[Massive ascites of unknown origin. Ovarian tumor].
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Biomedical subjects
Publications and source records attributed to Eckhart Georg Hahn.
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Obstructive sleep apnea syndrome (OSAS) is usually associated with conditions known to increase insulin resistance and cardiovascular risk, such as hypertension, obesity, and diabetes. Thus, investigating whether obstructive sleep apnea itself is an independent risk factor for increased insulin resistance and whether continuous positive airway pressure treatment (CPAP) might improve insulin sensitivity brings up considerable methodological problems. Even if insulin sensitivity improves, it is hard to distinguish between an effect of CPAP treatment, e.g. in the reduction of nocturnal sympathetic activity caused by the sleep disturbance, and concomitant factors, such as weight loss. Two recent investigations were able to prove that OSAS is an independent risk factor for insulin resistance: one study in a statistical approach, the other by demonstrating a significant improvement of insulin sensitivity already two days after onset of CPAP therapy, thus clearly ruling out such confounding factors as changes in lifestyle or weight loss. However, it is still not clear if this improvement in insulin sensitivity is accompanied by an improvement in the usually elevated cardiovascular risk of patients with OSAS. Since a decrease in elevated markers of subclinical inflammation--nowadays regarded as the main culprit of cardiovascular complications and atherosclerosis--such as Interleukin-6 and C-reactive protein has been reported during CPAP therapy, and since an improvement in left ventricular function and a decrease in blood pressure were also reported under CPAP treatment, there are several good reasons to assume an improvement in metabolical function in OSAS patients due to CPAP treatment.
BACKGROUND: The role of resistin, a "new" white adipose tissue hormone, still needs to be established. Its linkage to insulin sensitivity and body mass was controversial in previous studies. MATERIAL/METHODS: Twenty obese patients (BMI: 32.1+/-6.9 kg/m2 ) with obstructive sleep apnoea syndrome (OSAS) (Apnoea-Hypopnoea Index: 48.6+/-19.1, underwent measurements of resistin, interleukin-6 (IL-6), intracellular adhesion molecule-1 (ICAM-1), CRP and the insulin sensitivity index (ISI) by hyperinsulinaemic euglycaemic clamp before, 2 days and 2 months after onset of CPAP treatment. RESULTS: Resistin remained unchanged during CPAP-therapy and was negatively correlated to ISI (r=-0.359; p=0.006), the latter was significantly improved by CPAP (p<0.001). In a correlation matrix, IL-6 and ICAM-1 were significantly (p=0.001) correlated to resistin (p=0.614 and 0.427). Changes of inflammatory markers under CPAP treatment were related to AHI, as well as resistin changes. CONCLUSIONS: In agreement with previous investigations, we could only demonstrate a weak linkage between ISI and resistin. However, at least in obese patients with OSAS, there is a close relation to subclinical inflammation (IL-6) and endothelial activation (ICAM-1).
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The molecular mechanisms responsible for the progression of malignant transformation in Barrett's esophagus (BE) are still poorly understood. This study was undertaken (1) to investigate the gene and protein expression of cyclooxygenase-2 (COX-2), peroxisome proliferator-activated receptor-gamma (PPARgamma), interleukin-8 (IL-8), hepatocyte growth factor (HGF), gastrin, and its receptor (CCK-2) in the Barrett's epithelium; (2) to analyze the activity of NFkappaB in Barrett's esophagus with low-grade dysplasia; and (3) to assess the effects of PPARgamma ligand (ciglitazone) and gastrin on cell proliferation in the cell line derived from esophageal adenocarcinoma (OE-33). COX-2, PPARgamma, IL-8, HGF, gastrin, and CCK-2 expression levels relative to the control gene encoding GAPDH were analyzed by RT-PCR and Western blot in specimens of BE with low-grade dysplasia (n = 20) and compared with that in the normal squamous esophageal mucosa from the middle portion of the esophagus (n = 20). In vitro experiments included the incubation of cell line OE-33 with ciglitazone (1-15 microM) and gastrin (100 nM). NFkappaB activity in biopsies specimens was measured by highly sensitive ELISA. COX-2, PPARgamma, IL-8, HGF, gastrin, and CCK-2 expressions were significantly increased in BE compared with normal squamous esophageal mucosa. NFkappaB activity was significantly upregulated in BE. Ciglitazone inhibited cell proliferation of OE-33 cells as assessed by BrdU and this effect was attenuated partly by gastrin. (1) COX-2, PPARgamma, HGF, gastrin, and its receptor are significantly upregulated in BE, suggesting a possible role for these factors in Barrett's carcinogenesis; (2) the increased NFkappaB activity is probably linked to increased IL-8 and COX-2 expression; and (3) PPARgamma ligands might be useful as a new therapeutic option in the prevention and treatment of Barrett's carcinoma.
