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A Wirth

Publications and source records attributed to A Wirth.

At least 73 records · Page 4Linked to original sources
PubMed1996

[Metabolic syndrome].

The metabolic syndrome consists of a cluster of metabolic diseases which often coexist: abdominal obesity, glucoseintolerance, diabetes mellitus type II, dyslipidemia, hypertension and impaired fibrinolysis. The common pathophysiologic link of these diseases in insulin resistance. All clinical disorders of the metabolic syndrome are risk factors for the vascular system. Since several diseases are present at the same time the risk for atherosclerotic complications such as coronary artery disease and apoplexy is potentiated. As a consequence the costs for direct and indirect health care are high. Besides a genetic predisposition the metabolic syndrome is mainly caused by the typical life style in industrialized countries with high energy and fat intake, physical inactivity, alcohol consumption, smoking, and stress. Therefore, prophylaxis and therapy imply the removal of these factors. In order to be successful experienced physicians and motivated patients are prerequisites. Even more affective than therapy is prophylaxis which is, however, not established in Germany. The metabolic syndrome is up to now not identified as a major health problem neither by the medical profession nor by health insurances and politicians. An effective therapy and prophylaxis would induce far-reaching changes in our health system and diminish health costs.

Diabetes Mellitus, Type 2↗
PubMed1996

Quality assurance by specification and achievement of goals in palliative cancer treatment.

As the goals of palliative cancer treatments have not always been clearly specified, this paper describes how frequently the goals of palliative cancer treatment can be specified according to a given definition and how frequently those specified goals can be achieved. The clinical problems of 171 cancer patients were discussed in the Interdisciplinary Oncologic Conference (IOC) of the Cancer Centre University of Ulm (CCUU) and recommendations concerning further diagnostic treatments and/or therapy were provided. These recommendations had been documented and analysed retrospectively. The goals were classified as either cure or palliation or further investigation. If the goal was palliation, it was investigated whether or not the goal was specified as either alleviation of existing problems or prevention of impending problems. The achievement of the specified goals was assessed. Palliation was the goal of treatment in 119 (71%) of the 168 evaluable recommendations. In 83 of the 119 cases (70%), immediate treatment was recommended. The goal was specified in 57 (69%) of the 83 recommendations and could be realized in 24 of 57 specified cases (42%). Patients in this group survived longer (p < 0.01) than patients in whom the goals could not be achieved. Impending problems could be prevented more often (p = 0.001) in 14 out of 18 cases, while existing problems could be alleviated in only 10 out of 34 cases. It is concluded that specification of the goals of palliation is necessary because it is impossible to decide if a goal of treatment could be achieved or not unless the goal of treatment has been defined (as existing/impending problem). The prevention of impending problems could be investigated in prospectively controlled clinical trials.

Adult↗
PubMed1996

Atrial natriuretic peptide and plasma renin levels in assessment of mineralocorticoid replacement in Addison's disease.

Assessment of mineralocorticoid replacement therapy in Addison's disease relies on clinical features and laboratory measurements, including plasma renin and potassium. Previous studies have questioned the value of measuring the plasma renin concentration (PRC), particularly in the setting of fludrocortisone overreplacement. The aim of this study was to evaluate the usefulness of plasma atrial natriuretic peptide (ANP) measurements as a marker of sodium and volume status in Addison's disease. Fourteen patients with Addison's disease receiving their usual glucocorticoid doses were placed on various doses of fludrocortisone (FC; 0 mg, 0.05 mg, 0.1 mg and 0.2 mg) in random order for four 2-week periods. At the end of each period, blood pressure and clinical symptoms were assessed, and blood was drawn for measurement of PRC and ANP levels. PRC was significantly elevated in patients receiving placebo (54.2 +/- 57.9 ng/mL x h) compared with PRC in those receiving baseline FC (24.7 +/- 42.4 ng/mL x h), 0.1 mg FC (15.2 +/- 25.9 ng/mL x h), and 0.2 mg FC (5.5 +/- 5.7 ng/mL x h). ANP levels were measured by either an extraction method (ANP(ext)) or directly from plasma (ANP(dir)). ANP(dir) was significantly elevated at 0.2 mg FC (87.1 +/- 20.1 pg/mL) compared with baseline (63.3 +/- 8.1 pg/mL), placebo (56.1 +/- 5.5 pg/mL), 0.05 mg FC (60.5 +/- 16.0 pg/mL), and 0.1 mg FC (65.4 +/- 13.7 pg/mL) values. ANP(ext) was elevated in patients receiving 0.2 mg FC (42.7 +/- 41.8 pg/mL) compared with that in patients receiving placebo (7.9 +/- 5.4 pg/mL), 0.05 mg FC (16.2 +/- 11.2 pg/mL), or 0.1 mg FC (19.7 +/- 11.1 pg/mL). Our data suggest that PRC is of value in determining mineralocorticoid underreplacement, whereas ANP is a more sensitive index of FC overreplacement. ANP levels may, therefore, be complementary to PRC in adjustment of mineralocorticoid doses in the upper dose range, where clinical symptoms and signs appear to be of little value.

