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Biomedical subjects

B Nagai

Publications and source records attributed to B Nagai.

7 recordsLinked to original sources
PubMed1979

Metabolic acidosis in patients receiving anticonvulsants.

Blood pH, bicarbonate, PCO2, serum calcium, alkaline phosphatase and red cell carbonic anhydrase were measured in 37 selected patients receiving anticonvulsants. Patients with metabolic acidosis showed a high incidence of hypocalcemia with increased alkaline phosphatase and a significant reduction of carbonic anhydrase-B activity. High iPTH levels were found in 13 patients, but this was not correlated with acid-base balance status. Anticonvulsant drugs seemed to inactive carbonic anhydrase-B activity. Metabolic acidosis might be one of the factors causing a disturbance of calcium metabolism in these patients.

Acidosis↗
PubMed1979

Pseudohypoparathyroidism type II and anticonvulsant rickets.

A patient treated with anticonvulsants showed hypocalcemia and hyperphosphatemia in association with increased serum parathyroid hormone, reduced serum 25-hydroxy D3, diminished response in phosphorus excretion to exogenous parathyroid hormone and normal response in cyclic AMP excretion. Oral administration of Vitamin D3 resulted in normalization of serum 25-hydroxy D3, calcium, and phosphorus. At this stage, phosphorus excretion after parathyroid hormone returned to normal. These findings suggest that the patient had pseudohypoparathyroidism type II with anti-convulsant medication as a complicating factor.

Adolescent↗
PubMed1978

Glucose-6-phosphatase activity in liver and blood platelets of two patients with glycogen storage disease type I.

Glucose-6-phosphatase (G-6-Pase) activity in liver and blood platelets of two patients with glycogen storage disease (GSD) type I is described. Both patients had a reduced activity of G-6-Pase in liver. The km value for glucose 6-phosphate (G-6-P) of residual activity in liver of both patients was similar to that of control liver. We could not demonstrate any reduced activity of platelet G-6-Pase in the patients. Platelet G-6-Pase with our assay method seems to represent a nonspecific phosphatase activity. Our observation suggests that it is necessary to examine platelet G-6-Pase of many other patients with GSD type I to confirm that G-6-Pase deficiency can be diagnosed by enzyme assay performed on blood platelets.

Alanine↗
PubMed1977

The effects of oral alanine administration on blood glucose, pyruvate, lactate, serum glucagon and insulin in human newborns.

Alanine (500 mg/kg body weight) was given orally to 27 healthy full term newborn infants, and the changes in blood glucose, pyruvate, lactate, alanine, glucagon and insulin were determined. Significant increments in blood glucose were found in 15 infants with blood glucose levels below 60 mg/100 ml, 4 of whom showed significant elevation of serum glucagon levels on day 1. This observation suggests that hepatic gluconeogenesis is possible immediately after birth.

Age Factors↗
PubMed1977

Down syndrome with trisomy in one triplet.

The case presented here may be the first identified report of Down syndrome with 21 trisomy in one child of triplets. One triplet died at 1 month of age; his facial appearance was not typical of Down syndrome. Detailed testing of blood groups suggested identical origin in the remaining two children. However, the fluorescent banding technique of chromosome, one-way mixed lymphocyte culture test, and HLA typing were suggestive of dizygotic orgin. Skin transplant studies supported this contention.

Chromosomes, Human, 21-22 and Y↗
PubMed1975

Renal tubular acidosis and skeletal demineralization in patients on long-term anticonvulsant therapy.

Three children ranging from seven to 12 years of age from unrelated families were given long-term anticonvulsant therapy including acetazolamide (Diamox). These children had rickets and renal tubular acidosis. Investigations have suggested (1) secondary hyperparathyroidism due to hypocalcemia of rickets and (2) prolonged acetazolamide therapy were responsible for acidosis as a result of reduction of bicarbonate reabsorption in the kidney. A clear-cut recovery from acidosis and rickets was seen in two patients following medication with high doses of vitamin D, an oral supplement of phosphorus, and discontinuance of acetazolamide therapy.

Acetazolamide↗