OBJECTIVE: Can sonographic measurements of the transit time of an echo enhancer from the hepatic artery to the hepatic vein discriminate between patients with and without liver metastases? METHOD: The hepatic transit time (hepatic artery to hepatic vein delay) of an echo enhancer (Optison) was measured in pulse inversion mode on the basis of time intensity curves (TIC) in patients with gastrointestinal tumours with proven liver metastases and in patients without liver metastases. RESULTS: Sixty-four patients (46 males, 18 females, mean age 61 +/- 13 years) were admitted to the study. Fourteen patients had metastatic growth in the liver with a primary tumour in situ (group A). Fourteen patients had liver metastases following primary tumour resection (group B). Twenty-eight patients had a known primary tumour but no liver metastases (group C), and eight patients had neither liver symptoms nor a primary tumour (group D). The mean hepatic transit time in patients with liver metastases was 6.6 +/- 1.8 s in group A and 6.7 +/- 1.7 s in group B, whereas in patients without liver metastases it was significantly longer; namely, 15.7 +/- 4.4 s in group C and 15.0 +/- 2.0 s in group D (P < 0.001). The transit times in all patients with liver metastases were < or = 10 s, while in all patients without metastases except for four the times were > or = 12 s and one of the four had already developed liver metastases on early follow-up. CONCLUSIONS: Measurement of the hepatic transit time permits discrimination of patients with and without liver metastases.
OBJECTIVES: Chronic pancreatitis may lead to considerable reduction in health-related quality of life, but factors associated with a poor perceived health status have not been investigated. METHODS: We recruited 265 patients with chronic pancreatitis from a tertiary care gastroenterology clinic. Health-related quality of life was assessed using the Short Form-36 Health Survey. Data were compared with age- and gender-adjusted values from the German general population (6964 adults). Factors associated with poor perceived health status were identified by logistic regression. RESULTS: All domains of health-related quality of life were reduced in chronic pancreatitis. Decrements were most pronounced in role limitations caused by physical (-25%) and emotional health problems (-15%), and general health perceptions (-19%). Severity of abdominal pain, chronic pancreatic diarrhea, low body weight, and loss of work independently contributed to the physical component score of the Short Form-36 (adjusted R2= 33.8%) and were the factors most closely associated with poor health status perception. The etiology and duration of the disease or changes in pancreatic morphology had no impact on health-related quality of life. CONCLUSIONS: Patients with chronic pancreatitis experience substantial impairments in health-related quality of life. The severity of chronic pancreatitis-related symptoms is directly associated with patient function and well-being. These data offer further insight into the impact of chronic pancreatitis on patient health status and may serve as the basis for the development of disease-specific instruments, which are needed to measure the effect of therapeutic interventions on patient-derived health outcomes.
OBJECTIVE: To determine health-related quality of life in medical intensive care patients with multiple organ dysfunction. DESIGN: Prospective, observational study. SETTING: A 12-bed, noncoronary, medical intensive care unit of a university hospital. PATIENTS: Between June 1998 and May 1999, 318 consecutively admitted adult patients with an intensive care unit stay of >24 hrs were studied. MEASUREMENTS AND MAIN RESULTS: Health-related quality of life was assessed using a generic instrument, the Medical Outcomes Study Short Form-36 Health Survey, at admission and at 6-month follow-up. Patients who developed multiple organ dysfunction (n = 170) consumed 85% of the therapeutic activity provided in the intensive care unit. Compared with age- and sex-adjusted general population controls, multiple organ dysfunction patients had a worse preadmission health-related quality of life than other intensive care unit patients, predominantly due to a higher burden of comorbid disease. In a multivariate analysis, multiple organ dysfunction was the only variable independently associated with deteriorated physical health domains at follow-up (odds ratio, 4.4; 95% confidence interval, 1.3-14.6; p =.015), but it had no impact on dimensions of mental health. Analyzing the impact of different organ system failures, respiratory failure (odds ratio, 4.1; 95% confidence interval, 1.6-10.3; p =.002) and acute renal failure (odds ratio, 3.3; 95% confidence interval, 1.0-11.5; p =.05) increased the risk of deteriorated physical health at follow-up. No impact of the various organ system failures on mental health was noted. At 6-month follow-up, 83-90% of survivors had regained their previous health-related quality of life, and 94% were living at home with their families. CONCLUSIONS: This study has shown that preadmission health-related quality of life of our medical, noncoronary patients was substantially reduced compared with a matched general population. This demonstrates the need to take prehospitalization health-related quality of life into account when examining the outcomes of intensive care unit survivors. Multiple organ dysfunction was the major determinant of poor physical health at follow-up, but it had no impact on mental health domains.