Addison Disease↗
PubMed1996

[Obesity].

Explore the source record for details and available documents.

Adult↗
PubMed1995

[Non-pharmacological therapy of metabolic syndrome].

The metabolic syndrome usually goes along with abdominal obesity: diabetes type II, hypertension, dyslipidemia, and gout are often associated. The common characteristic is the resistance to insulin action. Reasons for the metabolic syndrome are--besides a genetic determination--overnutrition, physical inactivity, and alcohol consumption. Therefore, a causal therapy aims at the elimination of these factors. Consequently, the non-pharmacological therapy of the metabolic syndrome should be emphasized. The most important treatment is the reduction of body weight in the presence of obesity which is relevant for almost 90% of the patients. Body weight can rapidly be diminished by hypocaloric diets. Both, conventional reducing diets or formula diets may be used for weight reduction. Total fasting should not be performed for several reasons. For minor weight reduction or weight maintenance following a period of rapid weight loss with a hypocaloric diet, increased physical activity also lowers weight or prevents relapsing. Aims of therapeutical procedures are the elimination or amelioration of insulin resistance and subsequently the diseases of the metabolic syndrome. Both methods, reducing diet and physical training, act on various factors related to insulin resistance. For example, hypocaloric diets activate thyroxine kinase of the insulin receptor and reduce glucose and insulin in plasma. Physical training reduces not only insulin and glucose in plasma but also free fatty acids in addition and increases capillary density in skeletal muscle. Using the glucose clamp technique, diets and training are equally effective in improving glucose metabolism. Compared to these non-pharmacological methods drugs are less convincing. Since the non-pharmacological treatment implies behavioral changes with regard to nutrition, physical activity and alcohol consumption, simple instructions are not sufficient. Usually long-lasting changes in life style are necessary in order to achieve health improvement. Therefore, health care programs on individual or social basis are required in order to improve nutrition and increase physical activity. However, long-acting effects are difficult to achieve in adults; more promising is the prevention of insulin resistance.

Abdominal Muscles↗
PubMed1995

Improvement of left ventricular morphology and function in obese subjects following a diet and exercise program.

The aim of this work was to compare left ventricular performance during weight reduction induced by either physical training and diet or diet alone. Forty-three moderately obese subjects received a hypocaloric diet of 800 kcal/d for 4 weeks; 22 of them were also subjected to an exercise program. By means of echocardiography, left ventricular dimensions and systolic time intervals were determined. Heart rate and blood pressure were measured at rest and during exercise. The addition of physical training resulted in a more favourable change in weight loss (-8.3 vs -6.3 kg), heart rate (-14 vs -7 bpm), systolic (-17 vs -8 mm Hg), and diastolic (-11 vs -6 mm Hg) blood pressure. Left ventricular mass (LVM) was diminished more pronounced by combined therapy (-10.0%) as compared to diet alone (-4.7%). Changes in LVM were correlated with weight loss but not with alterations in heart rate and blood pressure. Fractional shortening and mean circumferential fiber shortening velocity did not improve significantly whereas the ratio of preejection period/left ventricular ejection time (PEPi/LVETi) was shortened in the diet and diet plus exercise group by -10.7 and -17.9%, respectively. It was concluded that exercise training in combination with a hypocaloric diet reduces left ventricular dimensions, LVM and PEPi/LVETi more distinctly than diet alone.

Adult↗
PubMed1993

MEG localization of interictal epileptic focal activity and concomitant stereotactic radiosurgery. A non-invasive approach for patients with focal epilepsy.

