{"id":1753,"date":"2003-10-01T01:00:00","date_gmt":"2003-10-01T00:00:00","guid":{"rendered":"https:\/\/angh.net\/abstracts\/hepatite-aigue-severe-a-la-pioglitazone\/"},"modified":"2018-10-20T18:39:30","modified_gmt":"2018-10-20T16:39:30","slug":"hepatite-aigue-severe-a-la-pioglitazone","status":"publish","type":"post","link":"https:\/\/angh.net\/abstracts\/hepatite-aigue-severe-a-la-pioglitazone\/","title":{"rendered":"H\u00e9patite aigu\u00eb s\u00e9v\u00e8re \u00e0 la pioglitazone"},"content":{"rendered":"

2003<\/strong><\/p>\n

Ramuntxo Arot\u00e7arena, Jean-Paul. Bigu\u00e9, Francine Etcharry et Alex Pariente, Centre Hospitalier, 64000 Pau<\/em><\/p>\n

H\u00e9patologie <\/strong>– \u00a02000-03-09 –\u00a0CO –<\/p>\n

________________________________<\/p>\n

Introduction : Les thiazolidinediones (glitazones) sont une nouvelle classe d\u2019 antidiab\u00e9tiques oraux, agonistes s\u00e9lectifs des r\u00e9cepteurs nucl\u00e9aires PPARg , r\u00e9duisant l\u2019 insulinor\u00e9sistance au niveau du tissu adipeux, du muscle squelettique et du foie. Le chef de file de cette famille, la troglitazone, commercialis\u00e9 en 1997 a \u00e9t\u00e9 retir\u00e9 du march\u00e9 en raison de son h\u00e9patotoxicit\u00e9. Deux autres glitazones, la pioglitazone et la rosiglitazone, ont \u00e9t\u00e9 r\u00e9cemment commercialis\u00e9es, et consid\u00e9r\u00e9es comme moins h\u00e9patotoxiques. Nous rapportons ici un cas d\u2019 h\u00e9patite aigu\u00eb s\u00e9v\u00e8re imputable \u00e0 la pioglitazone.
\nObservation : Un homme de 42 ans \u00e9tait hospitalis\u00e9 le 14 f\u00e9vrier 2003 pour ict\u00e8re. Dans ces ant\u00e9c\u00e9dents, une HTA depuis 1998, un accident isch\u00e9mique transitoire en juillet 2001, un suspicion d’embolie pulmonaire en mai 2002, une oesophagite ulc\u00e9ro-n\u00e9crotique en mai 2002 et un diab\u00e8te non insulino-d\u00e9pendant trait\u00e9 depuis 1998 par des antidiab\u00e9tiques oraux. Le malade \u00e9tait sous glibenclamide 15 mg\/j et metformine 3 g \/j depuis 1998. Il avait pris par ailleurs de l’amlodipine (10 mg par jour) depuis 6 ans, remplac\u00e9e par de la lercanidipine 20 mg par jour. Le 21 d\u00e9cembre 2002, le glibenclamide \u00e9tait arr\u00eat\u00e9, et remplac\u00e9 par de la pioglitazone (30 mg\/j). Le 27 d\u00e9cembre 2002, survenait une violente douleur abdominale sans fi\u00e8vre ni frisson. Cette douleur s’am\u00e9liorait spontan\u00e9ment, mais des douleurs abdominales vagues s’installaient, associ\u00e9es \u00e0 une asth\u00e9nie et une anorexie progressive. Un ict\u00e8re apparaissait le 5 f\u00e9vrier 2003. Le malade prenait 6 g\u00e9lules de dextropropoxyph\u00e8ne 30 mg-parac\u00e9tamol 400mg 4 jours apr\u00e8s l’installation de l’ict\u00e8re, puis, en l\u2019 absence d\u2019 am\u00e9lioration, \u00e9tait hospitalis\u00e9 le 13\/02\/2003. L’examen clinique notait un ict\u00e8re sans signe clinique d’ h\u00e9patopathie chronique, sans enc\u00e9phalopathie, sans fi\u00e8vre. Le bilan biologique montrait des ASAT \u00e0 2770 UI\/l (N<42), des ALAT \u00e0 2403 UI\/L (N<33), des phosphatases alcalines \u00e0 231 UI\/l (N<95), une gamma GT \u00e0 1141UI\/L (N<64), une bilirubin\u00e9mie \u00e0 270 \u00b5moles\/l dont 166 de bilirubine conjugu\u00e9e 166, un TP \u00e0 65%, un facteur V \u00e0 76%. L'albumin\u00e9mie \u00e9tait \u00e0 31,2 g\/l et les gamma-globulines \u00e0 7,5 g\/l. La num\u00e9ration formule sanguine, l\u2019 ionogramme sanguin et la fonction r\u00e9nale \u00e9taient normaux. L'Ag HBs, les anticorps anti-VHC, la recherche