OBJECTIVES: Serum immunoglobulin E (IgE) was investigated in patients with chronic pancreatitis in order to elucidate possible disease mechanisms linking pancreatitis, adverse reaction to foods and allergy. DESIGN AND METHODS: Serum IgE was analysed in 86 non-atopic patients with advanced chronic pancreatitis and 54 non-atopic controls. IgE detection was performed by enzyme-linked immunofluorescence. RESULTS: Mean IgE levels (+/- standard error of mean) in chronic pancreatitis patients (286.1+/-49 kU/l) were found to be significantly elevated compared to controls (67.7+/-11 kU/l; P<0.0001). Normal IgE levels (<100 kU/l) were present in 40/54 control patients (74.1%), but only 39/86 pancreatitis patients (45.3%). Of the patients with chronic pancreatitis, 47/86 (54.6%) had clearly elevated IgE levels of >100 kU/l and their IgE values did not show a Gaussian distribution. However, nine-fold higher IgE levels were found in chronic pancreatitis patients with alcohol consumption of >25 g/day and exocrine insufficiency (915.5+/-240 kU/l) than in pancreatitis patients with normal exocrine function and no alcohol consumption (103.4+/-43 kU/l; P<0.001). Moreover, acute episodes of chronic pancreatitis were found to increase serum IgE levels. CONCLUSIONS: In patients with chronic pancreatitis, serum IgE production is markedly enhanced, especially during acute inflammatory episodes or when alcohol is consumed. Since abstinence from alcohol and pancreatic enzyme substitution are associated with clearly lower IgE levels, it may be concluded that pancreatic insufficiency with reduced nutrient digestion and alcohol consumption stimulate IgE production. This finding gives rise to the speculation that, apart from pancreatic inflammation, cross-linking of IgE with alimentary or other antigens might be involved in the pathophysiology of a sub-population of patients with chronic pancreatitis and manifest pancreatic insufficiency.
BACKGROUND: The Launois-Bensaude syndrome (LBS) is a rare disease characterized by an accumulation of multiple lipomata with a preponderance at the thorax, abdomen, upper arms and the thighs. Frequently, the condition is associated with past or present alcohol abuse with no clear temporal coincidence between the onset and termination of lipomata growth and onset or termination of alcohol consumption. Due to the massive accumulation of adipose tissue, the patients frequently have features of the metabolic syndrome as hypertension, impaired fasting glucose or diabetes mellitus, hyperuricemia or hyperlipidemia. CASE REPORT: A 79-yr-old female observed an increase of fat mass especially at the upper arms, the thighs and the thorax in combination with a weight gain of 19 kg within 2 years without any changes in the nutrition habits. The unique features confirmed the diagnosis of LBS. Interestingly, she had diabetes mellitus, hypertension and hyperlipidemia before the manifestation of LBS and without any history of heavy alcohol consumption. Furthermore, the condition predominantly affects males. In her very case, treatment with sultanol, as successfully performed in some cases, could not be recommended due to her cardiac insufficiency. A surgical approach is of limited value due to the frequent relapses of the lipomata. CONCLUSIONS: Establishing the diagnosis of LBS is an important step for patients confronted with an inexplicable physical disfigurement that is not related to excessive nutrition. The disease is often not diagnosed because of its rareness, but its features are unique and easily to be distinguished from 'simple' truncal obesity.
BACKGROUND AND AIMS: We compared contrast-enhanced power Doppler sonography (CEPD) and phase-inversion harmonic imaging (PIHI) in the assessment of liver lesion vascularity and characterization of focal liver lesions. MATERIALS AND METHODS: We examined 101 focal liver lesions by CEPD and PIHI using Optison as echo-enhancing agent. Amount and architecture of lesion vascularity and the kinetics of contrast enhancement in the lesions were analyzed. A tumor diagnosis was assessed after each examination. RESULTS: Analysis of tumor vascularity was not possible in 30 liver lesions (30%) due to motion or blooming artifacts by CEPD. Vascularity was detected in 61% of liver lesions by CEPD and in 95% by PIHI. PIHI identified significantly more tumor vascularity pattern (93%) than CEPD (57%). Specific lesion diagnosis based on PIHI led to correct results in 92% compared to 59% by CEPD. CONCLUSION: PIHI is highly efficient in detecting tumor vascularity and is superior to CEPD in characterizing focal liver lesions.
