To analyze whether human leukocyte antigen (HLA)-E allelic variants are associated with and may predict response to peg-interferon (IFN) alpha and ribavirin treatment in HIV/hepatitis C virus (HCV)-coinfected patients.Retrospective follow-up study.We studied 321 naive patients who started HCV treatment. HLA-E genotyping was performed by restriction fragment length polymorphism. A sustained virological response (SVR) was defined as undetectable plasma HCV-RNA up through 24 weeks after the end of HCV treatment.The HLA-E*0101 allele increased the odds of achieving SVR for all patients [adjusted odds ratio (aOR) = 2.03 (95% confidence interval, 95% CI = 1.35-3.06); P = 0.001], for HCV genotype (GT) 1/4 patients (aOR = 1.62 (95% CI = 1.03-2.54), P = 0.035), and for GT2/3 patients [aOR = 9.87 (95% CI = 2.47-31.89), P = 0.001]. For decision tree analysis, the SVR rate increased from 0 to 82.6% and then to 92.5% in GT2/3 patients when the count of HLA-E*0101 alleles increased. In GT1/4 patients with rs8099917 TT genotype, the SVR rate increased from 33.3 to 54.8% and then to 61.8% when the count of HLA-E*0101 alleles increased. In GT1/4 patients with rs8099917 GT/GG genotype, the SVR rate increased from 15.4 to 22% and then to 44% when the count of HLA-E*0101 alleles increased. The overall percentage of patients correctly classified was 73.2% and the area under the receiver operating characteristic curve (AUROC) was 0.803 ± 0.024.The HLA-E*0101 allele was associated with increased odds of HCV clearance and could help to predict SVR among HIV/HCV-coinfected patients on HCV therapy. This would be helpful to avoid treatment in those less likely to respond to pegylated-interferon-alpha and ribavirin treatment.
Three patients with progressive multifocal leukoencephalopathy (PML) treated with highly active antiretroviral therapy (HAART) worsened clinically and radiologically. At the time of deterioration all three had reduced HIV viraemia and increased CD4 cell counts. Brain biopsy in all three disclosed PML and marked perivascular lymphoplasmacytic infiltration. We reviewed the slides of 28 brain biopsies diagnostic of PML. Inflammatory changes were observed in four out of nine patients on HAART and in one out of 19 patients not on HAART. Inflammatory reactions against several opportunistic pathogens after highly active antiretroviral therapy (HAART) have been described in individuals infected with HIV, and have been associated with pronounced reductions in plasma HIV viral load and increases in CD4 cell counts [1–3]. In this report, we describe the clinical and pathological findings that suggest the existence of an inflammatory reaction in patients with AIDS-associated progressive multifocal leukoencephalopathy (PML) related to immune recovery after HAART. In the past 6 years, 66 HIV-infected patients were diagnosed as having PML in our institution according to the following criteria: brain biopsy (n = 30), detection of JC virus DNA in the cerebrospinal fluid by polymerase chain reaction (n = 22), and clinical and neuroimaging manifestations compatible with PML and the exclusion of other aetiologies (n = 14). A total of 28 HIV-infected patients with PML have been treated with HAART. For this study, we reviewed the clinical records and neuroimaging studies of these 28 patients. We also reviewed 28 of the 30 brain biopsies diagnostic of PML performed in our institution. Two biopsies performed before 1995 were not reviewed because they were lost during a transfer of the pathology laboratory to another hospital facility. All the slides were reviewed by the same neuropathologist, who was blind to patient clinical information. The diagnosis of PML was established by the finding of foci of demyelination with scattered lipid-laden macrophages, enlarged oligodendrocytic nuclei with glassy amphophilic viral inclusions and characteristic bizarre giant astrocytes. Since the introduction of HAART in our institution, we found three patients with PML, who worsened clinically and radiologically shortly after the initiation of HAART (Table 1). At the time of deterioration all three had reduced HIV viral loads and increased CD4 cell counts. Brain biopsy in all three patients disclosed typical changes of PML, as well as a marked perivascular infiltration with lymphoplasmacytic cells. We reviewed 28 of the 30 brain biopsies diagnostic of PML performed in our institution. The diagnosis of PML was confirmed in all cases. However, in five patients a striking inflammatory reaction was observed and characterized by predominantly perivascular lymphomonocytic infiltrates. Immunohistochemical studies showed that most of the lymphoid cells were CD8 suppressor T cells and some were CD20 B cells. No CD4 helper T cells were observed. Infectious aetiologies other than JC virus were ruled out by appropriate stains and cultures of brain tissue. The absence of inflammation was observed in the biopsies from 23 patients. Four of the five patients with inflammation were receiving HAART, the fifth was receiving two