Vitamin prophylactic therapy

Idiopathic osteoporosis cannot be prevented by prophylactic therapy, but its development can be delayed. This requires a healthy lifestyle with plenty of physical exercise (sports, hiking), daily intake of calcium (lOOOmg/day Ca2+) and of vitamin D (1000 IU/day). The same principle holds for postmenopausal osteoporosis. Hormone Luellmann, Color Atlas of Pharmacology All rights reserved. Usage subject to terms... 

In the case of Vitamin K-deficency owing to bile obstruction, which has lowered the value for prothrombin complex, vitamin K1 is administered intravenously. In moderate vitamin K-deficiency induced by therapy with antibiotics or diarrhoeas of long duration, oral vitamin K therapy is needed. Prophylactically vitamin K is used for treatment of haemorrhage in the newborn and therapeutically in cases of overdosage of warfarin-type anticoagulants. 

A variety of antiinflammatory and sulfhydryl-scavenging agents (such as promethazine, vitamin E, heparin, and sodium thiosulfate) have been suggested as therapeutic drugs. Although animal studies suggest the value of these agents for prophylactic therapy (or therapy immediately after the exposure), there are no data to support their use after the lesions develop.85"87... 

If isoniazid is implicated in optic neuropathy or other neurologic signs, then pyridoxine (vitamin Bg), 25 to 100 mg/day, may be used. Prophylactic administration of this agent can be combined with isoniazid and monoamine oxidase inhibitor therapy. 

Although there are relatively few therapeutic indications for vitamin pharmaceutical preparations, diseases caused by certain vitamin deficiencies do respond favorably to vitamin therapy. Additionally, there are products indicated for prophylactic use as dietary supplements. An optimal diet provides all of the necessary nutrients in some cases of increased demands, however, vitamin and mineral supplementation is tecominended. ... 

Folate deficiency usually takes 3-5 years to evolve in patients with epilepsy. Therefore, prophylactic B vitamin supplements may be recommended for patients at risk. As long as physiological doses are used, vitamin therapy should be safe. 

It is perhaps surprising that megaloblastic anemia does not occur more frequently after total gastrectomy (Witts, 1962). MacDonald et al. (1947) traced 46 patients who had lived for three years or more after total gastrectomy and who were not known to have received prophylactic liver therapy. Only 12 patients had anemia of a pernicious type. This had seldom developed within 2 years, and two patients survived 10 and 20 years, respectively, without anemia. Witts compares these periods with the time (2 to 38 months) taken for idiopathic pernicious anemia to relapse after cessation of liver therapy (Schwartz and Legere, 1944). He remarks that cessation of substitution therapy in established pernicious anemia thus produces a prompter and more constant effect on blood formation than does complete removal of the stomach. This is perhaps because substitution therapy in the patients with pernicious anemia had not been intensive enough to maintain normal concentrations of vitamin Bi2 in the liver and other tissues. 

The answer is 4 iCh er 61B 2 c, 3 a]. Effective antidotal therapy m veterinary medi-ctne is limited toapprcadmately 12 to 14 drt. Of these, only atropine, vitamin K, and ascorbic acid are cleared for veterinary use. Others are effective, but not available accept from human source or by preparing the antidote from basic chemicals [e.g., 4-mediylpyrazole (4-MP), ammonium tetrathiomolybdate]. Adverse effects of antidotes are more likely when levels of the toxicant are low or nonexistent therefore, antidotes should not be used as prophylactic agents or when the toxicant has not clearly identified. General decontamination therapy should be carried out prior to antidote administration. 

In children at risk of vitamin A deficiency, vitamin A supplementation, given prophylactically or as therapy during illness, has significantly reduced the severity of measles and measles-related mortality (see Hypervitaminosis A and Vitamin A Toxicity ). 

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