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)

We have performed a side-to-side portacaval shunt as the treatment of choice in six cases of primary Budd-Chiari syndrome. All the patients (three men and three women, mean age 33 years) had marked hepatomegaly and massive ascites. Four patients had endoscopically proved esophageal varices with no episodes of bleeding. Preoperative angiographic studies, caval pressure measurement, laparoscopy, liver biopsy specimens, liver scanning, and liver function tests confirmed the diagnosis. A possible etiologic factor was evident in only two cases. A plain side-to-side portacaval shunt was performed in four patients, while two required the interposition of a graft. One patient died after surgery of hepatorenal syndrome. Four of the surviving patients are free of ascites and doing well at 29, 27, 25, and 6 months. The remaining patient subsequently developed cirrhosis and died 76 months after surgery. None of the patients who survived developed encephalopathy. Shunt patency was confirmed endoscopically by variceal decompression in the four patients with esophageal varices. We believe the side-to-side portacaval shunt is a reliable and effective procedure for the definitive management of primary budd-Chiari syndrome.
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PMID:Portacaval shunt in the treatment of primary Budd-Chiari syndrome. 402 24

Rather rapid and brief over-view of pathology of hepatocellular carcinoma has been made, where the connection between morphology and virology or biochemistry is stressed as the main focus of today's pathology. Thus, existence of some relation between hepatitis virus and hepatocellualr carcinoma seems to be definite for us. However, it is still very difficult to decide whether the relationship is a direct or indirect one. High incidence of hepatocellular carcinoma also in Budd-Chiari's cirrhosis and schistoma-induced cirrhosis seems to suggest existence of the high risk type of cirrhosis for hepatocellular carcinoma development, irrespective of the cause of cirrhosis itself, although HB antigen might be playing some role in these cases especially in the latter.
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PMID:Pathology of hepatocellular carcinoma. 615 15

Portal hypertension is defined as an increase of the portal venous pressure over 20 cm H2O or 7 mm Hg, respectively. It may be induced by different types of portal venous stenosis or obstruction, primarily by cirrhosis and fibrosis of the liver and, less frequent by posthepatic disorders such as the Budd-Chiari-syndrome or congestive heart failure. Portal hypertension is followed by ectasia and phlebosclerosis of the portal vein, by splenomegaly, ascites and by various types of collateral circulation. Among these, oesophageal varices, are most important since they often lead to acute upper gastrointestinal haemorrhage, the major complication of portal hypertension. Bleeding from oesophaeal varices is essentially based on atrophy of the squamous epithelium, caused by ischemia from local hypoxia and venous stasis. Portal hypertension and the frequently compromised blood clotting mechanism due to reduced synthesis of clotting factors in the liver aggravate the bleeding. Atrophy of the esophageal mucosa presents an area of decreased resistance likely to ulcerate with easy erosion of the varices--usually lying very superficially--; with mechanical irritation by food or peptic erosion from gastroesophageal reflux being frequent inducers of hemorrhage.
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PMID:[Pathologic-anatomic reflections on portal hypertension (author's transl)]. 624 21

To our knowledge, this is the first report of a patient for whom a successful radical treatment for both membranous obstruction of the inferior vena cava (MOVC) and coincident hepatocellular carcinoma (HCC) were simultaneously carried out. A 36 year old Japanese man with Budd-Chiari syndrome due to MOVC was found to have HCC in the right hepatic lobe during a shunt operation between the inferior vena cava (IVC) and the right atrium (RA), using a vascular prosthetic graft. He was referred to us from another institute for further operative procedures. Both the mediastinum and the abdomen were entered through a long midline incision with longitudinal splitting of the sternum. The graft that had been occluded by thrombus was removed. Transcardiac membranotomy was achieved by manual manipulation and then by Tubb's dilator. The hepatic tumor with an abundant surgical margin of the liver was resected. The tumor of 2.5 X 2.5 X 2.0 cm was a well differentiated clear cell type HCC associated with congestive liver cirrhosis. Postoperative contrast and pressure studies through IVC showed satisfactory results. Serum alfa-fetoprotein levels decreased from 503 to 12 ng/ml. The patient is well at least for 44 months after the surgery without any recurrence at the time of completion of this writing.
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PMID:Simultaneous radical surgical treatment for membranous obstruction of the inferior vena cava and the coincident hepatocellular carcinoma--the first successful case. 631 Jan 95

The diagnostic procedure to be followed in cases of Budd-Chiari syndrome and cardiac cirrhosis cannot be schematized. Although laparoscopy and histology can point the diagnostician in the right direction, they are not decisive for the localization of the occlusions. In the presence of lumen-constricting processes, the representation of the hepatic veins has reached its limits. In this situation, laparoscopic transhepatic segmental venography or portography may help. Here, a report is presented on 5 cases with a variety of problems.
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PMID:On the diagnosis of the Budd-Chiari syndrome and cardiac cirrhosis. 645 72

