1/10. Fits, pyridoxine, and hyperprolinaemia type II.The rare inherited disorder hyperprolinaemia type II presents with fits in childhood, usually precipitated by infection. A diagnosis of hyperprolinaemia type II and vitamin B(6) deficiency was made in a well nourished child with fits. It is thought that pyridoxine deficiency was implicated in her fits and was the result of inactivation of the vitamin by the proline metabolite, pyrroline-5-carboxylate.- - - - - - - - - - ranking = 1keywords = deficiency (Clic here for more details about this article) |
2/10. Neonatal pyridoxine responsive convulsions due to isoniazid therapy.A 17-day-old infant on isoniazid therapy 13 mg/kg daily from birth because of maternal tuberculosis was admitted after 4 days of clonic fits. No underlying infective or biochemical cause could be found. The fits ceased within 4 hours of administering intramuscular pyridoxine, suggesting an aetiology of pyridoxine deficiency secondary to isoniazid medication.- - - - - - - - - - ranking = 0.5keywords = deficiency (Clic here for more details about this article) |
3/10. Interrelationships between the B-vitamins in B12-deficiency neuromyelopathy. A possible malabsorption-malnutrition syndrome.Five patients presenting clinically with a form B12-deficiency neuromyelopathy, with cord involvement in all and proximal muscle weakness in two of them, were investigated for their neurologic, hematologic and vitamin status. Megaloblastosis and achlorhydria were present in all, and impaired absorption of 57Co vitamin B12 and of D-xylose was detected in four. Total cyanide extracted vitamin B12 (A) was lowered in all cases and noncyanide extractable (B) in four of the five, being zero in three. All five responded to injections of hydroxocobalamin. In two patients sequential estimations showed that both A and B, especially the latter, rose steeply initially, normalizing at 50% of A after some weeks. Moiety B is suggested to be physiologically the more active and dissociable form of vitamin B12. Markedly elevated initial serum folate levels, and their subsequent fall under treatment with B12, indicated the operation of the "methyltetrahydrofolate trap". blood levels of thiamin, nicotinic acid and pantothenic acid were within normal limits. However, serum riboflavin (B2) total vitamin B6 and pyridoxal were reduced in all where tested. Vitamin B6 deficiency could have resulted from its own malabsorption and have contributed to be B12 deficiency. Vitamin B2 and B6 levels also corrected themselves on B12 therapy. The B-vitamin deficiencies in our patients probably resulted from intestinal malabsorption, with a possible factor of malnutrition consequent to their strictly vegetarian diet.- - - - - - - - - - ranking = 3.5keywords = deficiency (Clic here for more details about this article) |
4/10. Vitamin B6 deficiency in patients with a clinical syndrome including the carpal tunnel defect. Biochemical and clinical response to therapy with pyridoxine.Ten individuals having a severe clinical status associated with the carpal tunnel syndrome were selected for treatment with pyridoxine. The status of vitamin B6, as pyridoxal phosphate, was determined by the specific activities of the glutamic oxaloacetic transaminase of the erythrocytes (EGOT). Before treatment, the patients showed a deficiency of vitamin B6 as determined by 1) a comparison of the specific activities of EGOT with those of a control group (P less than 0.001); and 2) a differential assay based upon the principle of unsaturation and saturation of a Coenzyme-Apoenzyme System (CAS), as applied to EGOT. These patients were treated with pyridoxine, and the specific activities of EGOT were determined after 2 and 4 weeks. Not only was there a disappearance of the deficiency of pyridoxal phosphate, but the level of EGOT activity increased 55-68% during 2-4 weeks, respectively. More apoenzyme was apparently biosynthesized, because the specific activities were significantly higher than before therapy (P less than 0.001/4 wks). Clinical evaluation showed a great improvement in their status, and anticipated surgery for some of the patients became unnecessary. It is concluded that patients with a severe syndrome including the carpal tunnel defect have a deficiency of vitamin B6, and that both the syndrome and the deficiency are relived by therapy with pyridoxine.- - - - - - - - - - ranking = 4keywords = deficiency (Clic here for more details about this article) |
5/10. Electrocardiographic changes due to pyridoxine deficiency.A young woman presented with marked alterations in the ECG without cardiological symptoms or evidence of structural heart disease after further evaluation. There was evidence of vitamin deficiency and the ECG normalized after 10 days of treatment with vitamins. Similar alterations have been described in several experimental studies with rats, but this is the first case reported in humans.- - - - - - - - - - ranking = 2.5keywords = deficiency (Clic here for more details about this article) |
