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Biomedical subjects

D Tschöpe

Publications and source records attributed to D Tschöpe.

At least 19 recordsLinked to original sources
PubMed2006

[Diabetics in secondary prevention].

It is well known that diabetics live with a significantly higher incidence of a cardiac insufficiency and that acute ischemia is the main cause of death in this group (75%). The risk of suffering a myocardial infarction after ischemic incidences is significantly higher for diabetics than for patients with normal carbohydrate metabolism. Diabetes mellitus is not only responsible for acute incidences, but also for a higher incidence of chronic coronary diseases. Furthermore a disturbed tolerance glucose value was detected in studies for two-thirds of the patients which could even be proven after complete rehabilitation. It has also been shown that the severity of hyperglycemia is in a close inverse relationship to the volume of the brain tissue which can be saved. For this reason hyperglycemia is possibly a therapeutic aim in case of acute ischemic incidences. Therefore the adjustment of blood sugar should be the primary aim to reduce risk in any cases of vascular incidences.

Blood Glucose↗
PubMed2005

[Cardiovascular protection in diabetic patients with heart disease in the doctor's office].

The long-term care of diabetic patients with heart disease poses a particular challenge. Various combinations of risk factors, progression of the coronary heart disease, and complications with further organic damage by the underlying diabetes, frequently necessitate a differentiated diagnostic work-up and management. This can be implemented only by close cooperation between the various specialities. Structured processes may be useful provided they are correctly applied and implemented. Guideline-based treatment of detected cardiovascular risk factors can improve quality of life, reduce morbidity and cardiovascular mortality and thus save costs over the long term.

Aged↗
PubMed2005

[Glucose metabolism].

The markedly increased peri-interventional risk (PCI and CABG) in patients with type-2 diabetes mellitus may be reduced by adjusting blood glucose values to a near-normal level. This adjustment should be realized acutely by glucose-insulin-potassium infusions. In long-term therapy, the target value should be achieved independent of the pharmacological principle of blood glucose reduction. Among the available oral antidiabetic agents, metformin, acarbose and glitazones seem to be cardioprotective via pleotropic effects. Given an optimal stent implantation and administration of GP IIb/IIIa inhibitors during coronary interventions, results are similar to those of non-diabetics.

Cardiotonic Agents↗
PubMed2004

[Diabetic patients after myocardial infarction].

Diabetes mellitus is not just another risk factor for cardiovascular events; it per se defines maximal risk for target organ damage including the cardiovascular system. Diabetes is one of the main drivers in the race towards a higher incidence in cardiovascular disease worldwide. In addition, it is also one of the often unrecognized predecessors of myocardial infarction and sudden cardiac death. About three quarters of patients post-MI show impaired glucose tolerance or full blown diabetes. The MONICA/KORA data have shown that the higher risk for mortality and morbidity in diabetics is maintained past the first event. However, the STENO-2 trial has shown that consequently managing diabetes and concomitant cardiovascular risk factors can significantly reduce the risk for cardiovascular events in this high-risk group.

Clinical Trials as Topic↗
PubMed2003

[Aim, design and methods of the "Hypertension and diabetes screening and awareness" -- (HYDRA) study].

Aim of the study is a comprehensive clinical-epidemiological description of the prevalence of arterial hypertension and diabetes among primary care patients along with an assessment of doctor's recognition rates and prescription behaviour. The paper describes methods and design of the study and provides background information on the sampling process, instruments used as well as characteristics of doctors and patients. The study is based on a nationally representative sample of 1,912 primary care doctors and 45,000 patients that attended the doctors' office on the target days. The patients were also characterized by laboratory tests. The first stage of study consisted of a comprehensive description of the doctors' characteristics in terms of psychosocial, qualification- and provider aspects as well as attitudes towards hypertension and diabetes and their management. In the second stage all patients completed a questionnaire to describe their health behaviour and attitudes as well as the treatment history and therapy. In the third stage all patients were characterized by their doctors in terms of their diagnostic status and their past and current interventions.

Adolescent↗
PubMed2003

[Management of diabetes and hypertension: how do primary care physicians judge their performance?].

With regard to the management of hypertension and diabetes, HYDRA reveals that doctors report multiple problems in their everyday practice. Being confronted with an average of 73 patients a day, with almost every second having either diabetes or hypertension, frequently associated with multiple comorbid conditions, the core obstacle is the time factor. Doctors do not have sufficient time to perform diagnostic tests and especially no time for non-drug interventions of any type. Further available treatment guidelines are only used in 1 out of 2 doctors. Further they seem not to affect doctors performance significantly.

Adult↗
PubMed2003

[Hypertension, diabetes mellitus and comorbidity in primary care].

Almost every second patient seeing a primary care doctor suffers from arterial hypertension and about every fifth has diabetes mellitus. These diseases often occur at the same time. They are associated in more than 80% of the cases with other severe concomitant and subsequent diseases (heart attack, stroke, renal failure, neuropathy etc.). The magnitude especially of subsequent and concomitant diseases, the dimension of the personal suffering and the immense diagnostic and therapeutic challenges for the doctors have been massively underestimated so far. The article informs about the prevalence of the above disease, and structure of the problem. Before the background of an extremely high patient load seen by German General Physicians, the mainstay challenge is highlighted how to achieve further improvements of the quality of care on the basis of scientific guidelines alone, without a concomitant change in the system structure.