nucleosides. In three of the four patients receiving HAART, the biopsy was performed to confirm the diagnosis of PML and to rule out other conditions because of serious clinical and radiological worsening (the three mentioned above). The fourth patient with a baseline CD4 cell count of 123/μl and an HIV viral load of 5.62 log copies/ml was biopsied 2 weeks after the initiation of HAART. He remains neurologically stable and medically well 2 years after the biopsy. In the 23 patients without inflammation, 11 were receiving monotherapy with a nucleoside, five were receiving HAART, and seven were not receiving antiretroviral agents. Inflammatory changes were observed in four out of nine patients receiving HAART and in one out of 19 patients not receiving HAART (difference 38.7%; 95% confidence interval 8.4–69%;P = 0.048).Table 1: Characteristics of patients with paradoxical worsening of AIDS-associated progressive multifocal leukoencephalopathy caused by an inflammatory reaction after the initiation of highly active antiretroviral therapy. In PML there is usually an absence of inflammation, although in rare instances lesions may exhibit a faint, peripheral, contrast enhancement on magnetic resonance imaging [4]. Little is known about inflammatory reactions after the addition of HAART in PML. In a recent case report [5], a patient with this disorder worsened clinically and the brain lesions enlarged and enhanced with contrast after HAART; brain biopsy showed demyelination and lymphoplasmacytic inflammation that was more prominent in the tissue from the contrast-enhancing region. In another report [6], lesions of PML were found in four patients after antiretroviral therapy using peripheral gadolinium enhancement. We found inflammatory changes in approximately half of the brain biopsies from patients with PML treated with HAART. We also found clinical and radiological deterioration of PML attributable to inflammatory reactions after HAART in three out of 28 patients (10.7%). Corticosteroid therapy was administered to two of the three patients; one died and the other, treated concurrently with cidofovir, survived and her neurological function improved. From a practical perspective, there is little doubt that HAART has had a major impact on the survival and probably of the clinical outcome of PML [7–10]. However, approximately one third of these patients follow a progressively deteriorating course and die despite HAART [11]. Clinicians caring for patients with AIDS-associated PML must be aware of this immune recovery syndrome, and consider the use of therapeutic measures that modulate the immune response, such as corticosteroids, when clinically appropriate, in order to prevent irreversible inflammatory damage to the brain. Acknowledgements The authors sincerely appreciate the help of Thomas O'Boyle in the preparation of the manuscript. Pilar Mirallesa Juan Berenguera Cesar Lacruzb Jaime Cosína Juan Carlos López Belén Padillaa Lucía Muñozc Darío García-de-Viedmaa
Although the short-term benefit of isoniazid prophylaxis in patients coinfected with human immunodeficiency virus (HIV) and tuberculosis has been shown, long-term benefits are unknown.Historical cohort study in an acquired immunodeficiency syndrome unit at a tertiary referral hospital. A sample of 121 HIV-infected patients with positive results on a purified protein derivative test were followed up for development of active tuberculosis and survival. Patients who received isoniazid prophylaxis were compared with patients who did not receive prophylaxis.Of the 121 patients examined, 29 (24%) completed a 9- to 12-month course of isoniazid prophylaxis (median follow-up, 89 months), and 92 (76%) did not receive the drug (median follow-up, 60 months). Active tuberculosis developed in 46 patients (38%). The incidence of tuberculosis was higher among patients with no prophylaxis (9.4 per 100 patient-years) than among patients with isoniazid prophylaxis (1.6 per 100 patient-years) (P = .006). Risk for development of tuberculosis was associated with the absence of isoniazid prophylaxis (relative risk [RR], 6.55; 95% confidence interval [CI], 2.02-21.19). Death during the period of study was more frequent in patients who did not receive isoniazid (50/92 or 54%) than in patients who received isoniazid (7/29 or 24%) (P = .008). Median survival was more than 111 months in patients who received isoniazid compared with 75 months in patients who did not receive isoniazid (P < .001). In a proportional hazards analysis, the development of tuberculosis (RR, 1.88; 95% CI, 1.09-3.27), the absence of isoniazid prophylaxis (RR, 2.68; 95% CI, 1.16-6.17), and a CD4+ cell count lower than 0.20 x 10(9)/L (RR, 3.03; 95% CI, 1.39-6.61) were independently associated with death. Patients who received isoniazid had a longer survival after stratifying for the CD4+ cell count.Preventive therapy with isoniazid confers long-term protection against tuberculosis and significantly increases survival in patients dually infected with HIV and Mycobacterium tuberculosis.
