Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0272170 (SDS)
 50,377 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

USA 10,434 children with End State Renal Disease or chronic renal insufficiency have been followed by NAPRTCS. 5958 renal transplants have been performed. Haemoidalysis preceeded Tx in 28%, PD in 47% and 24% were preemptive transplants. The most common diagnoses were obstructive uropathy, renal dysplasia, FSGN, reflux nephropathy and CGN. 20.4 were < 5 and 24.9% < 12 years or age a transplant. 57.7% had living related donors. The most common therapy is with prednisone, cyclosporine and mycophenalate mofetile. Time to 1st rejection episode is 755 days in LRD and 98 days in CD. 5 year patient survival is 93.5% and 5 year graft survival in LRD is 80% and in CD is 65%. 75 cases of PTLD have been reported. 3748 patients have had maintenance dialysis. Peritoneal dialysis was the main modality in 67% and hemodialysis in 39%. 0.86 episodes/year of peritonitis has occurred in PD patients. 94% of patients received EPO therapy and 15% received growth hormone therapy. 3 year patient survival on dialysis is 86.5% (69.5% in those < 1 to 92.4% in those > 12 yrs of age). 3863 patients with chronic renal insufficiency have been followed. Mean height by standard deviation score is -1.41 with one third -1.88. Growth hormone for one year increased SDS by -0.30.
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PMID:Treatment of children in the U.S. with end-stage renal disease (ESRD). 1176 43

Amelogenesis imperfecta (AI) is a diverse group of hereditary disorders that are characterized by a defect in the formation of the tooth enamel and a high degree of clinical diversity. X-linked, autosomal dominant and recessive inheritance have been demonstrated. Growth hormone (GH) has an effect on bone and soft tissue development. Dental and facial abnormalities associated with pituitary dwarfism have been reported, but GH deficiency with AI is very rare. We describe a 12 year-old pre-pubertal boy who was referred to our hospital with teeth deformities and growth retardation. His teeth had brown-yellow pigmented surfaces, and dental examination showed extensive enamel deficiency in his permanent teeth. He also had severe growth retardation; height SDS was -3.6. Laboratory examinations showed reduced GH levels, and he was diagnosed as having idiopathic isolated GH deficiency and AI.
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PMID:Amelogenesis imperfecta with growth hormone deficiency in a 12 year-old boy. 1201 27

Growth hormone (GH) treatment has been used in children with intrauterine growth retardation (IUGR) to promote growth with success in several short- and long-term clinical trials. Intermittent GH therapy has also been advocated in children with IUGR. This study was designed to evaluate the growth of children with IUGR after discontinuation of a two-year trial of GH treatment. Sixteen children (12 F, 4 M) who had received GH (Genotropin) at age 5.3 (1.3) years at a dose of 0.2 IU/kg/day for 2 years (Group 1) and 10 (6 F, 4 M) controls of age 4.3 (1.7) years without treatment (Group 2) were followed after completion of the trial over a median period of 4 years. Height SDS of the GH-treated group showed an increase from -3.0 (0.5) to -1.9 (0.7) (p <0.001) over 2 years of therapy. Off therapy, height SDS decreased to -3.5 (0.5) at a mean age of 11.2 (1.6) years. The difference between the initial and recent height SDS in this group was significantly different (p = 0.02). Height SDS of the control group, -2.7 (1.4) initially, did not change over the two-year observation period. At follow-up, seven control children received GH in a similar fashion for one year. In spite of an insignificant increase in height SDS on one year of GH, it decreased to -2.9 (1.6) at age 11.0 (2.1) years at the latest visit. There was no significant difference between the recent heights of the two groups at final examination. One girl in Group 1 developed acanthosis nigricans and type 2 diabetes mellitus at age 13.3 years, after the follow-up period. A second patient developed osteosarcoma in the left tibia at age 9.9 years, for which she received chemotherapy and surgery. In conclusion, height SDS showed a significant increase on GH therapy for 2 years in children with IUGR; however, it decelerated after discontinuation of therapy. At the final visit, GH therapy did not seem to have had any effect on height prognosis. This finding shows that GH should be given continuously to improve final height in children with IUGR.
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PMID:Follow-up height after discontinuation of growth hormone treatment in children with intrauterine growth retardation. 1209 89