6/10. Clinical results of a cross-over treatment with pyridoxine and placebo of the carpal tunnel syndrome.Clinical evaluation was made of cross-over treatments by pyridoxine and a placebo of patient 22 having the carpal tunnel syndrome. Extraordinary monitoring of the specific activities of the erythrocyte glutamic oxaloacetic transaminase proved a severe vitamin B6 deficiency, which was partially corrected by the Recommended Dietary Allowance of 2 mg, and completely corrected by 100 mg. The severity of the syndrome diminished on the recommended dietary allowances and the patient was asymptomatic at the higher dosage. On placebo, both the vitamin B6 deficiency and syndrome reappeared. retreatment with 100 mg again corrected both the deficiency and syndrome. Measurements (total n = 19) of flexion of proximal interphalangeal joints of the index fingers by a goniometer, and of pinch by the Preston gauge revealed objective normalization. Scores of 17 symptoms revealed reductions at both the 2- (P less than 0.01) and 100-mg (P less than 0.001) dosages. Conduction through the carpal tunnels had improved by electromyography. These and previous data on a total of 22 patients showed the concomitant presence of a deficiency of vitamin B6 and the carpal tunnel syndrome; a causal relationship is apparent.- - - - - - - - - - ranking = 2keywords = deficiency (Clic here for more details about this article) |
7/10. Vitamin B6 status and static muscle function. 2 case reports.2 young adult females, identified as vitamin B6 deficient based on xanthurenic acid excretion levels following a loading dose of tryptophan, were tested twice during each of 3 menstrual cycles for static muscle strength and endurance of the handgrip muscles. During each of the last 2 cycles either a 25-mg dose of pyridoxine hydrochloride or a placebo were administered daily in the double-blind fashion. Measurement of 24-hour xanthurenic acid and 4-pyridoxic acid excretion levels indicated correction of the biochemical indicators of vitamin B6 deficiency. Results of the tests of static muscle strength and endurance indicated no substantial improvement following vitamin B6 supplementation.- - - - - - - - - - ranking = 0.5keywords = deficiency (Clic here for more details about this article) |
8/10. pyridoxine deficiency and peripheral neuropathy associated with long-term phenelzine therapy.A 51-year-old, nonalcoholic, nondiabetic woman with sensorimotor peripheral neuropathy and pyridoxine deficiency associated with long-term phenelzine therapy is described. Since phenelzine, like hydralazine and isoniazid, is a hydrazine capable of reducing pyridoxine levels in the rat, it is suggested that phenelzine, like hydralazine and isoniazid, may cause a pyridoxine-responsive peripheral neuropathy in humans.- - - - - - - - - - ranking = 2.5keywords = deficiency (Clic here for more details about this article) |
9/10. pyridoxine deficiency with phenelzine.pyridoxine (vitamin B6) deficiency developed in two young men treated with phenelzine. Alleviation of symptoms possibly associated with this deficiency and correction of subnormal serum B6 levels occurred with the administration of pyridoxine. With the increased use of phenelzine, all physicians should be alert to this potential problem and instruct patients to eat an adequate amount of foods containing B6. If untoward reactions occur during phenelzine treatment, B6 deficiency should be considered.- - - - - - - - - - ranking = 3.5keywords = deficiency (Clic here for more details about this article) |
10/10. isoniazid-induced neurotoxicity in chronic dialysis patients: report of three cases and a review of the literature.This report describes an increased incidence of neurotoxic side effects secondary to isoniazid therapy in patients with end-stage renal disease. Toxicity was observed only in those patients receiving pyridoxine supplements of less than 100 mg/day. The increased sensitivity of the dialysis population to isoniazid neurotoxicity is predominantly due to abnormal metabolism of pyridoxine resulting in low serum levels of the active metabolite, pyridoxal phosphate. In addition, there is rapid clearance of pyridoxal phosphate by hemodialysis, resulting in a severer deficiency of this active metabolite. In order to prevent the neurotoxicity associated with isoniazid therapy, we recommend that 100 mg/day of pyridoxine be given as a supplement to hemodialysis patients requiring isoniazid therapy.- - - - - - - - - - ranking = 0.5keywords = deficiency (Clic here for more details about this article) |
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