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Biomedical subjects

A Sadeghi-Nejad

Publications and source records attributed to A Sadeghi-Nejad.

At least 37 records · Page 2Linked to original sources
PubMed1986

The incidence of late endocrine dysfunction following irradiation for childhood medulloblastoma.

A retrospective analysis of treatment in 20 patients who had received post-operative radiotherapy for medulloblastoma between 1969 and 1977 was completed. The patients were followed for a minimum of 60 months. Eleven patients survived for 5 or more years after treatment. The patients received 3600 cGy to the whole brain. The posterior fossa received 5600 cGY and the spinal axis 3600 cGY. Eight of eleven patients developed growth impairment; 6 of 7 patients had growth hormone deficiency. Since all endocrine gland failures are amenable to therapy, early attention to patients' growth rate and detection of hypothalamic-pituitary failure, would be of benefit to longterm survivors.

Adolescent↗
PubMed1986

Hypercalcemia: an unusual complication of hyperthyroidism in a child.

Although well known in adults the association of hypercalcemia with hyperthyroidism has not been reported in children. We described how its occurrence in a hyperthyroid child obscured the manifestations of hyperthyroidism and discuss the factors that led to its appearance and regression.

Child↗
PubMed1986

Value of computed tomographic scanning in patients with growth hormone deficiency.

In 18 of a series of 23 patients with growth hormone deficiency, computed tomographic scanning demonstrated a markedly small sellar volume. In four of the remaining five patients, the sella was enlarged. The cause of the enlargement was readily identifiable. Computed tomographic scanning of the sella appears to provide valuable supportive evidence of hypopituitarism.

Adolescent↗
PubMed1984

Ketonuria does not exclude hyperinsulinemic hypoglycemia.

We examined the relationship between serum beta-hydroxybutyrate (BOHB) and plasma glucose concentrations and between serum free fatty acid (FFA) and glucose concentrations in 34 normal children who fasted for up to 24 hours. The BOHB concentration correlated inversely with the glucose concentration, as did the FFA concentration. We compared these results with those in six patients with hypoglycemia due to hyperinsulinism. In the hyperinsulinemic children, hypoglycemia was invariably associated with relative hypoketonemia (glucose concentration, less than 40 mg/dL; BOHB concentration, less than 2mM; greater than 2 SDs below the mean). The FFA concentrations were also unduly low (greater than 2 SDs). However, despite being significantly hypoketonemic when hypoglycemic, four of the six hyperinsulinemic patients had ketonuria. Since it does not exclude hyperinsulinism, ketonuria may be a potentially misleading finding in a hypoglycemic child.

3-Hydroxybutyric Acid↗
PubMed1983

Hypoketonemia and age-related fasting hypoglycemia in growth hormone deficiency.

Body fuels were measured in 45 normal children and 17 growth hormone-deficient patients after 24 hours of fasting. After three months of therapy with human Growth Hormone (hGH) 16 of the patients were restudied. In all groups, beta-hydroxybutyrate (BOHB) concentrations correlated inversely with age and with glucose concentrations. When adjusted for these factors, the concentrations of BOHB were significantly lower in the growth hormone-deficient patients than in the control children, before (P less than 0.01) as well as after therapy (P less than 0.01). Only the five youngest patients became hypoglycemic. During fasting, ketones, which serve as an alternative fuel for the brain, spare glucose. Thus, a shortage of ketones would compromise the ability of the patient to conserve glucose and predispose the patient to fasting hypoglycemia. Accordingly, we propose that hypoketonemia is a critical factor in the genesis of fasting hypoglycemia in growth hormone deficiency.

Adolescent↗
PubMed1982

Fat-derived fuels during a 24-hour fast in children.

We examined the availability of fat-derived fuels in 23 normal children aged 1.9 to 16.7 years who fasted for 24 h. We found a rapid and progressive rise in the blood concentrations of free fatty acids (FFA) and ketones. There was a highly significant negative correlation between the concentrations of beta-hydroxybutyrate (beta OHB) and glucose and also between beta OHB and age. With time, the ratio of beta OHB to acetoacetate (AcAc) progressively increased. We briefly review the vital role of ketones in the adaptation to fasting and point out that qualitative tests of ketones can be misleading. Our results indicate that quantitative determinations are essential in the evaluation of suspected disorders of fuel metabolism and that the results must be interpreted according to the age of the child, the duration of fasting, and the concomitant concentrations of glucose.

Acetoacetates↗
PubMed1982

Hypoalaninemia and ketotic hypoglycemia: cause or consequence?

A shortage of alanine for gluconeogenesis is believed responsible for various forms of hypoglycemia and in particular ketotic hypoglycemia (KH). We examined the glucose-alanine relationship in two groups of fasting children, 18 with KH and 44 controls. Glucose levels declined in both groups but significantly more in KH; to 1.98 +/- 0.20 versus 3.26 +/-0.13 mM (mean +/- SEM; P less than 0.001). Alanine also fell in both groups, the concentrations correlating significantly with the concomitant glucose levels (KH: r = 0.64, P less than 0.001, and controls: r = 0.50, P less than 0.001). The relationship of alanine to glucose gave virtually identical regression equations, y = 0.054x + 0.063 for KH and y = 0.054x + 0.050 for controls. The differences in alanine levels between the two groups were too small to account for the greater decline in glucose in KH. The results indicate that hypoalaninemia rather than causing hypoglycemia results from it.

Acidosis↗
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↗
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↗
PubMed1974

A familial syndrome of isolated "aplasia" of the anterior pituitary. Diagnostic studies and treatment in the neonatal period.

A male newborn infant developed hypoglycemia, collapsed, and convulsed at eight hours of age. The diagnosis of pituitary "aplasia" was suspected, because of a previously affected female sibling, and treatment with glucocorticoids was instituted. Diagnostic studies revealed a deficiency of thyrotropin, growth hormone, and prolactin. He is now six months of age and is thriving on replacement therapy. Analysis of previous reports of this entity indicates that isolated "aplasia" of the anterior pituitary is a genetic syndrome with an autosomal recessive mode of transmission. The course in this patient suggests that this disorder, if diagnosed, is amenable to therapy.

Cortisone↗