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Background: Growth hormone deficiency is an important and treatable cause for short stature in early diagnosed cases. This study was conducted to determine the frequency of growth hormone deficiency in children with short stature referred. Methods: In a cross sectional descriptive study, all short stature children referred to endocrinology clinic of Golestan hospital in Ahvaz, Iran during 2005 to 2006 were included if they had height below 3rd percentile for age and sex, no any chronic disorder causing short stature and normal initial investigations. Standard growth hormone stimulation tests were performed and patients with growth hormone maximum level of less than 10 ng/dl (in two tests), were considered as growth hormone deficient. Findings: 202 cases (59.9% male and 40.1% female) with age range of 1 to 15 and mean age of 9.1 years were studied. Frequency of growth hormone deficiency was 11.8%. In growth hormone deficient group, male/female ratio was 2.4/1 and family history of short stature was positive only in 4.2%. Height standard deviation score (SDS) of 75% of these cases was ≤ -3 and weight for age in 79.2% was ≥ 10 percentile. These data showed significant difference between short and normal children (P < 0.05). Conclusion: In this study, frequency of growth hormone deficiency was average, compared to other studies. In children with standard deviation score < -3 and weight percentile ≥ 10, growth hormone deficiency should be more considered. Parents and health care providers should be urged to early referral of children with short stature. Key words: Short Stature, Children, Growth Hormone Deficiency.

To evaluate the prevalence of renal tubular dysfunction in children with β-thalassemia (β-T) major, we studied the glomerular and tubular function in 140 children with β-T major and compared them to a healthy control group at our center from May 2007 to April 2008. Fresh first morning samples were collected from each patient and analyzed for sodium, potassium, calcium (Ca), protein, uric acid (UA), creatinine (Cr), urine osmolality and urinary N-acetyl-β-D-glucosaminidase (UNAG) activity. Blood samples were also collected for complete blood count, blood urea nitrogen (BUN), fasting blood sugar, serum creatinine (SCr), electrolytes, and ferritin before transfusion. Among the study patients, 72 were males, and the mean age was 11.5 (ranging 7-16) years. SCr levels were all within normal limits and all of them had normal glomerular filtration rate (GFR). The mean UNAG was 17.8 IU/L in the study patients (normal 0.15-11.5 IU/L) and 3.2 IU/L in the control group (P < 0.001). Of the 82 study patients who had elevated level of UNAG, 58 (62.4%) had high blood levels of ferritin also (r = 0.2, P < 0.001) and 13 (15.9%) patients had hypercalciuria also (UCa/UCr > 0.21) (P = 0.006). Nine (6.4%) thalassemic patients with a mean age of 12 years had proteinuria (Upr/UCr > 0.2). Sixty-nine (49.3%) out of the 140 patients and 45 (65.2%) of the patients having UNAG had uricosuria also (UUA/UCr > 0.26). Ten (7%) patients had microscopic hematuria and 10 (7%) patients with a mean age of 13.5 years had glucosuria or diabetes mellitus. We conclude that tubular dysfunction is a relative common complication of the β-T major; UNAG and its index are the best to detect renal tubular dysfunction in these patients. Currently, periodic measurement of UCa/UCr and UUA/UCr ratios as well as urinalysis are recommended.