Objectives: To estimate the impact of interleukin 28B (IL28B) polymorphisms (rs12980275, rs8099917, rs7248668, and rs11881222) and their haplotypes on hepatitis C virus (HCV) treatment (peg-interferon-α and ribavirin) success in 324 HIV/HCV-coinfected patients. We also explore the behavior of plasma cytokine levels. Design: Retrospective follow-up study. Methods: Virologic response to HCV treatment was measured by plasma HCV viral load at different endpoints: rapid virologic response (RVR), early virologic response (EVR), end-of-treatment virologic response (ETVR) and sustained virologic response (SVR). IL28B polymorphisms were genotyped using GoldenGate assay. Finally, 13 cytokines were measured at baseline in 57 plasma samples using a multiplex immunoassay kit. Results: IL28B polymorphisms were strongly associated to virologic responses (RVR, EVR, ETVR, and SVR), although only for HCV genotypes 1 and 4 (P < 0.05). Strong linkage disequilibrium was detected for rs12980275/rs11881222 (r2 = 0.94) and rs8099917/rs7248668 (r2 = 0.99). IL28B haplotypes showed association but no improvement on treatment outcome prediction. Thus, the genotyping of only one single-nucleotide polymorphism was enough for predicting treatment response in GT1/4 patients with favorable rs12980275 (AA) genotype, while for subjects harboring unfavorable genotypes, the inclusion of rs8099917 was useful (SVR increased from 31 to 45%). Moreover, patients with rs12980275 (AA) that achieved SVR showed reduced plasma levels of Th1 (IFN-γ), Th2 (IL-6 and IL-9), and proinflammatory (TNF-α) cytokines. Conclusion: The presence of IL28B polymorphisms was significantly associated with HCV clearance during and after HCV therapy. The evaluated cytokine profile was much more favorable in patients with rs12980275 (AA) who achieved SVR.
Peroxisome proliferator-activated receptor gamma-2 gene (PPARγ2) rs1801282 (Pro12Ala) polymorphism has been associated with lower risk of metabolic disturbance and atherosclerosis. The aim of this study was to analyze the association between the Pro12Ala polymorphism and cardiometabolic risk factors in human immunodeficiency virus (HIV)/Hepatitis C virus (HCV)-coinfected patients.We carried out a cross-sectional study on 257 HIV/HCV coinfected patients. PPARγ2 polymorphism was genotyped by GoldenGate® assay. The main outcome measures were: i) serum lipids (cholesterol, triglycerides, high-density lipoprotein (HDL-C), low-density lipoprotein (LDL-C), LDL-C/HDL-C, and atherogenic index (AI)); ii) homeostatic model assessment (HOMA-IR) values; iii) serum adipokines (leptin, adiponectin, resistin, plasminogen activator inhibitor-1(PAI-1), hepatic growth factor (HGF), and nerve growth factor (NGF)). Generalized Linear Models (GLM) with gamma distribution (log-link) were used to investigate the association between PPARγ2 polymorphism and continuous outcome variables. This test gives the differences between groups and the arithmetic mean ratio (AMR) in continuous outcome variables between groups.The rs1801282 CG/GG genotype was associated with low values of cholesterol (adjusted arithmetic mean ratio (aAMR) = 0.87 (95% of confidence interval (95% CI) = 0.79; 0.96); p = 0.004) and LDL-C (aAMR = 0.79 (95% CI = 0.68; 0.93); p = 0.004). Furthermore, rs1801282 CG/GG was associated with low values of HOMA-IR (aAMR = 0.69 (95% CI = 0.49; 0.98); p = 0.038) among patients with significant liver fibrosis (F ≥ 2). Moreover, rs1801282 CG/GG was also associated with low serum values of hepatic growth factor (HGF) (aAMR = 0.61 (95% CI = 0.39; 0.94); p = 0.028), and nerve growth factor (NGF) (aAMR = 0.47 (95% CI = 0.26; 0.84); p = 0.010). The serum levels of leptin, adiponectin, resistin, and PAI-1 did not show significant differences.The presence of PPARγ2 rs1801282 G allele (Ala variant) was associated with a protective cardiometabolic risk profile versus CC genotype in HIV/HCV-coinfected patients. Thus, PPARγ2 rs1801282 polymorphism may play a significant role in the development of metabolic disorders in HIV/HCV coinfected patients, and might have an influence on the cardiovascular risk.