Adolescent↗
PubMed2003

Minimal metabolic data set for patients at high vascular risk.

Vascular events still represent the leading cause of death in the western world. The pathogenesis of atherothrombotic events is multifactorial. Epidemiological studies indicate that the presence of several concomitant risk factors, especially in the metabolic syndrome, markedly exacerbates the vascular risk. In the prevention and management of cardiovascular disease, a multi-dimensional risk factor approach is therefore required to reduce the "vascular burden". Consequently it is absolutely necessary to identify and to subsequently monitor these factors during intervention/therapy. The present MMDS represents a tool for the daily clinical routine to assess and document important cardiovascular risk factors. This data set is the result of a consensus of the two German working groups of the German Cardiology Society and the German Diabetes Society. The identification and detection of all relevant vascular risk factors should result in improved patient care and a more comprehensive documentation of cardiovascular risk factors in clinical studies.

Anthropometry↗
PubMed2001

Recovery of platelet function after discontinuation of clopidogrel treatment in healthy volunteers.

AIMS: To study the recovery of platelet function after discontinuation of clopidogrel treatment in healthy volunteers. METHODS: Ten healthy volunteers were treated with clopidogrel (75 mg day(-1)) for 7 days. CD62P expression and PAC-1 binding were measured by flow cytometry. RESULTS: Adenosine diphosphate (ADP, 30 microM)-induced platelet responses were almost completely inhibited by clopidogrel. After discontinuation of the drug, platelet function gradually increased and complete recovery was seen 7 days after the last clopidogrel dose. The mean difference (95% CI) for ADP-induced PAC-1 binding (fluorescence intensity) between baseline and 7 days after the last dose was 0.01 (0.61, -0.59). Single cell analysis provides direct evidence for an irreversible mode of action of clopidogrel. CONCLUSIONS: This is the first report to directly demonstrate irreversibility of clopidogrel action in humans.

Adenosine Diphosphate↗
PubMed2000

[Masked autoimmune polyendocrine syndrome caused by sequelae of diabetes mellitus].

BACKGROUND: In most cases Type I diabetes is immunologically mediated. Complications after long duration of the disease are commonly observed. Further autoimmune mediated diseases are rare, but more often diagnosed in diabetics than in the general population. The combination of 2 autoimmune endocrinopathies is subsumed under the term autoimmune polyendocrine syndrome (APS). Depending on the endocrine gland involved disorders are classified as APS Type I, II or III. CASE REPORT: We report on a 64-year-old diabetic patient presenting with repeated nightly hypoglycemia. Diabetes was first diagnosed 12 years before. Clinical examination revealed a café-au-lait like color of the skin and severe peripheral polyneuropathy. Surprisingly, laboratory testing revealed a hemoglobin concentration of 6.8 g/dl. Further examinations led to the diagnosis of pernicious anemia and funicular myelosis. Screening for potentially associated autoimmune diseases showed also features of autoimmune thyroid disease. CONCLUSION: Despite of late manifestation of disease Type I diabetes should be considered if the clinical features correspond to an autoimmune induced disorder. Associated autoimmunopathies have always to be considered. Early diagnosis of commonly with diabetes associated autoimmunopathies can prevent as severe manifestations of disease as reported in this case.

Diabetes Mellitus, Type 1↗
PubMed2000

Additive effect of coexistent type 2 diabetes and arterial hypertension on endothelial dysfunction in resistance arteries of human forearm vasculature.

Population studies suggest that vascular complications accumulate when arterial hypertension supervenes on diabetes mellitus. Although it has been demonstrated that endothelial function is impaired in patients with either diabetes mellitus or arterial hypertension it is unknown whether or not both diseases exert additive effects on endothelial dysfunction. The authors therefore investigated endothelium-dependent and endothelium-independent vasodilation in the forearm vasculature of 44 individuals: in 10 type 2 diabetic patients (DM), in 12 patients with arterial hypertension (HT), in 10 patients with both DM and HT (DM+HT), and in 12 healthy control subjects (C). Forearm blood flow (FBF) was measured by venous occlusion plethysmography at rest and following intraarterial infusion of acetylcholine (ACh) and the NO-donor sodium nitroprusside (SNP) at increasing doses. FBF at rest was significantly lower in diabetic patients: 2.2 +/- 0.1 (DM) and 2.6 +/- 0.2 (DM+HT) versus 3.1 +/- 0.1 (HT) and 3.4 +/- 0.2 (C) mL/min per 100 mL of tissue. ACh and SNP both increased FBF dose-dependently in each group. The maximum response to ACh was progressively decreased in DM and HT: 13.7 (C) > 8.1 (DM) > 7.6 (HT) > and 5.7 (DM+HT) mL/min per 100 mL of tissue. Reduction of the endothelium-dependent flow reserve assessed as percent increase in maximum FBF was also impaired following the same rank order: 349 (C) > 268 (DM) > 160 (HT) > 126 (DM+HT)%. The flow response to the NO-donor SNP amounted to: 327 (C), 306 (DM), 200 (HT), and 194% (DM+HT). In DM+HT the reduction of endothelium-dependent flow response was more pronounced compared with the endothelium-independent flow response. The present data provide evidence that type 2 diabetes and arterial hypertension impair endothelium-dependent dilation of resistance arteries in an additive manner suggesting that this progressive endothelial dysfunction might contribute to the increased incidence of cardiovascular complications when both diseases are coexistent.

