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 radiographic appearance of intestinal edema, including colonic edema, has been well described in the literature. Severe wall circumferential thickening can occur within the colon in a number of conditions. This includes edema secondary to colitis, allergy, ischemia, and infiltrative neoplastic processes. Edema may be secondary to low protein levels, as from protein losing enteropathy, nephrotic syndrome, and hepatic cirrhosis. The following case, in which there was severe ascending colonic wall thickening due to edema, is unusual in two respects: it had well-developed demonstrated "protective" right colonic varices and a normal protein level.
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PMID:CT demonstration of ascending colon varices. 818 Aug 60

Here, we describe the clinical course of an adult patient who had living-related liver transplantation (LRLT) from a donor with Gilbert's syndrome and problems of living-related liver transplantation to adult patients. A 22-year-old woman had been diagnosed as having liver cirrhosis at the age of 5. She had undergone devascularization and transsection of the esophagus, and splenectomy for esophageal varices at the age of 8. Complications such as spontaneous bacterial peritonitis and nonspecific colitis sometimes appeared from 17 years old, and icterus and ascites had appeared on all such occasions. Such complications had frequently occurred from 21 years old. Total bilirubin was 5.5 mg/dl and direct bil. was 4.2 mg/dl. The patient and her family members were informed that LRLT might be possible, and they indicated that the patient's 57-year old father was willing to act as the donor. His liver function was examined. His hepatic function was normal except for hyperbilirubinemia (T. Bil. 2.3 mg/dl, D. Bil. 0.3 mg/dl). He was diagnosed with Gilbert's Syndrome because of an increase of unconjugated bilirubin levels during low caloric intake and nicotinic acid test. The standard liver volume for the patient was calculated to be 900 ml on the basis of body weight. Volumetric analysis with computed tomography revealed that the left lobe volume of the donor's liver was 512 ml, corresponding to 56% of the recipient standard liver volume. This proposal was submitted to the ethical committee of Tokushima University School of Medicine and was accepted. In March 28, 1995, the patient underwent LRLT with the donor's left lobe as the graft. The graft weight was 440 g and the graft corresponded to 49% of the recipient's standard liver volume. Volumetric analysis showed rapid enlargement of graft to 683 ml as early as one week after the operation. The donor has returned to work after discharge from the hospital. The recipient is well 11 months after surgery. Total bilirubin was 1.8 mg/dl and D. Bil 0.5 mg/dl. LRLT may become an option for adult recipients, if graft of more than 30% of the recipient standard liver volume is transplanted even from a donor with Gilbert's syndrome.
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PMID:[Problems of living-related partial liver transplantation to adult patients]. 881 56

We prospectively evaluated 139 consecutive children presenting to the Sanjay Gandhi Postgraduate Institute of Medical Sciences (Lucknow, India) with gastrointestinal (GI) bleeding from January 1991 to November 1994. Our aims were to find out whether the causes of GI bleeding in a developing country differed from developed countries and how the application of newer diagnostic techniques would help in the diagnosis of GI bleeding. Barium studies, endoscopy, technetium-99m-labelled (erythrocytes and pertechnetate) scans, selective abdominal angiography using a digital subtraction technique and rectal endoscopic ultrasonography were performed. Upper GI bleeding (n = 75) was variceal in 71 (95%) children (extrahepatic portal venous obstruction in 65, cirrhosis in six) and non-variceal in four (5%) cases (Henoch-Schonlein purpura, idiopathic thrombocytopenic purpura, drug-induced gastric erosions and pseudoaneurysm of the gastroduodenal artery due to idiopathic chronic calcific pancreatitis). Causes of lower GI bleeding (n = 64) were colitis (27 cases; 42%), colorectal polyps (26 cases; 41%), enteric fever (n = 3), solitary rectal ulcer (n = 3), portal hypertensive colopathy (n = 2), colonic arteriovenous malformation (n = 1) and internal haemorrhoids (n = 1). One patient remained undiagnosed. Angiography performed in four children was diagnostic in two. In one child with massive lower GI bleeding from portal colopathy, the bleeding site (caecum) was localized by intra-operative colonoscopy, while in the other child with portal colopathy, rectal endoscopic ultrasonography was performed to substantiate the diagnosis. We conclude that the causes of upper GI bleeding in children in developing countries are different from those in developed countries (variceal bleeding due to extrahepatic portal venous obstruction is the most common cause, while peptic ulcer is rare). However, the spectrum of lower GI bleeding is similar to that of developed countries. Application of newer diagnostic techniques is helpful and safe in the identification of the cause of GI bleeding in children.
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PMID:Gastrointestinal bleeding in children. 891 24

