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Biomedical subjects

C Sekaran

Publications and source records attributed to C Sekaran.

5 recordsLinked to original sources
PubMed1986

Premarin priming does not alter growth hormone release following exercise.

We evaluated the usefulness of premarin priming on exercise induced growth hormone release and the value of combining several growth hormone screening agents in a large population of prepubertal children. Two hundred five short healthy prepubertal children growing below the 5th percentile in height were studied. One hundred forty-four were screened with exercise following glucose ingestion, while 61 were primed with estrogen prior to glucose and exercise testing. Premarin priming did not significantly increase the number of our patients who responded to exercise nor to glucose; 86% and 88.5% of non-primed and primed patients, respectively, responded with a growth hormone increase greater than or equal to 8 ng/ml following exercise and glucose. Glucose loading alone was not associated with a high enough growth hormone rise to rule out growth hormone deficiency in most of our children. Age (less than or equal to 5 yr) was associated with lower post-exercise growth hormone levels and a higher failure rate to testing in both primed and non primed children. Premarin priming does not seem to alter the growth hormone releasing capacity to exercise of prepubertal children. The combined use of exercise, glucose loading and premarin priming in a single screening test does not improve on the results obtained by growth hormone exercise screening alone.

Adolescent↗
PubMed1982

Glycerol-induced hypoglycemia: a syndrome associated with multiple liver enzyme deficiencies. Clinical and in vitro studies.

A 4 10/12 yr-old white male presented with a history of occasional grand mal seizures and hypoglycemic episodes after overnight fasting. Upon evaluation, he became hypoglycemic after 1 g/kg oral glycerol challenge (plasma glucose: 31 mg/dl in 45 min), but had normal glucose, alanine and fructose tolerance tests. He responded well to a glucagon challenge after 11 hr fast but he became hypoglycemic and could not normalize his blood glucose after a 2nd glucagon stimulation test after 17 hr of fasting. Studies conducted on a percutaneous liver biopsy, and compared with 3 non-hypoglycemic controls, showed reduced activities (20%-30% of normal) of alpha-glycerophosphate dehydrogenase, alpha-glycerophosphate oxidase and fructose-1,6-diphosphatase. Alpha glycerophosphate in the patient's liver was elevated. Two types of electrophoresis showed absence of one enzymatically active zone and overall decrease of staining intensity for alpha-glycerophosphate dehydrogenase. Other liver enzymes tested were normal. The 50% inhibition of the patient's liver fructose-1,6-diphosphatase by alpha-glycerophosphate occurred, in vitro, or lower concentration than in controls (11 versus 22-40 mM). Electron microscopy revealed hepatocytes with moderately swollen mitochondria that very occasionally contained dense inclusions in the inner mitochondrial matrix. After discharge from the hospital, the patient followed a normal course, with a regimen of multiple snacks and avoidance of high-fat food in the morning.

Child, Preschool↗