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)

Non-caseating epithelioid-cell granulomas named "sarcoid reactions" may occur rarely in regional lymph nodes of a malignant tumor. In this article, sarcoid reactions in a patient with hepatocellular carcinoma and two early gastric carcinomas are reported. A 78-year-old woman followed with a Hbs antigen positive liver cirrhosis from 1980 was admitted to our hospital to receive the operation for two early gastric carcinomas and hepatocellular carcinoma. Subsegmentectomy of the liver and subtotal gastrectomy were performed. Histologic examination of dissected lymph nodes revealed sarcoid reactions. There have been no reports regarding the association between sarcoid reactions and hepatocellular carcinoma combining early gastric carcinoma.
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PMID:[A case report of sarcoid reactions with hepatocellular carcinoma and two early gastric carcinomas]. 839 60

Asymptomatic patients with abnormal results on liver function test pose a diagnostic challenge. In general, determinations of routinely ordered tests of liver function are neither sensitive nor specific for liver disease. Fatty liver, alcohol-related liver damage and chronic viral hepatitis are the most common causes of abnormal liver function test results in asymptomatic patients. Causes of asymptomatic liver disease include hemochromatosis, Wilson's disease, drug toxicity, chronic autoimmune hepatitis, biliary cirrhosis, sclerosing cholangitis, alpha1-antitrypsin deficiency and sarcoidosis. The most efficient screening tests for liver damage are alanine transaminase, alkaline phosphatase and bilirubin. Repeat testing when results are abnormal, and use of ancillary tests, such as creatine phosphokinase or gamma-glutamyl-transferase, may confirm liver damage. Imaging studies help exclude biliary obstruction or neoplasm. Treatable illnesses should be ruled out. Three to six months of observation for progressive symptoms and liver dysfunction may follow. After the period of observation, further laboratory tests, a diagnostic liver biopsy and/or referral to gastroenterologist may be needed.
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PMID:Evaluating asymptomatic patients with abnormal liver function test results. 862 23

An acute transient swelling of the parotid glands is recorded after general anaesthesia in orthopaedic surgery. The first differential diagnosis is bacterial parotitis; other causes of gland enlargement are viral infections, lymphoma, leukemia, sarcoidosis, Sjogren's syndrome, malnutrition cirrhosis, vomiting, and poor oral hygiene. Excluding the above mentioned conditions, the most probably factors involved in our case are drugs used for anaesthesia, congestion of the venous drainage of the gland because of parasympathetic stimula during tracheal intubation and head positioning during surgery.
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PMID:[Transitory swelling of a parotid gland following general anesthesia. Description of a case]. 891 36

NCPH is a result of obliteration of portal veins. Many inflammatory conditions may initiate the process by causing endothelial injury. As obliteration progresses, there is local stasis and low-grade portal hypertension. In many cases, superimposed PVT occurs before portal hypertension becomes clinically evident. Hypercoagulability is an important cofactor. Diagnosis requires the exclusion of cirrhosis. Focal atrophy and nodular hyperplasia on biopsy may be a clue to the presence of small vessel obliteration. The distribution of vascular disease should be documented with Doppler ultrasound of both portal and hepatic veins. Investigation of cause should include tests for myeloproliferative and other hypercoagulable disorders, systemic diseases associated with vascular injury (eg, autoimmune diseases and toxin exposure) and local portal tract inflammatory diseases (primary biliary cirrhosis and sarcoidosis). Advances in this field will likely be made with improved diagnosis of acute and recanalized PVT using MRI, the new Acuson Sequoia ultrasound technology, and intravascular ultrasonography. Advances in the cause of PVT await studies using new and improved tests for the diagnosis of hypercoagulable states.
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PMID:Noncirrhotic portal hypertension: recent concepts. 905 82

Sarcoidosis often involves the liver with mild elevation of serum enzymes and granulomas histologically. Rarely, chronic cholestasis, portal hypertension, cirrhosis, or nodular hyperplasia may be found. The pathogenesis of the portal hypertension and of the cirrhosis are not understood, in part because large samples of tissue have seldom been described. We describe the clinical and anatomic findings of four patients with sarcoid liver disease in whom the whole livers were available for examination. One patient had cirrhosis, one had diffuse nodular hyperplasia, and two had small regions of parenchymal fibrosis. The first two of these had a history of variceal bleeding and healed portal vein thrombosis. One had chronic cholestasis without cirrhosis. We suggest that the cirrhosis and focal fibrosis were caused by ischemia secondary to primary granulomatous phlebitis of portal and hepatic veins. The portal hypertension in two patients was likely secondary to portal vein thrombosis, because cirrhosis was absent at the onset of variceal bleeding.
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PMID:The role of granulomatous phlebitis and thrombosis in the pathogenesis of cirrhosis and portal hypertension in sarcoidosis. 930 82

