Treatment of Chronic Hepatitis C in HIV-infected Patients With Compensated Liver Cirrhosis

L. Martín-Carbonero; P. Tuma, E. Vispo; J. Medrano, P. Labarga; J. González-Lahoz; P. Barreiro; V. Soriano


J Viral Hepat. 2011;18(8):542-548. 

In This Article


A total of 231 HIV–HCV-coinfected patients were included in the study, of whom 41 (17.8%) were considered as cirrhotics based on elastometric values. Median (interquartil) stiffness in patients with cirrhosis was 20 (16.6–26.3). Nearly 70% of all patients were men, with a median age of 43. Table 1 records the main characteristics of the study population, considering cirrhotics and noncirrhotics separately. Although most baseline features did not differ between both groups, cirrhotics showed significantly lower median CD4 counts than noncirrhotics despite the former were more often under antiretroviral therapy. HCV genotype 1 was the most prevalent in both groups, representing more than half of cases (51% in cirrhotics and 59% in noncirrhotics). Overall, 150 patients (65%) received peginterferon α2a, while 81 were treated with peginterferon α2b. The length of HCV therapy was as follows: 6 months for 22 (30%) subjects infected with HCV genotypes 2–3, 12 months for 195 patients and 15 or 18 months for 14 HCV genotypes 1–4 individuals. No significant differences were seen in the length of therapy comparing cirrhotics and noncirrhotics. Finally, as expected, cirrhotics had lower median haemoglobin and platelets than noncirrhotics. It should be noted that 10 (25%) of cirrhotics had <100 000 platelets/μL. All but two cirrhotics were classified as Child-Pugh A class. Other laboratory values related with cirrhosis as decrease in prothrombin time <75% or albumin level below 3.5 gr/dL were observed in 7 (22%) and 4 (14%) of patients with cirrhosis, respectively. Even more, in most of them, an abdominal ultrasonography was performed before treatment. In 18 (50%) of these patients, splenomegaly was detected, and in three of them, other portal hypertension signs were also present. Endoscopy was performed previously to treatment in 10 patients with stiffness values >22; in three of them, grade 1–2 oesophageal varices were present.

Sustained Virological Response

Both the intention to treat (ITT) and on-treatment (OT) analyses showed similar rates of SVR in cirrhotics compared to noncirrhotic patients (Fig. 1). In the ITT analysis, it was 39% (16/41) vs 44.9% (85/190), respectively (P = 0.48), while in the OT analysis it was 50% (16/32) vs 51.8% (85/164), respectively (P = 0.85). Results did not differ when considering HCV genotypes separately. The rate of SVR in subjects with HCV genotypes 1–4 was 33% (9/27) vs 34.6% (45/130), respectively (P = 0.89) in the ITT analysis. For HCV genotypes 2–3, these figures were 50% (7/14) vs 67.8% (40/59), respectively (P = 0.23).

Figure 1.

Sustained virological response in cirrhotic and noncirrhotic patients. (a) Intention to treat. (b) On treatment.

Variables associated with the achievement of SVR in a multivariate analysis were infection with HCV genotypes G2-3 (OR: 5, 95% CI: 2.9–11; P < 0.01) and lower baseline serum HCV-RNA (OR: 2, 95% CI: 1.4–3.03; P < 0.01, for every log decrease). Interestingly, liver cirrhosis was not significantly associated with a poorer treatment outcome (OR: 1.2, 95% CI: 0.4–3.6; P = 0.6). Other variables included in the multivariate analysis that were not associated with SVR were age, CD4 cell counts and being on highly active antiretroviral therapy (HAART).


Overall, 17% (7/41) and 12% (23/190) of patients with cirrhosis and noncirrhotic patients withdrew treatment prematurely because of adverse events, being the difference not statistically significant. One of the patients with cirrhosis suddenly died at home. Another woman with cirrhosis experienced oesophageal variceal bleeding while on HCV therapy. The remaining five early discontinuations occurred because of depression (two patients), thrombopenia (1), anaemia (1) and asthenia (1). Reasons for withdrawals among noncirrhotic were similar (Table 2). One patient also died of unknown origin. It should be noted that the main difference in toxicity when comparing cirrhotics and noncirrhotics was seen in the number of platelets. During the whole study, the number of platelets was significantly lower in cirrhotics, although only one individual discontinued the medication because of thrombocytopenia. Platelet counts <50 000 elements/μL were more frequently seen in cirrhotics than in the rest (8.5%vs 4% at week 12; P = 0.3 and 20%vs 3% at week 24; P < 0.01). Figure 2 depicts the changes in haemoglobin, neutrophils and platelets in the two groups of patients.

Figure 2.

Mean evolution of haemoglobin, leucocytes and platelets counts during treatment with pegylated interferon–ribavirin in the study population.


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