Growth hormone (GH), prostaglandins F (PGF) and prostaglandins E (PGE) are important regulators of ovarian function. Therefore, interrelationships between GH and these substances and their intracellular mechanisms might be of physiological significance in the ovary. The aims of this study on cultured porcine ovarian granulosa cells were to determine the effect of GH on the secretion of oxytocin (OT), PGF and PGE and whether MAP kinase could be involved in the mediation of GH action. Experiments were carried out with cultured porcine granulosa cells to investigate the effects of exogenous pGH (1-100 ng/ml) on the expression of MAP kinase (ERK-1, -2) and of PGH (1-100 ng/ml) and the MAP kinase blocker PD 98059 (1 microg/ml) on the secretion of PGF, PGE and OT. The cellular content of ERK-1 and -2 was analyzed by Western immunoblotting and immunocytochemistry, whilst PGF, PGE and OT accumulation in the medium was measured by RIA. Addition of GH to culture medium significantly altered the pattern of ovarian ERK MAP kinase on SDS-PA gels: the 44 and 42 kDa bands were reduced and additional 50 and 48 kDa bands appeared. Moreover, there was an increase in the percentage of cells containing ERK MAP kinase. GH stimulated the secretion of PGF (at a concentration of 1 ng GH per ml medium) and OT (100 ng GH per ml), but not PGE. The MAP kinase blocker alone did not affect PGF, PGE and OT secretion but did prevent the stimulatory effects of GH on PGF and induced stimulatory action of GH (10 ng/ml) on PGE. GH-stimulated OT secretion was unaffected. These observations confirm the role of GH in regulating porcine ovarian PGF, PGE and OT secretion and the presence of ERK MAP kinase in porcine granulosa cells. Furthermore, our studies demonstrate that MAP kinase-dependent intracellular mechanisms are dependent on GH, and that these mechanisms are involved in the mediation of GH action on ovarian PGF and PGE but not OT secretion.
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PMID:Involvement of MAP kinase in the mediation of GH action on ovarian granulosa cells. 1289 May 81

Growth hormone (GH) gene expression is not confined to pituitary somatotrophs and occurs in many extrapituitary tissues. In this study, we describe the presence of GH moieties in the chicken testis. GH-immunoreactivity (GH-IR), determined by ELISA, was found in the testis of immature and mature chickens, but at concentrations <1% of those in the pituitary gland. The immunoassayable GH concentration in the testis was unchanged between 4 and 66 weeks of age, and approximately 10-fold higher than that at 1-week of age and 25-fold higher than that in 1-day-old chicks and perinatal (embryonic day 18) embryos. This immunoreactivity was associated with several proteins of different molecular size, as in the pituitary gland, when analyzed by SDS-PAGE under reducing conditions. However, while most of the GH-IR in the pituitary ( approximately 40 and 15%, respectively) is associated with monomer (26 kDa) or dimer (52 kDa) GH moieties GH-IR in the testis is primarily (30-50%) associated with a 17 kDa moiety. GH bands between 32 and 45 kDa are also relatively more abundant in the testis than in the pituitary. During ontogeny the relative abundance of a 14 kDa GH and 40 kDa GH moieties in the testis significantly declined, whereas the relative abundance of the 17 and 45 kDa moieties increased with advancing age. In adult birds, GH-IR was widespread and intense in the seminiferous tubules. Although the GH-IR was not present in the basal compartment of Sertoli cells, nor in spermatogonia and primary spermatocytes, it was abundantly present in secondary spermatocytes and spermatids in the luminal compartments of the tubules as well as in some surrounding myocytes and interstitial cells. In summary, immunoreactive GH moieties are present in the chicken testis but at concentrations far less than in the pituitary. Age-related changes in the relative abundance of testicular GH variants may be related to local (autocrine/paracrine) actions of testicular GH. The localization of GH in spermatocytes and spermatids suggests hitherto unsuspected roles in gamete development.
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PMID:Growth hormone in the male reproductive tract of the chicken: heterogeneity and changes during ontogeny and maturation. 1509 34

