Vitamin drug induced

Parenteral Anticoagulant-induced prothrombin deficiency hypoprothrombinemia secondary to conditions limiting absorption or synthesis of vitamin K (eg, obstructive jaundice, biliary fistula, sprue, ulcerative colitis, celiac disease, intestinal resection, cystic fibrosis of the pancreas, regional enteritis) drug-induced hypoprothrombinemias due to interference with vitamin K metabolism (eg, antibiotics, salicylates) prophylaxis and therapy of hemorrhagic disease of the newborn. 

Spontaneous reports of osteoporosis, osteopenia, bone fractures, and delayed healing of bone fractures have been seen in the isotretinoin population. While causality to isotretinoin has not been established, an effect cannot be ruled out. Physicians should use caution when prescribing isotretinoin to patients with a genetic predisposition for age-related osteoporosis, a history of childhood osteoporosis conditions, osteomalacia, or other disorders of bone metabolism. This would include patients diagnosed with anorexia nervosa and those who are on chronic drug therapy that causes drug-induced osteoporosis/osteomalacia and/or affects vitamin D metabolism, such as systemic corticosteroids and any anticonvulsants. 

Pyridoxine [Vitamin B ] [Vitamin B Supplement] U e Rx prevention of vit B6 deficiency Action Vit supl Dose Adults. Deficiency 10-20 mg/d PO Drug-induced neuritis 100-200 mg/d 25-100 mg/d prophylaxis Peds. 5-25 mg/d x 3 wk Caution [A (C if doses exceed RDA), +] Contra Component aUCTgy Disp Tabs 25, 50, 100 mg inj 100 mg/mL SE Allergic Rxns, HA, N Interactions -1- Effects OF levodopa, phenobarbital, phenytoin EMS Can be used as an antidote for isoniazid poisoning OD May cause sensory nerve damage (numbness, tingling, reduced sensation) and coordination problems Sxs are usually revised aft stopping pyridoxine symptomatic and supportive... 

CNS toxicity occurs because isoniazid has structural similarities to pyridoxine (vitamin Be) and can inhibit its actions. This toxicity is dose-related and more common in slow acetylators. Manifestations include peripheral neuropathy, optic neuritis, ataxia, psychosis and seizures. The administration of pyridoxine to patients receiving INH does not interfere with the tuberculostatic action of INH but it prevents and can even reverse neuritis. Hematological effects include anaemia which is also responsive to pyridoxine. In some 20% of patients antinuclear antibodies can be detected but only in a minority of these patients drug-induced lupus erythematosus becomes manifest. 

Clinical trials have demonstrated that the use of the bisphosphonates, nasal calcitonin, or human rPTH combined with calcium and vitamin D supplementation is effective in preventing drug-induced osteoporosis. Thus, individuals receiving over the long term any medication that can induce osteomalacia should also take one of these compounds and have periodic bone density determinations. 

Finally, there has been considerable interest in the use of vitamin E to combat EPS, including TD, based on the oxidative-stress hypothesis. A randomized trial of 12 patients receiving supplementary vitamin E and haloperidol versus 12 receiving haloperidol alone revealed that vitamin E had no prophylactic effect on acute drug-induced EPS, nor did it interfere with the antipsychotic s therapeutic efficacy ( 455). 

If anticonvulsants are used, daily folate (1 mg per day) may decrease the risk of neural tube defects and vitamin K (20 mg per day) may prevent drug-induced bleeding. 

Corticosteroids are extremely useful in elderly patients who cannot tolerate full doses of NSAIDs. However, they consistently cause a dose- and duration-related increase in osteoporosis, an especially hazardous toxic effect in the elderly. It is not certain whether this drug-induced effect can be reduced by increased calcium and vitamin D intake, but it would be prudent to consider these agents (and bisphosphonates if osteoporosis is already present) and to encourage frequent exercise in any patient taking corticosteroids. 

Compared with healthy controls, 51 patients with epilepsy taking a variety of antiepileptic drugs (mostly carbamaze-pine) had higher mean plasma concentrations of homocysteine (130). This effect, which could be related to reductions in the concentrations of folate and vitamin B6, was likely to be drug-induced, but a causative role of the underlying disease could not be excluded. Although homocysteine is an experimental convulsant and a risk factor for atherosclerosis, the clinical relevance of these findings is uncertain. 

Vitamin E has been shown, in a wide range of studies, to be capable of affording considerable protection to cells exposed to free radical attack, either from pathological or drug-induced sources. In injured nervous tissue, vitamin E probably exerts its protective effect by scavenging free radicals, stabilizing cellular membranes and quenching the cascade of biochemical events that... 

Zhou C, Assem M, Tay JC, et al. Steroid and xenobiotic receptor and vitamin D receptor crosstalk mediates CYP24 expression and drug-induced osteomalacia. J Clin Invest 2006 116(6) 1703-1712. 

J2. Jounela, A. J., Pirttiaho, H., and Palva, P, Drug induced malabsorption of vitamin B12. 

This chapter considers primarily those prescription drugs that have been frequently implicated in OADRs. Some of the common OADRs noted in vitamin and herbal supplements are listed toward the end of the chapter. Clinically important drug effects are categorized in the ocular structure or fimction affected rather than in specific drug classes. A comprehensive review chart at the end of the chapter serves as a reference and study guide (Appendix 35-1). Recommendations for eye care practitioners for reporting suspected drug-induced ocular adverse effects are reviewed. 

Hemorrhagic states have been induced by rifampicin in pregnant women and their offspring because of drug-induced hepatic breakdown of vitamin K (39). 

All the cobalamins have the same pattern of adverse reactions. The adverse effects of high doses of cobalamins include urticaria, eczematous and exanthematous skin lesions, and anaphylactic reactions (SEDA-4, 265), but it is not clear whether the reactions are caused by the drug itself, a preservative, or possibly by contaminants. High oral or parenteral doses of vitamin Be and especially hydroxocobalamin are also on rare occasions suspected to induce acne which is, however, always benign (SEDA-5, 347) (1). Several cases of vitamin Bi2-induced folliculitis and acneiform eruptions have been described, in one case in connection with a patient receiving total parenteral nutrition (2). 

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