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Biomedical subjects

B Senior

Publications and source records attributed to B Senior.

At least 37 records · Page 2Linked to original sources
PubMed1980

Failure to thrive and metabolic alkalosis. Adverse effects of a chloride-deficient formula in two infants.

This report concerns two infants with failure to thrive and hypochloremic metabolic alkalosis. Both infants were fed exclusively with a soybean-based formula, which, as a result of a manufacturing error, was severely deficient in chloride. When an alternative formula containing an adequate amount of chloride was prescribed, the electrolyte abnormality was corrected, and the infants resumed their normal weight gain.

Alkalosis↗
PubMed1980

Hypoparathyroidism and pregnancy. Treatment with calcitriol.

Calcitriol was used successfully to treat a patient with hypoparathyroidism during pregnancy. Increasing dosage of calcitriol were needed during the last trimester with a prompt decrease in the requirement after delivery. The dosage changes appear to mirror the pattern of endogenous synthesis of calcitriol in normal pregnant women.

Adult↗
PubMed1979

Hypoglycemia in children.

The factors that sustain postabsorptive glucose concentrations have been analyzed and the adverse effects of various hypoglycemic disorders on these factors examined. The role of alanine has been reviewed and the importance of glycerol as a precursor of glucose and of ketones as a fuel substitute for glucose emphasized. Finally, we have suggested that fasting functional hypoglycemia replace ketotic hypoglycemia as a descriptive term and that we relinquish the concept of leucine-sensitive hypoglycemia as a specific entity.

Adult↗
PubMed1979

The diagnosis of insulinoma in a child in the absence of fasting hyperinsulinemia.

This report concerns an 8-year-old girl with fasting hypoglycemia caused by a functional islet cell adenoma. During two separate fasting studies the blood glucose concentrations decreased to abnormally low levels yet the serum concentrations of insulin were consistently within the accepted range of normal. This report illustrates the diagnostic value of three simple functional tests--the inhibitory effect of insulin on ketogenesis and on glycogenolysis and the stimulatory effect of leucine on insulin secretion.

Adenoma, Islet Cell↗
PubMed1978

Endocrine studies in a pubertal male pseudohermaphrodite with 17-ketosteroid reductase deficiency.

UNLABELLED: A 12 year old child (46,XY) with 17-ketosteroid reductase deficiency was investigated. The patient, reared as a female, was first noted to have clitoromegaly at 10 years of age. Increased facial hair, deepening of the voice, acne, increased body hair and minimal breast development were noted at 12 years. delta4-Androstenedione (delta4) in peripheral blood was markedly elevated (1913 ng/100 ml) whereas testosterone (T) was in the male range of Tanner III puberty (240 ng/100 ml). Thus, delta4/T in this patient was 9.4, compared to a normal ration of 0.15 to 0.25. T/DHT was normal (10.5). Oestrone (Oe1) level was slightly elevated (6 ng/100 ml, normal: 2.5-4.5 ng/100 ml). Oestradiol (Oe2) was normal (1.7 ng/100 ml, normal: 1.5-3 ng/100 ml. Oe1/Oe2 was slightly elevated (3.6, normal: 1-2). At laparotomy, testes were found and spermatic vein blood was obtained prior to castration. Androgen determinations of spermatic vein blood demonstrated extremely high delta4 levels (283 microgram/100 ml) and low levels of T (16 microgram/100 ml). delta4/T in spermatic vein was 17, higher than in the peripheral blood, suggesting intact peripheral conversion of delta4 to T. Incubation of testes slices with delta4 demonstrated severely impaired conversion to T. Conversion of Oe1 to Oe2 was impaired to a lesser degree. CONCLUSION: 17-ketosteroid reductase deficiency was documented in vivo by impaired conversion of precursor hormones resulting in higher than normal delta4T and Oe1/Oe2 ratios in blood. In vitro studies with testes slices confirmed the enzymatic defect.

17-Hydroxysteroid Dehydrogenases↗
PubMed1975

Studies in type I glycogenosis: the paradoxical effect of ethanol on lactate.

Paradoxically, ethanol, which raises lactate in normal individuals, lowers the elevated levels of lactate in patients with Type I glycogenosis. We found that, although lactate levels fell, pyruvate proportionately declined even more, resulting in an increased L/P ratio which indicates that, as in the normal, the oxidation of ethanol had generated NADH. In type I glycogenosis, the increased level of pyruvate-lactate derives from glycogenolysis. We found that, despite continued glycogenolysis, ethanol had caused less pyruvate-lactate to form. The effect of an increased NADH/NAD+ ratio on the flow of carbon through the Embden-Meyerhof pathway could account for the finding, presumably by its effect on the oxidation-reduction couples with diversion of carbon toward formation of triglyceride rather than pyruvate-lactate.

Adolescent↗