Several studies have demonstrated an association between low birth weight and impaired insulin sensitivity or even type 2 diabetes mellitus (DM2) in later life. Growth hormone (GH) is known to increase fasting and postprandial insulin levels. For that reason concern has been expressed regarding possible detrimental effects of GH therapy in children born SGA. In a Dutch trial the possible side effects of GH therapy on carbohydrate metabolism were assessed in short children born SGA after 6 years and at 6 months after discontinuation of GH therapy. This study included 79 prepubertal short children born SGA, participating in a multicenter double-blind, randomized, dose-response GH trial. Inclusion criteria were: 1) birth length SDS below -1.88, 2) age 3-11 years in boys and 3-9 years in girls, 3) height SDS < -1.88, 4) no spontaneous catch-up growth, and 5) an uncomplicated neonatal period. Mean (SD) value for age was 7.3 (2.1) years, birth length SDS -3.6, height SDS -3.0 (0.7) and BMI SDS -1.2 (1.3). All children were randomly assigned to either group A (n = 41) using 1 mg GH/m2/day or group B (n = 38) using 2 mg/m2/ d/ay (approximately 0.1 or 0.2 IU/kg/d, respectively). Standard oral glucose tolerance tests (OGTTs) were performed before and during 6 years of GH therapy and 6 months after discontinuation of GH therapy. Before GH therapy 8% of the children had impaired glucose tolerance (IGT) according to criteria of the WHO. After 6 years of GH therapy, IGT was found in 4% and after stopping GH in 10%. Mean fasting glucose increased significantly with 0.5 mMol/l after 1 year of GH therapy, without a further increase thereafter. GH therapy induced considerably higher fasting and glucose-stimulated insulin levels. None of the observed changes were different between the GH dosage groups. Children who remained prepubertal had similar glucose and insulin levels compared to children who entered puberty. HbA1c levels were always in the normal range and none of the children developed diabetes mellitus. After discontinuation of GH therapy the mean serum glucose levels remained normal and the mean serum insulin levels decreased significantly, to normal age reference values. Before the start of GH the mean systolic blood pressure was significantly higher compared to age-matched peers, whereas during GH therapy a significant decline in mean systolic blood pressure occurred, which remained similar after discontinuation of GH treatment. In conclusion, continuous, long-term GH therapy in short children born SGA has no adverse effects on glucose levels, even with GH dosages up to 2 mg/m2/day. However, as has been reported in other patient groups, GH induced higher fasting and glucose-stimulated insulin levels, indicating insulin resistance. After discontinuation of GH, serum insulin levels declined to normal age-matched reference levels. Since impaired insulin sensitivity and DM2 have been demonstrated in relatively young patients born SGA, long-term follow-up of children born SGA is advised, also after discontinuation of GH therapy.
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PMID:Small for gestational age (SGA): endocrine and metabolic consequences and effects of growth hormone treatment. 1513 8

Growth hormone (GH) expression is not confined to the pituitary and occurs in many extrapituitary tissues. Here, we describe the presence of GH-like moieties in chicken lymphoid tissues and particularly in the bursa of Fabricius. GH-immunoreactivity (GH-IR), determined by ELISA, was found in thymus, spleen, and in bursa of young chickens, but at concentrations <1% of those in the pituitary gland. Although the GH concentration in the spleen and bursa was approximately 0.82 and 0.23% of that in the pituitary at 9-weeks of age, because of their greater mass, the total GH content in the spleen, bursa, and in thymus were 236, 5.18, and 31.5%, respectively, of that in the pituitary gland. This GH-IR was associated with several proteins of different molecular size, as in the pituitary gland, when analyzed by SDS-PAGE under reducing conditions. While most of the GH-IR in the pituitary was associated with the 26 kDa monomer (40%), the putatively glycosylated 29 kDa variant (16%), the 52 kDa dimer (14%) and the 15 kDa submonomeric isoform (16%), GH-IR in the lymphoid tissues was primarily associated (27-36%) with a 17 kDa moiety, although bands of 14, 26, 29, 32, 37, 40, and 52 kDa were also identified in these tissues. The heterogeneity pattern and relative abundance of bursal GH-IR bands were determined during development between embryonic day 13 (ED13) and 9-weeks of age. The relative proportion of the 17 kDa GH-like band was higher (45-58%) in posthatched birds than in the 15 and 18-day old embryos (21 and 19%, respectively). The 26 kDa isoform was minimally present in embryos (<4% of total GH-IR) but in posthatched chicks it increased to 12-20%. Conversely, while GH-IR of 37, 40, and 45 kDa were abundantly present in embryonic bursa ( approximately 30% at ED13 and approximately 52-55% at ED15 and ED18, respectively), in neonatal chicks and juveniles they accounted for less than 5%. These ontogenic changes were comparable to those previously reported for similar GH-IR proteins in the chicken testis during development. In summary, these results demonstrate age-related and tissue-specific changes in the content and composition of GH in immune tissues of the chicken, in which GH is likely to be an autocrine or paracrine regulator.
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PMID:Heterogeneity of growth hormone immunoreactivity in lymphoid tissues and changes during ontogeny in domestic fowl. 1593 23

Growth hormone (GH) therapy has evolved rapidly over the past decade. Ongoing research has demonstrated a clear role for therapeutic GH in a wide spectrum of pediatric disorders involving both poor growth and abnormal body composition. Although guidelines for GH dosing are not fully established, a series of key studies has delineated the range of dosages that are useful in the treatment of children with growth disorders. The recent approval of idiopathic short stature (ISS) as an indication for GH therapy presents further challenges in optimizing the care of GH-treated patients. ISS is now recognized as a diverse collection of environmental and molecular abnormalities, some of which involve the GH-IGF axis. Emerging data indicate that serum IGF-I measurements are not only useful in the diagnosis of growth abnormalities but, in conjunction with auxological measurements, are also a powerful tool for assessing GH efficacy. While it is clear that many ISS patients respond to GH, some individuals will not show a satisfactory response. Monitoring IGF-I levels and change in height SDS during treatment can assist the physician in distinguishing those patients in whom GH successfully and safely induces statural growth from those with partial or complete GH insensitivity who might benefit from modified GH treatment protocols or alternate therapies. In addition, serum IGF-I measurements are increasingly used as part of a rational monitoring strategy to ensure safety of GH dosing in light of cumulative data associating high IGF-I levels with potential malignancy risk, and low IGF-I levels with cardiovascular disease risk.
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PMID:Insulin-like growth factor I (IGF-I) measurements in growth hormone (GH) therapy of idiopathic short stature (ISS). 1603 93

