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Biomedical subjects

J Ostman

Publications and source records attributed to J Ostman.

At least 19 recordsLinked to original sources
PubMed1992

Male predominance of type 1 (insulin-dependent) diabetes mellitus in young adults: results from a 5-year prospective nationwide study of the 15-34-year age group in Sweden.

The incidence of diabetes mellitus in Sweden in the 15-34 year age group was prospectively studied on a nationwide basis, beginning 1 January 1983. A total of 1,214 male and 720 female cases of newly-diagnosed (excluding gestational) diabetes were reported over a 5-year period. This corresponds to an incidence of 20.5 per 100,000/year in male subjects and 12.7 per 100,000/year in female subjects. Most cases were classified as Type 1 (insulin-dependent) diabetes, with an incidence of 15.9 in males and 8.6 in females. The incidence of Type 1 diabetes decreased gradually with age, while the incidence of Type 2 (non-insulin-dependent) diabetes increased. A male predominance was found in all age groups, with a male-to-female ratio of 1.8:1 for Type 1 diabetes and 1.3:1 for Type 2 diabetes. Maximum blood glucose concentration at diagnosis was significantly higher in males than in females in both Type 1 and Type 2 diabetic subjects. In contrast, the percent desirable weight was significantly higher in females, both in Type 1 and Type 2 diabetic subjects. The difference in diabetes incidence therefore cannot be attributed to any methodological error. The present finding of a marked male predominance after puberty in Type 1 diabetes in an ethnically quite homogeneous population supports the hypothesis that environmental risk factors and life-style are important for the development of the disease.

Adolescent↗
PubMed1992

Risk of developing insulin-dependent diabetes mellitus (IDDM) before 35 years of age: indications of climatological determinants for age at onset.

This study analyses data from two nationwide prospective diabetes registries now covering about 3400 cases from 19 million person-years of follow-up in the age group 0-34 years. The risk of developing insulin-dependent diabetes mellitus (IDDM) per 100,000 individuals before 15 years was 386 (95% confidence intervals (CI): 362-410) for boys and 391 (95% CI: 367-415) for girls and by 35 years 701 (95% CI: 671-731) for men and 562 (95% CI: 534-690) for women. The incidence rate showed a maximum for both boys and girls in early puberty. After pubertal years a sharp increase in the male to female incidence ratio of IDDM was notable. At 10-14 years it was 0.94, at 15-19 years 1.59 and at 20-24 years 2.08. A Cox regression model was used to analyse the effects on age at onset of sex, population density and climatological factors as measured by north-south area of residence and season at onset. The effect of sex was confirmed (P less than 0.001). A significant effect (P = 0.004) of season was shown when the four seasons were classified according to a four stage scale related to mean temperature. When dividing Sweden into 11 regions according to north-south gradient (Latitude 55 degrees, 56 degrees, 57 degrees, ..., 65 degrees) a significant effect (P = 0.038) was also found. However, no effects of population density or living near the coast versus in the interior were found. It is concluded that a large proportion of the young are at risk of developing this chronic disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Mortality of all incident cases of diabetes mellitus in Sweden diagnosed 1983-1987 at age 15-34 years. Diabetes Incidence Study in Sweden (DISS) Group.

From 1983 all incident cases of diabetes in the age group 15-34 years in Sweden have been recorded prospectively. The aim of the present study was to assess the mortality pattern of cases reported for 1983-87 and followed until the end of 1987. Eighteen deaths were identified by linkage to the national death register. When comparing the mortality in the cohort with Swedish males and females in general, an excess mortality was found in all the groups studied. It is, however, less pronounced if the analysis is restricted to those with Type 1 diabetes (standardized mortality ratio (SMR) and 95% confidence interval = 2.1; 0.8, 4.6), Type 2 diabetes (SMR = 4.8; 1.3, 12.3) or Type 1 + Type 2 (SMR = 2.7; 1.3, 5.0). Eight (44%) of the deaths were in patients with secondary diabetes, a diagnosis that applied to less than 3% of the cohort. Alcohol abuse was prevalent in six cases and suspected in another two. Hypoglycaemia was established as a cause of death in only one case but could not be excluded in a further six. Only one death was associated with ketoacidosis. No valid support for an increased risk of the 'dead in bed' syndrome was found. We suggest that diabetes was decisively important for the death in two cases and less important in 10. In the remaining six cases the existing documentation precludes a proper judgement.

