Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0239946 (liver fibrosis)
 8,268 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inspite of the fact that the haemodynamic changes in the right ventricle in schistosomal disease received proper attention, left ventricular changes were not equally assessed. That the left ventricle could suffer in bilharzial disease is a possibility, probably due to the development of shunts and toxic myocarditis. In this wor5, left ventricular functions were studied using the rate of maximum rise of intraventricular pressure (kp/dt) as an index of contractility. The study included 10 normal controls, 5 cases with bilharzial liver fibrosis and no ascites or cor pulmonale, 10 cases with BLF, and ascites but no cor pulmonale, and 10 cases with bilharzial cor pulmonale. Diminished dp/dt values were obtained in 8 out of the 10 cases of bilharzial cor pulmonale, in whom the left ventricular pressure curve also showed distortion and delay in the descending limb of the isometric relaxation phase, denoting defective contractility of the left ventricle, and probably a diastolic volume overload in these cases. In BLF with or without ascites, the dp/dt values were surprisingly increased possibly due to increased catecholamines in these cases secondary to ineffective destruction in the liver suffering from parenchymatous disease. The left ventricle is thus shown to suffer in bilharzial disease particularly in cases with bilharzial cor pulmonale.
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PMID:Assessment of left ventricular function in schistosomiasis. 102 51

A rare chronic course of Budd-Chiari syndrome associated with thrombosis of the portal vein was observed in a 30-year-old male patient suffering from postmyocarditic cardiosclerosis. At the age of 24 the patient had infectious allergic myocarditis, was hospitalized and rehospitalized for circulatory insufficiency. Upon 3 years since the disease onset the patient was admitted to a hematological department for progressive enlargement of the spleen. The diagnosis on discharge was idiopathic myelofibrosis with portal hypertension. The treatment included prednisolone, blood transfusions, myelosan. In 1987 the patient presented with enlarged liver and spleen, ascites, gastric and esophageal varicosis, augmenting hepatic insufficiency clinically evaluated as hepatic cirrhosis. Postmortem examination revealed macrofocal cardiosclerosis, splenomegaly, ascites, portal varicosis, enlarged nutmeg liver with smooth surface. Microscopically there was phlebosclerosis and phlebothrombosis varying in duration and involving predominantly medial branches of the hepatic and portal veins, liver fibrosis. The findings provided evidence for the final diagnosis of Budd-Chiari syndrome running an uncommon chronic course.
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PMID:[The chronic form of the Budd-Chiari syndrome]. 297 4

Aberrant expression of transforming growth factor beta 1 (TGF-beta 1) has been implicated in a number of disease processes, particularly those involving fibrotic and inflammatory lesions. To determine the in vivo effects of overexpression of TGF-beta 1 on the function and structure of hepatic as well as extrahepatic tissues, transgenic mice were generated containing a fusion gene (Alb/TGF-beta 1) consisting of modified porcine TGF-beta 1 cDNA under the control of the regulatory elements of the mouse albumin gene. Five transgenic lines were developed, all of which expressed the Alb/TGF-beta 1 transgene selectively in hepatocytes. The transgenic line 25 expressing the highest level of the transgene in the liver also had high (> 10-fold over control) plasma levels of TGF-beta 1. Hepatic fibrosis and apoptotic death of hepatocytes developed in all the transgenic lines but was more pronounced in line 25. The fibrotic process was characterized by deposition of collagen around individual hepatocytes and within the space of Disse in a radiating linear pattern. Several extrahepatic lesions developed in line 25, including glomerulonephritis and renal failure, arteritis and myocarditis, as well as atrophic changes in pancreas and testis. The results from this transgenic model strongly support the proposed etiological role for TGF-beta 1 in a variety of fibrotic and inflammatory disorders. The transgenic model may also provide an appropriate paradigm for testing therapeutic interventions aimed at neutralizing the detrimental effects of this important cytokine.
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PMID:Hepatic expression of mature transforming growth factor beta 1 in transgenic mice results in multiple tissue lesions. 770 87