Nodular regenerative hyperplasia, portal vein thrombosis, and avascular hip necrosis due to hyperhomocysteinaemia
A male patient with portal hypertension, portal vein thrombosis, spontaneous splenorenal shunt formation, and encephalopathy, thought to have post-hepatitis B cirrhosis, is described. His condition deteriorated and necessitated liver transplantation. In the explant liver, nodular regenerative hyperp...
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| Veröffentlicht in: | Gut 2005-07, Vol.54 (7), p.1021-1023 |
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| creator | Buchel, O Roskams, T Van Damme, B Nevens, F Pirenne, J Fevery, J |
| description | A male patient with portal hypertension, portal vein thrombosis, spontaneous splenorenal shunt formation, and encephalopathy, thought to have post-hepatitis B cirrhosis, is described. His condition deteriorated and necessitated liver transplantation. In the explant liver, nodular regenerative hyperplasia with pronounced vascular lesions both in portal venules and in arterioles was found instead of classical cirrhosis. Two years post-transplant he developed bilateral ischaemic femur head necrosis. The three disorders (portal vein thrombosis, nodular regenerative hyperplasia, and ischaemic hip necrosis) seemed to be due to a common vasculopathy induced by hyperhomocyteinaemia. Genetic studies showed that he carried a mutation in the gene encoding for formation of methylenetetrahydrofolate reductase. Treatment with folic acid combined with pyridoxine (vitamin B6) and cyanocobalamin (vitamin B12) normalised his serum homocysteine levels. |
| doi_str_mv | 10.1136/gut.2004.055921 |
| format | Article |
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His condition deteriorated and necessitated liver transplantation. In the explant liver, nodular regenerative hyperplasia with pronounced vascular lesions both in portal venules and in arterioles was found instead of classical cirrhosis. Two years post-transplant he developed bilateral ischaemic femur head necrosis. The three disorders (portal vein thrombosis, nodular regenerative hyperplasia, and ischaemic hip necrosis) seemed to be due to a common vasculopathy induced by hyperhomocyteinaemia. Genetic studies showed that he carried a mutation in the gene encoding for formation of methylenetetrahydrofolate reductase. Treatment with folic acid combined with pyridoxine (vitamin B6) and cyanocobalamin (vitamin B12) normalised his serum homocysteine levels.</description><identifier>ISSN: 0017-5749</identifier><identifier>EISSN: 1468-3288</identifier><identifier>EISSN: 1458-3288</identifier><identifier>DOI: 10.1136/gut.2004.055921</identifier><identifier>PMID: 15951553</identifier><identifier>CODEN: GUTTAK</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and British Society of Gastroenterology</publisher><subject>avascular hip necrosis ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Cardiovascular disease ; Case Report ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Enzymes ; Femur Head Necrosis - etiology ; Gangrene ; Gastroenterology. Liver. Pancreas. Abdomen ; Hepatitis ; homocystein ; Homocysteine ; Humans ; Hyperhomocysteinemia - complications ; Hyperplasia ; Hypertension ; Liver - pathology ; Liver cirrhosis ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Lupus ; Male ; Medical sciences ; Middle Aged ; Mortality ; Mutation ; nodular regenerative hyperplasia ; osteopenia ; Other diseases. Semiology ; Patients ; Plasma ; portal hypertension ; Portal Vein ; portal vein thrombosis ; Proteins ; Psoriasis ; Research parks ; Thrombosis ; Venous Thrombosis - etiology ; Vitamin B</subject><ispartof>Gut, 2005-07, Vol.54 (7), p.1021-1023</ispartof><rights>Copyright 2005 by Gut</rights><rights>2005 INIST-CNRS</rights><rights>Copyright: 2005 Copyright 2005 by Gut</rights><rights>Copyright © Copyright 2005 by Gut 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b553t-90820e32e25f0675d3deb5c5c66f945279ac952df5e7fc1edf16f1371cba4b933</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1774592/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1774592/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16893497$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15951553$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Buchel, O</creatorcontrib><creatorcontrib>Roskams, T</creatorcontrib><creatorcontrib>Van Damme, B</creatorcontrib><creatorcontrib>Nevens, F</creatorcontrib><creatorcontrib>Pirenne, J</creatorcontrib><creatorcontrib>Fevery, J</creatorcontrib><title>Nodular regenerative hyperplasia, portal vein thrombosis, and avascular hip necrosis due to hyperhomocysteinaemia</title><title>Gut</title><addtitle>Gut</addtitle><description>A male patient with portal hypertension, portal vein thrombosis, spontaneous splenorenal shunt formation, and encephalopathy, thought to have post-hepatitis B cirrhosis, is described. His condition deteriorated and necessitated liver transplantation. In the explant liver, nodular regenerative hyperplasia with pronounced vascular lesions both in portal venules and in arterioles was found instead of classical cirrhosis. Two years post-transplant he developed bilateral ischaemic femur head necrosis. The three disorders (portal vein thrombosis, nodular regenerative hyperplasia, and ischaemic hip necrosis) seemed to be due to a common vasculopathy induced by hyperhomocyteinaemia. Genetic studies showed that he carried a mutation in the gene encoding for formation of methylenetetrahydrofolate reductase. Treatment with folic acid combined with pyridoxine (vitamin B6) and cyanocobalamin (vitamin B12) normalised his serum homocysteine levels.