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Biomedical subjects

E Standl

Publications and source records attributed to E Standl.

At least 19 recordsLinked to original sources
PubMed1994

[How can primary prevention of coronary heart disease be improved in general practice?].

BACKGROUND: The basic issue of primary prevention strategies of coronary heart disease is an individually adapted cardiovascular risk factor management. However, transformation of these strategies by health care professionals is still insufficient, as was demonstrated by three studies performed in private practice. METHODS AND RESULTS: In oral glucose tolerance tests performed in 234 patients with essential hypertension who were under regular medical control, 25.6% turned out to have previously unknown diabetes and 41.4% had impaired glucose tolerance. In the remaining 33.3% with normal glucose tolerance, mean total serum cholesterol was 260 mg/dl. 82 patients with essential hypertension and known diabetes had a mean total serum cholesterol of 276 mg/dl. Neither cohort was under lipid lowering drugs. Out of 290 unselected patients treated for type II-diabetes in private practice, 62% were hypertensive. Of those, hypertension was not known untreated or not sufficiently treated in 78.2%. CONCLUSION: As a consequence, in patients at high cardiovascular risk, not only the "leading" disease (i.e. diabetes, hypertension, hyperlipidaemia), but also the concomitant constellation deserves attention and early intervention.

Adult↗
PubMed1994

Alterations of lymphocyte subsets in children of diabetic mothers.

To investigate the impact of diabetic mothers on the maturation of the immune system in their offspring, immunophenotypic markers of major lymphocyte subpopulations were evaluated by two-colour flow cytometric analysis in 160 healthy children of diabetic mothers (100 with insulin-dependent diabetes mellitus (IDDM): 48 with gestational diabetes), including 22 neonates, 45 infants aged 8-12 months, 46 children aged 1-2 years, 29 children aged 3-6 years and 18 children aged 7-17 years. Results were compared with 21 neonates of healthy mothers from our hospital and with 110 paediatric subjects of a reference population. In neonates of diabetic mothers, percentages of total lymphocytes (p = 0.044), T and B lymphocytes (p = 0.004, respectively) were significantly decreased compared to our neonates of healthy mothers. By subdividing the group of neonates in offspring of mothers with IDDM (n = 15) or gestational diabetes (n = 7), differences compared to normal neonates were mainly observed in neonates of mothers with IDDM (T lymphocytes: p = 0.006; B lymphocytes: p = 0.008). In cord blood, 45.5% of neonates had antibodies to islet cells, insulin or glutamic acid decarboxylase, most likely transmitted through the placenta of the diabetic mother. No association was found between alterations of lymphocyte subsets and antibody-positivity in cord blood, nor was there any correlation of lymphocyte counts and mean HbA1 during pregnancy, maternal age at delivery, diabetes duration, or neonatal birth weight, respectively. Comparisons among age groups from newborn infants through adolescents revealed higher percentages of total lymphocytes and lower percentages of activated T cells in children of diabetic mothers compared to children of the reference population between the age of 1 to 6 years (67-73% of the cases above and 62-77% below the interquartiles of the reference range, respectively). No significant differences in lymphocyte subpopulations between children of mothers with IDDM diabetes and gestational diabetes have been detected. In addition, there were no abnormalities of lymphocyte subsets in children who are at high risk for the development of IDDM. In summary, we suggest that the observed changes in children of diabetic mothers may reflect a cellular immune reaction to the particular maternal environment, characterized by both an abnormal metabolic state and persisting autoimmunity in the affected mother.

Adolescent↗
PubMed1994

[The metabolic syndrome. Pathophysiologic causes, diagnosis, therapy].

The individual components of the metabolic syndrome such as central obesity, dyslipidemia with increased triglycerides and decreased HDL-cholesterol, hyperuricemia, hypertension and progressive glucose intolerance are markers for an increased risk of atheroma and type 2 (non-insulin-dependent) diabetes. All components, with the exception of hyperuricemia, are associated with skeletal muscle insulin resistance, leading to compensatory chronic hyperinsulinemia. Insulin resistance/hyperinsulinemia, in turn, is associated with a series of hypertensiogenic and atherogenic side effects, aggravating the individual components of the metabolic syndrome. From a more pathophysiologically orientated point of view, early identification of individuals obviously at risk for atheroma and type 2 diabetes, as well as early intervention aimed at the improvement of reduced insulin action may play a central role in an integrated life-style approach of primary prevention of atherosclerosis and type 2 diabetes.

Arteriosclerosis↗
PubMed1993

Hypertension and insulin resistance. Glycaemia and insulinaemia in overweight hypertensive patients.