Adolescent↗
PubMed1991

Renal and splanchnic exchange of human biosynthetic C-peptide in type 1 (insulin-dependent) diabetes mellitus.

Biosynthetic human C-peptide or NaCl (154 mmol.l-1) was given intravenously to 13 Type 1 (insulin-dependent) diabetic patients to determine the renal and splanchnic exchange of C-peptide. Catheters were inserted percutaneously into an artery and a renal and hepatic vein. Infusions of C-peptide were given for 60 min at two dose levels (5 and 30 pmol.kg-1.min-1). Insulin was infused throughout the study (0.5 mU.kg-1.min-1) and plasma glucose was kept constant by a variable glucose infusion. The regional blood flows were measured by indicator dilution techniques. In 11 of the 13 patients basal C-peptide levels were not detectable. The arterial steady-state C-peptide concentration was 0.81 +/- 0.10 nmol.l-1 and 2.33 +/- 0.30 nmol.l-1 at the low and high rate infusions, respectively. Renal uptake was 124 +/- 18 pmol.min-1 at the low infusion corresponding to 39% of the infused amount. At the higher dose C-peptide infusion renal uptake increased to 155 +/- 21 pmol.min-1 (p less than 0.05). Urinary excretion of C-peptide was 7 +/- 2 pmol.min-1 at the low dose infusion and increased to 34 +/- 6 pmol.min-1 at the high dose infusion (p less than 0.01). The proportions of infused amount excreted were fairly constant and between 2% and 3%. No net exchange of C-peptide was found across the splanchnic vascular bed. The rate of glucose infusion had to be increased by 35% during the low dose C-peptide, but not during NaCl infusion in order to maintain a constant plasma glucose concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Normalization of hepatic glucose regulation despite systemic insulin delivery. Studies in patients with pancreatic transplantation for type 1 (insulin-dependent) diabetes mellitus.

With current surgical techniques for pancreatic transplantation, the graft is anastomosed to the iliac vessels, resulting in delivery of insulin to the systemic circulation rather than to the portal vein as in healthy man. The possible influence of the altered route of insulin delivery on the regulation of splanchnic glucose metabolism was studied in four patients with Type 1 (insulin-dependent) diabetes mellitus at 6-19 months after combined pancreatic and kidney transplantation. Four non-diabetic, age-matched renal transplant recipients and two groups of age-matched healthy subjects served as controls. The studies were carried out in the basal state and during two rates of intravenous glucose infusion (2 and 4 mg.kg-1.min-1). Fasting arterial glucose and splanchnic glucose output was similar in all groups. Basal hyperinsulinaemia was present in pancreatic graft recipients compared to healthy subjects. During low rate intravenous glucose infusion splanchnic glucose output decreased to a similar extent in all groups. With the higher glucose infusion rate (4 mg.kg-1.min-1) a net glucose uptake was observed which was similar in all three groups. Peripheral glucose uptake was unchanged at the lower glucose infusion rate but increased by 45-55% at the higher rate. It is concluded that despite systemic insulin delivery from a heterotopic pancreatic graft, hepatic glucose metabolism appears normal both in the post-absorptive state and in response to glucose-stimulated endogenous insulin secretion. Portal insulin delivery is thus not necessary for normal hepatic glucose metabolism in the Type 1 diabetic patient.

Adult↗
PubMed1991

The Stockholm experience with pancreatic transplantation using enteric exocrine diversion.

Between April 1974 and June 1990, 128 pancreatic transplantations were performed. Of these 117 were with pancreatico-enterostomy. In four consecutive series of combined transplantations in uraemic diabetic patients the 1-year graft survival rate have successively improved (27%, 65%, 68% and 73%). In three similar series of single pancreatic transplantations the results also improved but still remained inferior (0%, 33% and 33%). In a series of combined transplantations performed in preuraemic diabetic patients the 1-year actuarial graft survival rate was only 25%. The results with pancreatic transplantation with pancreatico-enterostomy are now satisfactory. However, immunological loss graft function still constitute a major problem in the non- or pre-uraemic recipients. The metabolic control in patients with functioning grafts is normal or near-normal in the majority of patients followed for at least 1 year.

