107 results on '"Schepke M"'
Search Results
102. Hemodynamic effects of the angiotensin II receptor antagonist irbesartan in patients with cirrhosis and portal hypertension.
- Author
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Schepke M, Werner E, Biecker E, Schiedermaier P, Heller J, Neef M, Stoffel-Wagner B, Hofer U, Caselmann WH, and Sauerbruch T
- Subjects
- Antihypertensive Agents adverse effects, Bilirubin blood, Biphenyl Compounds adverse effects, Double-Blind Method, Female, Humans, Hypotension chemically induced, Irbesartan, Kidney Function Tests, Liver Function Tests, Male, Middle Aged, Renin blood, Tetrazoles adverse effects, Angiotensin Receptor Antagonists, Antihypertensive Agents administration & dosage, Biphenyl Compounds administration & dosage, Hypertension, Portal drug therapy, Liver Circulation drug effects, Liver Cirrhosis complications, Tetrazoles administration & dosage
- Abstract
Background & Aims: Angiotensin II receptor antagonists have been proposed as new drugs for portal hypertension. This randomized, placebo-controlled, double-blind study aimed to assess the effect of the angiotensin II receptor antagonist irbesartan on portal and systemic hemodynamics and renal function in patients with cirrhosis., Methods: Thirty-six patients with cirrhosis and portal hypertension received 150 mg/d irbesartan or placebo for 1 week. Systemic hemodynamics, kidney and liver function parameters were recorded regularly; hepatic venous pressure gradient and plasma renin were assessed on days 0 and 7., Results: Irbesartan reduced the hepatic venous pressure gradient by 12.2% +/- 6.6% (P < 0.05) and mean arterial pressure by 5.3% +/- 4.0% in 13 of 18 verum patients. In 4 (22%) verum patients, arterial hypotension, accompanied by significant renal impairment, required withdrawal of irbesartan. In these patients, baseline plasma renin (P < 0.002) and cystatin C (P < 0.001) levels were higher, and creatinine clearance (P < 0.02), serum sodium (P < 0.01), and albumin (P < 0.05) were lower than in patients who tolerated irbesartan. Four of five patients with baseline renin >900 microU/mL developed treatment-limiting hypotension., Conclusions: The angiotensin II receptor antagonist irbesartan is not advisable in patients with advanced cirrhosis and high plasma renin because it may induce arterial hypotension and only moderately reduces portal pressure.
- Published
- 2001
- Full Text
- View/download PDF
103. Transjugular portosystemic stent shunt in treatment of liver diseases.
- Author
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Schepke M and Sauerbruch T
- Subjects
- Humans, Gastrointestinal Hemorrhage prevention & control, Liver Diseases surgery, Portasystemic Shunt, Transjugular Intrahepatic
- Published
- 2001
- Full Text
- View/download PDF
104. Comparison of portal vein velocity and the hepatic venous pressure gradient in assessing the acute portal hemodynamic response to propranolol in patients with cirrhosis.
- Author
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Schepke M, Raab P, Hoppe A, Schiedermaier P, Brensing KA, and Sauerbruch T
- Subjects
- Administration, Oral, Blood Flow Velocity drug effects, Blood Flow Velocity physiology, Female, Hemodynamics physiology, Hepatic Veins diagnostic imaging, Hepatic Veins physiopathology, Humans, Liver Cirrhosis diagnostic imaging, Liver Cirrhosis physiopathology, Male, Middle Aged, Portal Pressure physiology, Portal System diagnostic imaging, Portal System physiopathology, Portal Vein diagnostic imaging, Portal Vein physiopathology, Propranolol adverse effects, Sensitivity and Specificity, Treatment Outcome, Ultrasonography, Doppler drug effects, Hemodynamics drug effects, Hepatic Veins drug effects, Liver Cirrhosis drug therapy, Portal Pressure drug effects, Portal System drug effects, Portal Vein drug effects, Propranolol administration & dosage
- Abstract
Objective: The aim of this prospective study was to compare noninvasive Doppler sonography and invasive measurement of the hepatic venous pressure gradient (HVPG) to determine the acute portal hemodynamic response to propranolol in patients with liver cirrhosis., Methods: In a blinded study design, portal vein velocity (PVV) and HVPG were simultaneously assessed in 11 cirrhotic patients for 4 h after oral ingestion of 40 mg propranolol., Results: Both HVPG (17.2% +/- 4.3%, p < 0.0001) and PVV (15.6% +/- 2.1%, p < 0.0002) showed a highly significant reduction during the study period versus baseline. Based on HVPG measurements, four patients (36%) were classified as nonresponders. These patients had a significantly lower PVV reduction compared to the responders (responders: 18.8% +/- 2.0% vs nonresponders: 10.0% +/- 2.1%, p < 0.05). Nonresponders were identified by Doppler sonography with a sensitivity of 1.0, specificity of 0.86, and positive predictive value of 0.9 when a threshold of 20% PVV reduction 120 min after drug intake was applied., Conclusions: Doppler sonography is a useful tool for assessment of the acute portal hemodynamic effect of propranolol. To distinguish portal hemodynamic nonresponders from responders to propranolol, PVV measurements should be carried out 2 h after drug administration, and PVV reduction should be not <20% in propranolol responders.
- Published
- 2000
- Full Text
- View/download PDF
105. Altered adrenergic responsiveness of endothelium-denuded hepatic arteries and portal veins in patients with cirrhosis.
