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ABSTRACT: Chronic viral hepatitis is a leading cause of chronic hepatitis, liver cirrhosis, hepatic decompensation and hepatocellular carcinoma worldwide. Here, we will briefly review common indications and current therapies for chronic hepatitis B and C and discuss practical aspects of these therapies. Current therapies for hepatitis C aim at viral eradication. With the introduction of pegylated interferon and ribavirin viral eradication is successful in about 55% of treated patients. The goal of therapy of HBe antigen positive chronic hepatitis B is seroconversion to anti-HBe which can be achieved with interferon alpha in 25-45% of patients. A loss of HBs can be achieved in approximately 10%. Responders proceed significantly less to cirrhosis or hepatocellular carcinoma. Anti-HBe positive patients can be treated with interferon alpha or lamivudine. The former requires longer treatment and the results are disappointing. Lamivudine is a promising agent in the treatment of chronic hepatitis B, but the success is hampered by a high relapse rate and the emergence of viral resistance.
Therapeutische Umschau 11/2003; 60(10):651-6.
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ABSTRACT: The objective of this study was to investigate the spectrum and frequency of rare AIDS-defining diseases in the Swiss HIV Cohort Study. AIDS-defining diseases contributing less than 1% to the absolute number of all recorded AIDS-defining diseases in at least one of five periods (1988-1990, 1991-1992, 1993-1994, 1995-1996, 1997) were defined as being rare. A total of 9110 HIV-infected subjects were included in this study. Over the entire 9-year period, the following rare diseases were diagnosed: progressive multifocal leukoencephalopathy (n = 138), disseminated cryptococcosis (n = 67), visceral herpes simplex disease (n = 66), primary cerebral lymphoma (n = 65), indeterminate cerebral lesion (n = 50), cryptococcal meningitis (n = 34), Mycobacterium kansasii disease (n = 32), recurrent Salmonella septicemia (n = 22), intestinal isosporiasis (n = 21), candidiasis of the trachea, bronchi and lungs (n = 19), toxoplasma retinitis (n = 16), disseminated toxoplasmosis (n = 8), invasive cervical carcinoma (n = 8), extrapulmonary Pneumocystis disease (n = 5), disseminated histoplasmosis (n = 1) and disseminated coccidioidomycosis (n = 1). Rare diseases accounted for 7.3% of all AIDS-defining diseases over the entire 9-year period. Physicians should be aware of the likelihood of a broad spectrum of AIDS-defining diseases in HIV-infected patients.
European Journal of Clinical Microbiology 07/1999; 18(6):399-402. · 2.86 Impact Factor
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ABSTRACT: The objective of this study was to investigate the spectrum and frequency of rare AIDS-defining diseases in the Swiss HIV"Abs1"> The objective of this study was to investigate the spectrum and frequency of rare AIDS-defining diseases in the Swiss HIV
Cohort Study. AIDS-defining diseases contributing less than 1% to the absolute number of all recorded AIDS-defining diseases Cohort Study. AIDS-defining diseases contributing less than 1% to the absolute number of all recorded AIDS-defining diseases
in at least one of five periods (1988–1990, 1991–1992, 1993–1994, 1995–1996, 1997) were defined as being rare. A total of in at least one of five periods (1988–1990, 1991–1992, 1993–1994, 1995–1996, 1997) were defined as being rare. A total of
9110 HIV-infected subjects were included in this study. Over the entire 9-year period, the following rare diseases were diagnosed: 9110 HIV-infected subjects were included in this study. Over the entire 9-year period, the following rare diseases were diagnosed:
progressive multifocal leukoencephalopathy (n=138), disseminated cryptococcosis (n=67), visceral herpes simplex disease (n=66), primary cerebral lymphoma (n=65), indeterminate cerebral lesion (n=50), cryptococcal meningitis (n=34), Mycobacterium kansasii disease (n=32), recurrent Salmonella septicemia (n=22), intestinal isosporiasis (n=21), candidiasis of the trachea, bronchi and lungs (n=19), toxoplasma retinitis (n=16), disseminated toxoplasmosis (n=8), invasive cervical carcinoma (n=8), extrapulmonary Pneumocystis disease (n=5), disseminated histoplasmosis (n=1) and disseminated coccidioidomycosis (n=1). Rare diseases accounted for 7.3% of all AIDS-defining diseases over the entire 9-year period. Physicians should be awarees over the entire 9-year period. Physicians should be aware
of the likelihood of a broad spectrum of AIDS-defining diseases in HIV-infected patients. of the likelihood of a broad spectrum of AIDS-defining diseases in HIV-infected patients.
