Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From October 1982 to June 1985 158 hospitalized patients in the National Hospital of Niamey, Republic of Niger, were selected whenever one of the following signs was found: hepatomegaly, jaundice, ascites, oesophageal varices, abdominal venous pattern, or splenomegaly. Investigations included hepatic echography (158/158), needle liver biopsy (68/158), radioimmunoassays for serum hepatitis B surface antigen (HBsAg; 158/158), anti-HBs (152/158), anti-HBc (129/158) and anti-delta antibody (anti-HD; 158/158). 112 patients with liver diseases comprised 28 with chronic hepatitis, 55 with non-alcoholic hepatic cirrhosis, and 29 with hepatocellular carcinoma (HCC). 46 patients with other diagnoses were used as controls. 71/112 liver disease patients were positive for HBsAg in serum compared with 1/46 controls (P less than 10(-9)). Prevalences of delta superinfection in patients with serum HBsAg (+) and anti-HD (+) were 45/112 (40.2%) in liver disease patients versus 1/46 (2.2%) in controls (P less than 10(-9)). Delta superinfection was very frequent in chronic hepatitis (8/28), non-alcoholic cirrhosis (24/55) and HCC (14/29). In chronic hepatitis, delta superinfection was more frequent in the chronic active form than in the chronic persistent type (not significant). Cirrhosis patients with delta superinfection were younger (10 years in males, 11 years in females) than those without (P less than 0.05).
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PMID:Delta superinfection in patients with chronic hepatitis, liver cirrhosis and hepatocellular carcinoma in a Sahelian area. Study of 112 cases versus 46 controls. 284 9

A comparative study of portal hemodynamics was made in 79 cirrhotics (24 cirrhotics with a large spleen greater than or equal to 500 cm3 in volume, 55 cirrhotics with a spleen less than 500 cm3 in volume), 22 patients with idiopathic portal hypertension, and 63 healthy adults who served as the control for portal and splenic venous flows. Portal and splenic venous flows were significantly increased in the group order of the cirrhosis without splenomegaly group, the cirrhosis with splenomegaly group, and idiopathic portal hypertension group. Intrahepatic shunt index was significantly greater in the cirrhosis with splenomegaly group than in the cirrhosis without splenomegaly group, and it was negligible in the idiopathic portal hypertension group. Portal vein pressure was significantly elevated in the cirrhosis with splenomegaly group than in the cirrhosis without splenomegaly and idiopathic portal hypertension groups. Postsinusoidal resistances were significantly greater in the two groups of cirrhosis than in the idiopathic portal hypertension group, whereas presinusoidal resistance was significantly greater in the idiopathic portal hypertension group than in the two groups with cirrhosis. It is concluded that these differences are inconsistent with the view that cirrhosis with splenomegaly comes from idiopathic portal hypertension.
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PMID:Differences in portal hemodynamics in cirrhosis and idiopathic portal hypertension. 292 62

Three cases of idiopathic portal hypertension associated with Hashimoto's disease are described. All of the cases were middle-aged Japanese women showing splenomegaly, esophageal varices and pancytopenia in the absence of extrahepatic portal obstruction, and cirrhosis of the liver. Two patients were euthyroid with goiter, one of which revealed diffuse lymphocytic infiltration, obliteration of thyroid follicles, and fibrosis on histological examination of the thyroid; the third suffered from myxedema without goiter. Antithyroid microsomal antibody was positive in all patients and antithyroglobulin antibody was positive in none. These findings might imply an immunological role in the pathogenesis of idiopathic portal hypertension.
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PMID:Idiopathic portal hypertension associated with Hashimoto's disease: report of three cases. 294 77

A rare chronic course of Budd-Chiari syndrome associated with thrombosis of the portal vein was observed in a 30-year-old male patient suffering from postmyocarditic cardiosclerosis. At the age of 24 the patient had infectious allergic myocarditis, was hospitalized and rehospitalized for circulatory insufficiency. Upon 3 years since the disease onset the patient was admitted to a hematological department for progressive enlargement of the spleen. The diagnosis on discharge was idiopathic myelofibrosis with portal hypertension. The treatment included prednisolone, blood transfusions, myelosan. In 1987 the patient presented with enlarged liver and spleen, ascites, gastric and esophageal varicosis, augmenting hepatic insufficiency clinically evaluated as hepatic cirrhosis. Postmortem examination revealed macrofocal cardiosclerosis, splenomegaly, ascites, portal varicosis, enlarged nutmeg liver with smooth surface. Microscopically there was phlebosclerosis and phlebothrombosis varying in duration and involving predominantly medial branches of the hepatic and portal veins, liver fibrosis. The findings provided evidence for the final diagnosis of Budd-Chiari syndrome running an uncommon chronic course.
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PMID:[The chronic form of the Budd-Chiari syndrome]. 297 4