Acetylcholine↗
PubMed1999

High dose supplementation of RRR-alpha-tocopherol decreases cellular hemostasis but accelerates plasmatic coagulation in type 2 diabetes mellitus.

BACKGROUND: Diabetes mellitus is associated with increased generation of free oxygen radicals and depleted scavenging potential (oxidative stress), leading to increased LDL oxidation and platelet hyperreactivity, the major components of atherothrombotic vascular lesions. A main goal of antioxidant therapy is to protect the LDL particle from atherogenic oxidation and to reduce the activated cellular hemostasis. METHODS: We evaluated the influence of a high dose supplementation with 800 IU of the natural antioxidant RRR-alpha-tocopherol (vitamin E) per day for six months on serum levels, vitamin E load of LDL particles (HPLC), lag phase of LDL oxidation (Esterbauer's assay), platelet adhesion molecules, leukocyte-platelet coaggregation (flow cytometry, D-III protocol) and coagulation (INR/PTT) in a group of 36 patients with type 2 diabetes (f/m 22/14; age 58+/-8.0; HbA1 at baseline 10.25+/-1.7). RESULTS: Average vitamin E levels increased 2.65-fold accompanied by a 1.83-fold increase of LDL-associated vitamin E and a 12.3 min prolongation of the lag-phase of LDL oxidation (p<0.001 for all parameters at six months). Platelet expression of PECAM-1 (CD31) (-30.2% positive cells, p<0.001; antigen density -25%, p<0.001), ICAM-2 (CD102) (-2.9% positive cells, p<0.01; antigen density -10.6%, p<0.001) and fibrinogen (-1.6% positive cells, p<0.001; antigen density - 16.1 %, p<0.001) decreased. Concomitantly, platelet-leukocyte-coaggregation increased by 44% (p<0.001), correlating to an INR reduction of 10.4% (1.06+/-0.09 to 0.95+/-0.09, p<0.001, r = - 0.34). The PTT remained constant. CONCLUSION: The antioxidant protection from the increased vitamin E was accompanied by a decreased expression of constitutive and function-dependent platelet adhesion molecules. However, increases in platelet-leukocyte coaggregates and a shortened INR time suggest extrinsic coagulation activation, possibly by induction of a leukocyte tissue factor dependent mechanism. High dose supplements of alpha-tocopherol may override the available redox balance in well controlled type 2 diabetes. However, intrinsic effects of alpha-tocopherol must be discussed.

Aged↗
PubMed1998

Analysis of vessel wall morphology, blood flow velocity, and the hemostatic system in a patient with a large intracoronary thrombus.

A patient with AMI caused by a large thrombus in the proximal LAD was successfully treated with PTCA and an intracoronary lysis combined with the platelet-receptor antagonist c7E3. Analysis of cellular hemostasis after 1 and 6 months revealed a sustained platelet activation despite combined anti-platelet therapy with ASA and ticlopidine. A progredient slow-flow phenomenon appeared during control angiographies, confirmed by intracoronary Doppler examination.

Abciximab↗
PubMed1998

Introduction of apoptosis by high proinsulin and glucose in cultured human umbilical vein endothelial cells is mediated by reactive oxygen species.

There is much evidence that diabetes and hyperglycaemia contribute to the impairment of endothelial function and induce severe changes in the proliferation, the adhesive and synthetic properties of endothelial cells. Induction of apoptosis could represent one mechanism to prevent the new accumulation of those vascular defects and to allow generation of vascular endothelium. In this study, we demonstrate that high concentrations of glucose or proinsulin induce apoptosis in human umbilical endothelial cells by three independent methods (DNA fragmentation, fluorescence activated cell sorting analysis, and morphology). The number of apoptotic cells was increased by glucose (30 mmol/l or proinsulin (100 nmol/l) from less than 10% to about 30%. Activation of protein kinase C (PKC) largely prevented the induction of apoptosis, whereas inhibition of PKC further increased the number of apoptotic cells. Similar changes as induced by glucose were also observed after incubation of the cells with the non-metabolisable 3-O-methylglucose. These findings indicate that hyperglycaemic conditions stimulate the induction of apoptosis in endothelial cells by a mechanism which is independent from the formation of diacylglycerol and the activation of PKC. The induction of apoptosis by the non-metabolisable glucose suggests that formation of oxygen derived radicals by autoxidative processes is involved and may lead to an activation of transcription factors such as nuclear transcription factor-kappaB (NF-kappaB) transferring the activation signal into the nucleus and leading to changes in gene expression necessary for induction of apoptosis.

Apoptosis↗