Pyridoxine induced deficiency

Pyridoxine deficiency has been induced by administration of desoxy-pyridoxine to adults receiving a diet low in B complex vitamins. Seborrheic skin lesions developed about the eyes, nose, and mouth, and cheilosis, glossitis, and stomatitis were observed. Although these findings resemble those commonly seen in riboflavin and niacin deficiency, healing was dependent on administration of pyridoxine. The deficient subjects excreted large amounts of xanthurenic acid in the urine after a test dose of tryptophan, but ability to convert tryptophan to niacin was unimpaired. 

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... 

Pyridoxine is indicated in vitamin B deficiency, for the treatment of some pyridoxine responsive anemia s and for isoniazid-induced neuropathy. It may relieve symptoms of pellagra when niacin fails. Long-term administration of large doses may produce neurotoxicity manifesting itself in progressive peripheral sensory neuropathy. 

Although the MAOIs can have serious and potentially life-threatening adverse effects, it is the more common and less dramatic side effects that often lead to the discontinuation of MAOIs. These side effects include orthostatic hypotension, drowsiness, insomnia, edema, weight gain, sexual dysfunction, and precipitation of mania. Rare side effects include hepatitis and leukopenia. Parasthesias may develop secondary to a MAOI-induced pyridoxine deficiency, which responds to oral pyridoxine supplementation. Overall, phenelzine appears to be more sedating, whereas trancylpromine is more activating because of its stimulant-like properties. Meclobomide has more excitatory side effects, such as restlessness and insomnia. 

Isoniazid (isonicotinic acid hydrazide), a drug frequently used to treat tuberculosis, can induce a B6 deficiency by forming an iiactive derivative with pyridoxal phosphate. Dietary supplementation with B is, thus, an adjunct to isoniazide treatment. Otherwise, cletary deficiencies in pyridoxine are rare but have been observed in newborn infants fed formulas low in vitamin B6, in women taking oral contraceptives, and in alcoholics. 

Vitamin B6 (pyridoxine, pyridoxamine, and pyridoxal) has the active form, pyridoxal phosphate. It functions as a cofactor for enzymes, particularly in amino acid metabolism. Deficiency of this vitamin is rare, but causes glossitis and neuropathy. The deficiency can be induced by isoniazid, which causes sensory neuropathy at high doses. 

Excessive central stimulation, usually exhibited as tremors, insomnia and hyperhidrosis, can occur following therapeutic doses of the MAOIs, as can agitation and hypo manic episodes. Peripheral neuropathy, which is largely restricted to the hydrazine type of MAOI, is rare and has been attributed to a drug-induced pyridoxine deficiency. Such side effects as dizziness and vertigo (presumably associated with hypotension), headache, inhibition of ejaculation (which is often also a problem with the TCAs), fatigue, dry mouth and constipation have also been reported. These side effects appear to be more frequently associated with phenelzine use. They are not associated with any antimuscarinic properties of the drug but presumably arise from the enhanced peripheral sympathetic activity which the MAOIs cause. 

Pyridoxine was commenced to prevent any isoniazid-induced peripheral neuropathy, particularly as the patient was a vegetarian of Asian ethnicity and prone to this vitamin deficiency. 

Stewart JW, Harrison W, Quitkin F, Liebowitz MR. Phenelzine-induced pyridoxine deficiency. J Clin Psychopharmacol 1984 4(4) 225-6. 

When pyridoxine deficiency is induced in pregnant rats, spontaneous convulsions are seen in the offspring at 3-4 days of age. Seizures are of short duration. 

COMMENT Deficiency is rare, as B is so common in foods. Isoiazid, an antituberculosis drug, can interfere with B6 and induce symptoms of Be, deficiency. As pyridoxine is necessary in the steps that convert tryptophan to niacin (1-8), a deficiency of Be may result in niacin defi ciency. 

Faber et al. (FI) studied the effects of induced pyridoxine and pantothenic acid deficiency, obtained by use of a semisynthetic formula and deoxypyridoxine and co-methyl pantothenic acid supplements for six weeks, by determining in 5 men nitrogen retention and the urinary excretions of xanthurenic and oxalic acids during deficiency and recovery. They postulated that tissue catabolism releases suflBcient pyri-doxine to partially metabolize a tryptophan load, after which the amounts of urinary oxalic acid were sharply increased for 1-2 days. 

G9. Glazer, H. S., Mueller, J. F., Thompson, C., Hawkins, V. R., and Vilter, R. W., A study of urinary excretion of xanthurenic acid and other tryptophan metabolites in human beings with pyridoxine deficiency induced by desoxypyridoxine. Arch. Bio-chem. Biophys. 33, 243-251 (1951). 

Up to 30% of ingested zinc is absorbed from the small intestine however, a homeostatic mechanism controls the absorption. Nutritional status also influences zinc absorption deficiency of pyridoxine or tryptophan somewhat inhibits absorption. Zinc induces a zinc metallothionein, the form in which it is bound to the liver and other tissues. The pancreas is high in zinc, and in males the prostate gland contains the greatest store of zinc. Zinc is excreted in the feces. 

In rats fed a diet adequate in vitamin Bg, the fraction of total pyridoxal phosphate found in the nuclei of liver cells was 21%, and this increased to 39% in rats fed a vitamin Bg-deflcient diet, indicating a conservation of the vitamin in the nuclear compartment during deficiency. Pyridoxal phosphate in the cell nucleus is protein bound, and this protein has an apparent molecular mass of 50 to 55 kDa. Cells grown in the presence of 5 mM pyridoxine have a decreased glucocorticoid-dependent induction of enzymes such as tyrosine aminotransferase. Vitamin Bg regulates transcriptional activation of human glucocorticoid receptors in the HeLa cells. The modulatory role in transcription is not restricted to the glucocorticoid receptor but extends to other members of the steroid hormone super family. The intracellular concentration of PLP could have a profound influence on steroid hormone-induced... 

S.K. Sharma, B. Bolster, and K. Dakshinamurti. Picrotoxin and pentylene tetrazole induces seizure activity in pyridoxine-deficient rats. J. Neurolog. Sci. 121 1-9 (1994). 

Fears have been expressed [510, 511] that long-term administration of L-dopa may induce a state of pyridoxine deficiency, since excess dietary pyridoxine, which is rapidly converted in vivo to the decarboxylase coenzyme pyridoxine-5 -phosphate [512], can nullify the beneficial effects of the amino acid [513-515]. Pyridoxine apparently both complexes with L-dopa and produces an accelerated decarboxylation of the amino acid in extracerebral tissues, both processes effectively reducing the amount of available dopamine in the striatum [512, 516]. The decarboxylase inhibitor MK-485 (37) prevents this reversal of the therapeutic effect by pyridoxine [517] and, more significantly, pyridoxine actually enhances the effects of L-dopa when given in conjunction with such an inhibitor [518]. The mechanism involved in this potentiation reflects enhancement by pyridoxine of dopa decarboxylase activity within the striatum in the presence of complete inhibition of extracerebral decarboxylase. The use of combinations of L-dopa, pyridoxine, and inhibitors of aromatic L-amino-acid decarboxylase, may lead to a more... 

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