Eighty-five patients with chronic splenomegaly and proven oesophageal varices were studied at Kenyatta National Hospital, Nairobi. The major defined groups were hepatosplenic schistosomiasis (24%), cirrhosis (20%) and portal vein occlusion (11%). Hyper-reactive malarial splenomegaly (tropical splenomegaly syndrome) was considered as the cause of oesophageal varices in only one patient. In 26% of cases liver biopsy was non-diagnostic and the extrahepatic portal vein was demonstrated radiologically to be patent. Such patients were thought to be suffering from idiopathic portal hypertension, not previously described elsewhere in Africa. Hepatitis B surface antigen was detected in 12% of controls and in 58% of patients with cirrhosis (p less than 0.001). Some serological marker of previous hepatitis B virus infection was present in 92% of patients with cirrhosis and in 79% of controls. Kamba patients from Machakos and Kitui Districts were significantly more prevalent than expected among these 85 cases of portal hypertension.
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PMID:Chronic splenomegaly in Nairobi, Kenya. II. Portal hypertension. 312 51

A 64-year-old man with cirrhosis of the liver had a palpable, pulsatile palm-size mass over the upper abdomen. Splenic artery aneurysm was diagnosed by sonography, computed tomography scan, and celiac angiography. Operative findings showed a huge splenic artery aneurysm (20 X 30 X 20 cm) over the middle portion of the splenic artery. Such a huge splenic artery aneurysm may develop because changes in splenic circulatory dynamics after a portocaval shunt, resulting in compression of the splenic vein and congestive splenomegaly.
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PMID:Huge splenic artery aneurysm after portocaval shunt. 318 29

A retrospective study was designed to analyse the mode of presentation, clinical signs, haematological, biochemical and histological features in 46 Indian patients admitted with cirrhosis to R. K. Khan and King Edward VIII Hospitals, Durban, between 1977-1981. The commonest presenting feature was swelling of the body followed by pain in the right upper quadrant, most patients had hepatomegaly, jaundice and ascites, and splenomegaly was detected in one-third of cases. Biochemical investigations indicated that most patients had a high globulin and low albumin concentration. Liver function tests revealed raised bilirubin and gamma-glutamyltransferase values in most cases. On histological examination, micronodular cirrhosis predominated (95%) with a high incidence of fat and iron deposition. Changes consistent with alcoholic hepatitis were superimposed in one-third of cases while immunological and viral markers were absent. This study suggests that alcohol is the predominant cause of cirrhosis in Natal Indians.
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PMID:Patterns of cirrhosis in Natal Indians. 320 19

Fourteen patients had mesenteric, portal, or splenic venous thrombosis that was diagnosed primarily by contrast-enhanced CT. The group included five patients with coagulopathy, three with pancreatic carcinoma, two with cirrhosis and portal hypertension, one with pancreatitis, and one with hepatocellular carcinoma. In two patients, no etiology was determined. In all cases, CT easily identified low-density venous thrombosis, which frequently involved more than one vein. In four patients, all three splanchnic veins were involved; five patients had occlusion of two veins. In five patients, only one vein was involved. Additional CT findings included ascites, collateral veins, hepatomegaly, and splenomegaly. No venous wall enhancement was found. CT also was helpful in defining the cause of thrombosis in six of 14 patients. Mesenteric edema and/or bowel wall thickening was not identified. None of the patients had classic clinical evidence of splanchnic venous occlusion, and none died primarily of that disease. The major morbidity suffered by these patients stemmed from complications of splanchnic venous occlusion, and nine patients ultimately required sclerotherapy, splenectomy, and portal decompression. We conclude that CT is useful in the diagnosis of splanchnic venous thrombosis. Our experience suggests that mesenteric, splenic, and/or portal venous thrombosis may occur more commonly than has been previously thought and that the disease in many cases is not life threatening.
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PMID:Thrombosis of the splanchnic veins: CT diagnosis. 325 38

A 22-year-old man presented with pain in the right iliac fossa. Clinical examination suggested appendicitis and showed splenomegaly. Echography and abdominal CT-sca suggested the diagnosis of cystic fibrosis based on the association of signs of cirrhosis and pancreatic atrophy. The sweat test was positive. The hypothesis of a mucoid appendicular impaction with spontaneous regression was retained based on clinical and radiological signs. This atypical presentation of cystic fibrosis underscores the frequency of obstructive intestinal which occasionally reveals the disease in the adult, and on the absence in this case of otherwise frequently associated problems such as significant pulmonary disease and malnutrition.
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PMID:[Appendicular mucoid impaction disclosing mucoviscidosis with cirrhosis in a young adult without pulmonary lesion]. 340 94

We found a significantly lower plasma fibronectin concentration in cirrhotic patients than in controls, a significant inverse relationship between fibronectin and spleen size, but no correlation between fibronectin and hepatic blood flow, prothrombin time, or serum albumin. We suggest that the increased degradation in the enlarged spleen is more relevant than the decreased synthesis in reducing plasma fibronectin levels during liver cirrhosis with portal hypertension.
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PMID:Fibronectin decrease in liver cirrhosis is related to spleen size. 341 82


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