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At least 91 records · Page 5Linked to original sources
PubMed1974

Hypouricaemia and proximal renal tubular dysfunction in acute myeloid leukaemia.

Two patients with acute myeloid leukaemia developed hypouricaemia during the period of their illness. Renal clearance studies showed that the hypouricaemia was associated with an increased urate clearance, renal aminoaciduria, and an episodic increase in phosphate clearance. These findings together with an inadequate suppression of urinary urate exceretion after the administration of pyrazinamide suggest proximal tubular dysfunction affecting reabsorption of a wide variety of substances. Ten more patients with acute leukaemia were studied and the results indicate that this lesion develops in a large proportion of patients with acute myeloid leukaemia.

Amino Acids↗
PubMed1964

ESTIMATION OF ALPHA-AMINO NITROGEN IN PLASMA AND URINE BY THE COLORIMETRIC NINHYDRIN REACTION.

Methods are described for the estimation of plasma and urine alpha-amino nitrogen by the colorimetric ninhydrin reaction; in the method for urine, both ammonia and urea are separated by a rapid ion-exchange resin procedure. Two methods of estimation are given; one has the advantage of great simplicity, but involves the use of cyanide; in the other, cyanide is eliminated. Normal values are reported; they correspond well with those obtained by the gasometric ninhydrin method.

Amino Acids↗
PubMed1977

Hereditary mitochondrial myopathy with lactic acidemia, a De Toni-Fanconi-Debré syndrome, and a defective respiratory chain in voluntary striated muscles.

A patient suffering froma mitochondrial myopathy leading to severe insufficiency of the voluntary muscles is described. Severe cerebral damage was present. Major biochemical symptoms were extreme lactic acidemia, hypophosphatemia and hyperphosphaturia, and generalized aminoaciduria, renal glucosuria, and polyuria. Muscular insufficiency resulted in lethal asphyxiz. All therapeutic trials were insufficient. The patient and two other children of the same family with a similar clinical picture all died before the 4th month of life. The condition is probably inherited in an autosomal recessive way. A defective respiratory chain in the mitochondria of the striated muscles is proposed as the underlying mechanism. Cytochromes aa3 were absent, b was nearly absent, but cc1 was present. In heart muscle cytochromes aa3 and b were at the level of the controls.

Cytochromes↗