The state of bone health and the effect of growth hormone (GH) therapy on bone and body composition in children with idiopathic short stature (ISS) are largely unknown. A direct role of GH deficiency (GHD) on bone density is controversial. Using dual-energy X-ray absorptiometry, this study measured total body bone mineral content (TB BMC), body composition, and volumetric bone mineral density (vBMD) at the lumbar spine (LS) and femoral neck (FN) in 77 children (aged 3-17 years) with ISS (n = 57) and GHD (n = 20). Fifty-five children (GHD = 13) receiving GH were followed over 24 months including measurement of bone turnover. At diagnosis, size-corrected TB BMC SDS was greater (P <or= 0.002) and LSvBMD SDS lower (P < 0.03) than zero in both prepubertal ISS and GHD subjects, but FNvBMD SDS was reduced only in the GHD group (P < 0.05). The muscle-bone relation, as assessed by the BMC/lean mass (LTM) ratio SDS was not different between groups. During GH therapy, prepubertal GHD children gained more height (1.58 [0.9] SDS) and LTM (0.87 [0.63] SDS) compared to prepubertal ISS children (0.75 [0.27] and 0.17 [0.25] SDS, respectively). Percent body fat decreased in GHD (-5.94% [4.29]) but not in ISS children. Total body BMC accrual was less than predicted in all groups accompanied by an increase in bone turnover. Puberty led to the greatest absolute, but not relative, increments in weight, LTM, BMI, bone mass, and LSvBMD. Our results show that children with ISS and GHD differ in their response to GH therapy in anthropometry, body composition, and bone measures. Despite low vBMD values at diagnosis in both prepubertal groups, size-corrected regional or TB bone data were generally within the normal range and did not increase during GH therapy in GHD or ISS children. Growth hormone had great effects on the growth plate and body composition with subsequent gains in height, LTM, bone turnover, and bone mass accrual, but no benefit for volumetric bone density over 2 years.
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PMID:Effect of growth hormone therapy and puberty on bone and body composition in children with idiopathic short stature and growth hormone deficiency. 1613 78

Growth hormone releasing hormone is one of the hormones secreted by the hypothalamus. Because of its potential applications in agriculture and medicine, its short half-life and its expensive chemical synthesis, an analog with high GHRH activity and prolonged half-life has been looked for. The fusion partner gene with 127 amino acid residues of the C-terminus from L-asparaginase was recombined respectively with asp-pro-pro-hGHRH(1-44), asp-pro-hGHRH(1-44) or asp-1pro-GHRH(2-44) genes synthesized by PCR method to form three kinds of fusion proteins with unique acid labile linker Asp-Pro. The Pro-Pro-hGHRH(1-44), Pro-hGHRH(1-44), and 1Pro-GHRH(2-44) peptides were purified to homogeneity by means of cell disruption, washing of inclusion body, ethanol fraction precipitation, acid hydrolysis, SP-Sephadex C-25 and Sephadex G-10 column chromatography. The peptide molecular mass of 5235, 5139 or 4975 Da was determined by ESI mass spectroscopy and purity was determined by SDS-PAGE. In the study of in vitro activity, the antiserum kit against human GH and peptide doses of 0.1, 1.0 and 10 microg/ml were used. These peptides obviously increased GH releases both from human pituitary and from rat pituitary. The activity comparisons showed that there was significant difference between Pro-Pro-hGHRH(1-44)-Gly-Gly-Cys and Pro-Pro-hGHRH(1-44) at 1.0 microg/ml, or between 1Pro-hGHRH(2-44) and Pro-Pro-hGHRH(1-44) or Pro-hGHRH(1-44) at 10 microg/ml. The structure-activity relationships showed that at the original C-terminus, for rat pituitary the activity of the GHRH analog with 1Tyr-->Pro was more than that of Pro-Pro-hGHRH(1-44) or Pro-hGHRH(1-44). The results showed that the analogs had good GH-releasing activity and species specificity.
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PMID:Study on the constructions and activities of three novel hGHRH analogs with N-terminal prolyl modulation+. 1626 50


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