We present here three paediatric patients with primary sclerosing cholangitis. In case 1, the serum gamma-glutamyl transpeptidase was decreased only temporarily by ursodeoxycholic acid (UDCA) treatment and 34 months later, sulphasalazine was added because of microscopic colitis. The enzyme level decreased with dual therapy. Similarly, in case 3, first diagnosed as autoimmune hepatitis, the transpeptidase levels remained elevated for 18 months during treatment with UDCA, prednisolone and mizoribin. The enzyme decreased only after a diagnosis of primary sclerosing cholangitis complicated with ulcerative colitis was established and sulphasalazine was introduced. Case 2 also had Crohn's colitis and was put on UDCA and sulphasalazine from the start. The enzyme level was normalized within 1 month and has remained normal for the following 5 years. Liver biopsies were analysed repeatedly in these three patients. In case 1, periductal fibrosis remained unchanged while being treated by UDCA. There appeared to be no progression in liver cirrhosis in case 3 while being treated by UDCA, prednisolone, and mizoribin. In case 2, who has been treated with both UDCA and sulphasalazine from the start, periductal fibrosis and portal fibrosis were remarkably improved 45 months later. We suggest that sulphasalazine in addition to UDCA might be a viable treatment for children with primary sclerosing cholangitis.
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PMID:Three paediatric cases of primary sclerosing cholangitis treated with ursodeoxycholic acid and sulphasalazine. 973 77

Primary sclerosing cholangitis (PSC), a chronic inflammatory process affecting the extrahepatic and/or medium to large bile ducts, is not rare in children. It has features suggesting an autoimmune pathogenesis, although the mechanism of tissue damage remains unknown. The clinical presentation of childhood primary sclerosing cholangitis is highly variable and frequently without obvious features of cholestasis. Clinical similarity to autoimmune hepatitis is common. Association with chronic colitis is less common than in adults. Cholangiography is essential for the diagnosis and examination of the medium to large intrahepatic ducts is mandatory, as 40% of children lack extrahepatic duct involvement. Histological findings may help to distinguish childhood PSC from autoimmune hepatitis. In children, sclerosing cholangitis may also develop secondary to other disease processes, notably Langerhans histiocytosis, congenital immunodeficiencies and cystic fibrosis. Neonatal sclerosing cholangitis is chronic inflammatory disease of bile ducts which presents initially with neonatal cholestasis; its pathogenesis remains uncertain and may not be the same as for primary sclerosing cholangitis. Effective treatment modalities for childhood PSC remain undetermined. Liver transplantation is required for children who progress to biliary cirrhosis and hepatic decompensation.
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PMID:Primary sclerosing cholangitis in children. 1038 70

In 1983, a female patient born in 1963 presented with symptoms of ulcerative colitis and typical clinical and histological signs of primary sclerosing cholangitis (PSC). At this time only pANCA were positive while other marker antibodies for autoimmune liver disorders could not be detected. In summer 1987 the clinical picture changed and was replaced by laboratory and histological signs typical of autoimmune hepatitis (AIH). Thus, IgG levels increased considerably and cholestatic enzymes became normal. For the first time, anti-liver-pancreas antibodies (LP), a diagnostic marker for AIH type III could be detected. In the following years several relapses occurred also induced by repeated discontinuation of immunosuppressive therapy. Symptoms of colitis persisted but signs of cholestasis remained absent for the following ten years. In 1997, colitis exacerbated again and colectomy had to be performed together with liver transplantation. Surprisingly, histology of the explanted liver now showed the typical features of PSC stage III/IV while the significant criteria for AIH were now lacking. Thus, progression to cirrhosis was, probably, mainly induced by the biliary destructive and fibrotic process although biochemical and serological data were clearly indicative of an autoimmune, i.e. AIH-related manifestation.
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PMID:Sequential occurrence of primary sclerosing cholangitis and autoimmune hepatitis type III in a patient with ulcerative colitis: a follow up study over 14 years. 1095 14

Since the aetiopathogenesis of primary sclerosing cholangitis (PSC) in humans remains undefined, investigators have studied a variety of animal models to gain insights into immunopathogenetic mechanisms associated with obliterative fibrous cholangitis of intra- and extra-hepatic bile ducts. To date, no animal model has been developed that exhibits all of the attributes of PSC. Rodent models instigated by bacterial cell components or colitis are promising because they may help to explain the strong association between PSC and inflammatory bowel disease (IBD). Other models of direct injury to biliary epithelia, peribiliary vascular endothelia or portal venous endothelia indicate that inflammation, chemokines and cytokines can produce diffuse sclerosis of bile ducts. Models of toxic, infectious or intra-luminal injury of the biliary tract also exhibit focal biliary sclerosis mediated by inflammation and cytokines. The histopathology of several models suggests a sequence of events beginning with secretion of proinflammatory cytokines by activated hepatic macrophages followed by peribiliary infiltration with CD4 and CD8 T cells with a T helper 1 phenotype. These results strongly suggest co-ordinated, pathogenetic roles for both the innate and adaptive immune responses. However, the stimuli that initiate and perpetuate peribiliary fibrosis remain unknown. Interestingly, several models are also associated with the development of anti-neutrophil cytoplasmic antibodies that react in a perinuclear and cytoplasmic pattern similar to that observed in patients with ulcerative colitis and/or PSC. Finally, models of extra-hepatic biliary obstruction continue to provide important information about the pathogenesis of portal fibrosis and secondary biliary cirrhosis that occurs in PSC and other diseases with obstruction of bile flow. Future studies in either existing or new animal models should advance our understanding of the pathogenesis of PSC, the major prerequisite for the development of effective therapies.
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PMID:Animal models for primary sclerosing cholangitis. 1149 70

