[Physical endurance of patients with chronic hepatitis. The standardized treadmill test of 95 patients with liver biopsy verified disease].
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Biomedical subjects
Publications and source records attributed to J F Kalk.
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During a three-year period 145 consecutive patients with bleeding from oesophageal varices underwent immediate endoscopic sclerotherapy, by para- or intra- and paravascular injection of 4-40 ml 0.5% polidocanol. If the bleeding was not stopped within 15 minutes, a Linton-Nachlas tube was introduced. In case of bleeding recurrences from gastric varices or oesophageal ulcerations a gastro-oesophageal disconnection (after Hassab-Paquet) was performed as an emergency measure or electively. During the bleeding-free interval shunt criteria were examined and, if positive, an elective shunt operation was recommended. Hospital mortality was 16.5%, overall mortality during the period of the study was 29.5%. The results indicate that immediate sclerotherapy of bleeding oesophageal varices improves the prognosis, but it should be undertaken only in centres equipped for emergency endoscopy by an experienced immediately available team.
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Alcohol, hepatitis B, and Non A Non B hepatitis were the main aetiologies of 124 patients with hepatic encephalopathy (HE) due to histologically proven liver cirrhosis. All had severe portal hypertension (PH) and usually increased inflammatory activity of the liver. In stage I (n = 27) 7.4% died, in stage II (n = 28) 14.3%, in stage III (n = 32) 50% and in stage IV (n = 37) 94.6%. Even in cirrhotics without PH, serum albumin, cholinesterase activity and prothrombin time (PT) were significantly decreased. But only in the case of PT did the magnitude of the decrease parallel the stage of HE. Hyperammonaemia and serum creatinine were increased in parallel with the stage of HE. Therefore, in liver cirrhosis a quotient derived from decreased PT and increased serum creatinine has a good prognostic value. Early diagnosis of HE is possible on the basis of writing tests and the determination of free or toxic ammonia.
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Nowadays, both Anglo-Saxon and Middle European pathologists define chronic active hepatitis as synonymous with chronic aggressive hepatitis (CAH) without cirrhotic transformation. For its treatment, an accurate determination of the histological stage is necessary. CAH with slight to moderate activity (type 2a) requires merely general treatment, while corticosteroids and/or immunosuppressives are contraindicated. The latter drugs are indicated only for HBs- and HBeAG-negative CAH of type 2b with marked inflammatory activity. Every case should, however, be carefully assessed to determine whether these drugs might not be contraindicated. Our own experience with more than 600 patients with CAH shows that the prognosis is most favourable in HBs- and HBeAg-negative patients, in whom pre-existing chronic infections have been quickly recognized and eradicated, and in whom corticosteroids and/or immunosuppressives were not required. In the meantime, 13% of the CAH patients without cirrhotic transformation have been cured, and 42.5% improved. In contrast, CAH treatment with interferon, Virazol, arabinoside and immunostimulation remain disappointing.
560 patients with hepatic coma were treated during the years 1958 to 1982 in Homburg and Bad Kissingen . 82 patients had an endogeneous and 478 an exogeneous hepatic coma. Endogeneous hepatic coma was caused most frequently by fulminant virus hepatitis, intoxication, and hepatorenal syndrome accompanying serum hepatitis. Exogeneous hepatic coma in patients with cirrhosis of the liver was caused in most cases by gastrointestinal bleeding, by a diet too high in protein, or by excessive diuresis. Early clinical symptoms are changes in writing tests and ability to concentrate, whereas hepatic foetor occurs in coma stage III and IV. Clinical chemistry findings pointing to imminent hepatic coma are increase of arterial ammonia in exogeneous hepatic coma, and increase of free phenols in endogeneous hepatic coma. The increase of prothrombin time is prognostic for imminent hepatic coma in both types. Prognosis of endogeneous hepatic coma is still rather bad; 87% of the patients suffering from it died; in exogeneous hepatic coma prognosis has improved for stage I and II in the last 23 years, whereas however the total prognosis for all 4 stages is still unchanged, letality being 55%.
