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At least 19 recordsLinked to original sources
PubMed1975

[Vitamin B 6 deficiency anemia].

The course of spontaneous vitamin B6 deficiency anemia in a 57-year-old woman is reported. The anemia was characterized by hypochromasia of the erythrocytes, hyperferricemia, absence of hemolysis, and hyperplastic, ineffective, sideroblastic erythropoiesis of the bone marrow. It was corrected by oral vitamin B6 therapy. On interruption of the vitamin B6 therapy the anemia relapsed. On resumption of vitamin B6 medication it responded again with normalization of the hemoglobin and erythrocytes values. The hematological remission could be maintained under longterm vitamin B6 medication. The nosological significant of this rare anemia and its differentiation from other forms of anemia are discussed.

Anemia, Hypochromic↗
PubMed1977

[Influence of vitamin B 6 deficiency in early weaned piglets on the digestibility and conversion of protein and energy].

Early-weaned piglets were subjected during 2 metabolic periods (11th-18th and 32nd-39th days of the experiment) to conversion experiments to study the influence of vitamin B6 depletion on the digestibility of the crude nutrients, metabolizable energy and on nitrogen conversion using the difference procedure. The depleted piglets (0.4 mg vitamin B6/kh diet) and the pair-fed control animals raised under equal conditions (6.5 mg vitamin B6/kh diet) were first fed a pre-starter ration, and from the 24th experimental day, a starter feed. As the period of depletion increased, the vitamin B6 sub-provided piglets revealed deficiency symptoms such as reduced appetite, lethargic behaviour and less movement. Whilst in the first half of the experiment the control animals reached significantly higher weight gains at lower expenditure of dry matter and digestible energy per kg of weight gain, no differences were observed between both groups in the second period. On the other hand, during the 1st metabolic period the digestibility of all crude nutrients and energy in the depleted piglets proved slightly, but significantly higher than in the pair-fed control animals. In the second half of the experiment ther were just casual differences. After a 2-week vitamin B6 deficient nutrition, the piglets had a 4.1% lower nitrogen retention as compared with the pair-fed control. After a depletion period of 5 weeks, this difference reached 14.4%. As nitrogen excretion in the urine increased, a higher renal energy excretion was observed. Thus the vitamin B6 deficient animals had available less metabolizable energy (in % of digestible energy) than the control piglets.

Animal Feed↗
PubMed1976

[Secondary cystathioninuria due to vitamin B 6 deficiency in familial neuroblastoma].

In this study numerous amino acid analyses were performed in a family with increased incidence of tumors of the sympathetic nervous system. Since in 9 respectively 10 of a total of 13 surveyed persons an elevated urinary excretion of cystathionine was demonstrated with thin layer and column chromatographic methods, this constitutes the first report on cystathioninuria in familial neuroblastoma. Two family members also presented a homocystinuria in the spontaneously voided 24-hours urine. The only person whose plasma amino acids were analysed showed nearly normal levels. After oral loading with L-methionine the urinary excretion of cystathionine raised considerably. The different reaction of the two vitamin B6-dependent enzymes, cystathionine-synthetase and cystathionase, points at a different methionine induced sensitivity. The determination of pyridoxal phosphate and pyridoxal kinase detected a vitamin B6-deficiency, which corresponded well with an increased excretion of oxalic acid and a low normal urinary taurin excretion. Therefore these alterations of the amino acids are explained and thus urinary excretion of cystathionine can be interpreted as secondary cystathioninuria. Furthermore it was possible to provoke corresponding biochemical changes by oral administration of vitamin B6 such as reduction of the cystathioninuria and disappearance of the homocystinuria. In an infant the cystathioninuria could be observed over a period for 5 months, by which a transitory deficiency of the apoenzyme appears to be unlikely. The analysis of 24 hours urine samples of a gravida showed the persistance of cystathioninuria also during pregnancy. After radiation of a 5 year old girl with ganglioneuroblastoma an increase of the urinary cystathionine excretion and a first occurrence of homocystinuria was noted. These observations give rise to various considerations. The vitamin-B6-deficiency in familial neuroblastoma supports the assumption, that also the cystathioninuria in nonhereditary cases may be caused by vitamin-B6-deficiency. Since in this family the excretion of catecholamines was examined in a prior investigation a comparison of these two studies does not support the suggestion of a direct connection between the excretion of catecholamines and cystathioninuria, as it has been assumed to occur in sporadic neuroblastoma. The vitamin-B6-deficiency as seen in this family can also be considered in relation to tumor development. In the discussion about this possibility also the appearance of cystathioninuria in other tumors of early childhood is mentioned. Furthermore the relation of vitamin B6 to teratogenesis is commented on.

Child, Preschool↗
PubMedDate not supplied

Vitamin metabolism and therapy in ophthalmology.

Vitamin deficiency states are important in the genesis of many ocular disorders. Deficiencies may be due to poor dietary intake, or to alterations in metabolism produced by some commonly prescribed medications or by certain diseases. Furthermore, some vitamins may exert important pharmacologic effects on the normal eye. The ocular effects of deficiencies and excesses of specific vitamins, and the therapeutic uses of each vitamin, are reviewed.