Two patients with complex partial epilepsy and tumour of the temporal lobe scheduled for gamma knife radiosurgery were evaluated pre- and postoperatively by multichannel magnetoencephalography (MEG). Centers of epileptic dipole activity found preoperatively disappeared after the focal irradiation as did the epileptic seizures. Thus, to combine stereotactic MEG and gamma knife radiosurgery seems to be a non-invasive alternative to the conventional neurosurgery in focal epilepsy.

Adult↗
PubMed1993

[Concurrent and predictive correlations between emotions and cardiovascular and metabolic parameters in patients with myocardial infarct].

Amongst 86 patients with myocardial infarction, during their stay in a rehabilitation clinic, emotions (Gottschalk-Gleser speech content analysis), assessed at the beginning of the treatment, and cardiovascular (systolic and diastolic blood pressure, heart rate and reactivity during physical stress, performance) and metabolic parameters (triglycerides, HDL- and LDL-cholesterin, cholesterin/HDL, uric acid) assessed at the beginning (concurrent) and end (predictive) of the treatment, are examined. The emotion-factors "dejection" (anger in, shame and death anxiety) and "aggression" (anger out-open, anger out-hidden and ambivalent aggression) show the following association with the biological factors in stepwise regression analysis, taking into account age, body-mass-index, smoking and drugs: dejection is concurrent associated with lower systolic and diastolic blood pressure and lower HDL-cholesterin and predictive with lower uric acid, lower HDL-cholesterin and higher cholesterin/HDL. Aggression corresponds predictive with higher pulse rate and higher reactivity during physical stress, lower HDL-cholesterin and higher cholesterin/HDL.

Arousal↗
PubMed1993

[Food borne outbreak of a Salmonella enteritidis epidemic in a large pharmaceutical industry].

In summer 1991 an outbreak of a Salmonella enteritidis epidemic involving about 600 cases of gastroenteritis occurred at one of the leading pharmaceutical companies in southwestern Germany. The main source was a cold fruit soup, in addition Salmonella were isolated from meat strips and a curd cheese which were used for a salad dressing. A total of 2300 contaminated food portions were served resulting in an attack rate of about 25%. The possible origin could have been an asymptomatic Salmonella-positive member of the kitchen personnel who was the only one who was involved with the preparation of all the incriminated foods. A further spread of the epidemic and especially the possible contamination of pharmaceuticals was avoided by the timely and adequate reaction of the company's occupational medical service. This case exemplifies how classical crisis management, "increased initiative on one's own for prevention of infections in all areas of food processing" (Steuer) and finally the cooperation of the company with different institutions of the public health authorities contribute to the control of such a catastrophic scenario.

Adult↗
PubMed1992

Veratridine activates a silent sodium channel in rat isolated aorta.

To investigate the existence of silent Na+ channels, isolated rat aorta was treated with veratridine (0.1 mM) and the resulting Ca2+ uptake was determined. After 30-min incubation the total tissue uptake of Ca2+ and Ca2+ uptake increased from 2.325 +/- 0.017 to 2.614 +/- 0.080 nmol/mg wet weight (ww) and from 162.6 +/- 9.7 to 218.1 +/- 13.0 pmol/mg ww, respectively. The veratridine-induced Ca2+ uptake was blocked by tetrodotoxin (1 microM; to 17 +/- 5%) but not altered by amiloride (10 microM-1 mM). Activation of Na+/Ca2+ exchange by Na+ removal increased Ca2+ uptake from 74.2 +/- 4.5 to 97.3 +/- 5.3 pmol/mg ww, which was suppressed by amiloride (10 microM-1 mM). Nifedipine (10 nM) and verapamil (0.1 microM) at concentrations at which depolarization-induced Ca2+ uptake was diminished did not attenuate veratridine-induced Ca2+ uptake. Phenytoin at 0.1 mM reduced the Ca2+ uptake induced by veratridine or by depolarization. R 56865 (0.1 microM) and R 59494 (1 microM), novel anti-ischemic compounds inhibiting slowly inactivating Na+ channels, suppressed the veratridine-induced but not the depolarization-induced Ca2+ uptake. Guanidinium uptake was increased by veratridine (0.1 mM) from 371.2 +/- 7.2 to 574.8 +/- 45.9 pmol/mg ww. These results suggest that the rat aorta possesses a Na+ channel which is electrically silent under normal conditions but could be activated by veratridine.

Amiloride↗
PubMed1991

45Ca2+ movements induced by Ca2+ chloride in isolated rat aorta under K(+)-free conditions.

