The 1 μg cosyntropin test could be an adrenal function screening test in thalassemics. However, for definite diagnosis, ITT should be performed in those having peak total cortisol of less than 16 μg/dl after the 1 μg cosyntropin test.

Background: A test involving 100 μg of intravenous gonadotropin-releasing hormone (GnRH) is a gold standard for confirming the diagnosis of central precocious puberty (CPP). However, intravenous GnRH for testing is commercially limited. Objective: To develop subcutaneous GnRH agonist (GnRH-A) testing and define a peak luteinizing hormone (LH) cutoff value in diagnosing CPP. Methods: A retrospective study of 101 girls with sexual precocity was undertaken. All girls underwent 100 μg subcutaneous GnRH-A (triptorelin) testing. Blood samples before and 30, 60, 90 and 120 min after GnRH-A injection were analyzed for LH and follicle-stimulating hormone levels. Criteria for diagnosing CPP include accelerated height, advanced bone age and pubertal-sized uterus and ovaries. Results: Fifty-five girls were documented as having CPP. The remaining 46 girls were diagnosed with premature thelarche (PT). Peak LH concentration in the CPP group was significantly greater than that of the PT group with a median (range) of 10.0 IU/l (2.93–65.39) and 3.04 IU/l (0.19–8.82), respectively. Peak LH was achieved within 60 min following GnRH-A injection. Peak LH of 6 IU/l provided the most appropriate cutoff level in diagnosing CPP with a sensitivity of 89.1% and a specificity of 91.3%. Conclusion: Subcutaneous GnRH-A can be used as an alternative to confirm the diagnosis of CPP.

BACKGROUND: Pediatric obesity continues to rise and has become a major health problem worldwide. Vitamin D deficiency has been increasing among obese non-Asian children and is associated with abnormal glucose homeostasis in obese adults. However, data on the vitamin D status and its association with glucose homeostasis in obese children residing in tropical Asian countries are unavailable. OBJECTIVE: To assess vitamin D status and glucose homeostasis in obese Thai children. PATIENTS AND METHODS: A total of 150 obese, and 29 healthy non-obese children and adolescents were enrolled. Weight, height, body mass index (BMI) and waist circumference were obtained. All obese children underwent an oral glucose tolerance test with glucose and insulin measurements. Plasma 25-hydroxyvitamin D (25-OHD) and calciotropic blood chemistries were measured in all participants. Insulin sensitivity indices were calculated from the measured glucose and insulin levels. RESULTS: Approximately 25% of the obese children and adolescents had impaired glucose tolerance, impaired fasting plasma glucose (FPG) and diabetes. Seventeen out of 150 (11.3%) obese children and 3 out of 29 (10.3%) non-obese children had vitamin D deficiency, which was defined as a 25-OHD level of o50 nmol l À1 . Glucose tolerance and insulin sensitivity indices were comparable between obese children with sufficient vitamin D and those with vitamin D deficiency. There were no relationships among serum 25-OHD; weight, height, and BMI standard deviation scores; insulin sensitivity indices; FPG and insulin; and 2-h plasma glucose and insulin levels. CONCLUSION: Vitamin D deficiency is not as prevalent in obese Thai children as in obese non-Asian children from highlatitude countries. Adiposity per se is unlikely to be a determinant of vitamin D status in these obese individuals. There was no association between vitamin D deficiency and abnormal glucose homeostasis.