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At least 19 recordsLinked to original sources
PubMed1977

Hemoglobin E and glucose-6-phosphate deficiency in the Khmer Air Force (Cambodia).

This study was designed to investigate the use of primaquine in malaria control in the Khmer Republic (Cambodia). Blood was drawn from 106 male Khmer Air Force troops for analysis of hemoglobin E and glucose-6-phosphate (G-6-PD) deficiency. A test group of 15 men with G-6-PD deficiency and a group of 31 normal controls were given 15 mg of primaquine each morning for 14 days. The patients were followed for hemoglobinuria and changes in hematocrit. Primaquine induced a significant, but not a dangerous, hemolysis in G-6pD-deficient Khmer troops. The G-6-PD deficiency seen in Khmer Air Force subjects was G-6-PD Mahidol. Statistically, G-6-PD Mahidol was linked to hemoglobin E.

Cambodia↗
PubMed1979

[Acute polyneuropathy due to phosphate deficiency during parenteral feeding].

A malnourished M. Crohn-patient developed severe symptoms similar to those of an acute polyneuropathy associated with a period of marked decrease of serum phosphate concentration during intravenous high-caloric infusions. After the serum phosphate concentration was normalized recovery from all neurologic symptoms followed within a few days. Based on this observation the possible consequences of severe hypophosphatemia are discussed.

Adult↗
PubMed2026

Plant genetic and root-associated microbial diversity modulate Lactuca sativa responsiveness to a soil inoculum under phosphate deficiency.

Microbial-based approaches offer a promising strategy to decrease the use of chemical fertilizers in agriculture. Among them, arbuscular mycorrhizal fungi (AMF), which extend root surface area and enhance phosphate uptake, and phosphate-solubilizing bacteria (PSB) are particularly relevant. However, their effectiveness depends strongly on plant genetic diversity. To identify genetic markers underlying plant responses to beneficial soil microbes, we studied a panel of 128 fully sequenced Lactuca sativa varieties under controlled phosphate-starvation conditions and treated with AMF and PSB. Lettuce genetic variation showed a strong effect on physiological and morphological responses to microbial inoculation. Genome-wide association studies identified specific genomic regions associated with changes in leaf phosphate content and shoot biomass following treatment. Beyond genetic factors, we observed shifts in fungal β-diversity and increased bacterial α-diversity associated with phenotypic variation. We also identified 44 amplicon sequence variants associated with agriculturally relevant traits. Among these, six bacterial strains were experimentally validated through in vitro and pot experiments for their effects on leaf phosphate concentration and shoot biomass. Overall, we highlighted key genetic, microbial, and physiological mechanisms that may enhance microbial treatments for improved plant phosphate management in lettuce.

16S and ITS metabarcoding↗
PubMed1978

[Effect of a calcium-deficient, phosphate- or ammonia-rich diet on the development and mineral metabolism of growing miniature pigs].

The metaphylaxis of renal calculi in form of partial withdrawal of Ca and the nutrition rich in phosphate or NH4C1 in children was disputed and not ascertained by animal experiments. For this purpose growing female dwarf pigs got a semisynthetic ration with 1 g Ca and 23 g P, respectively, or 15 g NH4C1 per kg dry feeding mass during 168 days. The dwarf pigs fed poor in Ca had a reduced increase of body-weight of 30%, the pigs fed rich in P and NH4C1 a reduced increase of body-weight of 11 and 16%, respectively, compared with the control dwarf pigs. The feeding regime chosen has no significant influence on the Ca-, P-, Cu-, and Mn-state of the dwarf pigs (alpha greater than 0.05). Only the animals with deficiency of a Ca statistically ascertained stored more Zn in the liver than the control animals. The applied NH4C1 as well as the medicament Ammonchlor SSW contained traces of Cd. Concerning the lacking significant changes of metabolism on account of the retardation of growth conditioned by therapy it cannot be concluded that there is possible a metaphylaxis of the lithiasis in children by partial withdrawal of Ca or additions of P and NH4C1, respectively.

