dhg

Blut verbindet alle

Bericht über dramatischen Anstieg von Lebertumoren

28.08.2007

verursacht durch chronische Hepatitis C Infektionen

Bericht über dramatischen Anstieg von Lebertumoren

Über einen dramatischen Anstieg von Lebertumoren bei Hämophilen, verursacht durch  chronische Hepatitis C Infektionen berichteten Ärzte der Hämophiliebehandlungszentren von Frankfurt und Mainz auf dem im Juli in Genf stattgefundenen ISTH Kongress.
Von ungefähr 90 Patienten mit chronischer Hepatitis C Infektion erkrankten 7 Patienten in einem Beobachtungszeitraum von nur 15 Monaten an einem hepatozellulären Karzinom. Alle Patienten hatten zuerst eine Leberzirrhose entwickelt. Zwischen der Infektion mit dem Hepatitis C Virus und der Entwicklung des Tumors lagen im Durchschnitt 34 Jahre. Zwei der sieben Patienten sind leider an den Folgen der Tumorerkrankung inzwischen verstorben.

Kommentar: Auch in Thüringen verstarb erst vor wenigen Tagen ein Hämophiler an den Folgen seiner HCV Infektion. Diese dramatischen Zahlen belegen erneut, wie berechtigt die Forderungen der DHG nach einer Entschädigung für HCV infizierte Hämophile sind.
Dr. Uwe Schlenkrich

[P-W-115] RAPID INCREASE OF HEPATOCELLULAR CARCINOMA IN PATIENTS WITH    HAEMOPHILIA AND CHRONIC HCV- INFECTION                                                           

C. von Auer, S. Heinsdorf, M. Krause, W. Miesbach, I. Scharrer.       
Haematology and Oncology, J. Gutenberg-University Hospital, Mainz;   
Haemostaseology, J.W. Goethe-University Hospital, Frankfurt, Germany  
                                                                         
Introduction: Hepatocellular carcinoma (HCC) is an increasingly frequent cause of mortality in haemophiliacs with chronic hepatitis. In recent years we have observed a rapid increase in HCC development in  
our haemophilia treatment centre. We retrospectively analysed our data to investigate the impact of chronic hepatitis C virus infection in haemophilic patients nowadays.

Methods: In our centre we treated approximately 90 haemophilic patients with chronic HCV hepatitis. Seven patients developed a HCC. Their data were analyzed more detailed.                                          

Results: Median age at estimated infection was 24,5 years, median age at HCC detection was 60 years. HCV genotype was 1b (3), 3a (3), one unknown. The median estimated time between HCV infection and HCC development was 34 years. All patients had developed liver cirrhosis: two Child-Pugh A, one Child-Pugh B and four Child-Pugh C. All were regularly checked at least once a year in our centre with routine screening of AFP level and periodic ultrasound (US) scans. HCC was diagnosed either by elevated AFP levels and US findings (2) or MRT (2), by MRT and check of arterial hypervascularisation (1) plus liver biopsy  
(1). Two patients were co-infected (one with HIV, one with HIV and chronic HBV infection). Four patients had been treated with interferon alpha or peginterferon alone or in combination with ribavirin, only one  
achieved a virologic response. Transcatheter arterial chemoembolization was done repeatedly in three patients. Two patients died of hepatic failure.

Conclusions: The detection of seven HCC in our centre in only 15 months is striking. Our data confirm that HCC seems to be a more significant secondary disease for haemophilic patients than was formerly recognized. A close follow- up on haemophiliacs with chronic hepatitis C should result in early detection and consequently more easily treatable tumors and longer survival of our patients.                 

von Auer C, Heinsdorf S, Krause M, Miesbach W, Scharrer I. RAPID INCREASE OF HEPATOCELLULAR CARCINOMA IN PATIENTS WITH HAEMOPHILIA AND CHRONIC HCV- INFECTION. J Thromb Haemost 2007; 5 Supplement 2: P-W-115