The Lipoprotein(a). Significance and Relation to Atherosclerosis
ACTA Clinica Belgica, 1991;46(6):371-383.
Lipoprotein(a) is very similar to low density lipoprotein, but possesses a unique protein moiety called apolipoprotein (A). The plasma concentration of lipoprotein(a) is mainly under genetic control. Nicotinic acid (vitamin B3) and neomycin are able to reduce its concentration. Epidemiologic studies suggest that high levels of lipoprotein(a), greater than 30 mg per dl, are an independent risk factor for atherosclerosis of the coronary and carotid arteries. The risk is highest in those with hypercholesterolemia. High lipoprotein(a) levels could also favor thrombosis. Reducing hypercholesterolemia is important when lipoprotein(a) levels are greater than 30 mg per dl.
Protein/platelet interaction with an artificial surface: effect of vitamins and platelet inhibitors.
Thromb Res (UNITED STATES) Jan 1 1986, 41 (1) p9-22
Protein adsorption and platelet adhesion are two important biological processes arising at the blood-prosthetic interface. The effect of Vitamins and antiplatelet drugs to modulate the surface induced platelet adhesion to polycarbonate was investigated using washed calf platelets in presence and absence of fibrinogen. This study also demonstrated the effects of Vitamins and antiplatelet drugs towards protein adsorption to an artificial surface. It seems Vitamin B6, Vitamin E, combinations of Aspirin-Persantine, Aspirin-Vitamin C, a synthetic Polyelectrolyte and Galactosamine reduced the fibrinogen (fg) surface concentration from a mixture of proteins. These antiplatelet agents also enhanced the albumin surface concentration. This itself may be one of the parameters to reduce the platelet adhesion towards an artificial surface. A combination of Aspirin-Vitamin C-Vitamin B6-Vitamin E inhibited the fibrinogen surface binding, which might be beneficial to improve the blood compatibility of an artificial surface
Vitamins in psychiatry. Do they have a role?
DRUGS (AUSTRALIA), 1985, 30/1
IDeficiencies of specific vitamins produce consistent symptoms of psychiatric disorder. Thiamine deficiency, which is common in alcoholism, can produce confusion and psychotic symptoms, in addition to neurological signs. Vitamin Bsub 1sub 2 and folate deficiency may contribute symptoms of disorientation, depression or psychosis; their measurement is a part of routine dementia work-ups. Pyridoxine deficiency results in seizures, although the effects of exogenously administered pyridoxine are not clearly understood in depression and anxiety - the disorders in which it is most frequently used clinically. The use of vitamins has been most prominent in psychiatry in the treatment of schizophrenia, where large doses of nicotinic acid were initially given alone and later combined with other vitamins and minerals. Several theoretical models were described to support the use of vitamins in schizophrenia. These included: the parallels of schizophrenia to the psychiatric symptoms of pellagra; hypotheses of a defect in adrenaline metabolism; and the accumulation of psychotoxic substances which produce psychotic symptoms. Initially, positive results were reported over 30 years ago, but have not been replicated by thorough investigations. An extensive series of comprehensive placebo-controlled trials failed to show efficacy for any of the vitamin therapies tested. Although clearly less effective than antipsychotic drug treatment, vitamin therapy is not without risks - adverse effects have been reported with nicotinic acid, pyridoxine and vitamin C. Although the possible role of vitamins has played an important part in the development of biological psychiatry, vitamin therapy is no longer extensively practised, and claims for its efficacy have not been supported by objective scientific evidence.