Ammonia↗
PubMed1976

[Increase in the renal calcium-binding protein (CaBPr) in the presence of vitamin D in growing, phosphate deficient rats. Possible role in tubular calcium reabsorption].

Vitamin D-dependent CaBP isolated from Rat renal cortex (rCaBP) was measured in phosphorus-depleted (OP) and control (C) Rats, either vitamin D-deficient (OD) or vitamin D-supplemented (1 or 10 i. u.). A low molecular weight fraction was isolated from renal cortex by "Sephadex G-100" chromatography and rCaBP activity quantitated by saturation analysis using a 45 Ca chelex assay. The results indicated that phosphorus deprivation resulted in the increase in the vitamin D-dependent rCaBP as well as in the intestinal CaBP. As a marked hypercalciuria was noted in all OP Rats and as the rCaBP activity was high in vitamin D-supplemented Rats and hardly detectable in vitamin D-deficient Rats, the implication of the rCaBP in the large hypercalciuria can be definitely ruled out. Furthermore when vitamin D-supplementation ranged from 1 to 10 i. u. vitamin D, while the serum calcium level was increasing a decrease could be noticed in the large hypercalciuria. This deserves to be related to the increase in rCaBP activity. The high CaBP activity probably resulting from the renal synthesis of 1,25-dihydroxycholecalciferol stimulated by phosphorus-deprivation could represent the molecular basis of the calcium tubular reabsorption increased by vitamin D. Thus a vitamin D-dependent protein implicated in an ion-selective transport could be involved in the tubular calcium reabsorption as well as in the intestinal calcium absorption.

Animals↗
PubMed1978

Changes in organic matrix of bone and of bone and blood ATP in rats fed rachitogenic diets.

Vitamin D deficient and phosphate deficient states were produced in young rats by the use of synthetic diets. Whole blood ATP, serum calcium and phosphorus and the ash, phospholipid, hexosamine and hydroxyproline contents of metaphyseal bones of control and rachitic rats were measured after 4 weeks on the diets. There was a decrease in whole blood ATP and serum phosphorus of the rachitic rats, and in the contents of ash, phospholipid and hexosamine of the rachitic metaphyses, while the hydroxyproline contents of the rachitic bones were higher than those of the controls. Subcutaneous injection of ATP or inorganic phosphate in rats, fed a low phosphate diet deficient in vitamin D, caused an increase in serum phosphorus and blood ATP levels and in metaphyseal ash contents. It is suggested that some of the metabolic disturbances in rickets are due to alteration in ATP production.

Adenosine Triphosphate↗
PubMed1976

Long-term management of a case of carbamyl phosphate synthetase deficiency using ketanalogues and hydroxyanalogues of essential amino acids.

A 13-year-old girl with congenital deficiency of carbamyl phosphate synthetase has been treated intermittently for one year with a restricted protein diet supplemented by various mixtures of the alpha-ketoanalogues of valine, leucine, isoleucine, and phenylalanine, the D,L-alpha-hydroxyanalogue of methionine, and five amino acids (lysine, arginine, histidine, threonine and tryptophan). Numerous adjustments in the composition of this mixture were made. Eventually normal levels of plasma ammonia and most amino acids were achieved, with three exceptions: slightly increased glutamine, pronounced alloisoleucinemia, and persistently low phenylalanine. Alloisoleucine was shown not to be incorporated into plasma protein and not to be excreted in the urine; hence this abnormality was viewed as being clinically insiginificant. Hypophenylalaninemia was unexplained, and failed to respond to increased phenylpyruvate dosage or phenylalanine itself; renal clearance of phenylalanine was high but could not account for the low plasma level. Compared to the pretreatment period her clinical status has improved markedly. Physical and mental development has continued at the same rate. Temporary withdrawal of the supplements led to prompt increases in plasma ammonia, glutamine, and alanine. We conclude that this therapy provides safe and effective long-term management for this patient's disorder and may be useful in other cases of congenital hyperammonemia.

