[Diagnosis of chronic hepatitis].
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Biomedical subjects
Publications and source records attributed to W Rambach.
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HISTORY AND FINDINGS: A pale looking 33-year-old man with a history of perforated gastric ulcer and pancreatitis with surgically drained pseudocyst was admitted because of painless anal bleeding. Heart rate was 100/min, blood pressure 90/60 mm Hg. INVESTIGATIONS: Haemoglobin concentration (6.3 g/dl) and RBC count (2.4 mill./microliters) indicated anaemia due to bleeding. Sonography and computed tomography demonstrated chronic calcifying pancreatitis and thrombosis of splenic and mesenteric veins. There were grade 1 oesophageal varices on endoscopy. The source of bleeding was found by coloscopy to be a submucous pulsating tumour in the region of the left flexure, which on angiography was an aneurysm of the splenic artery. TREATMENT AND COURSE: The pseudoaneurysm of the splenic artery, which had perforated into the colon, was resected together with a partial pancreas excision and splenectomy. There were no complications and the patient was discharged symptom-free after 15 days, and there had been no further bleeding 6 months later. CONCLUSION: Pseudoaneurysm of a visceral artery is a rare, but life-threatening, complication of pancreatitis. Treatment options are operation and/or interventional catheter embolisation.
Of 1,756 liver biopsies performed in the years 1987-1991, in 139 cases the patients exhibited both a nearly normal liver histology and elevated GGT values. After exclusion of patients with known causes for an elevated GGT 15 patients were selected, who over at least one year, were documented as having at least 3 measured GGT values with an average of over 40 U/l. In the follow-up of 1-15 years a typical constellation was detectable: longterm elevation of GGT (average 47-156 U/l, moreover a smaller degree of elevation of GLDH and GPT), minimal deviations from norm in liver histology (periportal fibrosis and/or fatty liver degeneration), and functional abdominal complaints. This triad occurred predominantly in middle-aged males, did not exhibit laboratory-chemical or histological signs of progression or regression tendencies and could be interpreted as a "functional" liver disorder with parelleles to M. Gilbert-Meulengracht.
721 patients with liver cirrhosis were regularly screened by sonography and determination of alpha fetoprotein during a period of eleven years (1.1.1982-1.1.1993). In 137 of them hepatocellular carcinoma (HCC) was diagnosed; 28 (20.4%) had a unilocular HCC with a diameter up to 5 cm. Diagnosis was regularly verified by sonographic guided puncture, in rare cases by laparoscopy and biopsy. Beside a diameter of 5 cm the tumor should be localized at least 5 mm from the main structures in the hilus, and not in the centre of the liver; furthermore multilocular hepatocellular carcinomas and intra- and extrahepatic metastases were contraindications. Child-Pugh-classification should be A+B and urea synthesis rate at least 6 g per day. In 21 patients (75%) a portal hypertension was diagnosed; 19 (68%) had bled from esophageal varices; in case of one bleeding a therapeutic sclerotherapy and in case of recurrent variceal hemorrhage an elective shunt operation were performed. Surgical resection was carried out with controlled hypotension and temporary occlusion of the hepatoduodenal ligament. Tumor was removed by segmentectomy or bisegmentectomy and in rare cases by enucleation. There were 3 clinical deaths (10.7%); causes of death were liver failure and (2) sepsis (1). All patients could be followed up to January 1, 1993; there were 12 further deaths of liver failure, tumor recurrence or second tumor. 13 patients are still living. Thus the live expectancy for one year was 80, for 5 years 50 and for 10 years 30%. There is no doubt, that it is possible to detect hepatocellular carcinoma in patients with liver cirrhosis early by regular sonography and determination of alpha-fetoprotein.(ABSTRACT TRUNCATED AT 250 WORDS)
In 1984 Roark published the first report of a sucralfate treatment of esophageal ulcers after sclerotherapy. Because this was an uncontrolled trial we planned a prospective double-blind placebo-controlled study with 60 patients. After therapeutic paravariceal injection-sclerotherapy of esophageal varices, patients were randomly treated with sucralfate suspension or placebo. Time of treatment was limited to a maximum of 3 weeks and the dosage of sucralfate was 1 g q.i.d. (Ulcogant-Suspension). Healing was assessed by endoscopy at weekly intervals. Fifty-three patients (25 sucralfate, 28 placebo) were evaluable according to the protocol. No patient left the study because of side effects. At the start of the trial, the patients in the sucralfate group showed a larger ulcer area than the placebo group. There was a tendency to faster healing in the sucralfate group, especially in patients with deeper ulcerations. However, there was no significant difference in global healing between both treatment groups after 3 weeks. Sucralfate suspension may be of value in accelerating the healing process in esophageal ulcers after sclerotherapy, especially in patients with deep ulcers. These results should be confirmed in further trials, in which patients should be stratified with respect to their ulcer volume and severity of liver disease.
From 1 January 1983 to 1 January 1989 123 cirrhotic patients with hepatocellular cancer (n = 122) or cholangiocarcinoma (n = 1) were screened using liver function tests, alpha-fetoprotein determination, ultrasonography with biopsy (and in selected cases computed tomography or nuclear magnetic resonance), laparoscopy and angiography, Child-Pugh classification and urea-nitrogen synthesis rate. Twenty-three patients were selected for surgical resection because the tumour was smaller than 5 cm, not centrally located and at least 1 cm away from main structures; there was no evidence of multicentricity or metastatic disease; and the Child-Pugh classification was A or B and the urea-nitrogen synthesis rate at least 6 g/day. Upper gastrointestinal endoscopy was used routinely to identify oesophageal varices which were present in 17 cases; ten patients with a history of variceal haemorrhage (43 per cent) had preoperative endoscopic sclerotherapy. In cases with recurrent haemorrhage, surgery was used to prevent intraoperative and postoperative bleeding. Tumour resection was carried out using controlled hypotension and hepatoduodenal ligament clamping. Twelve bisegmentectomies, ten segmentectomies and one atypical resection were performed. The operative mortality rate was 13 per cent with liver failure and sepsis as the causes of death. The 'recurrence rate' was 26 per cent and the late mortality rate for the whole group up to 1 January 1990 was 30 per cent; 13 patients were still alive. The 12-month survival rate was 77 per cent and after 5 years it was 49 per cent. Thus, surgical resection of small liver tumours is the treatment of choice in this selected group of patients.
Endoscopic sclerotherapy has been used to control acute variceal haemorrhage which persists despite conservative therapy, prevent recurrent variceal haemorrhage in patients with a history of oesophageal haemorrhage, and to prevent a haemorrhage in patients with oesophageal varices who never bled. In this short paper I will cover our personal experience with more than 2000 patients receiving particularly paravariceal endoscopic sclerotherapy of bleeding esophageal varices, and especially present the results of our prospective and controlled randomized trials (Table 1) and underline the thesis that endoscopic sclerotherapy and surgical procedures for patients with portal hypertension are complementary supporting measures or options.
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