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Biomedical subjects

R Rosskamp

Publications and source records attributed to R Rosskamp.

At least 19 recordsLinked to original sources
PubMed2006

Inhaled insulin as adjunctive therapy in subjects with type 2 diabetes failing oral agents: a controlled proof-of-concept study.

AIM: This controlled proof-of-concept study investigated inhaled insulin (INH) as adjunctive therapy to existing oral antidiabetic agents in subjects with type 2 diabetes. METHODS: Twenty-four subjects with type 2 diabetes [19 men and 5 women, 56.1 +/- 6.6 years, body mass index 32.7 +/- 4.2 kg/m(2), glycosylated haemoglobin (HbA1c) 8.4 +/- 0.8% (mean +/- s.d.)] inadequately controlled by metformin and/or sulfonylureas were randomized to receive additional therapy with either INH administered preprandially using a metered-dose inhaler (MDI), or insulin glargine (GLA) injected subcutaneously at bedtime for 4 weeks. Both inhaled and injected insulin doses were titrated to predefined blood glucose (BG) targets. RESULTS: INH and GLA improved metabolic control to a similar extent. Mean daily BG decreased by 2.8 mmol/l in the INH group (p < 0.001) and by 2.4 mmol/l in the GLA group (p < 0.001). Accordingly, fasting BG (-2.7 vs. -3.6 mmol/l for INH vs. GLA), preprandial- and 2-h postprandial BG, HbA1c (-1.23 vs. -1.05%), body weight (-1.9 vs. -2.3 kg) and serum fructosamine were similarly and significantly reduced in both groups (p < 0.05). Triglycerides decreased significantly with INH (-1.15 micromol/l; p < 0.001) but not with GLA [-0.52 micromol/l; not significant (NS)]. Incidence rates of adverse events did not differ significantly, and there were no indications of respiratory tract irritation. CONCLUSIONS: In subjects with type 2 diabetes inadequately controlled by oral agents, preprandial administration of INH delivered by a MDI provided a comparable metabolic control to bedtime GLA and did not show any safety concerns during a 4-week treatment. These results warrant a more extensive investigation of preprandial treatment with INH in longer term studies.

Administration, Inhalation↗
PubMed2002

No evidence for accumulation of insulin glargine (LANTUS): a multiple injection study in patients with Type 1 diabetes.

AIMS: Insulin glargine is a long-acting insulin analogue that is metabolically active for at least 24 h. We investigated the multiple-dose pharmacokinetic properties of insulin glargine to determine whether daily injections lead to the accumulation of circulating insulin levels and a corresponding decrease in blood glucose levels in patients with Type 1 diabetes. METHODS: Fifteen patients using preprandial insulin lispro (mean age 36 +/- 9 years, body mass index 24.6 +/- 2.2 kg/m(2)) completed the study. Each patient's optimal insulin glargine dose was determined during a dose-finding phase. After a washout period, patients were treated over 12 days with a constant daily dose of insulin glargine injected in the abdominal subcutaneous adipose tissue at 22:00 h, and with preprandial insulin lispro. Free serum insulin (FSI) and blood glucose concentrations were assessed hourly after the first, fourth, and eleventh injection, after which patients fasted for 24 h and did not use any other insulin preparation. RESULTS: There were no changes in daily insulin doses during the dose-finding phase (insulin glargine: initial dose 24 +/- 6 IU, mean change 0 +/- 3 IU; insulin lispro: 18 +/- 9 IU, 0 +/- 7 IU). The time course of FSI was comparable on the three pharmacokinetic study days. Notably, the trough FSI at the end of the sampling periods was almost identical (day 1, 79 +/- 56 pmol/l, day 4, 77 +/- 56 pmol/l, day 11, 86 +/- 60 pmol/l). No changes occurred in any of the pharmacokinetic parameters studied. CONCLUSIONS: There is no evidence that insulin glargine accumulates after multiple injections over 12 days. These results indicate that the predetermined dose of insulin glargine will not need to be reduced after commencing treatment because of a risk of accumulation.

