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Biomedical subjects

R Rosskamp

Publications and source records attributed to R Rosskamp.

30 records · Page 2Linked to original sources
PubMed1986

Testing with growth hormone-releasing factor (GRF(1-29)NH2) and somatomedin C measurements for the evaluation of growth hormone deficiency.

Growth hormone (GH) responses to GRF (1 microgram/kg BW i.v.) were investigated. Comparison between GRF(1-40) and GRF(1-29)NH2 in 11 young adult volunteers gave identical results. One hundred and thirty-one children and adolescents (45 with idiopathic GHD) were tested with GRF (1-29)NH2. The maximal GH levels (max GH) in response to GRF during the 120 min test period were found suitable to characterize the response. In cases without GHD no correlation to age, sex and pubertal development was observed. A maximal GH level of above 10 ng/ml was found to be normal. In 3 out of 86 children without GHD (one with Turner syndrome; two with simple obesity) max GH fell short of 10 ng/ml, while 11 of 45 cases with GHD exceeded this margin. In GHD, max GH was inversely correlated with age. There was no difference in max GH between groups with or without perinatal pathology as a presumed cause of GHD. GH levels to GRF were positively correlated with maximal GH level during sleep in GHD, but not correlated with responses seen to insulin or arginine. The value of GRF testing for the confirmation of GHD is discussed in the light of other GH stimulatory tests and basal somatomedin C measurements. It is suggested that the combination of testing with GRF and the determination of a basal SmC level offers a safe and convenient way to diagnose GHD in clinically suspected cases, though in some cases further diagnostic tests may be needed.

Adolescent↗
PubMed1986

[Circulating somatostatin concentrations in childhood. Studies in normal weight and obese children and patients with growth hormone deficiency].

At present in childhood there is only few information about the importance concerning circulating somatostatin concentrations. We therefore investigated the plasma somatostatin response to a mixed meal, an oral glucose load, pentagastrin injection and insulin hypoglycemia in normal weight and obese children and patients with growth hormone deficiency. Results in normal weight children: 1. Following a 800 kcal mixed meal (50% carbohydrate, 35% protein, 15% fet) peak values of plasma somatostatin were reached within 30-180 min (37.6 +/- 4.2 pg/ml vs. 58.5 +/- 3.4 pg/ml; p less than 0.05) in 6 children. 2. In response to oral glucose load of 1.75 g/kg bw glucose no alterations of plasma somatostatin levels were observed in 13 children 3. Injection of 6 micrograms/kg bw pentagastrin s.c. in 10 children resulted in maximal increase of somatostatin concentrations between 5 and 15 min (32.0 +/- 4.5 pg/ml vs. 69.1 +/- 7.4 pg/ml; p less than 0.01). 4. Injection of 0.1 IU/kg bw insulin in 7 children induced hypoglycemia and stimulated peak values of plasma somatostatin within 15-60 min (32.0 +/- 6.6 pg/ml vs. 57.4 +/- 6.4 pg/ml; p less than 0.01). - Results in obese children: Following mixed meal ingestion in 7 obese children plasma somatostatin response was comparable to controls. Although integrated insulin response over 180 min was higher in this group (9694 +/- 1363 microU/ml vs. 5054 +/- 651 microU/ml; p less than 0.05) the integrated somatostatin response (9038 +/- 1852 pg/ml) did not differ from controls (8614 +/- 876 pg/ml). After oral glucose load no changes in circulating somatostatin concentrations were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

A randomized multicentre trial of insulin glargine compared with NPH insulin in people with type 1 diabetes.

BACKGROUND: To compare insulin glargine with NPH human insulin for basal insulin supply in adults with type 1 diabetes. METHODS: People with type 1 diabetes (n = 585), aged 17-77 years, were randomized to insulin glargine once daily at bedtime or NPH insulin either once- (at bedtime) or twice-daily (in the morning and at bedtime) according to their prior treatment regimen and followed for 28 weeks in an open-label, multicentre study. Both groups continued with pre-meal unmodified human insulin. RESULTS: There was no significant difference between the two insulins in change in glycated haemoglobin from baseline to endpoint (insulin glargine 0.21 +/- 0.05% (mean +/- standard error), NPH insulin 0.10 +/- 0.05%). At endpoint, self-monitored fasting blood glucose (FBG) had decreased similarly in each group (insulin glargine -1.17 +/- 0.12 mmol/L, NPH insulin -0.89 +/- 0.12 mmol/L; p = 0.07). However, people on >1 basal insulin injection per day prior to the study had a clinically relevant decrease in FBG on insulin glargine versus NPH insulin (insulin glargine -1.38 +/- 0.15 mmol/L, NPH insulin -0.72 +/- 0.15 mmol/L; p < 0.01). No significant differences in the number of people reporting >or=1 hypoglycaemic episode were found between the two groups, including severe and nocturnal hypoglycaemia. Insulin glargine was well tolerated, with a similar rate of local injection and systemic adverse events versus NPH insulin. CONCLUSIONS: A single, bedtime, subcutaneous dose of insulin glargine provided a level of glycaemic control at least as effective as NPH insulin, without an increased risk of hypoglycaemia.

Adolescent↗
PubMedDate not supplied

[Hormonal findings in obese children. A review].

Serum thyroid hormones in childhood obesity are not altered but caloric intake affects monoiodination of T4 to T3 and rT3. Plasma cortisol and urinary free cortisol concentrations are normal. Increase in cortisol production and secretion rate is reflected in increased values of urinary 17-hydroxycorticosteroids. Elevated urinary 17-ketosteroids are caused by increased androgen synthesis accounting for the increased height velocity in obese preadolescents and for the accelerated skeletal maturation. In both sexes earlier onset of puberty is noticed without remarkable alterations in gonadal steroids. Whether altered prolactin concentrations reflect neuroendocrine abnormalities remains unclear. Impairment of growth hormone release in face of normal or high somatomedins is not of clinical significance. Basal and stimulated insulin concentrations are high. Insulin resistance exists because glucose tolerance is simultaneously impaired. This is due to reduction in insulin receptor numbers and post-receptor defects in insulin action. Weight loss is effective in normalizing the above mentioned hormonal defects.

