adverse effects [ see warnings and precautions( 5.1, 5.2, 5.3, 5.6, 5.13) ] .  of the total number of subjects treated with diclofenac sodium topical gel in clinical studies, 498 were 65 years of age and over. no overall differences in effectiveness or safety were observed between these subjects and younger subjects, but greater sensitivity to the effect of nsaids in some older individuals cannot be ruled out. diclofenac, as with any nsaid, is known to be substantially excreted by the kidney, and the risk of toxic reactions to diclofenac sodium topical gel may be greater in patients with impaired renal function. because elderly patients are more likely to have decreased renal function, care should be taken when using diclofenac sodium topical gel in the elderly, and it may be useful to monitor renal function. diclofenac sodium topical gel, 1% important: use the dosing card that is inside the diclofenac sodium topical gel carton to correctly measure each dose. the dosing card is re-usable. do not throw the dosing card away. before you use diclofenac sodium topical gel for the first time, your healthcare provider or pharmacist should show you how to correctly measure your dose using the dosing card. read this instructions for use before you start using diclofenac sodium topical gel and each time you get a refill. there may be new information. this information does not take the place of talking to your healthcare provider about your medical condition or your treatment. your healthcare provider has prescribed diclofenac sodium topical gel to help relieve arthritis pain in some of your joints. diclofenac sodium topical gel may be used to treat arthritis pain in the arms (hands, wrists, and elbows) and in the legs (feet, ankles, and knees). it is not known if diclofenac sodium topical gel is safe and effective if used on your spine, hips, or shoulders. - use diclofenac sodium topical gel exactly how your healthcare provider prescribes it for you. do not apply diclofenac sodium topical gel anywhere other than where your healthcare provider tells you to. - do not use more than a total of 32 grams of diclofenac sodium topical gel each day. if you add up the amount of diclofenac sodium topical gel as directed by your healthcare provider, it should not be more than 32 grams in one day. the dose for your hands, wrists, or elbows is 2 grams of diclofenac sodium topical gel each time you apply it. - apply diclofenac sodium topical gel 4 times a day (a total of 8 grams each day). do not apply more than 8 grams each day to any one of your affected hands, wrists, or elbows. the dose for your feet, ankles, or knees is 4 grams of diclofenac sodium topical gel each time you apply it. - apply diclofenac sodium topical gel 4 times a day (a total of 16 grams each day). do not apply more than 16 grams each day to any one of your affected feet, ankles, or knees. some examples of diclofenac sodium topical gel application include : figure a - apply diclofenac sodium topical gel to clean, dry skin that does not have any cuts, open wounds, infections, or rashes. - do not use heating pads or apply bandages to where you have applied diclofenac sodium topical gel. - avoid exposing skin where you apply diclofenac sodium topical gel to sunlight and artificial light, such as tanning booths. - do not use sunscreens, cosmetics, lotions, moisturizers, insect repellants, or other topical medicines on the same skin areas where you have applied diclofenac sodium topical gel. - do not get diclofenac sodium topical gel in your eyes, nose, or mouth. diclofenac sodium topical gel is only to be used on your skin (topical use). if you get diclofenac sodium topical gel in your eyes, rinse your eyes right away with water or saline. talk with your healthcare provider if eye irritation lasts for more than one hour. what if i miss a dose? - if you miss a dose of diclofenac sodium topical gel, continue with your next scheduled dose using the prescribed amount of diclofenac sodium topical gel. do not double the dose. applying 2 grams (2 g) of diclofenac sodium topical gel to hands, wrists, or elbows: step 1. remove the dosing card that is attached inside the diclofenac sodium topical gel carton. use the dosing card to correctly measure each dose of diclofenac sodium topical gel. to measure the correct amount of diclofenac sodium topical gel, place the dosing card on a flat surface so that you can read the print. if the print is backwards, flip dosing card over (see figure a). if you lose or misplace your dosing card, you can ask your pharmacist for a new one or call. 1-833-285-4151. ask your healthcare provider or pharmacist to show you how to correctly measure your dose of diclofenac sodium topical gel while you are waiting to receive your new dosing card. figure b figure c figure d step 2 . squeeze diclofenac sodium topical gel onto the dosing card evenly, up to the 2 g line (a 2.25 inch length of gel). make sure that the gel covers the 2 g area of the dosing card (see figure b). put the cap back on the tube of diclofenac sodium topical gel. ask your healthcare provider or pharmacist if you are not sure how to correctly measure your dose of diclofenac sodium topical gel. step 3. apply the gel to your hand, wrist, or elbow. you can use the dosing card to apply the gel (see figure c). then, use your hands to gently rub the gel into the skin (see figure d). do not share your dosing card with another person. make sure to cover the entire affected hand, wrist, or elbow with the gel. remember that the hand includes the palm of your hand, the top of your hand, and your fingers. step 4. after using the dosing card, hold end with fingertips, rinse and dry. store the dosing card until next use. do not shower or bathe for at least 1 hour after applying diclofenac sodium topical gel. do not wash your treated hands for at least 1 hour after applying the diclofenac sodium topical gel. step 5. after applying diclofenac sodium topical gel, wait 10 minutes before covering the treated skin with gloves or clothing. applying 4 grams (4 g) of diclofenac sodium topical gel to feet, ankles, or knees: step 1. refer to step 1 above. step 2. squeeze diclofenac sodium topical gel onto the dosing card evenly up to the 4 g line (a 4.5 inch length of gel), making sure the gel covers the 4 g area of the dosing card (see figure e). put the cap back on the tube of diclofenac sodium topical gel. ask your healthcare provider or pharmacist if you are not sure how to correctly measure your dose of diclofenac sodium topical gel. step 3. apply diclofenac sodium topical gel to your foot, ankle, or knee. you can use the dosing card to apply the gel (see figure f). then, use your hands to gently rub the gel into the skin (see figure g). do not share your dosing card with another person. make sure to cover your entire foot, ankle, or knee area with the gel. for example, cover the skin above, below, inside and outside the knee cap. remember that the foot includes the sole of your foot, the top of your foot, and your toes. figure e figure f figure g refer to steps 4 and 5 above . wash your hands after applying diclofenac sodium topical gel to your foot, ankle, or knee. what are the ingredients in diclofenac sodium topical gel? active ingredient : diclofenac sodium inactive ingredients: carbomer homopolymer type c, cocoyl caprylocaprate, isopropyl alcohol, mineral oil, polyoxyl 20 cetostearyl ether, propylene glycol, purified water, strong ammonia solution. how should i store diclofenac sodium topical gel? - store at 68°f to 77°f (20°c to 25°c). - do not freeze diclofenac sodium topical gel. - store the dosing card with your diclofenac sodium topical gel. keep diclofenac sodium topical gel, the dosing card, and all medicines out of the reach of children . this medication guide and instructions for use have been approved by the u.s. food and drug administration. repackaged by / distributed by: remedyrepack inc. 625 kolter drive, indiana, pa 15701 (724) 465-8762

Jungtinės Valstijos - anglų - NLM (National Library of Medicine)

