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Query: UMLS:C0272170 (SDS)
 50,377 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of biosynthetic human growth hormone (b-hGH) treatment on rat skin collagen was investigated. Groups of rats were injected with b-hGH 0.16, 1.10 and 8.33 mg/kg/day for 90 days. The weight gain of the rats treated with b-hGH 1.10 and 8.33 mg/kg/day was 13% and 82% higher, respectively, compared with that of the placebo control group. The extractability of the skin collagen was studied by extraction with phosphate buffered saline (pH 7.4), followed by acetic acid (0.5 M) and acetic acid with pepsin. The reducible collagen cross-links were measured after reduction of the cross-links by KB3H4, followed by acid hydrolysis and ion-exchange chromatography. Furthermore, patterns of cyanogen bromide peptides were studied by SDS-poly-acrylamide-gel-electrophoresis. Peptides bound together by stable cross-links and the relative amounts of collagen type I and collagen type III were measured. Treatment with b-hGH 8.33 mg/kg/day resulted in increased extractability of the skin collagen in acetic acid, increased relative amounts of reducible collagen cross-links and reduced amounts of high molecular weight cyanogen bromide cleaved peptides of the collagen. These alterations probably reflect an increased synthesis of skin collagen induced by the highest dose of b-hGH. The relative amounts of collagen type I and collagen type III of the skin were not influenced by the b-hGH treatment.
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PMID:Alterations in the cross-links of skin collagen of rats treated with biosynthetic growth hormone. 206 Mar 8

A binding protein for growth hormone in serum from female rats has been identified and partially characterized. Serum was incubated with 125I-labelled human GH and fractionated on an agarose HPLC column. Complexes between the binding protein and 125I-hGH were detected as a peak eluted at a volume corresponding to a relative molecular weight of 159,000 +/- 11,000 (N = 8). The peak was not seen when the incubation was carried out in the presence of excess unlabelled hGH. The 125I-hGH bound with high affinity (Ka = 0.87 +/- 0.3 l/nmol; N = 3) and the binding was time- and dose-dependent. Bound 125I-hGH was displaced by rat GH and bovine GH, but not by rat prolactin. The protein was not detected in radioreceptor assay by the commonly used polyethylene glycol precipitation technique and was not recognized by a monoclonal antibody raised against lactogenic receptors from female rat liver. Covalent cross-linking of 125I-hGH to serum revealed in SDS electrophoresis two labelled complexes with molecular weights of 62,300 +/- 3900 and 77,600 +/- 4100, respectively (N = 10).
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PMID:Identification and partial characterization of a growth hormone-binding protein in rat serum. 215 95

Overnight physiological growth hormone (GH) secretion was evaluated in 95 short, prepubertal children (73 boys, 22 girls). All the children were below the 3rd centile for height and achieved GH levels greater than 15 mU/l following pharmacological stimulation. The mean average GH level was 7.1 mU/l and the mean sum of pulse amplitudes 80.4 mU/l. No relationship was found between age, height or height velocity and any of the parameters of GH secretion. The group was randomized to receive placebo, GH or remain under observation for the first 6 months and then all patients received GH treatment for a further 6 months. Those treated with GH, 0.27 IU/kg (0.1 mg/kg) three times weekly, in the first phase, demonstrated a mean increase in height velocity SDS of 3.24. There was no difference in growth response between the placebo or observation groups. In the second 6-month period, all children received GH according to the same dose regimen; they were then observed for a further 6 months following its discontinuation. In the 6 months following withdrawal of GH, all groups showed a significant fall in height velocity SDS, which returned to pretreatment levels, without demonstrating 'catch-down' growth. Repeat sampling of overnight GH secretion within 3 days of discontinuing GH showed normal secretory patterns with a small reduction in mean peak amplitude. These results suggest that short children without classic GH insufficiency respond well to exogenous GH in the short term and return to pretreatment height velocities afterwards. Consequently, it may be possible to increase final adult height in such children by GH treatment.
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PMID:Growth hormone treatment in non-growth hormone-deficient children: effects of stopping treatment. 220 5