Laparoscopic transhepatic measurement of pressures in the branches of the portal vein (and hepatic vein) were performed in 42 patients with hepatitic cirrhosis of the liver and compared with those obtained in patients with other defined causes of cirrhosis (alcohol, pigment, Budd-Chiari syndrome, right heart failure). Mean portal vein pressure was 27.2, mean hepatic vein pressure 14.5 mm Hg. A significant pressure difference (Kruskal-Wallis test) was present only between hepatitic cirrhosis and congestive cirrhosis, not alcohol or pigment cirrhosis. During the period of observation (1975-1978) there was a high incidence of deaths and complications in the hepatitic group compared with other forms of cirrhosis: 6 treatment-resistant and 2 successfully treated cases of bleeding from oesophageal varices. The risk of bleeding begins at a pressure above 27 mm Hg, but in individual cases it cannot be used to prognosticate.
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PMID:[Prognosis of portal hypertension in hepatitic cirrhosis of the liver (author's transl)]. 645 81

Twelve patients with the Budd-Chiari syndrome have been managed surgically. Ten of the patients were female, two were male, with a mean age of 40 years. Three of the patients had polycythemia vera, two had pre-existing cirrhosis, one had ingested estrogens, one had an occult tumor, and in four there were no associated factors. Ten patients presented with ascites and two with bleeding esophageal varices. The diagnosis was confirmed in all 12 patients by liver biopsy and hepatic vein catheterization. Inferior vena cavography revealed the abdominal vena cava to be thrombosed in six patients. The superior mesenteric vein was used to decompress the congested liver in all 12 patients. In five patients, a mesocaval shunt (MCS) was performed and in seven patients, a mesoatrial shunt (MAS) was carried out. There were four hospital deaths (two MCS, two MAS). One late death (MAS) occurred from liver failure following shunt thrombosis. Two additional patients (one MCS, one MAS) re-developed ascites immediately following surgery and angiography revealed a thrombosed shunt. Ascites has been controlled with a LeVeen shunt in these two patients, but liver biopsies showed progression to cirrhosis. The remaining five patients (three MAS, two MCS) did well, and angiography revealed patent shunts. Two of these patients, however, re-developed ascites at 4 and 10 months following MAS and required a second MAS. Follow-up ranges from 6 to 68 months. In three of the patients (two MCS, one MAS) with patent shunts, liver biopsy shows a remarkable return toward normal liver architecture and histology.
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PMID:The Budd-Chiari syndrome. Treatment by mesenteric-systemic venous shunts. 661 56

In vitro drug metabolism studies were carried out in 97 patients with liver disease. Drug-metabolizing enzymes (aminopyrine N-demethylase and bilirubin UDP-glucuronyl transferase) were estimated in livers obtained at the time of biopsy with a Menghini needle. The patients were divided into three groups depending on clinical, biochemical, radiologic, and histologic findings: (i) mild (non-cirrhotic portal fibrosis and extrahepatic portal vein obstruction), (ii) moderate (Budd-Chiari syndrome and amebic liver abscess), (iii) severe (acute hepatitis, chronic active hepatitis, and cirrhosis). Aminopyrine N-demethylase was decreased in all liver disorders as compared to ten control liver samples. Bilirubin UDP-glucuronyl transferase was significantly lower in all liver disorders except for amebic liver abscess and extrahepatic portal vein obstruction. Both the enzymes in (i) and (ii) groups were significantly higher than in group (iii). A significant correlation was obtained between the two enzymes.
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PMID:In vitro drug metabolism in humans with different liver diseases. 664 84

Membranous obstruction of the inferior vena cava (MOVC) is a rare clinical entity. The incidence is higher in Japan and Africa than that in USA and Europe. MOVC is considered to be different from the Budd-Chiari syndrome. There are differences in clinical manifestation and pathologic changes in the liver. Findings of the liver revealed cirrhosis in all patients but in one. Ascites and esophageal varices could be observed in 79% and in 58% of the patients, respectively. According to Sugiura's classification, they consisted of Type Ia in 63%, Type Ib in 11%, Type II in 11%, and Type III in 16%. Portopulmonary shunt by splenopneumopexy was successfully performed on 19 patients with MOVC in this clinic, of which diagnosis was established by cavography.
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PMID:Membranous obstruction of the inferior vena cava. 683 Mar 51

Arterioportal shunting is observed angiographically in a wide variety of pathologic conditions. The route of flow has classically been considered to be via the hepatic sinusoids (transsinusoidal). This route occurs in cases of cirrhosis or the Budd-Chiari syndrome, and results in retrograde hepatofugal flow in portal branches. More recently, a transvasal route has been recognized angiographically, in which portal flow often remains hepatopetal. The transvasal route occurs in cases of hepatocellular carcinoma, metastases, shock, hepatic arterial obstruction, and many other conditions. Histologic confirmation of this route has been sought for many years, with other partial success. Nevertheless, angiographic evidence, as presented here, is sufficiently compelling to justify description of this pathway and its significance. Arterioportal flow may also occur via a post-traumatic fistula (disruption of adjacent portions of hepatic artery and portal vein), and via benign tumor vessels in hemangioma or hemangioendothelioma.
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PMID:Arterioportal communications: observations and hypotheses concerning transsinusoidal and transvasal types. 706 71


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