European Journal of Clinical Microbiology 06/1999; 18(6):399-402. · 2.86 Impact Factor
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ABSTRACT: Emergencies in HIV-infected patients are a common complication which may occur at any stage of the disease. Opportunistic infections may lead to irreversible damages of organs such as the brain, the eye or the lung. With the widely use of antiretroviral therapy side effects of reverse transcriptease inhibitors and proteinase inhibitors and drug interactions are frequent causes of severe symptoms such as nausea and diarrhoea or of complications such as anaemia or leucopenia. As with Non-HIV-associated emergencies empiric therapy may be necessary to treat patients to prevent severe organ damage.
Therapeutische Umschau 06/1998; 55(5):295-301.
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ABSTRACT: The hypothesis that cholecystokinin release requires adequate dietary fat digestion in the small intestine was investigated in 10 healthy volunteers, and the consequences of reduced fat hydrolysis on pancreaticobiliary secretions were assessed.
Fat hydrolysis was inhibited by intraduodenal perfusion of tetrahydrolipstatin, an irreversible lipase inhibitor. An oil emulsion containing 0, 30, 60, or 120 mg tetrahydrolipstatin was perfused. After a 40-minute basal period, a test meal was eaten to stimulate cholecystokinin release and pancreaticobiliary responses.
In the control without tetrahydrolipstatin, lipase output increased threefold with meal ingestion and remained doubled for 4 hours. At the ligament of Treitz, free fatty acid concentration averaged 60% of total fatty acids. Increasing doses of tetrahydrolipstatin induced a dose-dependent inhibition of duodenal lipase activity (P < 0.01); 120 mg tetrahydrolipstatin eliminated the postprandial lipase peak activity, free fatty acid levels decreased to < 5% of total fatty acids, and plasma cholecystokinin levels were suppressed by 77% (P < 0.01). Amylase and trypsin outputs were reduced by 77% and 59%, respectively, and bilirubin secretion was virtually abolished (P < 0.01).
These findings show that tetrahydrolipstatin prevents triglyceride hydrolysis and that plasma cholecystokinin release, gallbladder emptying, and pancreatic enzyme secretion require adequate triglyceride digestion. These data also support the concept of negative feedback regulation of cholecystokinin secretion.
Gastroenterology 01/1998; 114(1):123-9. · 11.68 Impact Factor
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B Burckhardt
Praxis 04/1996; 85(11):348-50.
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ABSTRACT: CCK8 is a poor stimulant of gastric acid secretion in vivo, but is equipotent to gastrin-17 (G17) in in vitro systems. To further evaluate the role of cholecystokinin (CCK) in regulating acid output in humans, dose-response curves were constructed to CCK8 or G17 (6.4-800 pmol kg-1 per h) with and without a specific CCK-A receptor antagonist (loxiglumide). During loxiglumide infusion, G17-stimulated acid output was unchanged, whereas CCK8-stimulated secretion increased significantly. Gastric somatostatin-14 release increased fivefold with CCK8 alone, but was blocked with loxiglumide administration. These data suggest that CCK8 directly stimulates acid secretion by binding to a CCK-B/gastrin receptor on parietal cells, but at the same time inhibits acid responses by stimulating gastric somatostatin release to a CCK-A receptor-mediated pathway. To test which action of CCK is relevant under physiological circumstances, the effect of loxiglumide on fasting and post-prandial acidity was measured through continuous pH-metry. After eating, gastrin levels increased fourfold compared to controls with concomitant increases in acid secretion. These results suggest that post cibum, CCK is an inhibitor of acid secretion by regulating gastrin through local somatostatin; they support the hypothesis that CCK acts as an enterogastrone.