Adolescent↗
PubMedDate not supplied

[Idiopathic juvenile osteoporosis--report of 2 cases].

Idiopathic juvenile osteoporosis appears in temporal coherence with puberty leading to a reversible generalized osteoporosis of the skeletal system, spontaneous fractures and skeletal deformities. First symptoms in a 14 years old boy occurred as muscle pareses. A lymphocytic pleocytosis could be detected in cerebrospinal fluid. The next two years more than 20 spontaneous fractures occurred. Height was reduced by 15 cm. We first saw the boy at 17 years and could find decreased serum concentrations of calcitriol. Substitution with calcitriol resulted in regression of the pareses within days. Spontaneous fractures did not develop during the next two years of therapy. Subsequently serum calcitriol level was normalized. In a 10 years old boy first symptom occurred as fractures resulting from minimal traumas. In this case also during previous calcitriol therapy no new fractures occurred.

Adolescent↗
PubMedDate not supplied

[Growth hormone releasing hormone. Review].

Growth hormone-releasing hormone was isolated 1982 from human pancreatic tumours. They were found to consist of three peptides (GHRH1-44, GHRH1-40, GHRH1-37) which in vivo and in vitro were specific stimulators of pituitary growth hormone secretion. These tumor-derived GHRHs were demonstrated to be identical to human hypothalamic GHRHs. Extrahypothalamic GHRH is present in some brain regions and in the gastrointestinal tract. Circulating GHRH is detectable in human plasma, but little is known about its function. Above all binding of GHRH to a specific receptor stimulates growth hormone secretion through formation of cyclic AMP. GHRH secretion is modulated by somatostatin, the somatomedins and growth hormone itself. Following single injection of GHRH1-44 i.v. the equilibration half-time is 1.0 +/- 0.2 min and elimination half-time is 6.8 +/- 1.2 min. Maximal growth hormone response is achieved after injection of 1 microgram/kg GHRH. Using higher GHRH-doses growth hormone can be stimulated via subcutaneous or intranasal application. A single i.v. GHRH-test is not sufficient to prove a pituitary defect since growth hormone can be stimulated following repetitive injections in some cases. About 50% of patients with growth hormone deficiency have a hypothalamic defect of GHRH release. In some of these patients GHRH s.c. can promote linear growth to the same degree as growth hormone treatment.

Body Height↗
PubMedDate not supplied

[Adrenoleukodystrophy in a pair of siblings].

The diagnosis of adrenoleukodystrophy (ALD) in two brothers was confirmed by the analysis of long-chain fatty acids in cultured skin fibroblasts. The 23 year old brother was treated for Addison's disease at the age of 7 years. His first symptoms of ALD developed at the age of 22. These were lack of concentration and compulsive disorder. The younger brother was noted to show behavioural changes and a decreased performance at school at age 9. The disease then progressed rapidly. Variability and diagnostic procedures are discussed in this report.

Addison Disease↗
PubMedDate not supplied

[Thiamine-dependent anemia and thrombocytopenia, insulin-dependent diabetes mellitus and sensorineural deafness--case report and review].

Report of an 3 1/2 year old girl who because of resistant anemia and thrombocytopenia received blood transfusions since her third month of life. 15 months later she developed diabetes mellitus. Sensorineural deafness was noticed since her third year of life. Daily 25 mg thiamine prevented anemia and thrombocytopenia. The syndrome is compared with the 5 published cases of world literature.

Anemia↗
PubMedDate not supplied

[Myasthenia gravis following lupus erythematosus disseminatus].

Report on a 15 1/4 year old girl who developed Lupus erythematodes disseminatus when she was 9 years old. Four years later Myasthenia gravis occurred leading to myasthenic crisis in her 16th year of life. The special course of the disease and the diagnostic of Myasthenia gravis are discussed.

Adolescent↗
PubMedDate not supplied

[Erythropoietin as a biochemical parameter for fetal hypoxia].

The ability of parameters like umbilical arterial pH and Apgar-score to predict and/or to reflect fetal distress is limited. It is known that erythropoietin (EPO) increases due to hypoxic stimulation. Therefore we studied the levels of EPO in the cord blood of stressed neonates (n = 75). In addition, reference values for EPO were established in a group of healthy term infants (n = 54) (mean +/- SD: 20.02 +/- 6.4; median 17.8; range 8.7-40.3 (mU/ml]) and in premature infants (n = 77) according to gestational age (median/range: < 30 weeks 11.0, 5.5-17.5; 30-32 weeks 18.1, 5.5-136; 33-34 weeks 17.7, 8.3-422.9; 35-37 weeks 17.3, 5.5-272 [mU/ml]). EPO concentrations significantly increased in the stressed group: in acute stress (n = 27): mean 153.4, range 6.5-641.7 [mU/ml], p < 0.003; and in chronic stress (n = 48): mean 102.6, range 12.4-544 [mU/ml], p < 0.002. However, parameters like hemoglobin, hematocrit, umbilical arterial pH and Apgar-score did not correlate with EPO values. A sensitivity of 59% and a specificity of 92% was calculated. We conclude that serum EPO concentrations are capable of detecting acute and chronic stress. In part EPO also allows to grade stress in pregnancies, which are complicated by diseases like preeclampsia.

Asphyxia Neonatorum↗