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Biomedical subjects

M Kanayama

Publications and source records attributed to M Kanayama.

At least 109 records · Page 6Linked to original sources
PubMed1985

Renal handling of urate in the syndrome of inappropriate secretion of antidiuretic hormone.

Three patients with the syndrome of inappropriate secretion of antidiuretic hormone had elevated uric acid clearances. Their uric acid clearances decreased markedly after the administration of pyrazinamide. Probenecid was given to two of them and it produced large increases in uric acid clearance. These data suggest that enhanced secretion in the renal tubules was responsible for the increased clearance of uric acid. This article provides evidence that hypouricemia in the syndrome of inappropriate secretion of antidiuretic hormone is due to increased tubular urate secretion.

Aged↗
PubMed1984

Primary biliary cirrhosis. A patient with adverse reactions to tiopronin and autoimmune hemolytic anemia with reticulocytopenia.

A 32-year-old woman with asymptomatic primary biliary cirrhosis had autoimmune hemolytic anemia associated with reticulocytopenia and thrombocytopenia despite an intensely erythroid bone marrow. Her anemia was successfully treated with oral prednisolone and intravenous pulse methylprednisolone, with a rapid response of reticulocytosis and sustained erythrocytosis. Tiopronin therapy was later initiated and resulted in fever, rash, exacerbation of the liver disease, and positive direct and indirect antiglobulin tests.

Amino Acids, Sulfur↗
PubMed1984

Fatal intoxication by 1,2-dichloroethane--a case report.

This is a case report of acute fatal intoxication after accidental exposure to 1,2-dichloroethane in a 51-year-old man. Clinical manifestations, blood chemistry, and autopsy findings are described. High levels of lactate and ammonia in blood had been observed before the elevation of glutamic transaminases, lactic dehydrogenase, and creatine phosphokinase. Ornithine carbamyl transferase and glutamic oxaloacetic transaminase of mitochondrial origin (m-GOT) were remarkably high.

Accidents, Occupational↗
PubMed1983

Two cases of phosphofructokinase deficiency associated with congenital hemolytic anemia found in Japan.

Two kindreds of phosphofructokinase (PFK) deficiency associated with congenital nonspherocytic hemolytic anemia and mild myopathy were found in Japan. Both probands had jaundice, gallstones, and slight to moderate degree of exercise intolerance. They showed decreased level of red cell PFK activity and no increase of blood lactate in forearm ischemic exercise test. We studied these probands' red cell PFKs by partial purification and condensation. Muscle type isozyme of PFK in both cases was not demonstrable in starch gel electrophoresis and DEAE-Sephadex chromatography. The clinical symptoms are considered to be due to a defect of muscle type isozyme.

Adult↗
PubMed1982

Rifampicin-induced early phase hyperglycemia in humans.

Early phase hyperglycemia, associated with increased rates of insulin and C-peptide secretion after oral administration of 100 g glucose, was observed among patients with pulmonary tuberculosis who were taking rifampicin. This early phase hyperglycemia appeared shortly after rifampicin was started and it disappeared completely a few days after rifampicin was discontinued. No difference in oral glucose tolerance was noted between healthy normal subjects and patients with pulmonary tuberculosis who were not taking any medications. Antituberculous drugs other than rifampicin did not induce early phase hyperglycemia. Because intravenous glucose tolerance was normal in patients treated with rifampicin, it is suggested that rifampicin produces an early phase hyperglycemia possibly by augmenting intestinal absorption of glucose.

Administration, Oral↗
PubMed1982

Hypouricemia due to an increment in renal tubular urate secretion.

Two patients had hypouricemia due to increased uric acid clearance. Their daily urinary uric acid excretions were normal. In both patients, pyrazinamide decreased urinary uric acid clearance to almost while probenecid increased it markedly. No other renal tubular or metabolic abnormalities were found. The serum electrolytes and the urinary electrolytes excretions showed no abnormalities. It appears that increased secretion of uric acid in the renal tubule is most probably responsible for hypouricemia in these patients. This report adds to the list of hypouricemic conditions due to a new isolated renal tubular abnormality.

Adult↗