C-Peptide↗
PubMed1996

Clinical profile of the novel sulphonylurea glimepiride.

Glimepiride is a new generation sulphonylurea being prudently characterized in more than 2000 NIDDM patients. It has a short onset of action and a long duration of action. The same pharmacodynamic effect as with traditional sulphonylureas is achieved with secretion of less insulin, suggesting a possible extrapancreatic action. Glimepiride is given once daily in doses from 1-8 mg/day. 100% absolute bioavailability and the absence of a food interaction guarantee highly reproducible pharmacokinetics. Glimepiride is a remarkably safe drug especially in NIDDM patients at high risk e.g. the renally impaired, elderly or physically very active person. Hypoglycemia is less frequent in the first weeks of treatment than with glibenclamide. Ongoing studies are investigating the possible beneficial clinical effect of its different binding behavior to the potassium channel, especially in the heart.

Blood Glucose↗
PubMed1996

Long-term treatment of type 2 diabetic patients with the new oral antidiabetic agent glimepiride (Amaryl): a double-blind comparison with glibenclamide.

An international, prospective, double-blind trial compared the long-term therapeutic value of glimepiride with glibenclamide in patients with Type 2 diabetes mellitus. Patients stabilised on glibenclamide were randomised to 1 mg glimepiride (524 patients) or 2.5 mg glibenclamide (520 patients). The treatment groups were comparable at baseline with respect to age (60.2 years), body mass index (26.5 kg/m2), duration of diabetes (5.0 years) and fasting blood glucose levels (163 mg/dl [9.0 mmol/l]). Doses were increased stepwise, up to 8 mg for glimepiride (once-daily) and 20 mg for glibenclamide (> 10 mg as divided dose), until metabolic control (fasting blood glucose < or = 150 mg/dl [8.3 mmol/l]), or maximum dose was achieved. After one year of treatment, patients entered a long-term follow-up study. Primary endpoints for evaluation of metabolic control, mean glycated haemoglobin and mean fasting blood glucose, were 8.4% and 174 mg/dl (9.7 mmol/l) for glimepiride and 8.3% and 168 mg/dl (9.3 mmol/l) for glibenclamide. Differences between treatment groups were not considered clinically relevant (95% confidence intervals (-0.05, 0.19%) for glycated haemoglobin and (2, 11 mg/dl) [0.1, 0.6 mmol/l] for fasting blood glucose). Statistically significant lower fasting insulin and C-peptide values were observed in glimepiride patients compared with glibenclamide (differences: insulin, -0.92 microU/ml [p = 0.04]; C-peptide, -0.14 ng/ml [p = 0.03]). Both treatment groups showed an equivalent safety profile. Adverse events were consistent with the nature of the diabetic patient population studied. Fewer hypoglycaemic reactions occurred with glimepiride than with glibenclamide (105 versus 150 episodes). The long-term follow-up (457 patients) confirmed that glimepiride (1-8 mg) once daily provides equivalent metabolic control to a higher dosage (2.5-20.0 mg) of glibenclamide. Both treatments were well tolerated.

Adult↗
PubMed1991

Syndrome of developmental retardation, facial and skeletal anomalies, and hyperphosphatasia in two sisters: nosology and genetics of the Coffin-Siris syndrome.

We report on 2 sisters, 3 and 6 years old, with a possible new syndrome consisting of developmental retardation, facial and skeletal anomalies, and hyperphosphatasia. This disorder closely resembles the Coffin-Siris syndrome (McKusick number 135900). We describe the difficulties in achieving a diagnosis. A major diagnostic clue was the radiological recognition of hypoplasia/aplasia of the terminal phalanx of the 5th finger. Minor facial anomalies and mental retardation alone had not led to the proper diagnosis. Still, several diagnostic possibilities remain. For unknown reasons both children have an increased level of serum alkaline phosphatase activity.

Abnormalities, Multiple↗
PubMed1988

Plasma growth hormone-releasing hormone levels in type 1 (insulin-dependent) diabetic children following a mixed meal.