To the Editors: Coinfection by hepatitis C virus (HCV) is frequent in patients infected with human immunodeficiency virus (HIV) because both viruses share routes of transmission.1 Progression of chronic hepatitis C to cirrhosis and end-stage liver disease is more frequent and rapid among HIV-infected individuals than in those not infected by HIV.2 The major determinants of this accelerated fibrogenesis in HIV/HCV-coinfected patients are immunosuppression and alcohol consumption, although direct action of HIV may also be a contributing factor.3 Therefore, liver disease is a leading cause of hospital admissions and death after the introduction of combination antiretroviral therapy in areas where the prevalence of HIV/HCV coinfection is high.4 Decompensation in cirrhosis results primarily from portal hypertension, which is defined as a pathologic increase in the hepatic venous pressure gradient (HVPG), that is, the pressure gradient between the portal vein and the inferior vena cava.5 HVPG is the most accurate predictor of liver decompensation and hepatocellular carcinoma in patients with compensated cirrhosis.6 In addition, HVPG is an independent predictor of death in patients with decompensated cirrhosis.7 Therefore, HVPG is considered the best surrogate marker of the natural history of cirrhosis. Sustained virologic response (SVR) after anti-HCV therapy has been associated with improvements in liver fibrosis and with reversion of cirrhosis in one-third to half of patients with baseline cirrhosis included in randomized clinical trials of interferon plus ribavirin with pretreatment and posttreatment liver biopsies.8 SVR has also been associated with improved survival and reduced liver decompensation and hepatocellular carcinoma in patients with chronic hepatitis C with or without HIV infection.9,10 Although these findings support the notion that eradication of HCV can reduce HVPG in patients with HCV-related cirrhosis, this area has received little attention,11 particularly in coinfected patients. Our objective was to assess the effect of eradication of HCV after anti-HCV therapy on HVPG in HIV-infected patients with compensated HCV-related cirrhosis. The study population comprised all HIV/HCV-coinfected patients with compensated liver cirrhosis whose HVPG was measured before and after anti-HCV therapy between 2007 and 2012. HVPG was measured after an overnight fast as described elsewhere.12 The HVPG was calculated as the wedged hepatic venous pressure minus the free hepatic venous pressure. All patients signed an informed consent document before the portal hemodynamic study. Transient elastography (TE) was performed immediately before the determination of HVPG using a FibroScan device (Echosens, Paris, France). The median value [expressed in kilopascals (kPa)] of 10 successful acquisitions was considered the representative measurement of liver stiffness.13 We considered a cutoff value of liver stiffness ≥14 kPa as diagnostic of liver cirrhosis.14 Between 2007 and 2012, determination of HVPG and TE was performed in 60 HIV/HCV–coinfected patients with compensated cirrhosis confirmed by liver biopsy and/or TE. During this period, 27 of these 60 patients were treated with pegylated interferon (Peg-IFN) alpha-2a or alpha-2b plus ribavirin (programmed for 48 weeks), whereas 33 were not. A total of 15 treated patients achieved SVR, defined as undetectable HCV-RNA in serum at 24 weeks after discontinuation of anti-HCV therapy. The median [interquartile range (IQR)] baseline HVPG was 13 (10–15) mm Hg for untreated patients, 15 (10–18) mm Hg for treated patients with SVR, and 10 (9–14) mm Hg for nonresponders. The median (IQR) baseline liver stiffness was 30.4 (15.7–43.9) kPa for untreated patients, 23.9 (15.1–38.0) kPa for treated patients with SVR, and 14.6 (12.2–24.6) kPa for nonresponders. Eight of the 15 patients with SVR consented to have a second determination of HVPG and are the focus of this study. All 8 patients had clinically significant portal hypertension (HVPG ≥ 10 mm Hg), and 6 had severe portal hypertension (HVPG > 12 mm Hg). The second HVPG and TE determinations were performed a median of 18 (10–26) months after the discontinuation of anti-HCV