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)

The authors distinguish three kinds of hepatogenous polyglobulia: Polycythaemia caused by Budd-Chiari syndrome, polycythaemia caused by a Mosse syndrome (cirrhosis without liver venous thrombosis) and polyglobulia caused by liver tumours. In all three cases the same mechanism is likely to induce polycythaemia or polyglobulia respectively. In addition to the three cases of the Mosse syndrome published in 1966, the present paper deals with three cases of Budd-Chiari syndrome. Twice the Budd-Chiari syndrome was followed by a polycythaemia, once a Budd-Chiari syndrome was developed in the course of a polycythaemia vera.
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PMID:[Hepatogenic polyglobulinemias and polycythemias]. 7 34

Using baloon catheters in the inferior vena cava, post-hepatic blocks were produced in experimental animals. Subsequent liver perfusion scintigraphy showed marked reduction in portal flow. The significance of these findings in the diagnosis of the Budd-Chiari syndrome and its differentiation by scintigraphy from an intrahepatic block in cirrhosis of the liver is discussed.
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PMID:[Sequential hepato-splenic scintigraphy with 99mTc-pertechnetate in experimental post-hepatic block (author's transl)]. 14 7

A variety of indirect techniques has been claimed to provide evidence of spontaneous reversal of portal blood flow in hepatic cirrhosis but the existence of the phenomenon has been doubted by some who do not accept the validity of the indirect evidence. There are few reports of the demonstration of hepatofugal portal flow by selective hepatic arteriography, which is the only acceptable technique. We report three patients with histologically confirmed cirrhosis in whom hepatofugal portal blood flow was unequivocally demonstrated by arteriography, in whom no surgical portosystemic shunt had been performed and in whom there was no evidence of the Budd-Chiari Syndrome or hepatoma, situations accepted as associated with reversed portal blood flow. Theoretical considerations suggest that shunt surgery for bleeding esophageal varices should not be ruled out on the grounds of hepatofugal portal flow. However, end-to-side portacaval anastomosis and distal splenorenal shunt might predispose to the early redevelopment of esophageal varices when reversed portal flow is present. Side-to-side portacaval and conventional splenorenal shunts might be preferable in having less effect on hepatic parenchyma perfusion than when orthograde portal flow in the case.
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PMID:Hepatofugal portal blood flow in hepatic cirrhosis. 62 19

Sera of 184 patients were examined to determine the incidence of hepatitis B surface antigen (HBsAg). Ninety-two patients had primary liver cancer (PLC) and there were 92 matched controls. Thirty-one of the 92 patients with PLC and 8 of the 92 patients with no clinical evidence of liver disease had radio-immunoassay-positive tests for HBsAg. The difference was significant (P less than 0,01). In 56 of the patients with PLC it was possible to assess the nature of associated liver disease histologically. HBsAg was found in the sera of 66,6% of patients with postcollapse cirrhosis and in 22,2% of patients with chronic Budd-Chiari syndrome. It is likely that the role played by hepatitis B infection in the pathogenesis of PLC varies according to local circumstances in different geographical areas.
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PMID:Hepatitis B surface antigen and primary liver cancer. 71 32

This report concerns a young woman who, after taking a contraceptive preparation orally for three years, developed the Budd-Chiari syndrome as the result of a widespread chronic obliterative process involving the intrahepatic efferent venous system. Her prolonged course, which failed to respond to an end-to-side portacaval shunt procedure, mimicked chronic hepatitis evolving to cirrhosis. Additional noteworthy features were the presence of two small benign hepatic adenomas, observed both at biopsy and at necropsy, a lesion recently recognized as a complication of anovulatory drugs, and widespread hepatic calcifications found at autopsy.
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PMID:Veno-occlusive disease of the liver associated with oral contraceptives: case report and review of literature. 99 50

Symptomatic occlusion of hepatic veins, the Budd-Chiari syndrome (BCS), may be on the increase in women taking oral contraceptives. 17 liver scans in 7 patients with confirmed BCS over a 7-year period were studied. 6 of the 7 patients were women. When more than 1 vein is occluded BCS results, with hepatomegaly, abdominal pain, ascites, and hepatic histology showing centrizonal sinusoidal distention, hemorrhage, and necrosis. Mortality has been high. BCS is associated with polycythemia, oral contraceptive use, malignancy, trauma, and congenital abnormalities. The scintigram appearance with radiocolloid is usually characteristic but a similar appearance has rarely been reported in cirrhosis of the liver and in 1 case of contrictive pericarditis. Excessive uptake in the midline with markedly diminished activity at the periphery may be the 1st clue that BCS is present. Confusing conditions with incomplete BCS include partial hepatectomy, radiation injury, fortuitous segmental involvement by diffuse or focal liver disease, and rarely hepatic artery occlusion. Treatment is by the porto-caval shunting operation. Venous obstruction as shown venographically has had good correlation with liver scans. After the shunt procedure, hepatic artery flow to the affected lobes has increased as the pressure falls and underperfusion of the hypertorphied midline section. After 14 months, the midline area has shown no uptake, possibly because of atrophy. Radiocolloid uptake also appears in the ribs, spine, and lung. This uptake recedes when the liver function improves.
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PMID:Liver scan in Budd-Chiari syndrome. 126 39

