PURPOSE:Hypochondroplasia is a skeletal dysplasia characterized by poor childhood growth and an inadequate pubertal growth spurt. Final height attainment of hypochondroplasia has been reported to range between 120 and 152cm. Increased availability of growth hormone with the introduction of recombinant human growth hormone has allowed for clinical trials in a number of growth hormone sufficient children with growth problems. The purpose of this study was to assess the growth promoting effect of human growth hormone in children with hypochondroplasia. METHODS:Five patients with hypochondroplasia diagnosed by clinical and radiological findings between 1993 and 1997 at our hospital was aged 3 and 1/2 -11 and 1/2 years. Each patients continuously received human growth hormone 0.6-0.7U/Kg/week, intramuscularly or subcutaneously in 6-7 divided dose for 2 years. Standard auxologic assessment was carried out every 3 month interval in the first year after commencement of therapy and then same assessment was 6 monthly. Bone age was assessed 6 monthly using Gleurich-Pyle method. RESULTS:Mean height velocity of pretreatment and year 1 and 2 of GH treatment were 3.9+/-0.7, 6.5+/-1.8 and 5.7+/-1.5cm/year, respectively. Mean height standard deviation score for chronological age of pretreatment and year 1 and 2 of GH treatment were -2.7+/-0.3, -2.4+/-0.3 and -2.2+/-0.4, respectively. The increase in the height velocity diminishes over the subsequent year. The increment of bone age after GH treatment were same as the increments of chronological age. CONCLUSION: Short-term GH therapy increases the height velocity of children with hypochondroplasia, but the effect of GH therapy on final height remains unknown.
Child* ; Growth Hormone* ; Human Growth Hormone ; Humans

No abstract available.
Human Growth Hormone* ; Humans*

No abstract available.
Female* ; Human Growth Hormone* ; Humans*

Bilateral coronoid process hyperplasia is a rare condition characterized by an enlarged mandibular coronoid process. The painless progressive reduction of a mouth opening is caused by coronoid process impingement on the posterior aspect of the zygomatic bone. Hyperplasia of the bilateral coronoid process leads to the restriction of a mandibular opening consequent to the impingement of the enlarged coronoid process on the temporal surface of the zygomatic bone or with the medial surface of the zygomatic arch. The process has been diagnosed as developmental hyperplasia. Otherwise, the development of the coronoid process may be associated with growth hormone. This paper describes a case of trismus caused by coronoid hyperplasia in an idiopathic short-stature patient who received growth hormone therapy by somatropin injections.
Growth Hormone ; Human Growth Hormone ; Humans ; Hyperplasia ; Mouth ; Trismus ; Zygoma

Recombinant human growth hormone (GH) has been in use for over 30 years, and its indications have gradually expanded from the classical replacement therapy in GH deficiency (GHD) to pharmacological therapy in patients with normal GH secretion. The insulin-like growth factor-I (IGF-I ) is closely GH dependent and is the effector of GH biological actions in peripheral tissues. Since IGF-I has potent mitogenic and antiapoptotic effects, the use of GH, especially outside GHD, has raised safety concern regarding cancer risk. The results of experimental, epidemiological and observational studies are not univocal and a number of biases and confounders affect the interpretation of data. The aim of this review is to critically review the data linking GH therapy during childhood with cancer risk, highlighting strengths and weaknesses of the available evidence.
Bias (Epidemiology) ; Growth Hormone ; Human Growth Hormone ; Humans ; Humans ; Insulin-Like Growth Factor I

Child ; Humans ; Human Growth Hormone/therapeutic use* ; Growth Disorders/therapy*