Diabetes Mellitus, Type 1↗
PubMed1991

Long-term metabolic control after pancreas transplantation with enteric exocrine diversion.

Long-term metabolic control after pancreatic transplantation with enteric exocrine diversion was evaluated in 42 Type I (insulin-dependent) diabetic pancreas recipients with functioning grafts for 1 to 7 years. Glycaemic control (fasting blood glucose, glycosylated haemoglobin A1c, oral and intravenous glucose tolerance tests) was normal or near-normal in most patients, and showed no deterioration with time. In ten patients with functioning grafts for 5 years there was a small, but significant, improvement in the glucose control at 3 to 5 years as compared with that at 6 months post-operatively. In the latter recipients the number of acute rejection episodes correlated negatively with the intravenous glucose tolerance at 6 months (r = -0.64, p less than 0.01) and at 5 years (r = -0.60, p less than 0.01) after transplantation, respectively. The glycaemic control at 6 and 12 months after transplantation was similar whether segmental (n = 35) or whole-organ (n = 7) pancreatic grafts had been used. In six non-uraemic recipients who had received a pancreas transplant alone the serum cholesterol increased in all but one patient (0.05 less than p less than 0.1), and the LDL/HDL-cholesterol ratio was significantly higher (p less than 0.005) one year after transplantation than before. Conversely, in six diabetic patients who had lost the function of their single pancreatic grafts the lipid and lipoprotein profiles remained unaltered. It is concluded that the long-term glycaemic control after segmental or whole-organ pancreatic transplantation with enteric exocrine diversion remains essentially normal in most recipients, and it may even improve with time.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Effect of pancreas transplantation on glucose counterregulation in insulin-dependent diabetic patients prone to severe hypoglycaemia.

Pancreatic transplantation was performed in three patients with insulin-dependent diabetes mellitus in whom recurrent and severe episodes of hypoglycaemia had been found to be due to defective glucose counterregulation. Thus in these patients the spontaneous blood glucose recovery after insulin-induced hypoglycaemia (0.1 U kg-1 h-1 i.v. insulin until blood glucose levels fell below 2.8 mmol l-1) was delayed, and the responses of glucagon, epinephrine and growth hormone (GH) were absent or diminished. After pancreas transplantation the patients exhibited essentially normal blood glucose control. When the insulin infusion test was repeated 3 months after the transplantation, the blood glucose level recovered rapidly after insulin withdrawal. The glucagon response was restored, and the responses of epinephrine and GH were improved. Plasma C-peptide was suppressed by approximately 50%, which is less than is observed in normal subjects. It is concluded that glucose counterregulation improves after pancreas transplantation. This appears to be mainly due to an improvement in the hypoglycaemia-induced glucagon response, but an amelioration of sympatho-adrenal and hypothalamic-pituitary regulatory mechanisms may also be involved. The apparent failure to suppress completely the insulin release from the denervated pancreas transplant indicates that inhibition of beta-cell secretion during insulin-induced hypoglycaemia may be partly under neural control.

Adult↗
PubMed1990

Lack of relationship between glibenclamide metabolism and debrisoquine or mephenytoin hydroxylation phenotypes.

The pharmacokinetics of a single oral dose of 1.75 mg glibenclamide were studied in 15 healthy Caucasians including five poor metabolisers of debrisoquine and five poor metabolisers of S-mephenytoin. Plasma glibenclamide concentrations and the urinary concentrations of trans-4- and cis-3-hydroxyglibenclamide were analyzed by h.p.l.c. Thirty-six +/- 6% (mean +/- s.d., n = 15) of the given dose of glibenclamide was excreted in 48 h urine as hydroxylated metabolites, 27 +/- 4% as trans-4-hydroxyglibenclamide and 8 +/- 2% as cis-3-hydroxyglibenclamide. There were no differences in the plasma pharmacokinetics of glibenclamide or in the urinary excretion of the metabolites between poor and extensive metabolisers of debrisoquine, neither between the two mephenytoin hydroxylator phenotypes. The study thus indicates that the disposition of glibenclamide is not influenced by these two independent polymorphisms of drug oxidation.

Adult↗