d'ARN du VHC par PCR, les anticorps anti-nucl\u00e9aires, anti-mitochondries, anti-reticulum endoplasmique \u00e9taient absents du s\u00e9rum. Les anticorps anti-muscle lisse \u00e9taient postifs \u00e0 1\/80 de type non anti-actine. Une \u00e9chographie abdominale montrait un parenchyme h\u00e9patique d'\u00e9chostructure et de morphologie normales, et des voies biliaires normales. La pioglitazone \u00e9tait arr\u00eat\u00e9e \u00e0 l\u2019 entr\u00e9e. Les perturbations biologiques s'aggravaient jusqu'au 16\/02\/2003: ASAT 3467 UI\/l, ALAT 2797 UI\/l, bilirubine totale 297 \u00b5moles\/l, TP 57%. Le 21\/02\/2003 une \u00e9chographie abdominale retrouvait une ascite mod\u00e9r\u00e9e contenant 10 g de protides par litre , et 75 \u00e9l\u00e9ments par mm3 . L'\u00e9volution \u00e9tait ensuite favorable. Une biopsie h\u00e9patique \u00e9tait faite le 06\/03\/2003, apr\u00e8s la disparition de l\u2019 ascite. A cette date, ASAT 43 UI\/l, ALAT 88 UI\/l, phosphatases alcalines 76 UI\/l, gamma GT 150 UI\/l, bilirubine totale 74 \u00b5moles\/l, TP 78%. L\u2019 examen histologique montrait une architecture normale, les espaces porte \u00e9taient fibreux et oed\u00e9mateux avec une importante prolif\u00e9ration n\u00e9oductulaire et un infiltrat mod\u00e9r\u00e9 comportant \u00e0 pr\u00e9dominance lymphocytaire, avec des neutrophiles, sans \u00e9osinophiles, et une exocyose de polynucl\u00e9aires dans les canaux biliaires sans alt\u00e9ration \u00e9pith\u00e9liale. Les l\u00e9sions lobulaires \u00e9taient majeures avec ballonisation et clarification des h\u00e9patocytes, gros noyaux avec gros nucl\u00e9oles et inclusions glycog\u00e9niques, et nombreuses n\u00e9croses h\u00e9patocytaires entour\u00e9es de microgranulomes leucocytaires, cholestase intrah\u00e9patocytaire et intracanaliculaire, st\u00e9atose minime. Il y avait des d\u00e9pots de fer dans les macrophages portaux et les cellules de Kupffer. Les tests h\u00e9patiques \u00e9taient normaux un mois plus tard, \u00e0 l\u2019 exception de GGT \u00e0 2,7 fois la normale.
\nDiscussion : Quatre cas d\u2019 h\u00e9patite \u00e0 la pioglitazone1-4 ont \u00e9t\u00e9 rapport\u00e9s, chez trois hommes et une femme de 49 \u00e0 78 ans, apr\u00e8s 6 semaines \u00e0 7 mois de traitement, avec un profil d\u2019 h\u00e9patite mixte, des l\u00e9sions h\u00e9patocellulaires et cholangiolaires, et une \u00e9volution rapidement favorable \u00e0 l\u2019 arr\u00eat du m\u00e9dicament ; dans un cas4 il s\u2019 agissait d\u2019 une h\u00e9patite grave, r\u00e9gressive sous corticoth\u00e9rapie. Dans les \u00e9tudes r\u00e9alis\u00e9es avant la mise sur le march\u00e9, le taux d\u2019 \u00e9l\u00e9vation des transaminases au dessus de 3N \u00e9taient de 0,25% (non diff\u00e9rents du placebo), contre 3% avec la troglitazone. Le m\u00e9canisme de l\u2019 h\u00e9patotoxicit\u00e9 des glitazones est inconnu : la troglitazone a une toxicit\u00e9 mitochondriale in vitro, et est \u00e0 l\u2019 origine de la formation d\u2019 un epoxide quinonique ; elle poss\u00e8de une chaine lat\u00e9ral a-tocoph\u00e9rol dont sont d\u00e9pourvues les 2 autres glitazones. Des h\u00e9patites \u00e0 la rosiglitazone ont \u00e9galement \u00e9t\u00e9 d\u00e9crites. L\u2019 efficacit\u00e9 pr\u00e9ventive de la surveillance syst\u00e9matique des transaminases, qui avait r\u00e9duit de moiti\u00e9 la fr\u00e9quence des cas de toxicit\u00e9 s\u00e9v\u00e8re de la troglitazone reste \u00e0 \u00e9tablir, et l\u2019 intervalle de 2 mois actuellement propos\u00e9 semble insuffisant.<\/p>\n