Following a mixed meal, plasma hormone responses were measured in four type 1 diabetic children and in eight short normal children. Between 60 and 150 min after ingestion of the mixed meal there was a significant increase in circulating growth hormone-releasing hormone values both in diabetic and in normal children. Mean plasma GHRH peak values were not different between diabetic patients (27.0 +/- 3.9 ng/l) and controls (24.6 +/- 4.9 ng/l). No time relationship to spontaneous growth hormone peaks was observed. Whereas normal children showed a characteristic biphasic plasma somatostatin response, somatostatin plasma levels in diabetic children did not change. In normal children plasma insulin values increased between 30 and 150 min, but remained unchanged in type 1 diabetic patients. Blood glucose response was more pronounced in diabetic children than in short normal children. These results indicate that circulating growth hormone-releasing hormone does not play a dominant role in the regulation of insulin and somatostatin.

Adolescent↗
PubMed1988

Rapid effect of intravenous growth hormone (GH)-releasing hormone 1-44 on plasma GH levels in children.

Growth hormone releasing hormone (GHRH)-testing was performed in 24 short normal children (16 male, 8 female). Before and after administration of GHRH1-44 (1 microgram/kg body weight i.v.) blood samples for growth hormone (GH) determination were drawn at -30, 0, 1, 2, 3, 4, 6, 8, 10, 15, 30, 45, 60, and 90 min. Plasma GH increase was apparent 1 min after injection and in 12 patients (7 female) peak plasma GH values were reached within 15 min. In all patients plasma GH levels were greater than 10 ng/ml within the first 8 min following GHRH injection, but in 4 patients this level was not attained when considering only GH values obtained after 15 min. These results demonstrate the capability of the pituitary to rapidly secrete GH in response to GHRH1-44 in children. Therefore, in this age group blood samples for GH determination should be taken earlier when testing with GHRH1-44.

Adolescent↗
PubMed1988

Serum vitamin D metabolites do not change in response to intravenous injection of thyrotropin releasing hormone (TRH) and growth hormone releasing factor (GHRF 1-44) in children.

Several reports claim that thyroid hormones and growth hormone participate in the regulation of vitamin D synthesis. We investigated whether there was a direct effect of their releasing hormones on vitamin D metabolism. TRH (7 micrograms/kg) was injected iv in 8 children with euthyroid diffuse goiter and GHRF (1 microgram/kg) in 10 short normal children. TRH injection induced significant TSH elevations but no changes in serum vitamin D metabolites, calcium and phosphorus. GHRF administration resulted in marked growth hormone elevations without alterations in the serum vitamin D metabolites, calcium and phosphorus. These results indicate no direct effect of TRH or GHRF itself on vitamin D metabolism, as well as a lack of very short term effect of growth hormone and TSH.

Calcifediol↗
PubMed1987

Circulating somatomedin-C levels and the effect of growth hormone-releasing factor on plasma levels of growth hormone and somatostatin-like immunoreactivity in obese children.

The effect of growth hormone-releasing factor (GRF) 1-44 on growth hormone and somatostatin release in plasma has been studied in 20 obese children. Twenty age and sex-matched children with normal weight served as controls. Mean peak growth hormone response in obese children after 1 microgram/kg body wt. GRF 1-44 was significantly lower than in controls (23.7 +/- 3.6 ng/ml vs. 41.1 +/- 3.0 ng/ml; P less than 0.01), as were mean integrated growth hormone response areas (1544 +/- 272 ng X ml-1 X 2 h vs. 2476 +/- 283 ng X ml-1 X 2 h; P less than 0.01). Mean plasma levels of somatostatin-like immunoreactivity did not change after GRF in both groups. Mean somatomedin-C levels in obese children were significantly higher compared to controls (1.6 +/- 0.4 U/ml vs. 0.86 +/- 0.4 U/ml; P less than 0.01). Somatomedin-C levels were not related to the integrated growth hormone responses. In conclusion there is no relation between somatomedin-C levels and the reduced growth hormone-releasing effect of GRF in obese children. GRF does not alter peripheral somatostatin-like immunoreactivity levels either in normal or obese children.

