Although,most causes of SHORT STATURE are non pathologic but if pathological cause is diagnosed, medical treatment will be effective. This study was descriptive and crosssectional. The aim was to study the main cause of SHORT STATURE in patients aged 7-15years referring to Endocrine centers in Yazd. 125 patients were referred, 25 patients were excluded in this study because of severe malnutrition, Systemic disease . 100 patients including 48 males and 52 females were studied and most of them were in the age group of 13-15 years. 57% of the SHORT STATURE cases had non pathological causes (33% constitutional and 24% intrinsical, 43% of the SHORT STATURE cases had pathological causes in cluding 16% GH deficiency, 12% hypothyroidism, 7% turner syndrome, 5% chondrodysplasia, 4% rickets, 3 % hypoparathyroidism the most common cause of SHORT STATURE in males was constitutional SHORT STATURE (50%) and in females was Intrinsically (23.1%). The most common causes of SHORT STATURE were non pathological causes. and between inpathological causes, GH deficiency and hypothyroidism had more effects. Since, mean ages of patients referred to endocrine centers were high (13-15 Years),Therefore delayed of treatment affect on the final height of these patients. So, education of Patients and their parents with SHORT STATURE has important role in the treatment outcome .

Objective: SHORT STATURE is a common problem encountered by pediatricians and is the most common cause for referral to pediatric endocrinologists. Although most children referred with SHORT STATURE are normal and classified as normal variants of STATURE (constitutional growth delay and familial SHORT STATURE), it may sometimes be the only obvious manifestation of an endocrine or systemic disease. The objective of this study was to assess the characteristics of patients referred to pediatric endocrinology clinic because of SHORT STATURE and determination of the etiology. Methods: Three hundred-seventy nine children and adolescents were studied which referred with SHORT STATURE to pediatric endocrinology clinic. After complete clinical and paraclinical evaluation and appropriate treatment (if needed), patients were followed for at least six months. Findings: From 379 studied patients with a mean age of 9.7±3.7 years, 192 (50.7%) were girls and 187 (49.3%) boys (P=0.066); SHORT STATURE in 132 (34.8%) of patients was not approved. Normal variants of SHORT STATURE (familial and constitutional) constituted 53.3% of etiology in SHORT patients. In 11.5% of SHORT patients, no obvious etiology was found, and 9.8% were born with intra uterine growth retardation. Other causes were growth hormone deficiency, hypothyroidism, skeletal dysphasia, Turner syndrome, and malnutrition.Conclusion: A great number of children and adolescents referred with SHORT STATURE to pediatric endocrinology clinics are not really SHORT. Greater than half of SHORT patients are normal variants of SHORT STATURE.

Background & Aims: Combination of chelating therapy regimens with regular blood transfusion has significantly improved the life expectancy of thalassemic patients. Despite progresses in treatment of these patients, growth failure, and SHORT STATURE are found in significant number of them. Factors such as iron overload, desferal toxicity, and endocrine disorders play roles in growth failure, but other unknown factors may contribute too. We aimed to study SHORT STATURE and its contributing factors in our thalassemic patients. Materials & Methods: This descriptive-analytic study was conducted in 2006, on 71 patients with ß-thalassemia major who had regular visits and complete medical recordings. The patients were evaluated for STATURE, endocrine disorders, serum ferritin, pretransfusion hemoglobin, and liver enzymes. They were compared in two (SHORT STATURE and non SHORT STATURE) groups. Results: 45 boys and 26 girls with mean age of 12.9±5.2 years were studied. 45.1% of patients were SHORT STATURE and negative linear correlation between advancing of age and height SDS observed. Patients with endocrine anomaly were SHORTer and those with multiple endocrine anomalies had very severe growth retardation. Cases of hypersplenism were significant in SHORT STATURE group, but there were no significant differences in pretransfusion hemoglobin and serum ferritin levels between the groups. Although liver enzymes increased in significant number of patients, we didn't find any meaningful differences between two groups. Conclusion: Growth failure of patients with b-thalassemia major begins from first decades of life and aggravated with age advancement. For prevention of becoming SHORT STATURE, they need to be evaluated regularly for height velocity, and contributing factors in growth failure should be recognized earlier and treated appropriately. 

Background: Physiological growth is a sensitive long-term indicator of child health. Impaired growth of children may be the first manifestation of a serious chronic disease. SHORT STATURE is a common pediatric endocrine problem. The SHORT STATURE, although not a disease per se, is a manifestation of several diseases. Its early diagnosis and treatment is most of the time rewarding.Methods: Children between the age group of 2 to 15 years with growth retardation attending endocrine clinic in Loghman Hospital, Tehran, in October 2003 through October 2005 were evaluated for SHORT STATURE.Evaluation included: detailed medical history, physical examination and laboratory tests such as blood count, thyroid function, growth hormone screening, bone age estimation, and karyotypes. Centers for Disease Control (CDC) growth charts were used for percentiles.Findings: 188 children (110 boys, 78 girls) with growth retardation, whose heights were below 2 standard deviation score for age and gender, attended endocrine clinic. Normal variations accounted for 85.5% of all etiologies for reasons such as constitutional delay 49% and familial SHORT STATURE 26.5% and a combination of both 9%. The rest (14.5%) consisted of pathological SHORT STATURE. Growth hormone deficiency and hypothyroidism were the most common causes of pathological SHORT STATURE Conclusions: The most common cause of SHORT STATURE was a normal variance followed by SHORT STATURE caused by endocrine disturbances. In both sexes constitutional growth delay followed by familial SHORT STATURE counted to the most common non-endocrine causes of SHORT STATURE.

Fifty years ago, treatment of growth hormone deficiency with human growth hormone (hGH) was first reported by Raben from the Tufts Medical Center1. In the early years each pituitary supplied enough growth hormone for treating one child for one week. Thus the hormone available for therapy was very scarce. For the next 25 years demands far exceeded supplies and treatment was limited to severely affected children. In 1981 we reported a growth hormone deficient boy who developed a rare neurological disorder and postulated that the disease (presumed to be Creutzfeldt-Jacob) was transmitted by a “slow virus” (now called prion) via the administered pituitary derived growth hormone2. Other reports soon followed and four years later treatment with hGH was banned worldwide.

Background: When the pituitary gland is not seen within the sella turcica on radiologic imaging studies, is called empty sella syndrome. It’s an infrequent finding in childhood, but is more frequently seen in girls than boys. Pituitary hormones deficiency is present in less than 10% of such cases. The single most common endocrine abnormalities noted in children with primary empty sella is growth hormone deficiency.Case presentation: An 11.5-year-old girl was referred for evaluation of SHORT STATURE. Her weight was 22 kg and height 128 cm, which was -3.6 SD below the mean. She had also not any signs of breast development and puberty at this age. After ruling out systemic illness, the patient underwent specialized tests and radiologic evaluation. She was diagnosed to have GH deficiency by poor response to GH stimulation test, other endocrine evaluation revealed that LH, FSH and estradiol levels were prepubertal, and the rest pituitary hormone were all normal. MRI showed a partial empty sella on pituitary magnetic resonance imaging. On the above findings diagnosis of partial empty sella syndrome was made.Conclusion: Empty sella is sometimes associated with pituitary hypofunction and is most often discovered during imaging studies. MRI or CT scans are useful in differentiating empty sella from other etiologies of pathologic SHORT STATURE. Treatment involves replacing the hormones that are lacking.