CompositionEicosapentaenoic Acid (60 mg),Recombinant Hepatitis B Surface Antigen (90 mg),Tocopherol Acetate (400 mg)
SALT INFORMATIONEicosapentaenoic Acid (60 mg) TYPICAL USAGE To delay the progression and reduce symptoms of diabetic neuropathy and other associated symptoms of diabetes mellitus particularly in subjects with good blood sugar control and limited microangiopathy. SIDE EFFECTS Gastrointestinal disturbances, including nausea, eructation, vomiting, abdominal distension, diarrhoea and constipation. DRUG INTERACTION Do not start or stop any medicine without doctor or pharmacist approval. MECHANISM OF ACTION The omega-3 fatty acids eicosapentaenoic acid is long-chain n-3 polyunsaturated fatty acids, which compete with arachidonic acid for inclusion in cyclo-oxygenase and lipoxygenase pathways. It's actions include hypolipidaemic action (especially a reduction in plasma triglycerides) by reducing very-low-density lipoproteins; anti-inflammatory action, attributed to effects on leukotriene synthesis; and antiplatelet effect, attributed to effects on prostanoid synthesis, which promote vasodilatation, reduction in platelet aggregation, increased bleeding time and decreased platelet counts. Recombinant Hepatitis B Surface Antigen (90 mg) TYPICAL USAGE Hepatitis B prophylaxis. SIDE EFFECTS Convulsions, neuropathy, angioedema, meningitis, anaphylactic reactions, paralysis, weakness, dizziness, headache, fatigue, nausea, vomiting, diarrhea, fever, myalgia, abdominal pain, rashes, pruritus, pain, redness, malaise, hypotension. DRUG INTERACTION Hepatitis B prophylaxis. MECHANISM OF ACTION Hepatitis B vaccines are used for active immunisation against hepatitis B infection. Two types of vaccine have been available each containing hepatitis B surface antigen (HBsAg) adsorbed onto aluminium hydroxide or a similar adsorbent. Tocopherol Acetate (400 mg) TYPICAL USAGE Cardiovascular disease, dementia, haemolytic anaemia, hepatotoxin poisoning, metal poisoning, vitamin deficiency, malignant neoplasms, muscular spasm, parkinsonism, prophylaxis and treatment of angina, retinopathy, surgery. SIDE EFFECTS Thrombosis, bleeding in vitamin K deficient patients, necrotizing enterocolitis in premature infants, flatulence, weakness, dizziness, fatigue, nausea, diarrhea, abdominal pain, blurred vision, thrombophlebitis, myopathy, hypertension. DRUG INTERACTION Tocopherol (Vitamin E) is known to interact with other drugs like colestipol (HCl), desogestrel, retinol (Vitamin A), vitamin K, warfarin (Na). Always consult your physician for the change of dose regimen or an alternative drug of choice that may strictly be required. MECHANISM OF ACTION Vitamin E's anti-atherogenic activity involves the inhibition of the oxidation of LDL and the accumulation of oxLDL in the arterial wall. It also appears to reduce oxLDL-induced apoptosis in human endothelial cells. Vitamin E inhibits protein kinase C (PKC) activity. The inhibition of PKC results in inhibition of smooth muscle cell proliferation, which is involved in atherogenesis. Vitamin E's antithrombotic and anticoagulant activities involves the downregulation of the expression of intracellular cell adhesion molecule(ICAM)-1 and vascular cell adhesion molecule(VCAM)-1 which lowers the adhesion of blood components to the endothelium. Vitamin E upregulates the expression of cytosolic phospholipase A2 and cyclooxygenase (COX)-1 which in turn enhances the release of prostacyclin. Prostacyclin is a vasodilating factor and inhibitor of platelet aggregation and platelet release. Vitamin E has also been found in culture to decrease plasma production of thrombin, a protein which binds to platelets and induces aggregation. A metabolite of vitamin E called vitamin E quinone or alpha-tocopheryl quinone (TQ) is a potent anticoagulant. This metabolite inhibits vitamin K-dependent carboxylase, which is a major enzyme in the coagulation cascade. Many disorders of the nervous system are caused by oxidative stress. Vitamin E protects against this stress, thereby protecting the nervouse system.