Precocious puberty.

Puberty occurring before the age of 8 years in girls and 9 years in boys in considered precocious. The numerous causes of precocity can be classified as central or peripheral. Central or true precocious puberty (CPP) is due to premature activation of the hypothalamopituitary-gonadal axis and is isosexual. Peripheral or pseudoprecocious puberty (PPP) results from the production of sex steroids independent of the H-P-G axis and may be isosexual or heterosexual. CPP is the most common form of precocity involving more than 50% of children and is much more common in girls than boys. CPP is more common between 4 and 8 years. A peak serum LH levels > 10 iu/l following GnRH stimulation is the absolute evidence of CPP. Serum IGF-I levels are predictive of the outcome. Availability of CT and MRI has helped to determine the cause of CPP in most cases. Hypothalamic hamartoma is the most common tumour causing CPP especially in boys. Adrenal causes, particularly CAH, are the commonest cause of PPP in boys whereas ovarian causes are more likely in girls. Long acting GnRH analogues provide a safe and effective form of treatment of CPP.

Profile of growth hormone deficiency in Bombay.

Of the 430 children referred for the evaluation of short stature 100 (23%) were confirmed to have growth hormone deficiency. The male to female ratio was 1.94:1. Less than 10% belonged to the lower socio-economic group. Most of the cases (73%) presented between the ages of 6-15 years though growth failure was usually recognised earlier. Minimum of two stimulation tests were performed in each case. Seventy five GH deficient children had idiopathic GHD (IGHD) and 31% of these were familial. Fourteen had organic causes and 11 had GH resistance. Of 75 with IGHD, 18 had abnormal deliveries, breech or birth asphyxia. Multitropic pituitary hormone deficiency (MPHD) was found in 9/75 cases of idiopathic GHD and in three of the organic group. The height age was much more retarded than chronologic age in the GH resistant group (p less than 0.05) and the HA/BA ratio was also lowest in this group (p less than 0.001). Growth velocity was less than 4 cm/year in all the GHD children but was lowest in those with MPHD. The interesting feature of this study is the marked predominance of the familial cases 31% and a high incidence of growth hormone resistant cases (11%).

Identification of a child with short stature.

The objective of this study was to determine the utility of Indian Council of Medical Research's (ICMR) height percentile standards in comparison to Tanner's, in the evaluation of children with short stature. The study consisted of an initial survey of the heights of 500 consecutive new cases brought to the Out Patient Department. The heights were assessed by both ICMR and Tanner's standards. Only 10% were below the 5th percentile of ICMR standards while as many as 32% were below the 3rd percentile of Tanner's standards. Two hundred children who were referred to the endocrine clinic primarily for short stature and who were below the 3rd percentile of Tanner's standards were then evaluated. Of these 200 short children 132 (66%) were also below the 5th percentile of ICMR standards. The major causes of short stature in those below the 5th percentile of ICMR standards were endocrine (56.8%). In the group between the 5th percentile of ICMR standards and 3rd percentile of Tanner standards the major cause of growth retardation was normal variant short stature (67.8% of cases in this group). Correlation of the child's height with the mid-parental height was seen in 90.4% in this group but in only 16.6% of those below the 5th percentile of ICMR standards. The ICMR standards may, therefore, be more suitable than Tanner's standards for the identification of a short child from the lower socio-economic groups.