OBJECTIVE: The potential diagnostic value of performing Doppler measurements of liver vasculature to assess early stages of liver fibrosis has not been established. Due to the potential clinical impact, this study focused on the correlation between Doppler measurements and histologically proven liver fibrosis. METHODS: Forty-three consecutive patients with chronic viral hepatitis (79% hepatitis C) were enrolled. At the time of liver biopsy, two independent investigators measured maximum and mean blood flow velocity, resistance indices, vessel diameter and blood flow volume in the portal vein, hepatic artery and hepatic veins. All measurements were taken in triplicate. The mean values were correlated to the degree of liver fibrosis using the Ludwig score. RESULTS: Sixty-seven per cent of the patients in our study group had no or only mild fibrosis (Ludwig score stage I or II). Thirty-three per cent showed progressive fibrosis or cirrhosis (Ludwig score stage III or IV). There was a large overlap in the Doppler measurements and findings between the various disease stages. No significant changes of Doppler parameters were detected, even between patients with no or mild fibrosis and patients with severe fibrosis (Ludwig score stage III or IV). CONCLUSIONS: Doppler measurements of the portal vein, hepatic artery and hepatic vein(s) are not a valid surrogate marker of liver fibrosis. Nor are Doppler measurements a useful method to estimate the degree of liver fibrosis.
BACKGROUND: The main causative agents of cat-scratch disease are Bartonella henselae, tiny, gram-negative bacilli. The disease usually has a benign course with the development of a papule at the inoculation site, followed by regional lymphadenopathy. In most cases, complete resolution occurs, but in immunocompromised hosts, the course of the disease can be aggravated. CASE REPORT: A patient received methotrexate and corticosteroids for 3 months due to rheumatoid arthritis. He developed fever, exanthema and leukopenia under methotrexate therapy. Dark red indurations with central ulcerations at his right thigh revealed a further problem apart from the methotrexate-induced leucopenia and immunosuppression. The ulcerations were the remainders of recurrent scratches from the patient's cat. The patient's antibody titers against Bartonella henselae remained low and inguinal lymph node swelling was only for a short time to be observed, this reaction obviously weakened as a result of the immunosuppression. However, the typical course, the exclusion of other reasons for the exanthema and the rapid improvement of the patient's condition after antibiotic treatment ascertained the diagnosis. CONCLUSIONS: In immunocompromised hosts, diseases with a typically benign course can become severe and life-threatening illnesses. Ownership of pets should be taken into consideration before onset of an immunosuppressive therapy.
BACKGROUND: The obstructive sleep apnoea syndrome (OSA) is a frequent condition, as well as type 2 diabetes mellitus. Both diseases are characterized by insulin resistance. OBJECTIVES: The aim of this study was to establish whether OSA is an independent risk factor for increased insulin resistance in diabetics. For this purpose, we tested the hypothesis that the insulin sensitivity in patients with type 2 diabetes and OSA can be improved by 2 days or 3 months of continuous positive airway pressure (CPAP) treatment. METHODS: In 9 obese patients with type 2 diabetes and OSA [apnoea/hypopnoea index 43.1 +/- 21.3; body mass index (BMI) 37.3 +/- 5.6 kg/m2] and good glycaemic control on oral antidiabetics or on diet alone (HbA1c 6.4 +/- 0.7%), the insulin sensitivity index (ISI) was established by euglycaemic hyperinsulinaemic clamp tests at baseline, after 2 days and after 3 months of effective CPAP treatment. RESULTS: ISI was unchanged after 2 days of CPAP treatment, but was significantly improved after 3 months (4.38 +/- 2.94 vs. 2.74 +/- 2.25 at baseline; p = 0.021), without any significant changes in BMI. Glycaemic control was unaffected after 3 months (HbA1c 6.3 +/- 0.6%; not significant). Fasting leptin levels showed no significant changes. CONCLUSIONS: These results indicate that OSA itself is an independent risk factor for insulin resistance. This effect may be explained by the elevated sympathetic activity in OSA.