Adolescent↗
PubMed1979

Heterozygote detection in glucose-6-phosphate dehydrogenase deficiency: limitation of hair follicle analysis.

Glucose-6-phosphate dehydrogenase deficiency was demonstrated in a case of favism. The X-linked enzyme defect was expressed in erythrocytes but not in hair root cells. Predictably, the mother shown to be a heterozygous carrier on the basis of intermediate erythrocyte glucose-6-phosphate dehydrogenase activity could not be identified as a carrier by means of hair root study. It seems to be necessary to test the hair roots of at least one enzyme-deficient member of the family to exclude false negative results, if hair root analysis is used for carrier detection. Because of the more or less clonal origin of hair roots, they remain a convenient biopsy material with which to study heterozygosity in X-linked inborn errors of metabolism.

Child↗
PubMed1977

[Favourable erythrocyte rheology in patients with glucose-6-phosphate dehydrogenase deficiency (author's transl)].

The rheological properties of erythrocytes of 6 patients with glucose-6-phosphate dehydrogenase deficiency were studied. A method of filtration and measurements of viscosity of erythrocyte suspensions with a hematocrit of 80% were used. The erythrocytes of all patients were more flexible than the erythrocytes of healthy controls. The erythrocytes of the patients passed the polycarbonate filters with a pore diameter of 5 micron more rapidly and showed a lower viscosity of erythrocyte suspensions. The increased flexibility of erythrocytes was due to a lower hemoglobin content which was measured in isolated ghosts. After incubation of the cells with acetylphenylhydrazine, Heinz bodies formed in the erythrocytes of controls. The flexibility of these cells decreased markedly. Though more Heinz bodies were found in the erythrocytes of the patients when the cells were incubated under identical conditions, even these erythrocytes became less rigid than the erythrocytes of controls. From these results we condlude that the more flexible erythrocytes of the patients could pass the splenic sinus even when they contain Heinz bodies. The rheological properties of the erythrocytes explain why splenectomy is not efficient in glucose-6-phosphate dehydrogenase deficiency.

Blood Viscosity↗
PubMed1979

Clinical implications of sickle-cell trait and glucose-6-phosphate dehydrogenase deficiency in hospitalized black male patients.

To determine whether sickle-cell trait and glucose-6-phosphate dehydrogenase deficiency influence the course and fatality rates of certain diseases requiring hospitalization, especially those associated with thrombotic phenomena, we conducted a co-operative study of 65,154 consecutively admitted, black male patients in 13 Veterans Administration hospitals. The overall frequency of sickle-cell trait was 7.8 per cent and of glucose-6-phosphate dehydrogenase dificiency 11.2 per cent. Both conditions were present in 0.9 per cent of those examined. There were regional, but no age-dependent, differences in the frequency of sickle-cell trait. Sickle-cell trait had no effect on average age at hospitalization or death, overall mortality, length of hospitalization on medical and surgical wards and frequency of any diagnosis, except essential hematuria and pulmonary embolism. Although statistically significant (P less than 0.001), the differences for the latter were small (1.5 per cent of all patients with normal hemoglobin and 2.2 per cent of patients with sickle-cell trait). Glucose-6-phosphate dehydrogenase deficiency had no adverse effect.

Adult↗
PubMed1975

Treatment of carbamyl phosphate synthetase deficiency with keto analogues of essential amino acids.

Congenital carbamyl phosphate synthetase deficiency was diagnosed by liver biopsy in a 13-year-old girl, alpha-Keto analogues of essential amino acids have been shown to spare nitrogen by reducing urea formation; hence, they were given to this patient in the hope of reducing hyperammonemia and improving protein tolerance. After intravenous infusion of the keto analogues of valine, leucine, isoleucine, methionine and phenylalanine, the corresponding plasma amino acids, including alloisoleucine and tyrosine, rose sharply. Twenty-four hours later, fasting plasma ammonia had fallen from the preinfusion value of 0.050 to 0.028 mM. Protein intake was kept at 0.5 g per kilogram for two weeks. Addition of keto acids by mouth reduced plasma ammonia and alanine to normal or near normal levels. Seizures and episodes of vomiting and lethargy decreased in frequency. Urinary nitrogen decreased, suggesting that nitrogen balance improved. These data indicate that keto acids may be useful in the treatment of congenital hyperammonemia.