Adolescent↗
PubMed1987

Insulinhypoglycemia but not arginine infusion stimulates circulating plasma growth hormone-releasing hormone (GHRH) concentrations in children.

The effect of insulinhypoglycemia and arginine infusion on circulating concentrations of plasma growth hormone-releasing hormone (GHRH) and growth hormone (GH) has been studied in 24 children (4.4 to 14.3 years). Plasma GH and GHRH concentrations were determined by RIA. Basal plasma GHRH levels were detectable in the plasma of all patients ranging from 6.8 to 27.1 pg/ml. Injection of 0.1 U/kg body wt. insulin i.v. resulted in an increase of plasma GHRH levels (11.1 +/- 1.4 pg/ml vs. 18.8 +/- 2.6 pg/ml; P less than 0.01) preceding that of plasma GH (1.5 +/- 0.4 ng/ml vs. 13.6 +/- 1.3 ng/ml; P less than 0.01). Infusion of 0.5 gm/kg body wt. arginine hydrochloride did increase GH concentrations (2.0 +/- 0.6 ng/ml vs. 13.9 +/- 2.3 ng/ml; P less than 0.01) but did not change circulating plasma GHRH levels. Since the source of peripheral GHRH concentrations is not known the importance of these findings remains to be determined.

Adolescent↗
PubMed1987

Effect of insulin-induced hypoglycemia on circulating levels of plasma growth hormone-releasing hormone and somatostatin in children.

In response to insulin-induced hypoglycemia (0.1 U insulin/kg body weight, i.v.) plasma levels of growth hormone-releasing hormone (GHRH), somatostatin (SLI), and growth hormone (GH) were measured by radioimmunoassay in 10 children with short stature. Insulin injection resulted in a significant increase in plasma GHRH values at 15 min (10.0 +/- 0.5 vs. 17.1 +/- 3.1 pg/ml; p less than 0.05) preceding the increase in plasma GH levels (1.5 +/- 0.4 vs. 13.6 +/- 1.2 ng/ml; p less than 0.001). SLI concentrations peaked between 15 and 60 min after insulin injection (20.9 +/- 1.2 vs. 47.1 +/- 6.2 pg/ml; p less than 0.01). No correlation was present between plasma GHRH or SLI levels and plasma GH concentrations. A significant negative correlation could be established between maximum increments of plasma GHRH and SLI levels (r = -0.843; p less than 0.01) in response to insulin injection. This finding suggests a possible relationship between these two hormones at peripheral level.

Adolescent↗
PubMed1987

Plasma adrenocorticotropin, cortisol, and dehydroepiandrosterone response to corticotropin-releasing factor in normal children during pubertal development.

The adrenocorticotropin (ACTH), cortisol, and dehydroepiandrosterone responses to synthetic human corticotropin-releasing factor (CRF) were studied in 28 endocrinologically healthy children (age 1-16 yr) and in six adult volunteers (age 24-42 yr). CRF was given as an intravenous bolus (1 microgram/kg body weight) between 0900 and 1000 hr. Significant increments in ACTH and cortisol levels after CRF were observed in all subjects, with an ACTH peak value of 48.2 +/- 3.4 pg/ml at 10 min (p less than 0.001). The ACTH and cortisol response patterns after CRF did not change with age or pubertal maturation and did not differ in children and in adults. In contrast, the dehydroepiandrosterone response to CRF clearly was related to the stage of pubertal development. The peak value after CRF significantly increased from puberty stage 1 to puberty stage 5 (164 +/- 18 versus 779 +/- 86 ng/100 ml, p less than 0.001). In adults, the mean dehydroepiandrosterone peak value after CRF did not differ from that of P5 children. These results show that CRF can be given safely to children. The absence of age-dependent ACTH and cortisol responses and a dehydroepiandrosterone response changing with pubertal maturation points to the existence of factors involved in the control of adrenal androgen production other than ACTH.