remedyrepack inc. - meloxicam (unii: vg2qf83cgl) (meloxicam - unii:vg2qf83cgl) - meloxicam is indicated for relief of the signs and symptoms of osteoarthritis [ see clinical studies (14.1)]. meloxicam is indicated for relief of the signs and symptoms of rheumatoid arthritis [ see clinical studies (14.1) ]. meloxicam is indicated for relief of the signs and symptoms of pauciarticular or polyarticular course juvenile rheumatoid arthritis in patients who weighs ≥ 60 kg [ see dosage and administration ( 2.4) and clinical studies (14.2)]. meloxicam is contraindicated in the following patients: - known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to meloxicam or any components of the drug product [ see warnings and precautions ( 5.7, 5.9) ] - history of asthma, urticaria, or other allergic-type reactions after taking aspirin or other nsaids. severe, sometimes fatal, anaphylactic reactions to nsaids have been reported in such patients [ see warnings and precautions ( 5.7, 5.8) ] - in the setting of coronary artery bypass graft (cabg) surgery [ see warnings and precautions ( 5.1) ] risk summary use of nsaids, including meloxicam, can cause premature closure of the fetal ductus arteriosus and fetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment. because of these risks, limit dose and duration of meloxicam use between about 20 and 30 weeks of gestation, and avoid meloxicam use at about 30 weeks of gestation and later in pregnancy ( see   clinical considerations, data ). premature closure of fetal ductus arteriosus use of nsaids, including meloxicam, at about 30 weeks gestation or later in pregnancy increases the risk of premature closure of the fetal ductus arteriosus. oligohydramnios/neonatal renal impairment use of nsaids at about 20 weeks gestation or later in pregnancy has been associated with cases of fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. data from observational studies regarding potential embryofetal risks of nsaid use in women in the first or second trimesters of pregnancy are inconclusive. in animal reproduction studies, embryofetal death was observed in rats and rabbits treated during the period of organogenesis with meloxicam at oral doses equivalent to 0.65- and 6.5-times the maximum recommended human dose (mrhd) of meloxicam. increased incidence of septal heart defects were observed in rabbits treated throughout embryogenesis with meloxicam at an oral dose equivalent to 78-times the mrhd. in pre- and post-natal reproduction studies, there was an increased incidence of dystocia, delayed parturition, and decreased offspring survival at 0.08-times mrhd of meloxicam. no teratogenic effects were observed in rats and rabbits treated with meloxicam during organogenesis at an oral dose equivalent to 2.6 and 26-times the mrhd [see data] . based on animal data, prostaglandins have been shown to have an important role in endometrial vascular permeability, blastocyst implantation, and decidualization. in animal studies, administration of prostaglandin synthesis inhibitors such as meloxicam, resulted in increased pre- and post-implantation loss. prostaglandins also have been shown to have an important role in fetal kidney development. in published animal studies, prostaglandin synthesis inhibitors have been reported to impair kidney development when administered at clinically relevant doses. the estimated background risk of major birth defects and miscarriage for the indicated population(s) is unknown. all pregnancies have a background risk of birth defect, loss, or other adverse outcomes. in the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. clinical considerations fetal/neonatal adverse reactions premature closure of fetal ductus arteriosus: avoid use of nsaids in women at about 30 weeks gestation and later in pregnancy, because nsaids, including meloxicam, can cause premature closure of the fetal ductus arteriosus ( see data ). oligohydramnios/neonatal renal impairment: if an nsaid is necessary at about 20 weeks gestation or later in pregnancy, limit the use to the lowest effective dose and shortest duration possible. if meloxicam treatment extends beyond 48 hours, consider monitoring with ultrasound for oligohydramnios. if oligohydramnios occurs, discontinue meloxicam and follow up according to clinical practice ( see data ). labor or delivery there are no studies on the effects of meloxicam during labor or delivery. in animal studies, nsaids, including meloxicam, inhibit prostaglandin synthesis, cause delayed parturition, and increase the incidence of stillbirth. data human data premature closure of fetal ductus arteriosus: published literature reports that the use of nsaids at about 30 weeks of gestation and later in pregnancy may cause premature closure of the fetal ductus arteriosus. oligohydramnios/neonatal renal impairment: published studies and postmarketing reports describe maternal nsaid use at about 20 weeks gestation or later in pregnancy associated with fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. these adverse outcomes are seen, on average, after days to weeks of treatment, although oligohydramnios has been infrequently reported as soon as 48 hours after nsaid initiation. in many cases, but not all, the decrease in amniotic fluid was transient and reversible with cessation of the drug. there have been a limited number of case reports of maternal nsaid use and neonatal renal dysfunction without oligohydramnios, some of which were irreversible. some cases of neonatal renal dysfunction required treatment with invasive procedures, such as exchange transfusion or dialysis. methodological limitations of these postmarketing studies and reports include lack of a control group; limited information regarding dose, duration, and timing of drug exposure; and concomitant use of other medications. these limitations preclude establishing a reliable estimate of the risk of adverse fetal and neonatal outcomes with maternal nsaid use. because the published safety data on neonatal outcomes involved mostly preterm infants, the generalizability of certain reported risks to the full-term infant exposed to nsaids through maternal use is uncertain. animal data meloxicam was not teratogenic when administered to pregnant rats during fetal organogenesis at oral doses up to 4 mg/kg/day (2.6-fold greater than the mrhd of 15 mg of meloxicam based on bsa comparison). administration of meloxicam to pregnant rabbits throughout embryogenesis produced an increased incidence of septal defects of the heart at an oral dose of 60 mg/kg/day (78-fold greater than the mrhd based on bsa comparison). the no effect level was 20 mg/kg/day (26-fold greater than the mrhd based on bsa conversion). in rats and rabbits, embryolethality occurred at oral meloxicam doses of 1 mg/kg/day and 5 mg/kg/day, respectively (0.65- and 6.5-fold greater, respectively, than the mrhd based on bsa comparison) when administered throughout organogenesis. oral administration of meloxicam to pregnant rats during late gestation through lactation increased the incidence of dystocia, delayed parturition, and decreased offspring survival at meloxicam doses of 0.125 mg/kg/day or greater (0.08-times mrhd based on bsa comparison). risk summary there are no human data available on whether meloxicam is present in human milk, or on the effects on breastfed infants, or on milk production. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for meloxicam and any potential adverse effects on the breastfed infant from the meloxicam or from the underlying maternal condition. data animal data meloxicam was present in the milk of lactating rats at concentrations higher than those in plasma. infertility females based on the mechanism of action, the use of prostaglandin-mediated nsaids, including meloxicam, may delay or prevent rupture of ovarian follicles, which has been associated with reversible infertility in some women. published animal studies have shown that administration of prostaglandin synthesis inhibitors has the potential to disrupt prostaglandin-mediated follicular rupture required for ovulation. small studies in women treated with nsaids have also shown a reversible delay in ovulation. consider withdrawal of nsaids, including meloxicam, in women who have difficulties conceiving or who are undergoing investigation of infertility. the safety and effectiveness of meloxicam in pediatric jra patients from 2 to 17 years of age has been evaluated in three clinical trials [ see dosage and administration ( 2.3), adverse reactions ( 6.1) and clinical studies ( 14.2) ]. elderly patients, compared to younger patients, are at greater risk for nsaid-associated serious cardiovascular, gastrointestinal, and/or renal adverse reactions. if the anticipated benefit for the elderly patient outweighs these potential risks, start dosing at the low end of the dosing range, and monitor patients for adverse effects [ see warnings and precautions ( 5.1, 5.2, 5.3, 5.6, 5.14) ]. no dose adjustment is necessary in patients with mild to moderate hepatic impairment. patients with severe hepatic impairment have not been adequately studied. since meloxicam is significantly metabolized in the liver and hepatotoxicity may occur, use meloxicam with caution in patients with hepatic impairment [ see warnings and precautions ( 5.3) and clinical pharmacology ( 12.3) ]. no dose adjustment is necessary in patients with mild to moderate renal impairment. patients with severe renal impairment have not been studied. the use of meloxicam in subjects with severe renal impairment is not recommended. in patients on hemodialysis, meloxicam should not exceed 7.5 mg per day. meloxicam is not dialyzable [ see dosage and administration ( 2.1) and clinical pharmacology ( 12.3) ].