Initially liver morphology of chronic destructive non-suppurative cholangitis (CDNC) is rather atypical. Therefore, early morphological diagnosis is difficult. First symptoms are severe pruritus and an increase of IgM, AP and gamma-GT. Own investigation of 101 CDNC patients showed that antimitochondrial antibodies (AMA) are generally later present than the increase of the a/m enzymes. Also remarkable is the fact that among 101 patients are 13 men generally observed during the last 3 years. The most difficult problem is the treatment of CDNC. Here we have to differentiate between symptomatic basic treatment and so-called specific treatment. As basic treatment, ammonia-reducing amino acids, phenobarbital and finally cholestyramine are administered in order to diminish the severe pruritus. The diet must be rich on pectine. Lactulose and bifidum milk improve the diminished detoxication function of the liver. As specific treatment prednisolone and/or azathioprin have disappointed. D-penicillamine can influence CDNC at least temporarily. Because of the frequent side-effects D-penicillamine should be administered only in low doses (100-200 mg daily together with 300 mg vitaminee B6). Until not it is uncertain if the extremely bad prognosis of CDNC can be improved by medical treatment of its early stages.
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The results of a prospective series using the mesocaval interposition shunt (MIS) over a period of 13 years is reviewed: 100 patients were selected for the operation using strict criteria and in 98 cases the operation was performed electively. Selection criteria included liver volume between 1000-2500 mL, portal perfusion between 15-30%, no active liver disease and no stenosis of hepatic artery or coeliac axis as well as a good functional CHILD-PUGH classification (A-B). In all the cases preoperative sclerotherapy was performed so many times as needed by each individual patient with the goal of controlling the active bleeding episodes at admission and of diminishing the pre and postoperative bleeding probability. Intraoperative postshunt measurements showed residual portal perfusion in all studied patients. Early mortality was 10% and the follow up mortality 38.8%. Main causes of death were liver failure and hepatocellular carcinoma. Five and ten years survival rates were 63.9% and 35.1% respectively. The total encephalopathy rate was 12.2%. Rebleeding was observed in 5.5% of the cases and long term shunt patency rate among survivors was 90%. Angiography and sequential scintigraphy showed residual portal perfusion in 75% of cases soon after operation, in 60% after 6 months and 38% after 2 years, showing the tendency of the derivation to diminish the portal perfusion rate in the late postoperative period. The results show that MIS still has a place in the treatment of portal hypertension and that it is an excellent alternative choice to the selective shunts and the devascularization procedures.(ABSTRACT TRUNCATED AT 250 WORDS)
From January 1st, 1975, up to January 1st, 1986, a meso-caval interposition shunt was performed in 86 patients (electively with one exception), using a 16 or 18 mm lumen Dacron prosthesis. The criteria for selection for operation were a liver volume of 1000-2500 ml, a residual portal perfusion of 15 to 30%, exclusion of an activity of the liver process and stenosis of the hepatic artery or coeliac trunk. The cause of portal hypertension was liver cirrhosis in 77 patients (89.5%), prehepatic block in five (4.5%), liver fibrosis in three patients (3.5%), and myeloproliferative disease in one patient (1%). The study represents a prospective assessment and included 52 men and 32 women with a mean age of 43 years. Intraoperative flow measurement demonstrated a residual portal perfusion in all 17 patients measured after the shunt. In-hospital mortality was 8%, late mortality 39%; the fate of four patients is unknown. The main causes of death were liver failure and hepatocellular carcinoma. The rate of encephalopathies over the whole period was 10.5%. The actual survival rate was over 70% for five and over 50% for ten years. Postoperative angiographic studies confirmed by sequential scintigraphy demonstrated a residual portal perfusion in 75% of the patients postoperatively, 60% after six months and in 38% after two years. Thus it could be demonstrated that the meso-caval interposition shunt is converted to a total shunt in the long term. The total shunt patency rate was 90%. The meso-caval interposition shunt is certainly no ideal procedure but is useful in the selective or semiurgent management of patients with liver cirrhosis and portal hypertension.
Mesocaval interposition shunt, using a 14 or 16 mm Dacron prosthesis, was electively performed on 86 patients (male/female ratio 52/34, aged 15-73, mean 43 years) with portal hypertension mainly due to liver cirrhosis. The selection criteria included liver volume 1,000-2,500 ml, residual portal perfusion 15-30%, no active liver disease and no stenosis of hepatic artery or celiac trunk. Intraoperative measurements showed residual portal perfusion in all studied patients. The early mortality was 8% and the follow-up mortality (1-11 years) 39%. The main causes of death were liver failure and hepatocellular carcinoma. The actuarial survival rate was c. 70% after 5, and greater than 50% after 10 years. The total encephalopathy rate was 10%. Angiography and sequential scintigraphy showed residual portal perfusion in 75% of cases soon after operation, in 60% after 6 months and 38% after 2 years. Reduction of residual portal perfusion was not associated with rising encephalopathy rate. Mesocaval interposition shunt thus was converted to total shunt during long-term follow-up. Overall shunt patency was 90%. Mesocaval interposition shunt has a place in elective or semiurgent management of portal hypertension.