Generic Information
VITAMIN A
Effective for: Vitamin A deficiency. Taking vitamin A by mouth is effective for preventing and treating symptoms of vitamin A deficiency. Vitamin A deficiency can occur in people with protein deficiency, diabetes, over-active thyroid, fever, liver disease, cystic fibrosis, or an inherited disorder called abetalipoproteinemia. Possibly Effective for: Breast cancer. Premenopausal women with a family history of breast cancer who consume high levels of vitamin A in their diet seem to have reduced risk of developing breast cancer. It is not known if taking vitamin A supplements has the same benefit. Cataracts. Research suggests that high intake of vitamin A in the diet is linked to a lower risk of developing cataracts. Diarrhea related to HIV. Taking vitamin A along with conventional medicines seems to decrease the risk of death from diarrhea in HIV-positive children with vitamin A deficiency. Malaria. Taking vitamin A by mouth seems to decrease malaria symptoms in children less than 3 years-old living in areas where malaria is common. Measles. Taking vitamin A by mouth seems to reduce the risk of measles complications or death in children with measles and vitamin A deficiency. Precancerous lesions in the mouth (oral leukoplakia). Research suggests that taking vitamin A can help treat precancerous lesions in the mouth. Recovery from laser eye surgery (photoreactive keratectomy). Taking vitamin A by mouth along with vitamin E seems to improve healing after laser eye surgery. Complications after pregnancy. Taking vitamin A seems to reduce the risk of diarrhea and fever after pregnancy in malnourished women. Complications during pregnancy. Taking vitamin A by mouth seems to reduce the risk of death and night blindness during pregnancy in malnourished women. Eye disease affecting the retina (retinitis pigmentosa). Research suggests that taking vitamin A can slow the progression of an eye disease that causes damage to the retina.
Vitamin-A preparations
Vinpocetine increases cerebral metabolism; it increases glucose and O2 consumption; improves cerebral hypoxia tolerance; shifts glucose metabolism to the energetically more favourable aerobic pathway, but it increases the anaerobic pathway as well; it elevates the ATP concentration and the ATP/AMP ratio in the brain, and elevates the cerebral norepinephrine, dopamine and serotonin levels. Vinpocetine considerably improves cerebral microcirculation by inhibiting platelet aggregation, reducing the pathologically increased blood viscosity, and increases erythrocyte deformability. It also promotes O2 transport into the tissues by reducing the O2 affinity of erythrocytes. It selectively and intensely increases cerebral blood flow and the share of the brain in cardiac output, it reduces cerebral vascular resistance without affecting systemic circulation (blood pressure, heart rate, cardiac output, total peripheral resistance). It does not elicit steal phenomenon; on the contrary, it primarily improves the blood supply of the injured and ischaemic area while it remains unchanged in the intact areas (inverse steal effect). It further increases blood flow which is already increased as a result of hypoxia.
Vitamin A deficiency For severe deficiency with corneal changes: 500,000 unit/day for 3 days, followed by 50,000 unit/day for 2 wk and then 10,000-20,000 unit/day for 2 mth as follow-up therapy. For cases without corneal changes: 10,000-25,000 unit/day until clinical improvement occurs (usually 1 -2 wk).
Decreased absorption with neomycin. Increased risk of hypervitaminosis A with synthetic retinoids eg, acitretin, isotretinoin and tretinoin. Increased risk of toxicity when used with alcohol.
Hypervitaminosis A; pregnancy (dose exceeding RDA).
Hypervitaminosis A characterised by fatigue, irritability, anorexia, weight loss, vomiting and other Gl disturbances, low-grade fever, hepatosplenomegaly, skin changes, alopoecia, dry hair, cracking and bleeding lips, SC swelling, nocturia, pains in bones and joints.
Pregnancy Category A. Adequate and well-controlled human studies have failed to demonstrate a risk to the fetus in the first trimester of pregnancy (and there is no evidence of risk in later trimesters).
Cholestatic jaundice; fat-malabsorption conditions. Monitor patients closely for toxicity. Liver impairment and children.