Acquired hypochromic and microcytic sideroblastic anaemia responsive to pyridoxine with low value of free erythrocyte protoporphyrin: a possible subgroup of idiopathic acquired sideroblastic anaemia (IASA)

Patients with idiopathic acquired sideroblastic anaemia (IASA) usually show macrocytic or normocytic anaemia and increased free erythrocyte protoporphyrin (FEP). The mean cell haemoglobin concentration is normal or slightly low. Here we report a pyridoxine-responsive IASA patient with microcytic and hypochromic anaemia and low FEL level; these features are usually seen in cases of hereditary sideroblastic anaemia. Microcytosis increased during therapy.
There may be a subgroup of IASA with microcytic and hypochromic anaemia, low normal FEP and some response to pyridoxine like hereditary sideroblastic anaemia.     

Photoallergic Drug Eruption Due to Pyridoxine Hydrochloride

Photoallergy to vitamin B₆ is very rare; only a few cases of contact dermatitis and one case of photosensitive dermatitis due to pyritinol have been reported. We report here the first case of photoallergy drug eruption due to pyridoxine hydrochloride. A 71-year-old man developed papulo-squamous erythemata which were confined to sun-exposed sites. Photopatch testing, together with the clinical course, was helpful in reaching the initial diagnosis; this was confirmed by an oral challenge test. Photoallergic drug eruption due to vitamin B₆ should be considered a rare cause of photosensitive dermatitis.     

Effect of avitaminosis B6 in mice on T-lymphocyte function in vitro

The effect of different degrees of avitaminosis B₆ in mice on the cytolytic activity of T lymphocytes, measured as the quantity of Na₂Cr⁵¹O₄ released from lysed target cells, was studied on a model of the primary immune response in a mixed lymphocyte culture in vitro. Keeping animals for 3 weeks on a diet without pyridoxine did not affect the ability of the lymphocytes to proliferate in vitro or their cytolytic activity. In animals receiving a diet without pyridoxine for 45 days the content of pyridoxal-5-phosphate in the spleen was 55% lower than in the control. Lymphocytes taken from these animals, when cultured in vitro, showed sharply weakened ability to incorporate [³H]thymidine into DNA in response to the alloantigen. The cytolytic activity of these lymphocytes also was reduced. The ability of different forms of pyridoxine to restore the functions of T lymphocytes, when disturbed by avitaminosis B₆, was studied.Laboratory of Systemic Blood Diseases, Oncologic Scientific Center, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR N. A. Kraevskii.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 84, No. 8, pp. 185–188, August, 1977.     

Pineal response after pyridoxine test in children

Summary To characterize the pineal response to pyridoxine, plasma melatonin was measured in one hundred and twenty children 3 hours after vitamin B₆ administration. The children, aged between 1.5 and 8 years, were divided in four groups as follows: a) control day group, grouping 27 children sampled at 9:00 and at 12:00; b) control night group, grouping 29 children sampled at 21:00 and at 24:00; c) pyridoxine day group, grouping 30 children sampled at 9:00, then intravenously (i.v.) injected with 3mg/kg of pyridoxine, and sampled at 12:00; and d) pyridoxine night group, grouping 34 children sampled at 21:00, i.v. injected with 3mg/kg of pyridoxine, and sampled at 24:00. Melatonin concentration was measured by radioimmuno assay. The data obtained showed a significant increase in melatonin levels after pyridoxine administration in the pyridoxine night group (39.87 ± 8.02pg/ml basal vs 88.45 ± 9.21 pg/ml after pyridoxine, p < 0.001). The other groups did not showed significant differences in melatonin concentrations. Statistical analysis shows that the administration of pyridoxine during the nocturnal hours represents a stimulating factor to increase the pineal production of melatonin in children.     

Coma caused by isoniazid poisoning in a patient treated with pyridoxine and hemodialysis

Isoniazid is widely used to treat tuberculosis. In populations with a high prevalence rate of tuberculosis, acute ingestion of isoniazid has been reported as a potential cause of coma. In this study, we present the diagnosis and treatment of isoniazid poisoning in a case with acute coma as the major clinical presentation.A 32-year-old male who ingested 12 g isoniazid (2 hours prior to medical attention) was brought to the emergency department while in a coma and experiencing frequent seizures. Initial treatment with large doses of pyridoxine (for 6 hours) failed to awaken this patient. The patient was then given hemodialysis and pyridoxine; after 3 days he awoke from coma, with no further reported seizures.Isoniazid poisoning should be suspected in patients whose major symptoms are coma and seizure, especially those who have access to isoniazid. Monitoring the blood level of isoniazid will establish the diagnosis and help clinical management. A combination of hemodialysis and pyridoxine is effective in treating isoniazid poisoning.     

VITAMIN B6 TOXICITY: A NEW MEGAVITAMIN SYNDROME

Seven young adults developed ataxia and sensory nervous system dysfunction after daily ingestion of 2–6 grams of pyridoxine for 2 to 40 months.     

Effect of pyridoxine deficiency on the exploratory behavior of rats

Malnutrition early in life impairs the development of brain as well as behavior. In the present study the behavioral effects of preweaning pyridoxine deficiency in rats, as reflected by their exploratory score, have been investigated. The results clearly indicated that the body weight of pyridoxine-deficient rats was significantly less when compared to the control rats. Besides this, the sign of maturation of sensory perceptual mechanisms like the first day of eye opening and signs of maturation of neuromotor coordination like the day of supported standing are delayed in vitamin-deficient rats. The open-field activity reflected by the exploratory score was observed to be significantly less in vitamin-deficient rats. In short, considerable effects of prenatal pyridoxine deficiency were observed in the neonatal pups as stunting of growth and in the delayed onset of neuromotor coordination as well as a low level of open-field activity. The importance of maternal pyridoxine supplementation during pregnancy has been emphasized.