17-Ketogenic Steroid Excretion in Obese Children Before and After Weight Reduction
Authors: H. Cohen
Journal: BMJ (1958)

Obesity must be due to overeating, although it may result indirectly from other abnormalities.Simpson (1951) described a type of obesity in children as a minor endocrine disorder, and named the syndrome " adipose gynandrism" in boys and "adipose gynism" in girls.On the other hand, Wilkins (1957) states that endocrine abnormality is rarely encountered in obese children; and Newburgh (1942), in a review of the subject, found no evidence that obesity in children was directly due to endocrine imbalance.The case histories recorded in this paper are of four patients, children and adolescents, who were very fat, and who, when first investigated, had a daily excretion of 17-ketogenic steroids in excess of the normal for their age.This finding led to a suspicion that the con- dition was due to endocrine imbalance, although in each case the clinical diagnosis was that of simple obesity.However, with dietary restriction alone the 17-ketogenic steroid excretion fell to normal. MethodsThe 17-ketosteroid and 17-ketogenic steroid excretion was determined by the method of Norymberski, Stubbs, and West (1953) with the modification of Gibson and Norymber- ski (1954).The 17-ketosteroids are the products of testi- cular and adrenal cortical hormones excreted as 17-ketones.The 17-ketogenic steroids are steroids in which the side chain on C17 is oxidized to a ketone group by the method of Norymberski et al. (1953).The 17-ketogenic steroid assay therefore involves, of necessity, estimation of the 17- ketosteroids.Levell et al. (1957) estimated the normal range using this method and discussed the clinical value of the 17-ketosteroid and 17-ketogenic steroid assays.They considered that the 17-ketogenic steroid excretion probably gave a measure of the adrenal function concerned with the production of hydrocortisone and that it was the assay of choice in following changes in adrenal function, as, for example, in observing the response to corticotrophin. Case IA boy aged 14 attended the out-patient clinic at the Sheffield Royal Hospital in June, 1956.He had no symp- toms, but was extremely obese.His weight was 12 st. 12lb.(81.6 kg.).His mother stated that he had always been big for his age, but had started to become fat after he had a tonsillectomy at the age of 7.He had always been a big eater, particularly of bread.He did not play much with his contemporaries, partly because he found it difficult to run about and partly because of the derision that he had to contend with.He preferred adult company.He attended a secondary modern school and had no difficulty with the work.Apart from tonsillectomy and an operation for a deviated septum at the age of 7 there was no previous illness of note.He was an only child.Both parents were small and thin.The father died of heart disease in 1947.Physical examination showed an obese boy with kyphosis.Red striae were seen over his thighs and buttocks.There was no axillary hair, but pubic hair was present.His testes were descended and his genital development was normal.He had a thyroglossal cyst, but there was no other abnorm- ality.The blood pressure was 120/80.His height was 66 in.(167.5 cm.), and span 68+ in.(174 cm.).Investigations.-Urine, blood count, E.S.R., and chest and skull x-ray films were normal.B.M.R. approximately +5%.Bone age between 13 and 15 years.Excretion uro- gram, no abnortnality.17-Ketosteroid excretion, 17-keto- genic steroid excretion, weight reduction, and progress are