The effect of 3 years of growth hormone (GH) treatment on growth rate, predicted height, carbohydrate and metabolic status, and thyroid function was studied in 16 short prepubertal children growing with a normal pretreatment growth rate. The height velocity SDS increased from a pretreatment value of -0.44 +/- 0.33 (mean +/- SD) to a value of +2.20 +/- 1.03 during the first year of treatment. It was maintained at a value above zero over the subsequent 2 years. By the end of the third year of treatment, the predicted final height had increased by 6.8 cm in the boys and by 4.2 cm in the girls (p less than 0.001 and p less than 0.01, respectively). Increasing the dose of GH on a body surface area basis reduced the deceleration of growth observed during the second year of treatment, leading to an improvement in height prognosis over that year. Glucose homoeostasis was achieved initially at the expense of an elevation in fasting serum insulin concentration, but this had returned to pretreatment values by the end of the second year of therapy.
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PMID:Effects of 3 years of growth hormone therapy in short normal children. 220 7

Preliminary results from an ongoing multicentre study on pubertal growth and sexual maturation in chronic renal failure are presented. Puberty was delayed by approximately 2.5 years in both sexes in children with chronic renal failure. There was also an irreversible decline in height SDS during puberty. The pulsatile secretion of growth hormone (GH) and luteinizing hormone (LH) were disrupted in patients on conservative treatment or dialysis compared with those in patients with renal transplants; the mean nocturnal GH level and the mean GH peak amplitude were increased, while the number of pulses and peak amplitude of LH were decreased. The biopotency of LH, expressed as the ratio of bioactive to immunoreactive LH, was suppressed in patients with renal transplants.
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PMID:Growth and development of children with chronic renal failure. Study Group on Pubertal Development in Chronic Renal Failure. 220 11

Placental lactogen (PL) was isolated from goat cotyledonary tissue by a combination of mild alkaline extraction, anion and cation exchange chromatography, chromatofocussing and molecular filtration. The product, enriched 15,000-fold from the initial extract, was homogeneous when examined by SDS-gel electrophoresis (Mr 22,500) and isoelectricfocussing indicated a pI of 8.35 with a trace contaminant of pI 8.0. When assessed by relative binding activity in radioreceptor assays (RRA), goat PL exhibited somatotropic activity equivalent to 2.2 units/mg dry weight and lactogenic activity equivalent to 28.5 units/mg. A radioimmunoassay (RIA) for goat PL is described that is highly sensitive (190 pg/tube) and has acceptable repeatability within and between assays (6 and 13%, respectively). The assay is not affected by goat pituitary extracts or partly purified goat growth hormone and prolactin. Despite the marked increase in sensitivity of the RIA over that previously available when goat PL was measured by RRA, the hormone was not detected in jugular plasma of goats before Day 44 of pregnancy; concentrations increased thereafter and highest levels were measured during the last third of pregnancy in animals bearing triplets. Measurements by RIA are in general agreement with those obtained earlier in several studies in which RRAs were used. The hormone was detected in amniotic fluid. Maternal concentrations of goat PL declined before parturition and were undetectable by 18 h post partum.
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PMID:Purification, partial characterization, and development of a specific radioimmunoassay for goat placental lactogen. 223 47

The present demographic data from the Kabi International Growth Study (KIGS) database are summarized. Of the 2580 patients included, 85% have growth hormone deficiency (GHD) and 15% have other causes of growth failure. Idiopathic GHD is present in 78.5% of the patients, the remaining 21.5% have organic GHD. Isolated GHD is common in idiopathic GHD whereas multiple pituitary hormone deficiencies occur in at least 50% of the organic GHD patients. A preponderance of boys is observed in most groups of patients. Median chronological age (CA) at start of treatment is 10 years and median duration of therapy is 2.3 years. However, a wide range is observed. In most cases growth retardation is severe. In most patients with GHD height SDS for chronological age at start of therapy is at or below -3. The median difference between idiopathic and organic GHD is 1 SDS. Most patients have 6 or 7 injections of growth hormone (GH) per week. The median total weekly dose is approximately 0.5 IU/kg/week, but it is lower in older patients. It is concluded that steadily increasing numbers of patients with idiopathic and organic GHD are being treated with human GH (hGH). In addition, many patients with other growth disorders not necessarily associated with GHD receive hGH therapy. Chronological age at start of treatment still appears to be (too) high in most patients and growth retardation severe. The frequency of hGH injections has been increased to nearly daily administration. However, the total weekly dose appears to be low, especially in the older patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Who is treated with growth hormone today? The Executive Scientific Committee of the Kabi International Growth Study. 226 Apr 48