The relationship between insulin resistance and hyperinsulinaemia on one hand and hypertension on the other hand has become apparent during the last few years. Insulin resistance, which may be genetically determined, is, according to our present understanding, the 'key player' in the metabolic syndrome. However, the pathophysiology of the combination of factors has not yet been fully elucidated. Early therapeutic intervention for insulin resistance, hyperinsulinaemia and hypertension may prevent the clinical manifestation of non-insulin-dependent (type 2) diabetes. Preliminary results of an ongoing study investigating the effects of trandolapril or the diuretic combination of hydrochlorothiazide and triamterene on serum glucose and insulin levels are presented.

Antihypertensive Agents↗
PubMed1992

Involvement of dendritic cells in early insulitis of BB rats.

In this study, subsets of mononuclear infiltrates in pancreatic islets of BB rats at different stages of insulitis were determined by various monoclonal antibodies against rat lymphoid cells, including a mouse monoclonal IgM antibody that distinguishes between macrophages and dendritic cells (mAb 1F119). 1F119+ dendritic cells were absent in and around islets of Wistar control rats. In BB rats, the first alteration of islets detectable by immunohistochemistry when compared with normal islets was the enhanced expression of 1F119 antigen around and in the islets (17% 1F119+ islets). At disease stage 1 (i.e. no leukocyte infiltration after HE staining), lymphocytes and macrophages were almost absent. At disease stage 2 (leukocyte infiltration < 20 cells), a more intense form of dendritic cell infiltration was seen (stage 1 versus stage 2, P < 0.0001). In addition, ED2+ and ED3+ cells were present around the islets (50% of islets were infiltrated with 1F119+ cells versus 16% with ED2+, 19% with ED3+, 11% with W3/25+ cells, and 11% with OX8+ cells, P < 0.0001). At disease stage 3 (> 20 cells), a clear increase of ED2+ and ED3+ macrophages and of W3/25+ and OX8+ T-lymphocytes in the infiltrates was observed. These observations suggest a role for antigen presenting dendritic cells in the initiation of immune reaction in type 1 diabetes of BB rats.

Animals↗
PubMed1992

[Clinical sequelae of hyperinsulinemia in diabetes mellitus].

Surprisingly enough, insulin has recently been suspected of promoting cardiovascular complications, provided it becomes effective in excess concentrations at the vascular walls. This applies to both endogenous hyperinsulinemia and insulin substitution performed exogenously with high insulin doses. Several large population studies in non-diabetics - carried out in Helsinki, Busselton and Paris - have proved recently that serum insulin concentration is an independent risk predictor for the occurrence of coronary heart disease. According to in vitro trials, insulin stimulates the proliferation of the smooth muscle cells in vascular media and the lipid synthesis, as well as lipid incorporation into the vascular wall. Very recent large-scale population studies in randomly selected type II diabetics (the Schwabing Study and one performed at Oxford) have revealed a close association between an endogenous insulin requirement, on the one hand, and the risk of macroangiopathy or coronary heart disease on the other.

Coronary Artery Disease↗
PubMed1991

[Insulin autoantibodies and islet cell antibodies in recently appearing diabetes mellitus type I. Association with age of manifestation and HLA phenotype].

Insulin autoantibody (IAA) and islet cell antibody (ICA) titres were measured in 108 newly diagnosed type I diabetics (49 male, 59 female, mean age 20 [1-38] years) and 103 non-diabetic controls (41 male, 62 female, mean age 23 [16-46] years). IAA titres in the controls were normally distributed, with a mean of 5 +/- 11 nU/ml. The upper limit of normal was established as 49 nU/ml (mean + 4 standard deviations). Raised IAA and ICA titres were present in 45% and 44% of type I diabetics, respectively, with 59% positive for either IAA or ICA or both. IAA were markedly age-dependent, being positive in 70% (26 out of 37) of diabetics under the age of 15 years, and in 32% (23 out of 71) at the age of 15 years or more (P = 0.0004). There was a less marked difference for ICA titres (positive in 62% of patients less than 15 years, and in 35% of those of 15 years of older; P less than 0.01). IAA were significantly more common in HLA DR4 positive patients than in HLA DR4 negative patients (56% vs 11%; Pc less than 0.00015). With regard to age a significant association between IAA and HLA DR phenotype was present only in homozygous (Pc less than 0.03) and heterozygous (P less than 0.0003) patients aged 15 years or older. By contrast, ICA was not significantly correlated with HLA phenotype. These data suggest a genetic predisposition for the development of IAA.

Adolescent↗
PubMed1991

[Insulin level--a parameter for risk of arteriosclerosis?].

Surprisingly enough, insulin has recently been suspected of promoting cardiovascular complications provided it becomes effective in excess concentrations at the vascular walls. This applies to both endogenous hyperinsulinemia and insulin substitution performed exogenously with high insulin doses. Several large population studies in non-diabetics--carried out in Helsinki, Busselton and Paris--proved recently that serum insulin concentration is an independent risk predictor for the occurrence of coronary heart disease. According to in-vitro trials, insulin stimulates the proliferation of the smooth muscle cells in vascular media and the lipid synthesis as well as lipid incorporation into the vascular wall. Very recent large-scale population studies in randomly selected type II-diabetics (the Schwabing Study and one performed at Oxford) have revealed a close association between endogenous hyperinsulinemia respectively high exogenous insulin requirement on the one hand and the risk of macroangiopathy or coronary heart disease on the other.