Sarcoidosis is a chronic multisystem disorder of unknown cause characterized by the presence of noncaseating epitheloid granulomas and derangement of the normal skin architecture. Though an array of organs may be affected by the disease the most common site of affection is the lung. An extrathoratic manifestation is rare. We describe a 66-year-old patient who was admitted to our hospital because of weight loss and hepatomegaly. A thorough examination revealed the diagnosis of a granulomatous hepatitis characterized by a markedly elevated alkaline phosphatase concentration of 1,490 U/I. A drug-induced hepatitis could be excluded and no evidence was found for the existence of a bacterial or viral infection or an autoimmune disorder. An ERCP revealed a normal common bile duct and normally branching small intrahepatic ducts. The patient was discharged with the diagnosis of a biliary cirrhosis. Half a year later the patient was readmitted to the hospital because of severe intestinal bleeding due to pancytopenia. A bone marrow biopsy showed infiltration of the marrow by granulomas. A histiocytosis X could be ruled out. The diagnosis of an extrathoracic sarcoidosis was assumed and a therapy with prednisone was started. Within six weeks the blood count normalized. After 18 months the serum alkaline phospatase concentration also normalized and no granulomas were found in the bone marrow. The case demonstrates that pancytopenia in sarcoidosis is not due to bone marrow failure.
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PMID:[Granulomatous hepatitis and myelitis: an unusual manifestation of extrapulmonary sarcoidosis]. 1019 Feb 49

Hepatopulmonary syndrome is the most widely recognized of the processes associated with end-stage liver disease. Chronic liver dysfunction is associated with pulmonary manifestations due to alterations in the production or clearance of circulating cytokines and other mediators. Hepatopulmonary syndrome results in hypoxemia due to pulmonary vasodilatation with significant arteriovenous shunting and ventilation-perfusion mismatch. Hepatic hydrothorax may develop in patients with cirrhosis and ascites. Rarely, pulmonary hypertension occurs in the setting of portal hypertension. A second group of disorders may primarily affect the lungs and liver (the hepatopulmonary axis). Among these are the congenital conditions alpha(1)-antitrypsin deficiency and cystic fibrosis. Autoimmune liver disease may be associated with lymphocytic interstitial pneumonitis, fibrosing alveolitis, intrapulmonary granulomas, and bronchiolitis obliterans with organizing pneumonia. Sarcoidosis affects the lung and liver in up to 70% of patients. Medications such as amiodarone can result in a characteristic radiologic appearance of pulmonary and hepatic toxic effects. Knowledge of these associations will assist the radiologist in forming a meaningful differential diagnosis and may influence treatment decisions.
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PMID:Diseases of the hepatopulmonary axis. 1083 22

A few cases of sarcoidosis are associated with progressive liver disease, with a wide variety of clinicopathologic features. Herein, we report an autopsy case (65-year-old man). During an examination for liver dysfunction, cirrhosis with cholestatic dysfunction and splenomegaly were found. Needle liver biopsy revealed cirrhosis with lymphocytic piecemeal necrosis, dense septal fibrosis, and ductopenia. In addition, noncaseating epithelioid granuloma was also seen in the periportal region. Ductal enzymes and immunoglobulin M (IgM) levels were elevated, although antimitochondrial antibodies were negative. Instead, angiotensin-converting enzyme was elevated. He died of pulmonary failure and lung cancer. The autopsy liver (1,220 g) showed multinodular cirrhosis with broad and dense septa that divided the parenchyma. Mild lymphoid cell infiltration was seen in the periportal region. About a half of the interlobular bile ducts were lost, and the remaining bile ducts showed prominent periductal fibrosis, resembling sclerosing cholangitis. Interestingly, a few interlobular bile ducts showed chronic nonsuppurative cholangitis with epithelioid granulomas. Intrahepatic portal veins showed luminal narrowing with prominent phlebosclerosis. Hepatobiliary pathologies that resemble primary biliary cirrhosis and primary sclerosing cholangitis and that are followed by vanishing bile duct syndrome, chronic active hepatitis-related cirrhosis, and intrahepatic portal venous phlebosclerosis occur in a single case of sarcoidosis.
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PMID:Hepatic sarcoidosis with vanishing bile duct syndrome, cirrhosis, and portal phlebosclerosis. Report of an autopsy case. 1120 61

A 57-year-old woman with sarcoidosis was referred because of the appearance of multiple small low-attenuation areas in the liver on computed tomography (CT). A liver biopsy specimen showed chronic active hepatitis accompanied by sarcoid granulomas. The patient received prednisolone and, later, interferon-alpha. CT at 5 months of prednisolone treatment showed disappearance of the hepatic low-attenuation nodules. During long-term follow-up, however, these nodules reappeared on CT and liver cirrhosis finally developed. We present this case for two reasons: (1) hepatic sarcoidosis was associated with chronic active hepatitis C; (2) hepatic nodular lesions were evaluated by CT throughout the entire course, with CT scans having been taken from 2 years prior to their appearance.
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PMID:Hepatic sarcoidosis associated with chronic hepatitis C. 1216 17

We report the identification of a novel mutation in ferroportin1 in an Australian family with autosomal dominant iron overload. The phenotype of iron overload in one member of this family is associated with high serum ferritin concentration and elevated transferrin saturation. The pattern of iron overload in the liver shows accumulation predominantly in parenchymal cells with some Kupffer cell iron loading. Although some cases of type 4 haemochromatosis have been associated with the development of liver fibrosis this is the first report of a patient with fully established cirrhosis at a relatively young age (32 years). The coexistence of sarcoidosis in this patient may contribute to the more severe phenotype. This report highlights the phenotypic variability that can occur in type 4 haemochromatosis. Some patients have predominant reticuloendothelial iron loading and normal transferrin saturation whereas others have predominant parenchymal iron loading and elevated transferrin saturation. The reasons for this variability remain to be determined. Interestingly this is the third mutation to affect asparagine 144, reinforcing the important role for this amino acid in the function of ferroportin1.
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PMID:Autosomal dominant iron overload due to a novel mutation of ferroportin1 associated with parenchymal iron loading and cirrhosis. 1503 Sep 91


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