Jungtinės Valstijos - anglų - NLM (National Library of Medicine)

remedyrepack inc. - meloxicam (unii: vg2qf83cgl) (meloxicam - unii:vg2qf83cgl) - meloxicam is indicated for relief of the signs and symptoms of osteoarthritis [ see clinical studies (14.1)]. meloxicam is indicated for relief of the signs and symptoms of rheumatoid arthritis [ see clinical studies (14.1) ]. meloxicam is indicated for relief of the signs and symptoms of pauciarticular or polyarticular course juvenile rheumatoid arthritis in patients who weighs ≥ 60 kg [ see dosage and administration ( 2.4) and clinical studies (14.2)]. meloxicam is contraindicated in the following patients: - known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to meloxicam or any components of the drug product [ see warnings and precautions ( 5.7, 5.9) ] - history of asthma, urticaria, or other allergic-type reactions after taking aspirin or other nsaids. severe, sometimes fatal, anaphylactic reactions to nsaids have been reported in such patients [ see warnings and precautions ( 5.7, 5.8) ] - in the setting of coronary artery bypass graft (cabg) surgery [ see warnings and precautions ( 5.1) ] risk summary use of nsaids, including meloxicam, can cause premature closure of the fetal ductus arteriosus and fetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment. because of these risks, limit dose and duration of meloxicam use between about 20 and 30 weeks of gestation, and avoid meloxicam use at about 30 weeks of gestation and later in pregnancy ( see   clinical considerations, data ). premature closure of fetal ductus arteriosus use of nsaids, including meloxicam, at about 30 weeks gestation or later in pregnancy increases the risk of premature closure of the fetal ductus arteriosus. oligohydramnios/neonatal renal impairment use of nsaids at about 20 weeks gestation or later in pregnancy has been associated with cases of fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. data from observational studies regarding potential embryofetal risks of nsaid use in women in the first or second trimesters of pregnancy are inconclusive. in animal reproduction studies, embryofetal death was observed in rats and rabbits treated during the period of organogenesis with meloxicam at oral doses equivalent to 0.65- and 6.5-times the maximum recommended human dose (mrhd) of meloxicam. increased incidence of septal heart defects were observed in rabbits treated throughout embryogenesis with meloxicam at an oral dose equivalent to 78-times the mrhd. in pre- and post-natal reproduction studies, there was an increased incidence of dystocia, delayed parturition, and decreased offspring survival at 0.08-times mrhd of meloxicam. no teratogenic effects were observed in rats and rabbits treated with meloxicam during organogenesis at an oral dose equivalent to 2.6 and 26-times the mrhd [see data] . based on animal data, prostaglandins have been shown to have an important role in endometrial vascular permeability, blastocyst implantation, and decidualization. in animal studies, administration of prostaglandin synthesis inhibitors such as meloxicam, resulted in increased pre- and post-implantation loss. prostaglandins also have been shown to have an important role in fetal kidney development. in published animal studies, prostaglandin synthesis inhibitors have been reported to impair kidney development when administered at clinically relevant doses. the estimated background risk of major birth defects and miscarriage for the indicated population(s) is unknown. all pregnancies have a background risk of birth defect, loss, or other adverse outcomes. in the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. clinical considerations fetal/neonatal adverse reactions premature closure of fetal ductus arteriosus: avoid use of nsaids in women at about 30 weeks gestation and later in pregnancy, because nsaids, including meloxicam, can cause premature closure of the fetal ductus arteriosus ( see data ). oligohydramnios/neonatal renal impairment: if an nsaid is necessary at about 20 weeks gestation or later in pregnancy, limit the use to the lowest effective dose and shortest duration possible. if meloxicam treatment extends beyond 48 hours, consider monitoring with ultrasound for oligohydramnios. if oligohydramnios occurs, discontinue meloxicam and follow up according to clinical practice ( see data ). labor or delivery there are no studies on the effects of meloxicam during labor or delivery. in animal studies, nsaids, including meloxicam, inhibit prostaglandin synthesis, cause delayed parturition, and increase the incidence of stillbirth. data human data premature closure of fetal ductus arteriosus: published literature reports that the use of nsaids at about 30 weeks of gestation and later in pregnancy may cause premature closure of the fetal ductus arteriosus. oligohydramnios/neonatal renal impairment: published studies and postmarketing reports describe maternal nsaid use at about 20 weeks gestation or later in pregnancy associated with fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. these adverse outcomes are seen, on average, after days to weeks of treatment, although oligohydramnios has been infrequently reported as soon as 48 hours after nsaid initiation. in many cases, but not all, the decrease in amniotic fluid was transient and reversible with cessation of the drug. there have been a limited number of case reports of maternal nsaid use and neonatal renal dysfunction without oligohydramnios, some of which were irreversible. some cases of neonatal renal dysfunction required treatment with invasive procedures, such as exchange transfusion or dialysis. methodological limitations of these postmarketing studies and reports include lack of a control group; limited information regarding dose, duration, and timing of drug exposure; and concomitant use of other medications. these limitations preclude establishing a reliable estimate of the risk of adverse fetal and neonatal outcomes with maternal nsaid use. because the published safety data on neonatal outcomes involved mostly preterm infants, the generalizability of certain reported risks to the full-term infant exposed to nsaids through maternal use is uncertain. animal data meloxicam was not teratogenic when administered to pregnant rats during fetal organogenesis at oral doses up to 4 mg/kg/day (2.6-fold greater than the mrhd of 15 mg of meloxicam based on bsa comparison). administration of meloxicam to pregnant rabbits throughout embryogenesis produced an increased incidence of septal defects of the heart at an oral dose of 60 mg/kg/day (78-fold greater than the mrhd based on bsa comparison). the no effect level was 20 mg/kg/day (26-fold greater than the mrhd based on bsa conversion). in rats and rabbits, embryolethality occurred at oral meloxicam doses of 1 mg/kg/day and 5 mg/kg/day, respectively (0.65- and 6.5-fold greater, respectively, than the mrhd based on bsa comparison) when administered throughout organogenesis. oral administration of meloxicam to pregnant rats during late gestation through lactation increased the incidence of dystocia, delayed parturition, and decreased offspring survival at meloxicam doses of 0.125 mg/kg/day or greater (0.08-times mrhd based on bsa comparison). risk summary there are no human data available on whether meloxicam is present in human milk, or on the effects on breastfed infants, or on milk production. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for meloxicam and any potential adverse effects on the breastfed infant from the meloxicam or from the underlying maternal condition. data animal data meloxicam was present in the milk of lactating rats at concentrations higher than those in plasma. infertility females based on the mechanism of action, the use of prostaglandin-mediated nsaids, including meloxicam, may delay or prevent rupture of ovarian follicles, which has been associated with reversible infertility in some women. published animal studies have shown that administration of prostaglandin synthesis inhibitors has the potential to disrupt prostaglandin-mediated follicular rupture required for ovulation. small studies in women treated with nsaids have also shown a reversible delay in ovulation. consider withdrawal of nsaids, including meloxicam, in women who have difficulties conceiving or who are undergoing investigation of infertility. the safety and effectiveness of meloxicam in pediatric jra patients from 2 to 17 years of age has been evaluated in three clinical trials [ see dosage and administration ( 2.3), adverse reactions ( 6.1) and clinical studies ( 14.2) ]. elderly patients, compared to younger patients, are at greater risk for nsaid-associated serious cardiovascular, gastrointestinal, and/or renal adverse reactions. if the anticipated benefit for the elderly patient outweighs these potential risks, start dosing at the low end of the dosing range, and monitor patients for adverse effects [ see warnings and precautions ( 5.1, 5.2, 5.3, 5.6, 5.14) ]. no dose adjustment is necessary in patients with mild to moderate hepatic impairment. patients with severe hepatic impairment have not been adequately studied. since meloxicam is significantly metabolized in the liver and hepatotoxicity may occur, use meloxicam with caution in patients with hepatic impairment [ see warnings and precautions ( 5.3) and clinical pharmacology ( 12.3) ]. no dose adjustment is necessary in patients with mild to moderate renal impairment. patients with severe renal impairment have not been studied. the use of meloxicam in subjects with severe renal impairment is not recommended. in patients on hemodialysis, meloxicam should not exceed 7.5 mg per day. meloxicam is not dialyzable [ see dosage and administration ( 2.1) and clinical pharmacology ( 12.3) ].