1May LD, Lefkowitch JH, Kram MT. Mixed hepatocellular-cholestatic liver injury after pioglitazone therapy. Ann Intern Med 2002; 136:449-52
\n2Maeda K. Hepatocellular injury in a patient receiving pioglitazone. Ann Intern Med 2001; 135: 306
\n3Pinto AG, Cummings OW, Chalasani N. Severe but reversible cholestatic liver injury after pioglitazone therapy. Ann Intern Med 2002;137:857.
\n4Chase MP, Yarze JC. Pioglitazone-associated fulminant hepatic failure. Am J Gastroenterol 2002; 97:502-3<\/p>\n","protected":false},"excerpt":{"rendered":"

2003 Ramuntxo Arot\u00e7arena, Jean-Paul. Bigu\u00e9, Francine Etcharry et Alex Pariente, Centre Hospitalier, 64000 Pau H\u00e9patologie – \u00a02000-03-09 –\u00a0CO – ________________________________ Introduction : Les thiazolidinediones (glitazones) sont une nouvelle classe d\u2019 antidiab\u00e9tiques oraux, agonistes s\u00e9lectifs des r\u00e9cepteurs nucl\u00e9aires PPARg , r\u00e9duisant l\u2019 insulinor\u00e9sistance au niveau du tissu adipeux, du muscle squelettique et du foie. Le chef […]<\/p>\n","protected":false},"author":2,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_exactmetrics_skip_tracking":false,"_exactmetrics_sitenote_active":false,"_exactmetrics_sitenote_note":"","_exactmetrics_sitenote_category":0,"footnotes":""},"categories":[3],"tags":[14],"class_list":["post-1753","post","type-post","status-publish","format-standard","hentry","category-hepatologie","tag-14"],"yoast_head":"\nH\u00e9patite aigu\u00eb s\u00e9v\u00e8re \u00e0 la pioglitazone - Abstracts des congr\u00e8s de l'ANGH<\/title>\n<meta name=\"description\" content=\"ANGH R\u00e9sum\u00e9s congr\u00e8s H\u00e9patologie Gastroent\u00e9romogie Hepatology Gastroenterology Etudes cliniques Clinical study\" \/>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/angh.net\/abstracts\/hepatite-aigue-severe-a-la-pioglitazone\/\" \/>\n<meta property=\"og:locale\" content=\"fr_FR\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"H\u00e9patite aigu\u00eb s\u00e9v\u00e8re \u00e0 la pioglitazone - 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