Background:Eutropin is a recombinant human growth hormone preparation and has been used in patients with growth hormone deficiency. Short stature is a characteristic feature of Turner syndrome, which is caused by sexual chromosomal anomalies. Growth hormone therapy would increase growth velocity and increase the ultimate final height in patients with Turner syndrome. The purpose of this study was to evaluate the clinical effects and safety in patients with Turner syndrome with Eutropin treatment. Subjects and METHODS:60 patients with Turner syndrome,who were diagnosed by chromosome study,were treated with Eutropin 1IU/kg/week for 12 months and followed up every 3 month. The height and weight were evaluate at 0, 3, 6, 9, 12 months. A complete blood count, ESR, urinary analysis and chemistry studies were done every 3 month. IGF- I , T4, TSH & anti-GH antibody were measured at 6 months and 12 months. Chest X-ray was checked at 0, 6 ,12 months. RESULTS:60 patients were enrolled but 10 patients were lost or treated irregularly and excluded in the study of growth effect. but included all cases in safety analysis. At the onset of Eutropin therapy,their mean age was 10.8+/-2.9 years old(range 4.2- 14.9yr)and the height was 121.1+/-13.7cm(-3.1+/-0.9 SDS) and yearly growth velociy was 3.4+/-1.5cm. Their weight was 30.5+/-10.6kg and bone age 9.1+/-3.0 yrs. After Eutropin treatment, mean height was increased to 123.2+/-13.5cm at 3 months, 125.2+/-13.1cm at 6 months, 127.5+/-12.4cm at 9 months, 128.3+/-12.8cm at 12 months. Height velocity were increased to 8.3+/-3.1cm at 3 months, 8.1+/-2.6cm at 6 months, 7.6+/-1.9cm at 9 months and 7.1+/-1.9cm at 12 months(P<0.001). Height SDS at 0, 3, 6, 9, 12 months were -3.1+/-0.9, -2.9+/-1.0, -2.7+/-0.9, -2.7+/-0.9 respectively(P>0.001).Their bone age were 9.1+/-3.0yr, 9.6+/-2.9yr, 10.2+/-2.7yr before and 6 & 12 months after treatment respectively. HA/BA were 0.84+/-0.15, 0.87+/-0.13, 0.88+/-0.12 at before and 6 & 12 months after treatment respectively(P<0.05). Growth velocity of 4-8 yrs group was most prominent compared to other groups. Serum IGF- I concentration was increased from 167.4+/-85.8ng/ml to 368.4+/-158.1ng/ml at 6 months and 423.2+/-181.0ng/ml at 12 month(P<0.001) after treatment. No significant changes were observed in thyroid function, CBC, ESR, Blood chemistry and urinalysis. Anti-hGH antibody were positive in 2 patients, but these didnot attenualte the growth velocity. CONCLUSION: Treatment with Eutropin increased significantly height velocity in patients with Turner syndrome. No specific adverse events were observed during Eutropin therapy.
Blood Cell Count ; Chemistry ; Growth Hormone ; Human Growth Hormone ; Humans* ; Thorax ; Thyroid Gland ; Turner Syndrome* ; Urinalysis

PURPOSE: Short stature is the most common finding in patients with Turner syndrome. Improving the final adult height in these patients is a challenge both for the patients and physicians. We investigated the clinical response of patients to growth hormone treatment for height improvement over the period of three years. METHODS: Review of medical records from 27 patients with Turner syndrome treated with recombinant human growth hormone for more than 3 years was done. Differences in the changes of height standard deviation scores according to karyotype were measured and factors influencing the height changes were analyzed. RESULTS: The response to recombinant human growth hormone was an increase in the height of the subjects to a mean value of 1.1 standard deviation for subjects with Turner syndrome at the end of the 3-year treatment. The height increment in the first year was highest. The height standard deviation score in the third year was negatively correlated with the age at the beginning of the recombinant human growth hormone treatment. Different karyotypes in subjects did not seem to affect the height changes. CONCLUSION: Early growth hormone administration in subjects with Turner syndrome is helpful to improve height response to the treatment.
Adult ; Growth Hormone ; Human Growth Hormone ; Humans ; Karyotype ; Medical Records ; Treatment Outcome ; Turner Syndrome

We investigated the acute effect of recombinant human growth hormone (rhGH) on the activity of polymorphoneuclear leukocyte (PMN). We selected 6 patients of growth hormone deficient and 5 normal control children. In both groups, 0.15 IU/kg of rhGH was administered subcutaneously. The plasma growth hormone level were measured by radioimmunoassay on 0, 2, and 6 hours after administration of rhGH. To determined PMN activity, peripheral blood PMN were separated by discontinuous density-gradient centrifigation. Isolated PMN were stimulated hy fMLP and PMA and then respiratory burst activity of PMN was determined. The average growth hormone level of growth horrnone deficient and normal group were increased to the level of 41.6+/-23.7 and 96.3+/-46.5 ng/ml respectively, 2 hours after rhGH injection and decreased to the level of 18.5+/-10.6 and 42.2+/-5.5 ng/ml respectively, 6 hours after rhGH injection. Superoxide (O ) production by PMN which was stimulated by PMA was increased from 9.98+/-5.18 to 38.67+/-19.19 (x 10'cpm) after 6 hours of rhGH injection in control group children. It seemed that administration of the rhGH do not made a any effects acutely on PMN activity in growth hormone deficient group. But in a normal control children, extemal administration of rhGH acutely increased activity of PMN.
Child* ; Growth Hormone ; Human Growth Hormone* ; Humans* ; Leukocytes ; Neutrophils* ; Plasma ; Radioimmunoassay ; Respiratory Burst ; Superoxides

Growth hormone deficiency (GHD) is a clinical syndrome associated with increased morbidity and possibly mortality. Many clinical studies over the past decade show beneficial effects of replacement therapy with recombinant human growth hormone in GHD in adults. GH replacement in patients with GHD induces reduction of cardiovascular risk factors, improvement of lipid profile, normalization of body composition and improvement of exercise capacity, as well as enhanced psychological well-being. To make a diagnosis of GHD, insulin-induced hypoglycemia is recommended as a standard test, but the arginine-GH-releasing hormone test achieves comparable separation between normal and hypopituitary subjects in most groups. GHD should be always confirmed by the results of biochemical, especially provocative, tests, and therapy should be limited to those with biochemically proven growth hormone deficiency.
Adult ; Body Composition ; Growth Hormone ; Human Growth Hormone ; Humans ; Hypoglycemia ; Hypopituitarism ; Risk Factors