EVITOL 200 MG

Country: Iżrael

Lingwa: Ingliż

Sors: Ministry of Health

Ixtrih issa

Ingredjent attiv:

TOCOPHEROL (VIT E) (AS TOCOPHERYL ACETATE)

Disponibbli minn:

TEVA PHARMACEUTICAL INDUSTRIES LTD, ISRAEL

Kodiċi ATC:

A11HA03

Għamla farmaċewtika:

TABLETS

Kompożizzjoni:

TOCOPHEROL (VIT E) (AS TOCOPHERYL ACETATE) 200 MG

Rotta amministrattiva:

PER OS

Tip ta 'preskrizzjoni:

Not required

Manifatturat minn:

TEVA PHARMACEUTICAL INDUSTRIES LTD, ISRAEL

Grupp terapewtiku:

TOCOPHEROL (VIT E)

Żona terapewtika:

TOCOPHEROL (VIT E)

Indikazzjonijiet terapewtiċi:

For the prevention and treatment of diseases caused by Vitamin E deficiency.

Data ta 'l-awtorizzazzjoni:

2013-10-31

Karatteristiċi tal-prodott

                                Evitol Tablets, 1 4. 2014, RH
"
ע עבקנ הז ןולע טמרופ
"
רשואו קדבנ ונכותו תואירבה דרשמ י
."
רשואמ ןולע
:
31/3/2014
“This leaflet form
at has been determined by the Ministry of Health and the content
thereof has
been checked and approved.” Date of approval: 31/3/2014
EVITOL
®
TABLETS
COMPOSITION
Each tablet contains:
_Active Ingredient _
dl-alpha-Tocopherol acetate 100 mg or 200 mg (Vitamin E)
_Other Ingredients _
Microcrystalline cellulose, silicon dioxide, hydrogenated vegetable
oil, povidone,
gelatin, sucrose
*
, maize starch, sodium alumino-silicate.
*
_Each Evitol 100 mg tablet contains 9.4 mg sucrose_.
_* Each Evitol 100 mg tablet contains 1.74 mg sodium. _
_ _
_*_
_ Each Evitol 200 mg tablet contains 18.8 mg sucrose. _
_* Each Evitol 200 mg tablet contains 3.5 mg sodium. _
_ _
MECHANISM OF ACTION
Vitamin E is a fat-soluble intracellular antioxidant. It plays an
important role in
preventing
oxidation
of
essential
cellular
constituents,
thereby
preventing
the
formation of toxic oxidation products, such as the peroxides formed
from unsaturated
fatty acids. These lipid peroxides are known to damage cell membranes.
Vitamin E deficiency plays a significant role in the pathogenesis of
hemolytic anemia
in premature infants. Its antioxidant property is important for the
maintenance of red
cell viability. It is also quite likely that vitamin E deficiency
predisposes to the
development of retrolental fibroplasia in premature infants exposed to
higher oxygen
tensions than those of the intrauterine environment.
The need of the body for vitamin E is considerably increased by diets
that contain
foods rich in polyunsaturated fatty acids. This explains vitamin E
deficiency in infants
fed
on
formulas
rich
in
such
fatty
acids.
This
deficiency
is
corrected
by
the
administration of vitamin E. In fact, it has been shown that levels of
vitamin E rise
much slower in artificially-fed infants than in those who are
breastfed.
Human atheromatous lesions contain lipid peroxides. F
                                
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