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Advanced fibrosis raised risk for decompensation in HIV/HCV coinfection
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Hepatitis C therapy is necessary in patients with advanced fibrosis who are coinfected with hepatitis C and HIV because they are at risk for liver decompensations, researchers reported in Clinical Infectious Diseases
“HIV/HCV-coinfected patients with advanced fibrosis, but still without cirrhosis, should be treated with the currently available drugs,” Juan Macías, MD, of the Hospital Universitario de Valme in Seville, Spain, told Infectious Disease News. “Because current triple drug regimens are poorly tolerated, complex and inconvenient, especially for those with HIV, the strategy recommended in many countries is immediate therapy for patients with advanced fibrosis or cirrhosis, but the high cost of boceprevir and telaprevir has limited their used mostly to individuals with cirrhosis in some countries.”
Juan Macías
The retrospective cohort study included 892 patients with HIV/HCV coinfection who were treated from November 1990 to June 2012. They had not previously received HCV therapy or had received treatment but not reached sustained virological response. All patients had advanced fibrosis diagnosed by liver biopsy or liver stiffness measurement. The researchers evaluated the number of liver decompensations recorded during the follow-up period.
Among the 317 patients who had liver biopsy, 40 patients experienced liver decompensation, with a rate of 2.3 decompensations per 100 person-years. At 5 years, the probability of remaining free of liver decompensation was 90%. Twelve patients with fibrosis stage 3 at baseline developed liver decompensation, for an incidence of 1.4 per 100 person-years. Twenty-eight patients with cirrhosis at baseline developed liver decompensation, for an incidence of 3.1 per 100 person-years.
Among the 575 patients who had liver stiffness measurement, 53 patients experienced liver decompensation, with a rate of 3.98 decompensations per 100 person-years. At 5 years, the probability of remaining free of liver decompensation was 77%. Six individuals with a liver stiffness measurement of ≥9.5 kiloPascal (KPa) and <14.5 KPa and 47 patients with a measurement of ≥14.6 KPa at baseline experienced decompensations of cirrhosis. The incidence rates were 0.9 per 100 person-years and 4 per 100 person-years, respectively.
“Clinicians should be more proactive prescribing anti-HCV therapy to patients with bridging fibrosis in the liver biopsy or liver stiffness values between 9.5 KPa and 14.6 KPa,” Macías said. “The likelihood of liver decompensations among these patients could be high in a short period of time. If close follow-up with serial liver stiffness measurements is feasible, individuals with early increasing liver stiffness values and progression to cirrhosis could be detected and treated. If shorter and safer new regimens can be prescribed in the short term, liver stiffness follow-up could also be used to identify individuals who can wait for new drugs.”
Juan Macías, MD, can be reached at: Unidad de Enfermedades Infecciosas y Microbiología, Hospital Universitario de Valme, Avda. Bellavista s/n, 41014 Seville, Spain; email: jmacias@cica.es.
Disclosure: Some of the researchers report financial relationships with Abbott, Boehringer Ingelheim, Bristol-Myers Squibb, Gilead, GlaxoSmithKline, Jansen Cilag, Merck Sharp & Dome, Roche, Schering-Plough and ViiV.
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