Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Portal hypertension, widely recognized as a complication of cirrhosis, may also develop as an intrahepatic consequence of numerous hepatic disorders in the absence of cirrhosis. When gastrointestinal bleeding occurs in such cases, ruptured esophageal varices must be considered. Among chronic liver diseases, some, such as schistosomiasis, are commonly associated with portal hypertension and its complications. In others, including tuberculosis, amyloidosis, and polycystic disease, well-documented portal hypertension has been reported in only a small minority of cases. Nevertheless, because of the ever-present possibility of variceal hemorrhage whenever portal hypertension occurs, clinicians should be aware of these disorders. Acute conditions associated with noncirrhotic intrahepatic portal hypertension include acute (and particularly fulminant) viral or drug-induced hepatitis, acute alcoholic hepatitis, acute veno-occlusive disease, and acute fatty liver of pregnancy. Portal hypertension may be reversible following recovery in these settings. Particular attention is called to the increasing frequency of acute veno-occlusive disease on bone marrow transplant units, presumably as a complication of high-dose chemo- and radiotherapy.
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PMID:Noncirrhotic intrahepatic portal hypertension. 354 26

Hepatic manifestations are a common phenomenon in patients with systemic lupus erythematosus (SLE). However, their cause may be difficult clinically to determine. A significantly increased frequency of anti-ribosomal P antibody has recently been found in patients with SLE-associated hepatitis. Thus, we examined the prevalence of anti-ribosomal P antibody and clinical differences between anti-ribosomal P antibody positive and negative SLE patients with liver dysfunction using ELISA kits against recombinant ribosomal P0 protein. Sera of 61 patients with SLE and 20 patients with autoimmune hepatitis (AIH) were assayed. Of 34 SLE patients with liver dysfunction, anti-ribosomal P antibody was detected in 15 (44.1%), consisting of 11 (68.8%) of 16 patients with SLE-associated hepatitis, 2 (28.6%) of 7 patients with fatty liver, 1 (16.7%) of 6 patients with drug-induced hepatitis, and 1 (20.0%) of 5 patients with SLE complicated by AIH. This antibody was not detected in patients with AIH. Except for those with SLE-associated hepatitis, anti-ribosomal P antibody positive patients were complicated by renal dysfunction and CNS lupus. The positive rate of anti-ribosomal P antibody was significantly higher in patients with SLE-associated hepatitis (68.8%) than in patients with SLE complicated by AIH (20%) ( [Formula: see text] ) and AIH (0%) ( [Formula: see text] ). These findings suggest that anti-ribosomal P antibody may be a useful marker of SLE-associated hepatitis to differentiate it from AIH and other liver dysfunctions in SLE patients without renal dysfunction or CNS lupus.
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PMID:High frequency of anti-ribosomal P antibody in patients with systemic lupus erythematosus-associated hepatitis. 1503 69

Diseases involving the hepatopancreatobiliary (HPB) system are frequently encountered in patients with inflammatory bowel disease (IBD). Hepatobiliary manifestations constitute some of the most common extraintestinal manifestations of IBD. They appear to occur with similar frequency in patients with Crohn's disease or ulcerative colitis. HPB manifestations may occur in following settings: 1) disease possibly associated with a shared pathogenetic mechanism with IBD including primary sclerosing cholangitis (PSC), small-duct PSC/pericholangitis and PSC/autoimmune hepatitis overlap, acute and chronic pancreatitis related to IBD; 2) diseases which parallel structural and physiological changes seen with IBD, including cholelithiasis, portal vein thrombosis, and hepatic abscess; and 3) diseases related to adverse effects associated with treatment of IBD, including drug-induced hepatitis, pancreatitis (purine-based agents), or liver cirrhosis (methotrexate), and reactivation of hepatitis B, and biologic agent-associated hepatosplenic lymphoma. Less common HPB manifestations that have been described in association with IBD include autoimmune pancreatitis (AIP), IgG4-associated cholangitis (IAC), primary biliary cirrhosis (PBC), fatty liver, granulomatous hepatitis, and amyloidosis. PSC is the most significant hepatobiliary manifestation associated with IBD and poses substantial challenges in management requiring a multidisciplinary approach. The natural disease course of PSC may progress to cirrhosis and ultimately require liver transplantation in spite of total proctocolectomy with ileal-pouch anal anastomosis. The association between AIP, IAC, and elevated serum IgG4 in patients with PSC is intriguing. The recently reported association between IAC and IBD may open the door to investigate these complex disorders. Further studies are warranted to help understand the pathogenesis of HPB manifestations associated with IBD, which would help clinicians better manage these patients. An interdisciplinary approach, involving gastroenterologists, hepatologists, and, in advanced cases, general, colorectal, and transplant surgeons is advocated.
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PMID:Hepatopancreatobiliary manifestations and complications associated with inflammatory bowel disease. 2019 12