Esophageal strictures are characterized by excess deposition of collagen in the esophageal wall. Polyunsaturated phosphatidyl-choline (PPC) stimulates collagen breakdown in experimental models of liver cirrhosis and colitis. This study was done in order to investigate the therapeutical effect of PPC in preventing esophageal strictures due to alkali-induced esophageal burns in rats. Fifty-five albino rats were divided into four groups as follows: control group (Group A, 10 rats), rats with sham operation and treated with saline (Group B, 15 rats), rats with esophageal burns only (Group C, 15 rats), and PPC-fed rats with esophageal burns (Group D, 15 rats). A standard esophageal burn was produced as described by Gehanno. PPC was administered orally to Group D rats in doses of 100 mg/day for four weeks. All animals were sacrificed on the 28th day of the experiment. Hydroxyproline levels in esophageal tissue was determined in each rat, and histopathologic evaluation was performed for each group. Hydroxyproline levels were significantly lower in the PPC-fed rats than in the rats with pure esophageal burns (p < 0.001). Histopathologically, collagen deposition in the submucosa and tunica muscularis was lower in Group D rats (PPC-fed rats with esophageal burn) than Group C rats (pure esophageal burn) (p < 0.05). As a result of our study, we concluded that PPC has an ameliorating effect on stricture formation after alkali-induced corrosive esophageal burns in rats.
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PMID:Polyunsaturated phosphatidylcholine lowers collagen deposition in a rat model of corrosive esophageal burn. 1196 52

Five autopsy cases of Vibrio vulnificus infection with liver disease are reported. All five patients ate raw seafood 24 h before the onset of illness. The clinical presentation was of primary septicemia, with positive cultures in both the blood and cutaneous lesions. Stool cultures were positive for the organism in one patient with gastrointestinal symptoms. Autopsy examination revealed liver cirrhosis in three cases and alcoholic liver disease in two; all showed portal hypertension. Gastrointestinal mucosal changes were seen in four patients: edema, hemorrhagic necrosis, and lymphocyte infiltration. One case was of an human immunodeficiency virus infected patient in which histology showed a rare intestinal disease, phlegmonous colitis. We believe this is the first description of a case of concomitant phlegmonous enterocolitis and V. vulnificus infection. Patients with liver disease should be warned about the possibility of life-threatening infections and complications associated with the consumption of raw seafood.
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PMID:Vibrio vulnificus infection in patients with liver disease: report of five autopsy cases. 1211 Dec 6

Within the colonic mucosa of rats with portal hypertension and liver cirrhosis, there is an increased generation of inflammatory mediators, such as leukotriene B4 and endothelin-1, and increased generation of nitric oxide. Nitric oxide overproduction may induce tissue injury. This study was undertaken to assess whether the colonic mucosa of rats with portal hypertension and liver disease have increased susceptibility to damage by noxious agents. In this study, acetic acid colitis was induced in rats with portal vein ligation and in control groups, and iodoacetamide colitis was induced in rats with partial portal vein ligation and cirrhosis due to bile duct ligation and in control groups. Rats with acetic acid colitis and those with iodoacetamide-induced colitis were studied 24 and 72 hours, respectively, after induction of colitis. Portal hypertension alone and portal hypertension with cirrhosis were present in the portal vein ligation and bile duct ligation models, respectively. In the rats with acetic acid, colitis lesion area, colonic mucosal myeloperoxidase activity, and prostaglandin E2 generation were not different between the portal vein ligation groups with and without colitis. Nitric oxide activity was higher only in the groups with colitis, irrespective of the presence of portal hypertension. In the group of rats with iodoacetamide colitis, colonic lesion area and colonic mucosal myeloperoxidase activity were similar in all groups with colitis. Colonic mucosal prostaglandin E2 generation was lower in the portal vein ligation and bile duct ligation rats with colitis compared with a control group. We concluded that rats with experimental portal hypertension do not have increased damage when induced by either acetic acid or iodoacetamide.
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PMID:Experimental colitis in rats with portal hypertension and liver disease. 1265 33


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