Adolescent↗
PubMed1987

Circulating serum phenylalanine concentrations and the effect of arginine infusion on plasma levels of growth hormone and insulin in treated phenylketonuric children.

According to desired phenylalanine (Phe) levels of 50-80 mg/l during treatment, three groups of patients with classical phenylketonuria (PKU) (5.3-17.1 years) were formed. They were investigated for their growth hormone (GH) and insulin response to arginine infusion: Group I (N = 5) had Phe levels below (22 +/- 4 mg/l), group II (N = 3) within (61 +/- 6 mg/l), and group III (N = 3) above therapeutic limits (156 +/- 3 mg/l). Nine children (5.2-14.5 years) with short stature served as controls. Whereas group I and II PKU children showed normal GH response to arginine infusion, group III children exhibited impaired GH response expressed as integrated GH response (218 +/- 38.6 micrograms X 1(-1) X 2 h vs 911 +/- 145 micrograms X 1(-1) X 2 h; P less than 0.01) or peak GH response (6.6 +/- 1.2 micrograms/l vs 18.7 +/- 2.3 micrograms/l; P less than 0.05). Integrated insulin responses did not differ between the three PKU groups but were significantly higher in all PKU patients compared with controls (4903 +/- 421 mU/l vs 2750 +/- 378 mU/l; P less than 0.01). However, this reflects impaired insulin secretion in children with constitutional delay of growth and adolescence rather than hyperinsulinism in PKU patients.

Adolescent↗
PubMed1987

Plasma levels of growth hormone-releasing hormone and somatostatin in response to a mixed meal and during sleep in children.

Following a mixed meal, plasma levels of GHRH, GH, SRIH and insulin were measured in 7 prepubertal children with constitutional delay of growth and adolescence (CDGA) and in 3 children with proven GH-deficiency which responded to GHRH-injection. In children with CDGA, plasma levels of GHRH increased between 60 and 120 min (10.1 +/- 1.2 ng/l vs 25.5 +/- 4.4 ng/l; P less than 0.01). Although no GH increase occurred in patients with GH-deficiency, their plasma GHRH increases were comparable to those in CDGA children. No time relationship was present between circulating GHRH and GH, SRIH, or insulin, nor was there any correlation between their integrated hormone response areas. Sleep-induced plasma GHRH, GH and SRIH values were determined in 10 prepubertal children with CDGA. Spontaneous variations of plasma GHRH and GH values occurred with no temporal or quantitative relationship. SRIH values did not change during nocturnal sleep. In one child with GH-deficiency, comparable GHRH plasma fluctuations occurred, although GH values were all below 1 microgram/l. Our results support the concept that circulating GHRH does not only represent hypothalamic GHRH, but derives mainly from extrahypothalamic sources, possibly from the gastrointestinal tract.

Adolescent↗
PubMed1987

[Therapy of constipation with wheat bran in infancy and early childhood].

In 22 infants and children aged 6 to 62 months (mean = 23 months) with severe constipation a commercially produced solid food containing 4.2 g wheat bran was used for 41 days. Acceptance was satisfactory, compatibility was reported to be good. In 86% of the children normal bowel movements appeared within 8.2 days of therapy. Blood levels of hemoglobin, calcium, phosphathase, alkaline phosphatase, iron, transferrin, total protein, cholesterol, and carotene were controlled in monthly intervals. Under wheat bran there was only a slight decrease of carotene concentrations by 13.5 mg/dl (p less than 0.05) and a minimal increase of alkaline phosphatase activity by 14.5 U/l (p less than 0.1). In 8 healthy infants aged 4.5-9 months (mean = 6.7 months) the bran preparation induced an increase of stool weight by 21.5% (p less than 0.05), whereas the frequency of bowel actions did not change. The results indicate that bran preparations may be used in severe constipation even in early childhood.

Child, Preschool↗