Jungtinės Valstijos - anglų - NLM (National Library of Medicine)

remedyrepack inc. - meloxicam (unii: vg2qf83cgl) (meloxicam - unii:vg2qf83cgl) - meloxicam is indicated for relief of the signs and symptoms of osteoarthritis [ see clinical studies (14.1)]. meloxicam is indicated for relief of the signs and symptoms of rheumatoid arthritis [ see clinical studies (14.1) ]. meloxicam is indicated for relief of the signs and symptoms of pauciarticular or polyarticular course juvenile rheumatoid arthritis in patients who weighs ≥ 60 kg [ see dosage and administration ( 2.4) and clinical studies (14.2)]. meloxicam is contraindicated in the following patients: - known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to meloxicam or any components of the drug product [ see warnings and precautions ( 5.7, 5.9) ] - history of asthma, urticaria, or other allergic-type reactions after taking aspirin or other nsaids. severe, sometimes fatal, anaphylactic reactions to nsaids have been reported in such patients [ see warnings and precautions ( 5.7, 5.8) ] - in the setting of coronary artery bypass graft (cabg) surgery [ see warnings and precautions ( 5.1) ] risk summary use of nsaids, including meloxicam, can cause premature closure of the fetal ductus arteriosus and fetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment. because of these risks, limit dose and duration of meloxicam use between about 20 and 30 weeks of gestation, and avoid meloxicam use at about 30 weeks of gestation and later in pregnancy ( see   clinical considerations, data ). premature closure of fetal ductus arteriosus use of nsaids, including meloxicam, at about 30 weeks gestation or later in pregnancy increases the risk of premature closure of the fetal ductus arteriosus. oligohydramnios/neonatal renal impairment use of nsaids at about 20 weeks gestation or later in pregnancy has been associated with cases of fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. data from observational studies regarding potential embryofetal risks of nsaid use in women in the first or second trimesters of pregnancy are inconclusive. in animal reproduction studies, embryofetal death was observed in rats and rabbits treated during the period of organogenesis with meloxicam at oral doses equivalent to 0.65- and 6.5-times the maximum recommended human dose (mrhd) of meloxicam. increased incidence of septal heart defects were observed in rabbits treated throughout embryogenesis with meloxicam at an oral dose equivalent to 78-times the mrhd. in pre- and post-natal reproduction studies, there was an increased incidence of dystocia, delayed parturition, and decreased offspring survival at 0.08-times mrhd of meloxicam. no teratogenic effects were observed in rats and rabbits treated with meloxicam during organogenesis at an oral dose equivalent to 2.6 and 26-times the mrhd [see data] . based on animal data, prostaglandins have been shown to have an important role in endometrial vascular permeability, blastocyst implantation, and decidualization. in animal studies, administration of prostaglandin synthesis inhibitors such as meloxicam, resulted in increased pre- and post-implantation loss. prostaglandins also have been shown to have an important role in fetal kidney development. in published animal studies, prostaglandin synthesis inhibitors have been reported to impair kidney development when administered at clinically relevant doses. the estimated background risk of major birth defects and miscarriage for the indicated population(s) is unknown. all pregnancies have a background risk of birth defect, loss, or other adverse outcomes. in the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. clinical considerations fetal/neonatal adverse reactions premature closure of fetal ductus arteriosus: avoid use of nsaids in women at about 30 weeks gestation and later in pregnancy, because nsaids, including meloxicam, can cause premature closure of the fetal ductus arteriosus ( see data ). oligohydramnios/neonatal renal impairment: if an nsaid is necessary at about 20 weeks gestation or later in pregnancy, limit the use to the lowest effective dose and shortest duration possible. if meloxicam treatment extends beyond 48 hours, consider monitoring with ultrasound for oligohydramnios. if oligohydramnios occurs, discontinue meloxicam and follow up according to clinical practice ( see data ). labor or delivery there are no studies on the effects of meloxicam during labor or delivery. in animal studies, nsaids, including meloxicam, inhibit prostaglandin synthesis, cause delayed parturition, and increase the incidence of stillbirth. data human data premature closure of fetal ductus arteriosus: published literature reports that the use of nsaids at about 30 weeks of gestation and later in pregnancy may cause premature closure of the fetal ductus arteriosus. oligohydramnios/neonatal renal impairment: published studies and postmarketing reports describe maternal nsaid use at about 20 weeks gestation or later in pregnancy associated with fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. these adverse outcomes are seen, on average, after days to weeks of treatment, although oligohydramnios has been infrequently reported as soon as 48 hours after nsaid initiation. in many cases, but not all, the decrease in amniotic fluid was transient and reversible with cessation of the drug. there have been a limited number of case reports of maternal nsaid use and neonatal renal dysfunction without oligohydramnios, some of which were irreversible. some cases of neonatal renal dysfunction required treatment with invasive procedures, such as exchange transfusion or dialysis. methodological limitations of these postmarketing studies and reports include lack of a control group; limited information regarding dose, duration, and timing of drug exposure; and concomitant use of other medications. these limitations preclude establishing a reliable estimate of the risk of adverse fetal and neonatal outcomes with maternal nsaid use. because the published safety data on neonatal outcomes involved mostly preterm infants, the generalizability of certain reported risks to the full-term infant exposed to nsaids through maternal use is uncertain. animal data meloxicam was not teratogenic when administered to pregnant rats during fetal organogenesis at oral doses up to 4 mg/kg/day (2.6-fold greater than the mrhd of 15 mg of meloxicam based on bsa comparison). administration of meloxicam to pregnant rabbits throughout embryogenesis produced an increased incidence of septal defects of the heart at an oral dose of 60 mg/kg/day (78-fold greater than the mrhd based on bsa comparison). the no effect level was 20 mg/kg/day (26-fold greater than the mrhd based on bsa conversion). in rats and rabbits, embryolethality occurred at oral meloxicam doses of 1 mg/kg/day and 5 mg/kg/day, respectively (0.65- and 6.5-fold greater, respectively, than the mrhd based on bsa comparison) when administered throughout organogenesis. oral administration of meloxicam to pregnant rats during late gestation through lactation increased the incidence of dystocia, delayed parturition, and decreased offspring survival at meloxicam doses of 0.125 mg/kg/day or greater (0.08-times mrhd based on bsa comparison). risk summary there are no human data available on whether meloxicam is present in human milk, or on the effects on breastfed infants, or on milk production. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for meloxicam and any potential adverse effects on the breastfed infant from the meloxicam or from the underlying maternal condition. data animal data meloxicam was present in the milk of lactating rats at concentrations higher than those in plasma. infertility females based on the mechanism of action, the use of prostaglandin-mediated nsaids, including meloxicam, may delay or prevent rupture of ovarian follicles, which has been associated with reversible infertility in some women. published animal studies have shown that administration of prostaglandin synthesis inhibitors has the potential to disrupt prostaglandin-mediated follicular rupture required for ovulation. small studies in women treated with nsaids have also shown a reversible delay in ovulation. consider withdrawal of nsaids, including meloxicam, in women who have difficulties conceiving or who are undergoing investigation of infertility. the safety and effectiveness of meloxicam in pediatric jra patients from 2 to 17 years of age has been evaluated in three clinical trials [ see dosage and administration ( 2.3), adverse reactions ( 6.1) and clinical studies ( 14.2) ]. elderly patients, compared to younger patients, are at greater risk for nsaid-associated serious cardiovascular, gastrointestinal, and/or renal adverse reactions. if the anticipated benefit for the elderly patient outweighs these potential risks, start dosing at the low end of the dosing range, and monitor patients for adverse effects [ see warnings and precautions ( 5.1, 5.2, 5.3, 5.6, 5.14) ]. no dose adjustment is necessary in patients with mild to moderate hepatic impairment. patients with severe hepatic impairment have not been adequately studied. since meloxicam is significantly metabolized in the liver and hepatotoxicity may occur, use meloxicam with caution in patients with hepatic impairment [ see warnings and precautions ( 5.3) and clinical pharmacology ( 12.3) ]. no dose adjustment is necessary in patients with mild to moderate renal impairment. patients with severe renal impairment have not been studied. the use of meloxicam in subjects with severe renal impairment is not recommended. in patients on hemodialysis, meloxicam should not exceed 7.5 mg per day. meloxicam is not dialyzable [ see dosage and administration ( 2.1) and clinical pharmacology ( 12.3) ].