Arteriosclerosis↗
PubMed1991

Follow-up of cyclosporin A treatment in type 1 (insulin-dependent) diabetes mellitus: lack of long-term effects.

In the Canadian/European randomized controlled study on cyclosporin A (CsA) in recent onset Type 1 (insulin-dependent) diabetes, treatment with the immunosuppressive drug had increased and maintained Beta-cell function and clinical remission during the first 12 months. Following discontinuation of the study drug and double-blinding after a mean of 13.8 months former CsA patients doubled the daily insulin dose within 6 months reaching the level of former placebo patients. The difference in Beta-cell function between the two groups was also lost. Metabolic control (HbA1c) was transiently worse in the former CsA group. Adverse effects of cyclosporin A on systolic blood pressure, haemoglobin levels, serum potassium and creatinine levels also remitted during that time. We conclude that treatment with cyclosporin A for a mean of 13.8 months had no long-lasting effect on the course of Type 1 diabetes persisting beyond drug discontinuation.

Adolescent↗
PubMed1991

HLA-associated insulin autoantibody formation in newly diagnosed type I diabetic patients.

To assess a possible HLA association with anti-insulin autoantibodies (IAAs) in human insulin-dependent (type I) diabetes, 51 newly diagnosed type I diabetic patients (mean age 22 +/- 8 yr) were typed for HLA-DR and HLA-DQ and studied for IAAs before exogenous insulin therapy with a competitive radioimmunoassay (normal range less than or equal to 49 nU/ml). The level of IAAs in 16 patients exceeded our upper limit of normal, and 18 had high-titer islet cell antibodies (ICAs; greater than or equal to 40 Juvenile Diabetes Foundation U). A striking association with HLA-DR4 (DQw3) in both the prevalence and the level of IAAs was found (IAA positivity in patients with DR4/4 vs. DR4 heterozygous vs. non-DR4: 90 vs. 29%, corrected [c] P less than 0.01, vs. 5%, Pc less than 0.0001; IAA positivity in patients with DR4 vs. non-DR4: 50 vs. 5%, Pc less than 0.005; IAA level in patients with DR4/4 vs. DR4 heterozygous vs. non-DR4: 111 vs. 17 nU/ml, Pc less than 0.01, vs. 20 nU/ml, Pc less than 0.0001; IAA level in patients with DR4 vs. non-DR4: 45 vs. 20 nU/ml, Pc less than 0.01). In contrast, none of the DR3+ subjects had IAAs above normal range, except in conjunction with DR4 (DR3 vs. non-DR3: 12 vs. 42%, Pc less than 0.05). However, there was no significant relationship between DR3 and IAAs after correcting for the number of DR4 alleles. No relationship was seen between age of onset, IAA level, and HLA typing in our population, and no relationship was found between ICA positivity and HLA antigens.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Changes of vitamin D3 serum concentrations at the onset of immune-mediated type 1 (insulin-dependent) diabetes mellitus.

Several hormones such as 1,25-dihydroxy-vitamin D3 (1,25-(OH)2D3), alpha-MSH, or ACTH have been found to interact extensively with the immune system. In view of the immune-mediated nature of Type 1 (insulin-dependent) diabetes mellitus, 49 recently diagnosed diabetic patients were investigated in terms of serum 1,25-(OH)2D3-levels, 25-hydroxyvitamin D3(25-(OH)D3), alpha-MSH and ACTH, and compared with 42 healthy controls. A marked decrease of 1,25-(OH)2D3-levels was found at onset of Type 1 (insulin-dependent) diabetes compared to normal controls (39 +/- 2 vs 55 +/- 4 pg/ml, p less than 0.01). Grouping patients according to season (winter or summer) of diabetes onset and blood sampling, it was demonstrated that the decrease of 1,25-(OH)2D3 was primarily present during summer and due to a loss of the seasonal rhythm of this hormone observed in healthy controls (summer: patients vs controls 41 +/- 2 vs 63 +/- 4 pg/ml, p less than 0.001; winter: 37 +/- 3 vs 33 +/- 3 pg/ml, n.s.). Serum concentrations of 25-(OH)D3 were closely correlated with those of 1,25-(OH)2D3, both in controls (r = 0.55, p less than 0.002) and diabetic patients (r = 0.41, p less than 0.05), yielding a similar loss of seasonal variation also of this vitamin D3 metabolite in Type 1 (insulin-dependent) diabetic patients. No difference was found in the mean and median values of alpha-MSH and ACTH between IDDM patients and controls, although patients exhibited much higher variation of alpha-MSH levels than did controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