Increasing the extracellular Ca2+ concentration induced a dihydropyridine-insensitive contraction in the isolated rat aorta bathed in K(+)-free solution. To obtain further insight into the mechanism of this contraction 45Ca2+ uptake measurements were carried out with isolated rat aorta. Increasing the extracellular Ca2+ concentration from 0.63 to 5.0 mM enhanced the 45Ca2+ uptake from 186 +/- 3 to 359 +/- 12 dpm/mg ww (n = 8). Under K(+)-free conditions increasing the extracellular Ca2+ concentration from 0.63 to 5.0 mM enhanced the 45Ca2+ uptake from 184 +/- 4 to 541 +/- 6 dpm/mg ww (n = 12) and elicited an increase in tension of 10.0 +/- 0.4 mN (n = 9). The Ca2(+)-induced 45Ca2+ uptake was not affected by the Ca2% channel antagonists, nifedipine (L-type), flunarizine (L- and T-type) and omega-conotoxin (N-type). Amiloride, a blocker of the Na+/Ca2+ exchange, indomethacin, a blocker of prostaglandin synthesis, the local anaesthetic, lidocaine, and the Ca2+ overload blocker. R 56865, had no effect on Ca2(+)-induced 45Ca2+ uptake. Additionally, R 56865 did not affect the Ca2(+)-induced contractile response. The inorganic Ca2+ entry blocker, lanthanum, reduced both the non-stimulated and stimulated 45Ca2+ uptake and inhibited the Ca2(+)-induced contractile response. We would like to suggest that the 45Ca2+ uptake induced by Ca2+ under K(+)-free conditions enters the cell via the leakage Ca2+ channel, because lanthanum was an effective antagonist and a significant contribution of any other Ca2+ pathway could not be demonstrated.

Amiloride↗
PubMed1991

Veratridine-induced intoxication in the isolated left atrium of the rat: effects of some anti-ischemic compounds.

Veratridine-induced Na+ and Ca2+ uptake was used as a simulation of ischemia-induced Na+ and Ca2+ uptake. Therefore, electrically driven (1 Hz) isolated left atria of the rat were intoxicated with veratridine and the 45Ca2+ uptake was determined. Veratridine (10(-4) mol/l) increased the 45Ca2+ uptake from 575 +/- 13 to 2320 +/- 86 dpm/mg ww (n = 20). The total tissue content of 45Ca was elevated from 4328 +/- 132 to 5136 +/- 303 dpm/mg ww (n = 13). The veratridine-induced 45Ca2+ uptake was completely suppressed by tetrodotoxin (10(-7) and 10(-6) mol/l), whereas amiloride (6.10(-6) mol/l) and phentolamine (10(-6) and 10(-5) mol/l) exhibited no effect on the veratridine-induced 45Ca2+ uptake. Nifedipine (10(-7) and 10(-6) mol/l) was ineffective on veratridine-induced 45Ca2+ uptake. Verapamil (10(-5) mol/l) suppressed the veratridine-induced 45Ca2+ uptake, but the 45Ca2+ uptake in the absence of veratridine was also suppressed by verapamil (10(-6) and 10(-5) mol/l). The novel anti-ischemic compounds R 56865 (10(-8)-10(-5) mol/l) and R 59494 (10(-8)-10(-5) mol/l) totally abolished veratridine-induced 45Ca2+ uptake. It is speculated that Ca2+ enters the cell via a Na+ channel which changes its selectivity upon veratridine treatment. Consequently, R 56865 and R 59494 could display their protective effect by either inhibiting the modified Na+ channel or preventing the transition of the normal Na+ channel to its altered state.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Adjuvant therapy of colorectal cancer: an overview.

The substantial recurrence rate of colorectal cancer following potentially curative resection has fuelled the search for effective adjuvant therapy. Previous trials using 5-fluorouracil (5-FU) as a single agent or in combination chemotherapy regimens have not demonstrated meaningful benefits, an impression reflected in the results of a meta-analysis encompassing large patient numbers. Newer developments utilizing intraportal chemotherapy and the combination of 5-FU and levamisole have resulted in lower recurrence rates and improved survival in patients with colon cancer. In advanced disease, the biochemical modulation of 5-FU by Leucovorin has been shown to prolong survival in some studies. Combined chemotherapy and radiotherapy or chemotherapy alone have showed promising results in rectal cancer. These developments have now been incorporated into ongoing trials.

Antineoplastic Agents↗