- Author
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Heller J, Schepke M, Gehnen N, Molderings GJ, Müller A, Erhard J, Spengler U, and Sauerbruch T
- Subjects
- Adrenergic alpha-Agonists pharmacology, Adrenergic beta-Agonists pharmacology, Adult, Case-Control Studies, Endothelium, Vascular, Female, Humans, In Vitro Techniques, Isoproterenol pharmacology, Liver Cirrhosis surgery, Liver Transplantation, Male, Methoxamine pharmacology, Middle Aged, Vasoconstrictor Agents pharmacology, Vasodilator Agents pharmacology, Adrenergic Agonists pharmacology, Hepatic Artery drug effects, Hepatic Artery physiopathology, Liver Cirrhosis physiopathology, Portal Vein drug effects, Portal Vein physiopathology, Receptors, Adrenergic drug effects
- Abstract
Background & Aims: Patients with cirrhosis are characterized by a reduced splanchnic vascular resistance and a hyporeactivity to adrenergic vasoconstrictors. So far, their adrenergic splanchnic vascular responsiveness has not been evaluated in vitro. We compared responses to alpha1- and beta2-adrenoceptor stimulation of hepatic arteries and portal veins of patients with cirrhosis undergoing transplantation with those of organ donors., Methods: Isometric contractions of endothelium-denuded vessel rings were induced cumulatively by methoxamine and relaxations by isoproterenol. Results are expressed as percentage of the contraction obtained by 85 mmol/L KCl or of the relaxation obtained by 100 micromol/L papaverine, respectively., Results: Maximal methoxamine-induced contractions were reduced in cirrhotic hepatic arteries (cirrhosis, 51.8% +/- 6.8%; donor, 89.9% +/- 6.6%; P < 0.01) and portal veins (cirrhosis, 49.2% +/- 6.4%; donor, 94.0% +/- 5.3%; P < 0.01). In cirrhosis, isoproterenol induced a less marked relaxation of hepatic arteries (cirrhosis, 46.6% +/- 3.2%; donor, 100.3% +/- 4.4%; P < 0. 01) but an increased relaxation of portal veins (cirrhosis, 41.9% +/- 6.2%; donor, 26.2% +/- 2.8%; P < 0.01)., Conclusions: In cirrhosis, endothelium-free hepatic arteries are hyporeactive to alpha1- and beta2-adrenoceptor agonists, and portal veins are hyporeactive to alpha1- but hyperreactive to beta2-adrenoceptor agonists. These findings support the in vivo findings of a hyporesponsiveness to adrenergic vasoconstrictors in patients with cirrhosis.
- Published
- 1999
- Full Text
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106. [The Churg-Strauss syndrome with cerebral seizures and terminal kidney failure].
- Author
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Terjung B, Paar WD, Schepke M, Klehr HU, Hufnagel A, and Sauerbruch T
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- Aged, Asthma complications, Asthma diagnosis, Asthma therapy, Churg-Strauss Syndrome diagnosis, Churg-Strauss Syndrome therapy, Combined Modality Therapy, Diagnosis, Differential, Disease Progression, Eosinophilia complications, Eosinophilia diagnosis, Eosinophilia therapy, Humans, Kidney Failure, Chronic diagnosis, Kidney Failure, Chronic therapy, Male, Seizures diagnosis, Seizures therapy, Churg-Strauss Syndrome complications, Kidney Failure, Chronic etiology, Seizures etiology
- Abstract
History and Clinical Findings: A 67-year-old man with known bronchial asthma was admitted to hospital because of deteriorating general state of health, fever, progressive renal failure and confusional states., Investigations: Erythrocyte sedimentation rate was 70/95 mm and the concentration of C-reactive protein raised to 30 mg/dl. WBC count was 19,000/microliter with 39% eosinophilia. Anticytoplasmatic antibodies (cANCA) had a high titre (1:160). On admission the creatinine level was 5.6 mg/dl. Renal biopsy indicated marked glomerular and tubulo-interstitial scarring. Chest radiograms showed transient pulmonary infiltrates. Churg-Strauss syndrome (CSS) was diagnosed on the basis of the clinical and biochemical findings., Treatment and Course: Haemodialysis was instituted to counteract the renal failure with water retention. Inflammatory parameters and clinical symptoms rapidly responded to administration of corticosteroids (prednisolone, initially 250 mg/d for 3 days, then 150 mg/d for 5 days followed by slowly decreasing doses). Two weeks after starting prednisolone he had secondary generalised seizures. Magnetic resonance imaging (MRI) of the skull demonstrated marked hyperintense focal changes which in their pattern were characteristic of cerebral vasculitis. As a steroid-refractory condition had to be assumed, cyclophosphamide was also given (100 mg/d). Within 6 weeks the clinical symptoms gradually regressed and the MRI changes became practically normal., Conclusion: Early combined immunotherapy should be given if CSS runs a complicated course, rather than the usually recommended corticosteroid monotherapy.
- Published
- 1997
- Full Text
- View/download PDF
107. [Endoscopy in patients at risk for bleeding].
- Author
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Schepke M, Unkrig C, and Sauerbruch T
- Subjects
- Gastrointestinal Hemorrhage therapy, Hemorrhagic Disorders therapy, Humans, Risk Factors, Endoscopy, Gastrointestinal methods, Gastrointestinal Hemorrhage etiology, Hemorrhagic Disorders etiology
- Published
- 1997
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