Production of Microcytic Hypochromic Anemia in Puppies on Synthetic Diet Deficient in Rat Antidermatitis Factor (Vitamin B6)

1938 ◽  
Vol 16 (2) ◽  
pp. 197-207 ◽  
Author(s):  
Paul J. Fouts ◽  
O. M. Helmer ◽  
S. Lepkovsky ◽  
T. H. Jukes
Blood ◽  
1961 ◽  
Vol 17 (5) ◽  
pp. 547-561 ◽  
Author(s):  
LUIS SANCHEZ MEDAL ◽  
JORGE ELIZONDO ◽  
JESUS TORRES GALLARDO ◽  
CARLOS GITTLER

Abstract The clinical and laboratory findings in two brothers with severe anemia are presented. These findings were very similar in both cases. Evidence that at least one of them suffered from a pyridoxine-responsive anemia is presented. It was assumed that the other had the same disorder since, in addition to the striking similarity in the clinical and laboratory abnormalities, the latter’s anemia disappeared completely with the parenteral administration of vitamin B complex, which provided him with 2 mg. of pyridoxine daily. These patients have not relapsed 1.5 and 6 years after stopping the therapy. A review of the reported cases with anemia responding to vitamin B6 administration is presented. Common factors observed in some of these cases are: (1) severe anemia, microcytic and hypochromic in type, chiefly due to a striking maturation erythroblastic arrest at the basophilic stage with no defect in leukocytes or thrombocytes; (2) hyperferremia and hemosiderosis; (3) an abnormal tryptophan-loading test; and (4) complete or almost complete correction of all abnormalities with administration of vitamin B6, even at small doses. These data were considered to suggest that the patients had a true deficiency in pyridoxine. In other patients, no increased excretion of xanthurenic acid has been observed after a tryptophan-loading dose, and pyridoxine administration has improved the anemia only partially and has not reversed the serum iron parameters to normality. All of these other patients suffered from a familial hypochromic anemia not due to iron deficiency or from a "sidero-achrestic" or "refractory normoblastic" anemia. The cause of the disorder in patients in the first group is unknown, but, by exclusion, increased requirement of vitamin B6 seems to be the most likely possibility.


Blood ◽  
1962 ◽  
Vol 19 (3) ◽  
pp. 304-312 ◽  
Author(s):  
JOHN N. BICKERS ◽  
CHARLES L. BROWN ◽  
CHARLES C. SPRAGUE ◽  
Katherine Karst

Abstract A patient is reported with pyridoxine responsive anemia superimposed upon a chronic hypochromic anemia with excess iron storage. A specific response to pyridoxine was demonstrated on several occasions with restoration of the blood picture to its original state. Dietary estimates of vitamin B6 intake demonstrated an increased requirement for the vitamin, approximately 2.5 mg. per day being required for hematologic remission. Splenectomy was followed by high circulating siderocyte levels and severe thromboembolic problems. The possible mechanisms for the development of pyridoxine responsive anemia are discussed briefly.


Author(s):  
V.J. Montpetit ◽  
S. Dancea ◽  
L. Tryphonas ◽  
D.F. Clapin

Very large doses of pyridoxine (vitamin B6) are neurotoxic in humans, selectively affecting the peripheral sensory nerves. We have undertaken a study of the morphological and biochemical aspects of pyridoxine neurotoxicity in an animal model system. Early morphological changes in dorsal root ganglia (DRG) associated with pyridoxine megadoses include proliferation of neurofilaments, ribosomes, rough endoplasmic reticulum, and Golgi complexes. We present in this report evidence of the formation of unique aggregates of microtubules and membranes in the proximal processes of DRG which are induced by high levels of pyridoxine.


2018 ◽  
Vol 88 (1-2) ◽  
pp. 80-89 ◽  
Author(s):  
Zahra Shakibay Novin ◽  
Saeed Ghavamzadeh ◽  
Alireza Mehdizadeh

Abstract. Branched chain amino acids (BCAA), with vitamin B6 have been reported to improve fat metabolism and muscle synthesis. We hypothesized that supplementation with BCAA and vitamin B6 would result in more weight loss and improve body composition and blood markers related to cardiovascular diseases. Our aim was to determine whether the mentioned supplementation would affect weight loss, body composition, and cardiovascular risk factors during weight loss intervention. To this end, we performed a placebo-controlled randomized clinical trial in 42 overweight and obese women (BMI = 25–34.9 kg/m2). Taking a four-week moderate deficit calorie diet (–500 kcal/day), participants were randomized to receive BCAA (6 g/day) with vitamin B6 (40 mg/day) or placebo. Body composition variables measured with the use of bioelectrical impedance analysis, homeostatic model assessment, and plasma insulin, Low density lipoprotein, High density lipoprotein, Total Cholesterol, Triglyceride, and fasting blood sugar were measured. The result indicated that, weight loss was not significantly affected by BCAA and vitamin B6 supplementation (–2.43 ± 1.02 kg) or placebo (–1.64 ± 1.48 kg). However, significant time × treatment interactions in waist to hip ratio (P = 0.005), left leg lean (P = 0.004) and right leg lean (P = 0.023) were observed. Overall, supplementation with BCAA and vitamin B6 could preserve legs lean and also attenuated waist to hip ratio.


2007 ◽  
Vol 37 (23) ◽  
pp. 30
Author(s):  
SHERRY BOSCHERT
Keyword(s):  

2009 ◽  
Vol 09 (05) ◽  
pp. 289-293
Author(s):  
B. Reulecke ◽  
J. Denecke

ZusammenfassungDie Homocystinurie ist eine seltene angeborene Erkrankung des Methioninstoffwechsels, die mit einer pathologischen Erhöhung der nicht proteinogenen Aminosäure Homocystein und der Ausscheidung ihres Disulfids Homocystin über den Urin einhergeht. Mehrere biochemische und genetische Defekte können zu einer deutlichen Homocysteinerhö-hung führen, darunter Störungen des Vita-min-B6-, Folsäure- und Vitamin-B12-Stoffwechsels, sodass der Terminus Homocystinurie eine Erkrankungsgruppe zusammenfasst. Die häufigste Ursache der Homocystinurie, auch klassische Homocystinurie oder Homo-cystinurie Typ I genannt, stellt die hereditäre Cystathionin-β-Synthase-Defizienz dar, die mit einer Erhöhung von Homocystein und Methionin im Blut einhergeht. Die Diagnose wird durch Bestimmung von Homocystein im Plasma gestellt und kann biochemisch und genetisch gesichert werden. Unbehandelt zeigen sich eine erhebliche Morbidität und Mortalität, die durch Ausschöpfung der therapeutischen Optionen, bestehend aus Vitamin B6, Folsäure, Vitamin B12, Betain und einer Proteinrestriktion mit Aminosäuresupplementie-rung, erheblich reduziert werden können.


2018 ◽  
Author(s):  
Martin Hildebrandt ◽  
Kai-Nils Pargac
Keyword(s):  

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