This study analyses gestational age, mode of delivery and size at birth in children who later developed idiopathic or organic growth hormone deficiency (GHD). A data register of children on growth hormone (GH) treatment in Sweden was compared with the Swedish Medical Birth Register during a 14-year period (1973-1986) comprising 1.4 million newborn children. Size at birth was evaluated using a new Swedish reference standard based on data from around 500,000 newborn children. It was found that the children who later develop idiopathic GHD (IGHD) were born with a normal distribution of gestational age. They were more often born with breech delivery (7.1% versus 2.8%) or caesarean section (16.6% versus 10.4%) compared with normal children. The children's condition at birth was poorer than normal, as shown by the frequency of Apgar scores below 7 at 5 minutes (5.2% versus 1.2%). Finally, it was found that children who later develop IGHD (n = 220) had a median birth length of 0.87 SDS below the mean and a median birth weight of 0.60 SDS below the mean of the standard. In contrast, both the birth length and weight of the children who later develop organic GHD (OGHD) (n = 92) did not differ from that of the reference.
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PMID:Birth data for patients who later develop growth hormone deficiency: preliminary analysis of a national register. The Executive Scientific Committee of the Kabi International Growth Study and the Swedish Paediatric Study Group for Growth Hormone Treatment. 226 Apr 49

In order that children with growth hormone deficiency (GHD) reach the goal of normal adult stature, treatment modalities need to be optimized. From the large database of patients enrolled in the Kabi International Growth Study (KIGS), 257 prepubertal patients with idiopathic GHD undergoing their first year of growth hormone (GH) substitution therapy were selected. A multiple regression analysis was performed to determine both auxiological factors characterizing the patients and the factors related to the chosen treatment modalities which are of significance for the observed magnitude of the growth response. Due to the structure of the data, pretreatment height velocity and bone age-derived auxiological data were not considered. It was observed that the magnitude of the growth response was inversely correlated with chronological age and relative height (HT SDS) at the start of GH treatment but was positively correlated with mid-parental height. The growth response was also positively correlated with the GH dose (IU/kg/week) and the frequency of GH injections per week. A regression equation using these five parameters was derived, allowing the growth response of these patients to be predicted. The extension of this analytical approach in the future will allow the treatment of patients with GHD to be tailored to individual requirements.
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PMID:Growth response in prepubertal children with idiopathic growth hormone deficiency during the first year of treatment with human growth hormone. Analysis of the Kabi International Growth Study. 226 Apr 50

Growth retardation is common in children with chronic renal disease. Final adult height is often reduced, even in children with a functioning renal transplant. The five European studies considered here aim to investigate the efficacy and safety of recombinant human growth hormone therapy (rhGH) in two groups of short children with chronic renal disease. The first group comprises 29 prepubertal children with preterminal chronic renal failure (i.e. before renal transplantation), and the second group comprises 39 prepubertal and pubertal children with functioning renal transplants. The median bone age retardation in the groups at the start of treatment was between 2.2 and 3.7 years; this did not change during the first year of treatment. This interim report concentrates on patients who have been treated for at least 1 year (i.e. 22 children from the first group, and 28 children from the transplant group (15 prepubertal and 13 pubertal children). The median height velocity increased from 4.8 cm/year to 10.0 cm/year in the first group (the chronic renal failure group), from 2.6 cm/year to 6.2 cm/year in prepubertal children with renal transplants and from 3.8 cm/year to 6.7 cm/year in pubertal children with renal transplants. The corresponding changes in height velocity SDS were from -1.3 to 5.1 for the chronic renal failure group and -2.8 to 2.3 for the prepubertal children with renal transplants. Renal function declined in the chronic renal failure group but this decline corresponded to expected progression of the disease. Some of the children with renal transplants showed a decreased renal function, which in most cases was explained by non-compliance or chronic rejection.
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PMID:Recombinant human growth hormone treatment in short children with chronic renal disease, before transplantation or with functioning renal transplants: an interim report on five European studies. 226 Apr 56


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