Animals↗
PubMed1975

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.

Achlorhydria↗
PubMed1976

Biochemical assessment of the nutritional status of low-income pregnant women of Mexican descent.

Biochemical parameters of nutritional status were investigated in 300 women of Mexican descent during the first and second trimesters of pregnancy. Blood samples were obtained from the women during clinic visits, and measurements were made of serum iron, hemoglobin, hematocrit, serum protein, and transferrin saturation. Additionally, the nutritional status of seven vitamins was determined either by direct assay of the vitamin levels in blood or by measurement of erythrocyte enzyme stimulation. Thiamin and riboflavin were also determined in causal urine samples. Very few women, 8% or less, were classified as being low or deficient in hemoglobin, serum protein, iron, transferrin saturation, vitamin C, carotene, vitamin A, or vitamin B12. Thirty-one percent had low or deficient hematocrit values according to the guidelines used. Folic acid was the most prevalent vitamin deficiency, with 69% of the women having low or deficient serum levels. Based on the erythrocyte enzyme stimulation tests, 22% of the women were low or deficient in thiamin, 29% were low or deficient in riboflavin, and 9% were deficient in pyridoxine. None of the women had a low urinary excretion of thiamin, but 8% had excretion values of riboflavin below the acceptable level. Fewer deficiencies of thiamin and serum folic acid were observed in women taking vitamin and mineral supplements than in those who were not.

Adolescent↗
PubMed1977

Influence of norethindrone on drug-metabolizing enzymes of female rat liver in various B-vitamin deficiency states.

Ingestion of high levels of thiamin significantly decreased the activity of cytochrome P-450, NADPH cytochrome c reductase, and the metabolism of aniline and ethylmorphine. Apparent VmaxS for ethylmorphine N-demethylase and aniline hydroxylase were decreased by high levels of riboflavin even though NADPH cytochrome c reductase was elevated. High levels of dietary pyridoxine significantly decreased only the Vmax for aniline hydroxylase. Generally, norethindrone produces either no change or slight depression of cytochrome P-450 regardless or diet, whereas the administration of norethindrone produced no change or an increase in activity of c reductase and ethylmorphine N-demethylase. Norethindrone induces aniline hydroxylase in animals fed all diets except those deficient in thiamin and riboflavin. The activities of the four parameters of the drug metabolizing system measured in these studies as well as the effects of norethindrone are clearly affected by the dietary status of the animal.

Aniline Hydroxylase↗
PubMed1975

Nutrition and experimental carcinogenesis: a review.

Restriction of the total diet or the number of calories fed to rats and mice inhibits the formation of tumors in several tissues. Unless animals are fed equivalent levels of food, or attain equivalent body weights, it is difficult to assess the significance of the effect of other nutritional modifications on carcinogenesis. The effects of altering the levels of protein or fat are much less than those seen with dietary restriction. Feeding a protein-free diet is tolerated for a limited period and can alter the metabolism of carcinogens. It may thus affect the tumor incidence induced by one-shot carcinogens. Vitamins have specific effects on the activity of certain carcinogens, the fullest information being available for vitamin A, which has been shown to inhibit or enhance carcinogenesis, and vitamin C, which by reducing sodium nitrite, prevents nitrosation of secondary and tertiary amines occurring in acidic conditions of the stomach. Inorganic substances, such as iodine (thyroid) and copper (liver), may affect the tumor incidence in specific tissues. The metabolic activation of carcinogens is modified by enzyme induction and the administration of antioxidants. The relevance of these results to the induction of cancer in humans is briefly discussed.

Animals↗
PubMed1975

Oral contraceptives and vitamins: a review.

The literature concerning the influence of estrogen-containing oral contraceptives on vitamins is reviewed. The appearance of an elevated plasma concentration of vitamin A is probably without clinical importance, while there seems to be a clear connection between disturbances of vitamin B6 metabolism and mental symptoms. Low levels of folic acid and vitamin B12 have also been noted. Despite this, it is very rare that hematologic abnormalities develop during hormonal contraception. A reduced concentration of vitamin C in plasma and blood corpuscles has been reported. The clinical significance of these alterations is unknown.

Ascorbic Acid↗
PubMed1979

Drugs and vitamin deficiency.

During the past 10 to 20 years it has become increasingly clear that a certain number of drugs may lead to increased vitamin requirements. However, it is unusual for symptomatic avitaminosis to develop, and then only when circumstances are present which in themselves increase the risk of vitamin deficiency. Therapeutic doses of drugs will interfere with the vitamin status only to a restricted degree, provided they are administered for brief periods and to patients receiving a normal supply of vitamins. Most cases of vitamin deficiency have in fact been described in connection with drugs usually taken for a longer period of time by patients who were already in negative vitamin balance as a result of disease or marginal supply of the necessary vitamins. This review describes some of the more important articles covering this topic.

Ascorbic Acid Deficiency↗