European Journal of Clinical Investigation 07/1994; 24(6):370-6. · 3.02 Impact Factor
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ABSTRACT: Studies were designed to establish the acid inhibitory potency and plasma kinetics of somatostatin-28 (S-28) in humans and to determine whether the amount of S-28 released into the circulation after a meal is sufficient to regulate gastric acid secretion. A liquid meal induced a significant increase of S-28 (P < 0.01) whereas S-14 levels did not change. Postprandial S-28 concentrations were then mimicked by exogenous infusions and tested on basal and pentagastrin-stimulated gastric acid secretion. Expressed in terms of circulating plasma concentrations measured by specific radioimmunoassays, S-14 was 10 times more potent than S-28 in inhibiting gastric acid production. The plasma half-life of S-28 (1.86 min) was longer than that of S-14 (1.00 min) due to a slower plasma clearance rate. S-28 did neither affect basal and stimulated gastric acid secretion nor postprandial intragastric acidity. These studies suggest that postprandial plasma concentrations of S-28 are unlikely to regulate gastric acid secretion in man. They also show that S-28 is several times less potent than S-14 with respect to inhibition of gastric acid output.
European Journal of Clinical Investigation 02/1994; 24(1):50-6. · 3.02 Impact Factor
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ABSTRACT: To evaluate the compliance for a breast cancer screening program in the region of Basel, a mammography and a clinical examination has been offered free of charge to women between 40 and 60 years of age, especially to women with familial breast cancer. From September to November 1989, 602 women participated. Results were obtained from an epidemiologic questionnaire and a two-view mammography. The median age was 55.1 years. 70.2% of the women never had a mammography before. 28.8% indicated a history of familial breast cancer. So far 444 women have been evaluated. No pathological results were obtained in 84.8% In 10.7% a second examination has been recommended in the near future. In 4.5% the mammography led to an aspiration biopsy or surgical lumpectomy where 5 (1.2%) neoplasms have been detected. Due to the limited duration of the campaign and the invitation especially addressed to women at risk, our results are not comparable with large-scale screening campaigns known from the literature. Nevertheless, we succeeded to sensitize the female population for this kind of breast care. The overwhelming success shows that the basis for a large-scale screening program may exist.
Helvetica chirurgica acta 06/1992; 59(1):203-8.
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ABSTRACT: Twenty-two para- and tetraplegic patients with chronic spinal cord injuries were examined with magnetic resonance imaging (MRI). The clinical course in the entire rehabilitation period was recorded and an attempt was made to associate the functional status of the patients with the morphologic findings on MRI. Small and large spinal cord cysts and syringomyelia, cord atrophy, and spinal stenosis were found. Additionally, in a number of patients regions of increased signal intensity within the cord, interpreted as myelomalacia, and obliteration of the intradural extramedullary space, interpreted as arachnopathy, were noted. The large number (13/22) of cystic lesions in our patients was unexpected. It was in contrast to the rate reported in autopsy studies of paraplegics which note only few cysts. Whereas a direct association of morphologic findings with neurologic symptoms and the clinical course was difficult, it was found that patients with large cysts and spinal cord atrophy generally showed no tendency to improve in spite of the measures taken during the rehabilitation period. It is difficult to decide whether the initial trauma with cord hemorrhage is limiting the chance of neurological improvement or if a sequence of events leading from hemorrhage to gliosis and cystic necrosis is the determining factor.
Neurosurgical Review 02/1991; 14(3):169-79. · 2.04 Impact Factor