Transatrial membranotomy was performed in a patient with membranous obstruction of the hepatic segment of the inferior vena cava, manifesting as longstanding varicosity and edema of the legs, chronic type of Budd-Chiari syndrome, liver cirrhosis and hypersplenism. The course in this patient and similar ones reported in the literature suggests a conservative approach.
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PMID:Advisability of surgical treatment for chronic membranous obstruction of the hepatic portion of the inferior vena cava. 126 64

The authors performed 20 liver transplantations from living related donors between June 1990 and July 1991. The 20 pediatric patients (14 biliary atresia, two Budd-Chiari syndrome, one liver cirrhosis after hepatitis C viral infection (HCV hepatitis), 1 progressive intrahepatic cholestasis, 1 liver cirrhosis, 1 protoporphyria) were transplanted with 11 left lobes, eight left lateral segments, and one right lobe. The choice of donors was restricted to the parents of the recipients. The immunosuppressive treatment consisted of FK 506 and steroids. Seventeen recipients are alive, 15 of whom are well and at home. Two recipients, who underwent emergency transplantation, died of postoperative complications. Another recipient died of accidental asphyxia at 6 months after the transplantation. All 20 donors had uneventful postoperative courses and were able to resume their normal social lives. The arterial ketone body ratio (AKBR) increased to above 1.0 within 2 days after the transplantation in all cases. Relatively mild rejection episodes were encountered in only two cases transplanted with ABO-compatible grafts, and these were treated successfully with steroids and FK 506.
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PMID:An appraisal of pediatric liver transplantation from living relatives. Initial clinical experiences in 20 pediatric liver transplantations from living relatives as donors. 128 74

Primary Budd-Chiari syndrome, obstruction of the hepatic portion of the inferior vena cava (IVC), is a rare disorder, but relatively prevalent in the Far East, northern India and Africa. Ultrasound examination was carried out on 9 patients with primary Budd-Chiari syndrome. There were 5 men and 4 women aged 27-60 years. In all the 9 cases, the diagnosis was confirmed by cavography and liver histology. Moreover, 7 of the 9 subsequently underwent radical operation using a patch graft. Ultrasonic study showed several characteristic findings suggestive of the syndrome, and frequencies of the main findings were as follows: 1) an echogenic obstructing membrane; 22.2%, 2) segmental obstruction of the IVC; 77.8%, 3) occlusion of the major hepatic veins at the juxtacaval portion; 100%, 4) enlarged inferior right hepatic veins; 55.6%, 5) abnormal intrahepatic venous structures and collaterals; 88.9%. Of these findings, 5) was the most prominent and most characteristic in the diagnosis of the syndrome. It is necessary for early detection of this entity to evaluate carefully intrahepatic venous abnormalities and patency of either the IVC or major hepatic veins on ultrasonic examination. The careful examination for Budd-Chiari syndrome should be done in cases with cryptogenic liver cirrhosis, particularly in countries where the prevalence of the syndrome is high.
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PMID:Ultrasound study in the diagnosis of primary Budd-Chiari syndrome (obstruction of the inferior vena cava). 131 85

The incidence of portal vein thrombosis was examined in 885 patients who received orthotopic liver transplantations for various end-stage liver diseases between 1989 and 1990. The thrombosis was classified into four grades. Grade 1 was thrombosis of intrahepatic portal vein branches, grade 2 was thrombosis of the right or left portal branch or at the bifurcation, grade 3 was partial obstruction of the portal vein trunk, and grade 4 was complete obstruction of the portal vein trunk. Among the 849 patients without previous portosystemic shunt, 14 patients (1.6%) had grade 1, 27 patients (3.2%) had grade 2, 27 patients (3.2%) had grade 3 and 49 patients (5.8%) had grade 4 portal vein thrombosis. The incidence of portal vein thrombosis was highest (34.8%) in the patients with hepatic malignancy in the cirrhotic liver, followed by those with Budd-Chiari syndrome (22.2%) and postnecrotic cirrhosis of various causes (15.7%). The patients with encephalopathy, ascites, variceal bleeding, previous splenectomy and small liver had significantly higher incidences of portal vein thrombosis than the others. The total incidence of portal vein thrombosis among the 36 patients with previous portosystemic shunt was 38.9%, which was significantly higher than that (13.8%) of those without shunt.
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PMID:The incidence of portal vein thrombosis at liver transplantation. 142 58


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