</description><subject>avascular hip necrosis</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular disease</subject><subject>Case Report</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Enzymes</subject><subject>Femur Head Necrosis - etiology</subject><subject>Gangrene</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Hepatitis</subject><subject>homocystein</subject><subject>Homocysteine</subject><subject>Humans</subject><subject>Hyperhomocysteinemia - complications</subject><subject>Hyperplasia</subject><subject>Hypertension</subject><subject>Liver - pathology</subject><subject>Liver cirrhosis</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Lupus</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mortality</subject><subject>Mutation</subject><subject>nodular regenerative hyperplasia</subject><subject>osteopenia</subject><subject>Other diseases. Semiology</subject><subject>Patients</subject><subject>Plasma</subject><subject>portal hypertension</subject><subject>Portal Vein</subject><subject>portal vein thrombosis</subject><subject>Proteins</subject><subject>Psoriasis</subject><subject>Research parks</subject><subject>Thrombosis</subject><subject>Venous Thrombosis - etiology</subject><subject>Vitamin B</subject><issn>0017-5749</issn><issn>1468-3288</issn><issn>1458-3288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkc1v1DAQxSMEokvhzA1ZQnBAzdYfcRxfKqEtBaSqgChcLceZ7HpJ4tROVt3_HoesWuDSkw_zm-f35iXJS4KXhLD8dD0OS4pxtsScS0oeJQuS5UXKaFE8ThYYE5Fykcmj5FkIW4xxUUjyNDkiXHLCOVskN1euGhvtkYc1dOD1YHeANvsefN_oYPUJ6p0fdIN2YDs0bLxrSxdsOEG6q5De6WD-7G9sjzowfpqhagQ0uFlm41pn9mGI6xpaq58nT2rdBHhxeI-THxcfrlef0ssvHz-v3l-mZTQ2pBIXFAOjQHmNc8ErVkHJDTd5XsuMUyG1kZxWNQdRGwJVTfKaMEFMqbNSMnacnM26_Vi2UBnoBq8b1Xvbar9XTlv176SzG7V2O0WEyOIxo8Dbg4B3NyOEQbU2GGga3YEbg8qFpBQX4kGQEsowoziCr_8Dt270XbzC9Gn0THhWROp0pqZjBg_1nWeC1dS6iq2rqXU1tx43Xv0d9Z4_1ByBNwcg1qWb2uvO2HDP5YVkmZySpDNnY1-3d3Ptf8W0THB19XOlLsT56tv11-9qsvpu5st2-6DL37R51MU</recordid><startdate>20050701</startdate><enddate>20050701</enddate><creator>Buchel, O</creator><creator>Roskams, T</creator><creator>Van Damme, B</creator><creator>Nevens, F</creator><creator>Pirenne, J</creator><creator>Fevery, J</creator><general>BMJ Publishing Group Ltd and British Society of Gastroenterology</general><general>BMJ</general><general>BMJ Publishing Group LTD</general><general>Copyright 2005 by Gut</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20050701</creationdate><title>Nodular regenerative hyperplasia, portal vein thrombosis, and avascular hip necrosis due to hyperhomocysteinaemia</title><author>Buchel, O ; Roskams, T ; Van Damme, B ; Nevens, F ; Pirenne, J ; Fevery, J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b553t-90820e32e25f0675d3deb5c5c66f945279ac952df5e7fc1edf16f1371cba4b933</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>avascular hip necrosis</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular disease</topic><topic>Case Report</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Enzymes</topic><topic>Femur Head Necrosis - etiology</topic><topic>Gangrene</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Hepatitis</topic><topic>homocystein</topic><topic>Homocysteine</topic><topic>Humans</topic><topic>Hyperhomocysteinemia - complications</topic><topic>Hyperplasia</topic><topic>Hypertension</topic><topic>Liver - pathology</topic><topic>Liver cirrhosis</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Lupus</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Mortality</topic><topic>Mutation</topic><topic>nodular regenerative hyperplasia</topic><topic>osteopenia</topic><topic>Other diseases. 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His condition deteriorated and necessitated liver transplantation. In the explant liver, nodular regenerative hyperplasia with pronounced vascular lesions both in portal venules and in arterioles was found instead of classical cirrhosis. Two years post-transplant he developed bilateral ischaemic femur head necrosis. The three disorders (portal vein thrombosis, nodular regenerative hyperplasia, and ischaemic hip necrosis) seemed to be due to a common vasculopathy induced by hyperhomocyteinaemia. Genetic studies showed that he carried a mutation in the gene encoding for formation of methylenetetrahydrofolate reductase. Treatment with folic acid combined with pyridoxine (vitamin B6) and cyanocobalamin (vitamin B12) normalised his serum homocysteine levels.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and British Society of Gastroenterology</pub><pmid>15951553</pmid><doi>10.1136/gut.2004.055921</doi><tpages>3</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | avascular hip necrosis Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cardiovascular disease Case Report Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Enzymes Femur Head Necrosis - etiology Gangrene Gastroenterology. Liver. Pancreas. Abdomen Hepatitis homocystein Homocysteine Humans Hyperhomocysteinemia - complications Hyperplasia Hypertension Liver - pathology Liver cirrhosis Liver. Biliary tract. Portal circulation. Exocrine pancreas Lupus Male Medical sciences Middle Aged Mortality Mutation nodular regenerative hyperplasia osteopenia Other diseases. Semiology Patients Plasma portal hypertension Portal Vein portal vein thrombosis Proteins Psoriasis Research parks Thrombosis Venous Thrombosis - etiology Vitamin B |
| title | Nodular regenerative hyperplasia, portal vein thrombosis, and avascular hip necrosis due to hyperhomocysteinaemia |
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