Jungtinės Valstijos - anglų - NLM (National Library of Medicine)

remedyrepack inc. - meloxicam (unii: vg2qf83cgl) (meloxicam - unii:vg2qf83cgl) - meloxicam is indicated for relief of the signs and symptoms of osteoarthritis [ see clinical studies (14.1)]. meloxicam is indicated for relief of the signs and symptoms of rheumatoid arthritis [ see clinical studies (14.1) ]. meloxicam is indicated for relief of the signs and symptoms of pauciarticular or polyarticular course juvenile rheumatoid arthritis in patients who weighs ≥ 60 kg [ see dosage and administration ( 2.4) and clinical studies (14.2)]. meloxicam is contraindicated in the following patients: - known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to meloxicam or any components of the drug product [ see warnings and precautions ( 5.7, 5.9) ] - history of asthma, urticaria, or other allergic-type reactions after taking aspirin or other nsaids. severe, sometimes fatal, anaphylactic reactions to nsaids have been reported in such patients [ see warnings and precautions ( 5.7, 5.8) ] - in the setting of coronary artery bypass graft (cabg) surgery [ see warnings and precautions ( 5.1) ] risk summary use of nsaids, including meloxicam, can cause premature closure of the fetal ductus arteriosus and fetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment. because of these risks, limit dose and duration of meloxicam use between about 20 and 30 weeks of gestation, and avoid meloxicam use at about 30 weeks of gestation and later in pregnancy ( see   clinical considerations, data ). premature closure of fetal ductus arteriosus use of nsaids, including meloxicam, at about 30 weeks gestation or later in pregnancy increases the risk of premature closure of the fetal ductus arteriosus. oligohydramnios/neonatal renal impairment use of nsaids at about 20 weeks gestation or later in pregnancy has been associated with cases of fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. data from observational studies regarding potential embryofetal risks of nsaid use in women in the first or second trimesters of pregnancy are inconclusive. in animal reproduction studies, embryofetal death was observed in rats and rabbits treated during the period of organogenesis with meloxicam at oral doses equivalent to 0.65- and 6.5-times the maximum recommended human dose (mrhd) of meloxicam. increased incidence of septal heart defects were observed in rabbits treated throughout embryogenesis with meloxicam at an oral dose equivalent to 78-times the mrhd. in pre- and post-natal reproduction studies, there was an increased incidence of dystocia, delayed parturition, and decreased offspring survival at 0.08-times mrhd of meloxicam. no teratogenic effects were observed in rats and rabbits treated with meloxicam during organogenesis at an oral dose equivalent to 2.6 and 26-times the mrhd [see data] . based on animal data, prostaglandins have been shown to have an important role in endometrial vascular permeability, blastocyst implantation, and decidualization. in animal studies, administration of prostaglandin synthesis inhibitors such as meloxicam, resulted in increased pre- and post-implantation loss. prostaglandins also have been shown to have an important role in fetal kidney development. in published animal studies, prostaglandin synthesis inhibitors have been reported to impair kidney development when administered at clinically relevant doses. the estimated background risk of major birth defects and miscarriage for the indicated population(s) is unknown. all pregnancies have a background risk of birth defect, loss, or other adverse outcomes. in the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. clinical considerations fetal/neonatal adverse reactions premature closure of fetal ductus arteriosus: avoid use of nsaids in women at about 30 weeks gestation and later in pregnancy, because nsaids, including meloxicam, can cause premature closure of the fetal ductus arteriosus ( see data ). oligohydramnios/neonatal renal impairment: if an nsaid is necessary at about 20 weeks gestation or later in pregnancy, limit the use to the lowest effective dose and shortest duration possible. if meloxicam treatment extends beyond 48 hours, consider monitoring with ultrasound for oligohydramnios. if oligohydramnios occurs, discontinue meloxicam and follow up according to clinical practice ( see data ). labor or delivery there are no studies on the effects of meloxicam during labor or delivery. in animal studies, nsaids, including meloxicam, inhibit prostaglandin synthesis, cause delayed parturition, and increase the incidence of stillbirth. data human data premature closure of fetal ductus arteriosus: published literature reports that the use of nsaids at about 30 weeks of gestation and later in pregnancy may cause premature closure of the fetal ductus arteriosus. oligohydramnios/neonatal renal impairment: published studies and postmarketing reports describe maternal nsaid use at about 20 weeks gestation or later in pregnancy associated with fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. these adverse outcomes are seen, on average, after days to weeks of treatment, although oligohydramnios has been infrequently reported as soon as 48 hours after nsaid initiation. in many cases, but not all, the decrease in amniotic fluid was transient and reversible with cessation of the drug. there have been a limited number of case reports of maternal nsaid use and neonatal renal dysfunction without oligohydramnios, some of which were irreversible. some cases of neonatal renal dysfunction required treatment with invasive procedures, such as exchange transfusion or dialysis. methodological limitations of these postmarketing studies and reports include lack of a control group; limited information regarding dose, duration, and timing of drug exposure; and concomitant use of other medications. these limitations preclude establishing a reliable estimate of the risk of adverse fetal and neonatal outcomes with maternal nsaid use. because the published safety data on neonatal outcomes involved mostly preterm infants, the generalizability of certain reported risks to the full-term infant exposed to nsaids through maternal use is uncertain. animal data meloxicam was not teratogenic when administered to pregnant rats during fetal organogenesis at oral doses up to 4 mg/kg/day (2.6-fold greater than the mrhd of 15 mg of meloxicam based on bsa comparison). administration of meloxicam to pregnant rabbits throughout embryogenesis produced an increased incidence of septal defects of the heart at an oral dose of 60 mg/kg/day (78-fold greater than the mrhd based on bsa comparison). the no effect level was 20 mg/kg/day (26-fold greater than the mrhd based on bsa conversion). in rats and rabbits, embryolethality occurred at oral meloxicam doses of 1 mg/kg/day and 5 mg/kg/day, respectively (0.65- and 6.5-fold greater, respectively, than the mrhd based on bsa comparison) when administered throughout organogenesis. oral administration of meloxicam to pregnant rats during late gestation through lactation increased the incidence of dystocia, delayed parturition, and decreased offspring survival at meloxicam doses of 0.125 mg/kg/day or greater (0.08-times mrhd based on bsa comparison). risk summary there are no human data available on whether meloxicam is present in human milk, or on the effects on breastfed infants, or on milk production. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for meloxicam and any potential adverse effects on the breastfed infant from the meloxicam or from the underlying maternal condition. data animal data meloxicam was present in the milk of lactating rats at concentrations higher than those in plasma. infertility females based on the mechanism of action, the use of prostaglandin-mediated nsaids, including meloxicam, may delay or prevent rupture of ovarian follicles, which has been associated with reversible infertility in some women. published animal studies have shown that administration of prostaglandin synthesis inhibitors has the potential to disrupt prostaglandin-mediated follicular rupture required for ovulation. small studies in women treated with nsaids have also shown a reversible delay in ovulation. consider withdrawal of nsaids, including meloxicam, in women who have difficulties conceiving or who are undergoing investigation of infertility. the safety and effectiveness of meloxicam in pediatric jra patients from 2 to 17 years of age has been evaluated in three clinical trials [ see dosage and administration ( 2.3), adverse reactions ( 6.1) and clinical studies ( 14.2) ]. elderly patients, compared to younger patients, are at greater risk for nsaid-associated serious cardiovascular, gastrointestinal, and/or renal adverse reactions. if the anticipated benefit for the elderly patient outweighs these potential risks, start dosing at the low end of the dosing range, and monitor patients for adverse effects [ see warnings and precautions ( 5.1, 5.2, 5.3, 5.6, 5.14) ]. no dose adjustment is necessary in patients with mild to moderate hepatic impairment. patients with severe hepatic impairment have not been adequately studied. since meloxicam is significantly metabolized in the liver and hepatotoxicity may occur, use meloxicam with caution in patients with hepatic impairment [ see warnings and precautions ( 5.3) and clinical pharmacology ( 12.3) ]. no dose adjustment is necessary in patients with mild to moderate renal impairment. patients with severe renal impairment have not been studied. the use of meloxicam in subjects with severe renal impairment is not recommended. in patients on hemodialysis, meloxicam should not exceed 7.5 mg per day. meloxicam is not dialyzable [ see dosage and administration ( 2.1) and clinical pharmacology ( 12.3) ].