Adolescent↗
PubMed1979

An examination of the role of vitamin E in glucose-6-phosphate dehydrogenase deficiency.

The effect of vitamin E on erythrocyte glutathione stability was studied both in vitro and in vivo on subjects with glucose-6-phosphate dehydrogenase deficiency. The results suggest that lipid membrane peroxidation in glucose-6-phosphate dehydrogenase deficient erythrocytes, which has been postulated to occur under conditions of oxidative stress, does not result in significant depletion of erythrocyte reduced glutathione pools. Vitamin E supplementation in these individuals was shown to have little or no effect on the response of their erythrocytes to oxidative stress.

Erythrocytes↗
PubMed1979

Glucose-6-phosphate dehydrogenase deficiency and neonatal jaundice in Jamaica.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency was detected in 16 (69.6%) of a group of 23 neonates who had unexplained moderate or severe jaundice. This proportion is significantly more than the 9.4% observed or the 22.2% expected in Jamaican neonates who are not moderately or severely jaundiced (P less than 0.003), and significantly more than the 12.6% observed or the 21.0% expected in older Jamaican children and adults (P less than 0.003). Phenobarbitone therapy and phototherapy reduced the need for exchange transfusion but this was necessary in eight patients. Two babies developed kernicterus and one died. On the other hand, only two of 21 neonates who were identified as G6PD deficient at birth subsequently became moderately or severely jaundiced, and this could be attributed to other causes in both cases. These findings indicate that apparently spontaneous neonatal jaundice is important in infants who have the G6PD A--enzyme. However, the jaundice is probably precipitated by unknown factors to which the G6PD deficient neonate is more susceptible than the infant who is not G6PD deficient. THere is also a slightly increased incidence of G6PD deficiency in neonates who develop jaundice because of ABO or Rh(D) iso-immune disease, infection or prematurity.

Adolescent↗
PubMed1976

Drug-induced haemolysis in glucose-6-phosphate dehydrogenase deficiency.

People with the variants of glucose-6-phosphate dehydrogenase (GPD) deficiency common in the southern Chinese (Canton, B(-)Chinese, and Hong Kong-Pokfulam) have a moderate shortening of red-cell survival but no anaemia when they are in the steady state. With a cross-transfusion technique, primaquine, nitrofurantoin, and large doses of aspirin were found to aggravate the haemolysis while sulphamethoxazole did so only in some people. Individual differences in drug metabolism may be the reason for this. Many commonly used drugs reported to accentuate haemolysis in GPD deficiency did not shorten red-cell survival.

Aspirin↗
PubMed1979

Congenital haemolytic anaemia resulting from glucose phosphate isomerase deficiency: genetics, clinical picture, and prenatal diagnosis.

Glucose phosphate isomerase (GPI) deficiency with severe haemolysis and hydrops fetalis was found in the first child of unrelated, healthy Caucasian parents. The child died at 3 hours. Both parents were found to have 50% of normal red cell GPI activity and qualitative tests on their red cells and white cells showed that each was heterozygous for a different GPI variant allele associated with enzyme deficiency. Tests on the placenta showed that the propositus was a 'compound' heterozygote. Examination of amniotic cells obtained by amniocentesis on the mother at 28 weeks in her second pregnancy led to the prenatal diagnosis of GPI deficiency. This second child, a 'compound' heterozygote at the GPI locus indistinguishable from the first, was successfully treated by immediate exchange transfusion and subsequent blood transfusions.

Adult↗