Jungtinės Valstijos - anglų - NLM (National Library of Medicine)

remedyrepack inc. - meloxicam (unii: vg2qf83cgl) (meloxicam - unii:vg2qf83cgl) - meloxicam is indicated for relief of the signs and symptoms of osteoarthritis [ see clinical studies (14.1)]. meloxicam is indicated for relief of the signs and symptoms of rheumatoid arthritis [ see clinical studies (14.1) ]. meloxicam is indicated for relief of the signs and symptoms of pauciarticular or polyarticular course juvenile rheumatoid arthritis in patients who weighs ≥ 60 kg [ see dosage and administration ( 2.4) and clinical studies (14.2)]. meloxicam is contraindicated in the following patients: - known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to meloxicam or any components of the drug product [ see warnings and precautions ( 5.7, 5.9) ] - history of asthma, urticaria, or other allergic-type reactions after taking aspirin or other nsaids. severe, sometimes fatal, anaphylactic reactions to nsaids have been reported in such patients [ see warnings and precautions ( 5.7, 5.8) ] - in the setting of coronary artery bypass graft (cabg) surgery [ see warnings and precautions ( 5.1) ] risk summary use of nsaids, including meloxicam, can cause premature closure of the fetal ductus arteriosus and fetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment. because of these risks, limit dose and duration of meloxicam use between about 20 and 30 weeks of gestation, and avoid meloxicam use at about 30 weeks of gestation and later in pregnancy ( see   clinical considerations, data ). premature closure of fetal ductus arteriosus use of nsaids, including meloxicam, at about 30 weeks gestation or later in pregnancy increases the risk of premature closure of the fetal ductus arteriosus. oligohydramnios/neonatal renal impairment use of nsaids at about 20 weeks gestation or later in pregnancy has been associated with cases of fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. data from observational studies regarding potential embryofetal risks of nsaid use in women in the first or second trimesters of pregnancy are inconclusive. in animal reproduction studies, embryofetal death was observed in rats and rabbits treated during the period of organogenesis with meloxicam at oral doses equivalent to 0.65- and 6.5-times the maximum recommended human dose (mrhd) of meloxicam. increased incidence of septal heart defects were observed in rabbits treated throughout embryogenesis with meloxicam at an oral dose equivalent to 78-times the mrhd. in pre- and post-natal reproduction studies, there was an increased incidence of dystocia, delayed parturition, and decreased offspring survival at 0.08-times mrhd of meloxicam. no teratogenic effects were observed in rats and rabbits treated with meloxicam during organogenesis at an oral dose equivalent to 2.6 and 26-times the mrhd [see data] . based on animal data, prostaglandins have been shown to have an important role in endometrial vascular permeability, blastocyst implantation, and decidualization. in animal studies, administration of prostaglandin synthesis inhibitors such as meloxicam, resulted in increased pre- and post-implantation loss. prostaglandins also have been shown to have an important role in fetal kidney development. in published animal studies, prostaglandin synthesis inhibitors have been reported to impair kidney development when administered at clinically relevant doses. the estimated background risk of major birth defects and miscarriage for the indicated population(s) is unknown. all pregnancies have a background risk of birth defect, loss, or other adverse outcomes. in the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. clinical considerations fetal/neonatal adverse reactions premature closure of fetal ductus arteriosus: avoid use of nsaids in women at about 30 weeks gestation and later in pregnancy, because nsaids, including meloxicam, can cause premature closure of the fetal ductus arteriosus ( see data ). oligohydramnios/neonatal renal impairment: if an nsaid is necessary at about 20 weeks gestation or later in pregnancy, limit the use to the lowest effective dose and shortest duration possible. if meloxicam treatment extends beyond 48 hours, consider monitoring with ultrasound for oligohydramnios. if oligohydramnios occurs, discontinue meloxicam and follow up according to clinical practice ( see data ). labor or delivery there are no studies on the effects of meloxicam during labor or delivery. in animal studies, nsaids, including meloxicam, inhibit prostaglandin synthesis, cause delayed parturition, and increase the incidence of stillbirth. data human data premature closure of fetal ductus arteriosus: published literature reports that the use of nsaids at about 30 weeks of gestation and later in pregnancy may cause premature closure of the fetal ductus arteriosus. oligohydramnios/neonatal renal impairment: published studies and postmarketing reports describe maternal nsaid use at about 20 weeks gestation or later in pregnancy associated with fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. these adverse outcomes are seen, on average, after days to weeks of treatment, although oligohydramnios has been infrequently reported as soon as 48 hours after nsaid initiation. in many cases, but not all, the decrease in amniotic fluid was transient and reversible with cessation of the drug. there have been a limited number of case reports of maternal nsaid use and neonatal renal dysfunction without oligohydramnios, some of which were irreversible. some cases of neonatal renal dysfunction required treatment with invasive procedures, such as exchange transfusion or dialysis. methodological limitations of these postmarketing studies and reports include lack of a control group; limited information regarding dose, duration, and timing of drug exposure; and concomitant use of other medications. these limitations preclude establishing a reliable estimate of the risk of adverse fetal and neonatal outcomes with maternal nsaid use. because the published safety data on neonatal outcomes involved mostly preterm infants, the generalizability of certain reported risks to the full-term infant exposed to nsaids through maternal use is uncertain. animal data meloxicam was not teratogenic when administered to pregnant rats during fetal organogenesis at oral doses up to 4 mg/kg/day (2.6-fold greater than the mrhd of 15 mg of meloxicam based on bsa comparison). administration of meloxicam to pregnant rabbits throughout embryogenesis produced an increased incidence of septal defects of the heart at an oral dose of 60 mg/kg/day (78-fold greater than the mrhd based on bsa comparison). the no effect level was 20 mg/kg/day (26-fold greater than the mrhd based on bsa conversion). in rats and rabbits, embryolethality occurred at oral meloxicam doses of 1 mg/kg/day and 5 mg/kg/day, respectively (0.65- and 6.5-fold greater, respectively, than the mrhd based on bsa comparison) when administered throughout organogenesis. oral administration of meloxicam to pregnant rats during late gestation through lactation increased the incidence of dystocia, delayed parturition, and decreased offspring survival at meloxicam doses of 0.125 mg/kg/day or greater (0.08-times mrhd based on bsa comparison). risk summary there are no human data available on whether meloxicam is present in human milk, or on the effects on breastfed infants, or on milk production. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for meloxicam and any potential adverse effects on the breastfed infant from the meloxicam or from the underlying maternal condition. data animal data meloxicam was present in the milk of lactating rats at concentrations higher than those in plasma. infertility females based on the mechanism of action, the use of prostaglandin-mediated nsaids, including meloxicam, may delay or prevent rupture of ovarian follicles, which has been associated with reversible infertility in some women. published animal studies have shown that administration of prostaglandin synthesis inhibitors has the potential to disrupt prostaglandin-mediated follicular rupture required for ovulation. small studies in women treated with nsaids have also shown a reversible delay in ovulation. consider withdrawal of nsaids, including meloxicam, in women who have difficulties conceiving or who are undergoing investigation of infertility. the safety and effectiveness of meloxicam in pediatric jra patients from 2 to 17 years of age has been evaluated in three clinical trials [ see dosage and administration ( 2.3), adverse reactions ( 6.1) and clinical studies ( 14.2) ]. elderly patients, compared to younger patients, are at greater risk for nsaid-associated serious cardiovascular, gastrointestinal, and/or renal adverse reactions. if the anticipated benefit for the elderly patient outweighs these potential risks, start dosing at the low end of the dosing range, and monitor patients for adverse effects [ see warnings and precautions ( 5.1, 5.2, 5.3, 5.6, 5.14) ]. no dose adjustment is necessary in patients with mild to moderate hepatic impairment. patients with severe hepatic impairment have not been adequately studied. since meloxicam is significantly metabolized in the liver and hepatotoxicity may occur, use meloxicam with caution in patients with hepatic impairment [ see warnings and precautions ( 5.3) and clinical pharmacology ( 12.3) ]. no dose adjustment is necessary in patients with mild to moderate renal impairment. patients with severe renal impairment have not been studied. the use of meloxicam in subjects with severe renal impairment is not recommended. in patients on hemodialysis, meloxicam should not exceed 7.5 mg per day. meloxicam is not dialyzable [ see dosage and administration ( 2.1) and clinical pharmacology ( 12.3) ].

Jungtinės Valstijos - anglų - NLM (National Library of Medicine)

remedyrepack inc. - gabapentin (unii: 6cw7f3g59x) (gabapentin - unii:6cw7f3g59x) - gabapentin is indicated for: • management of postherpetic neuralgia in adults • adjunctive therapy in the treatment of partial onset seizures, with and without secondary generalization, in adults and pediatric patients 3 years and older with epilepsy gabapentin is contraindicated in patients who have demonstrated hypersensitivity to the drug or its ingredients. pregnancy exposure registry there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to antiepileptic drugs (aeds), such as gabapentin, during pregnancy. encourage women who are taking gabapentin during pregnancy to enroll in the north american antiepileptic drug (naaed) pregnancy registry by calling the toll free number 1-888-233-2334 or visiting http://www.aedpregnancyregistry.org/. risk summary there are no adequate data on the developmental risks associated with the use of gabapentin in pregnant women. in nonclinical studies in mice, rats, and rabbits, gabapentin was developmentally toxic (increased fetal skeletal and visceral abnormalities, and increased embryofetal mortality) when administered to pregnant animals at doses similar to or lower than those used clinically [see data]. in the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. the background risk of major birth defects and miscarriage for the indicated population is unknown. data animal data   when pregnant mice received oral doses of gabapentin (500, 1000, or 3000 mg/kg/day) during the period of organogenesis, embryofetal toxicity (increased incidences of skeletal variations) was observed at the two highest doses. the no-effect dose for embryofetal developmental toxicity in mice (500 mg/kg/day) is less than the maximum recommended human dose (mrhd) of 3600 mg on a body surface area (mg/m 2 ) basis. in studies in which rats received oral doses of gabapentin (500 to 2000 mg/kg/day) during pregnancy, adverse effect on offspring development (increased incidences of hydroureter and/or hydronephrosis) were observed at all doses. the lowest dose tested is similar to the mrhd on a mg/m 2 basis. when pregnant rabbits were treated with gabapentin during the period of organogenesis, an increase in embryofetal mortality was observed at all doses tested (60, 300, or 1500 mg/kg). the lowest dose tested is less than the mrhd on a mg/m 2 basis. in a published study, gabapentin (400 mg/kg/day) was administered by intraperitoneal injection to neonatal mice during the first postnatal week, a period of synaptogenesis in rodents (corresponding to the last trimester of pregnancy in humans). gabapentin caused a marked decrease in neuronal synapse formation in brains of intact mice and abnormal neuronal synapse formation in a mouse model of synaptic repair. gabapentin has been shown in vitro to interfere with activity of the α2δ subunit of voltage-activated calcium channels, a receptor involved in neuronal synaptogenesis. the clinical significance of these findings is unknown. risk summary gabapentin is secreted in human milk following oral administration. the effects on the breastfed infant and on milk production are unknown. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for gabapentin and any potential adverse effects on the breastfed infant from gabapentin or from the underlying maternal condition. safety and effectiveness of gabapentin in the management of postherpetic neuralgia in pediatric patients have not been established. safety and effectiveness as adjunctive therapy in the treatment of partial seizures in pediatric patients below the age of 3 years has not been established  [see clinical studies (14.2)]. the total number of patients treated with gabapentin in controlled clinical trials in patients with postherpetic neuralgia was 336, of which 102 (30%) were 65 to 74 years of age, and 168 (50%) were 75 years of age and older. there was a larger treatment effect in patients 75 years of age and older compared to younger patients who received the same dosage.    since gabapentin is almost exclusively eliminated by renal excretion, the larger treatment effect observed in patients ≥ 75 years may be a consequence of increased gabapentin exposure for a given dose that results from an age-related decrease in renal function. however, other factors cannot be excluded. the types and incidence of adverse reactions were similar across age groups except for peripheral edema and ataxia, which tended to increase in incidence with age. clinical studies of gabapentin in epilepsy did not include sufficient numbers of subjects aged 65 and over to determine whether they responded differently from younger subjects. other reported clinical experience has not identified differences in responses between the elderly and younger patients. in general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy. this drug is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function. because elderly patients are more likely to have decreased renal function, care should be taken in dose selection, and dose should be adjusted based on creatinine clearance values in these patients [see dosage and administration (2.4), adverse reactions (6), and clinical pharmacology (12.3)] . dosage adjustment in adult patients with compromised renal function is necessary [see  dosage and administration (2.3) and clinical pharmacology (12.3)] . pediatric patients with renal insufficiency have not been studied. dosage adjustment in patients undergoing hemodialysis is necessary [see dosage and administration (2.3) and clinical pharmacology (12.3)] . gabapentin is not a scheduled drug. abuse is the intentional, non-therapeutic use of a drug, even once, for its desirable psychological or physiological effects. misuse is the intentional use, for therapeutic purposes, of a drug by an individual in a way other than prescribed by a health care provider or for whom it was not prescribed. gabapentin does not exhibit affinity for benzodiazepine, opioid (mu, delta or kappa), or cannabinoid 1 receptor sites. gabapentin misuse and abuse have been reported in the postmarketing setting and published literature. most of the individuals described in these reports had a history of polysubstance abuse. some of these individuals were taking higher than recommended doses of gabapentin for unapproved uses. when prescribing gabapentin, carefully evaluate patients for a history of drug abuse and observe them for signs and symptoms of gabapentin misuse or abuse (e.g., self-dose escalation and drug-seeking behavior). the abuse potential of gabapentin has not been evaluated in human studies. physical dependence is a state that develops as a result of physiological adaptation in response to repeated drug use, manifested by withdrawal signs and symptoms after abrupt discontinuation or a significant dose reduction of a drug. there are rare postmarketing reports of individuals experiencing withdrawal symptoms shortly after discontinuing higher than recommended doses of gabapentin used to treat illnesses for which the drug is not approved. such symptoms included agitation, disorientation and confusion after suddenly discontinuing gabapentin that resolved after restarting gabapentin. the dependence potential of gabapentin has not been evaluated in human studies.

Jungtinės Valstijos - anglų - NLM (National Library of Medicine)

remedyrepack inc. - gabapentin (unii: 6cw7f3g59x) (gabapentin - unii:6cw7f3g59x) - gabapentin tablets are indicated for: - management of postherpetic neuralgia in adults - adjunctive therapy in the treatment of partial onset seizures, with and without secondary generalization, in adults and pediatric patients 3 years and older with epilepsy gabapentin is contraindicated in patients who have demonstrated hypersensitivity to the drug or its ingredients. pregnancy exposure registry there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to antiepileptic drugs (aeds), such as gabapentin, during pregnancy. encourage women who are taking gabapentin during pregnancy to enroll in the north american antiepileptic drug (naaed) pregnancy registry by calling the toll free number 1-888-233-2334 or visiting http://www.aedpregnancyregistry.org/. risk summary there are no adequate data on the developmental risks associated with the use of gabapentin in pregnant women. in nonclinical studies in mice, rats, and rabbits, gabapentin was developmentally toxic (increased fetal skeletal and visceral abnormalities, and increased embryofetal mortality) when administered to pregnant animals at doses similar to or lower than those used clinically [see data] . in the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2 to 4% and 15 to 20%, respectively. the background risk of major birth defects and miscarriage for the indicated population is unknown. data animal data when pregnant mice received oral doses of gabapentin (500, 1000, or 3000 mg/kg/day) during the period of organogenesis, embryofetal toxicity (increased incidences of skeletal variations) was observed at the two highest doses. the no-effect dose for embryofetal developmental toxicity in mice (500 mg/kg/day) is less than the maximum recommended human dose (mrhd) of 3600 mg on a body surface area (mg/m 2 ) basis. in studies in which rats received oral doses of gabapentin (500 to 2000 mg/kg/day) during pregnancy, adverse effect on offspring development (increased incidences of hydroureter and/or hydronephrosis) were observed at all doses. the lowest dose tested is similar to the mrhd on a mg/m 2 basis. when pregnant rabbits were treated with gabapentin during the period of organogenesis, an increase in embryofetal mortality was observed at all doses tested (60, 300, or 1500 mg/kg). the lowest dose tested is less than the mrhd on a mg/m 2 basis. in a published study, gabapentin (400 mg/kg/day) was administered by intraperitoneal injection to neonatal mice during the first postnatal week, a period of synaptogenesis in rodents (corresponding to the last trimester of pregnancy in humans). gabapentin caused a marked decrease in neuronal synapse formation in brains of intact mice and abnormal neuronal synapse formation in a mouse model of synaptic repair. gabapentin has been shown in vitro to interfere with activity of the α2δ subunit of voltage-activated calcium channels, a receptor involved in neuronal synaptogenesis. the clinical significance of these findings is unknown. risk summary gabapentin is secreted in human milk following oral administration. the effects on the breastfed infant and on milk production are unknown. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for gabapentin and any potential adverse effects on the breastfed infant from gabapentin or from the underlying maternal condition. safety and effectiveness of gabapentin in the management of postherpetic neuralgia in pediatric patients have not been established. safety and effectiveness as adjunctive therapy in the treatment of partial seizures in pediatric patients below the age of 3 years has not been established [see clinical studies ( 14.2)] . the total number of patients treated with gabapentin in controlled clinical trials in patients with postherpetic neuralgia was 336, of which 102 (30%) were 65 to 74 years of age, and 168 (50%) were 75 years of age and older. there was a larger treatment effect in patients 75 years of age and older compared to younger patients who received the same dosage. since gabapentin is almost exclusively eliminated by renal excretion, the larger treatment effect observed in patients ≥75 years may be a consequence of increased gabapentin exposure for a given dose that results from an age-related decrease in renal function. however, other factors cannot be excluded. the types and incidence of adverse reactions were similar across age groups except for peripheral edema and ataxia, which tended to increase in incidence with age. clinical studies of gabapentin in epilepsy did not include sufficient numbers of subjects aged 65 and over to determine whether they responded differently from younger subjects. other reported clinical experience has not identified differences in responses between the elderly and younger patients. in general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy. this drug is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function. because elderly patients are more likely to have decreased renal function, care should be taken in dose selection, and dose should be adjusted based on creatinine clearance values in these patients [see dosage and administration ( 2.4), adverse reactions ( 6), and clinical pharmacology ( 12.3)] . dosage adjustment in adult patients with compromised renal function is necessary [see dosage and administration ( 2.3) and clinical pharmacology ( 12.3)] . pediatric patients with renal insufficiency have not been studied. dosage adjustment in patients undergoing hemodialysis is necessary [see dosage and administration ( 2.3) and clinical pharmacology ( 12.3)] . gabapentin is not a scheduled drug. abuse is the intentional, non-therapeutic use of a drug, even once, for its desirable psychological or physiological effects. misuse is the intentional use, for therapeutic purposes, of a drug by an individual in a way other than prescribed by a health care provider or for whom it was not prescribed. gabapentin does not exhibit affinity for benzodiazepine, opioid (mu, delta or kappa), or cannabinoid 1 receptor sites. gabapentin misuse and abuse have been reported in the postmarketing setting and published literature. most of the individuals described in these reports had a history of polysubstance abuse. some of these individuals were taking higher than recommended doses of gabapentin for unapproved uses. when prescribing gabapentin, carefully evaluate patients for a history of drug abuse and observe them for signs and symptoms of gabapentin misuse or abuse (e.g., self-dose escalation, and drug-seeking behavior). the abuse potential of gabapentin has not been evaluated in human studies. physical dependence is a state that develops as a result of physiological adaptation in response to repeated drug use, manifested by withdrawal signs and symptoms after abrupt discontinuation or a significant dose reduction of a drug. there are rare postmarketing reports of individuals experiencing withdrawal symptoms shortly after discontinuing higher than recommended doses of gabapentin used to treat illnesses for which the drug is not approved. such symptoms included agitation, disorientation and confusion after suddenly discontinuing gabapentin that resolved after restarting gabapentin. the dependence potential of gabapentin has not been evaluated in human studies.