therapy. The median (IQR) HVPG was 15.50 (11.25–17.62) mm Hg at baseline and 8.75 (6.25–12.00) mm Hg after SVR (P = 0.01) (Figure 1). After SVR, 7 patients experienced a reduction in HVPG from baseline of ≥20%, and all 7 had HVPG values ≤12 mm Hg. Likewise, the median (IQR) liver stiffness was 27.75 (18.20–38.60) kPa at baseline and 12.80 (7.30–17.05) kPa after SVR (P = 0.01) (Figure 1). After a median follow-up time of 60 months, all 8 patients were alive and free from decompensation and hepatocellular carcinoma.FIGURE 1: A, Median and IQR values and individual values of HVPG at baseline and after SVR. B, Median and IQR values and individual TE values at baseline and after SVR.The effect of anti-HCV therapy on HVPG in patients with HCV-related cirrhosis has received little attention hitherto. In one study, HVPG was measured in 5 patients immediately before and immediately after the discontinuation of a 48-week course of interferon monotherapy and in 5 control patients.15 In treated patients, HVPG decreased from a mean of 13.8 mm Hg at baseline to 11.1 mm Hg at the end of therapy, whereas in controls, it increased from a mean of 13.2 to 14.6 mm Hg; neither of these changes was statistically significant.15 In a second study, HVPG measurements were performed immediately before and immediately after discontinuation of Peg-IFN plus ribavirin in 20 patients with compensated chronic hepatitis C and portal hypertension, defined as an HVPG > 5 mm Hg.16 The authors found a greater reduction in HVPG in patients who achieved end-of-treatment virologic response than in nonresponders. The effect of SVR on portal pressure in 33 patients with HCV-related cirrhosis was assessed at baseline and after 6 months of treatment-free follow-up in 33 patients with cirrhosis by Roberts et al,11 who found that after treatment, there was a significant decrease in HVPG in sustained responders (from a mean of 9.0 mm Hg to a mean of 6.9 mm Hg) compared with relapsers and primary nonresponders. Our findings and those of others bring a pathophysiological correlate to the observation of clinical benefits obtained with SVR in patients with HCV-related compensated liver cirrhosis with or without HIV infection.9,10 It is important to remark that the achievement of an adequate reduction in HVPG after pharmacological treatment of portal hypertension in patients with variceal bleeding reduces not only the probability of recurrent bleeding but also the probability of developing other severe manifestations of end-stage liver cirrhosis such as spontaneous bacterial peritonitis, hepatorenal syndrome, and even death.17 This adequate reduction in portal pressure has been estimated as a decrease in HVPG of ≥20% from baseline or an absolute reduction of HVPG to ≤12 mm Hg.17 We found that 7 of the 8 patients met both these requirements for reduction of portal pressure and, therefore, were at less risk of decompensation and death. The remaining patient had a reduction of 10% in HVPG from baseline, and his HVPG value after SVR was 13.5 mm Hg. However, he was also the patient with the shortest interval between drug discontinuation and the second HVPG determination (only 7 months). Roberts et al11 found that among patients with portal hypertension, a higher proportion of responders achieved a ≥20% reduction in HVPG compared with nonresponders (71% vs. 20%, respectively). According to our experience and that of others, most patients with HCV-related compensated cirrhosis and portal hypertension achieve adequate reductions in HVPG after SVR following anti-HCV therapy, although a small fraction do not achieve that goal. These patients probably remain at risk of developing complications related to portal hypertension despite eradication of HCV.10,18 HVPG determinations or even TE19 could help to identify patients with HCV-related cirrhosis who remain at risk for decompensation or hepatocellular carcinoma despite having achieved SVR. This issue should be addressed in prospective studies. The main limitation of this study is the small sample size and the lack of a control group comprising HIV-infected patients with HCV-related cirrhosis who are nonresponders to anti-HCV therapy and whose HVPG was determined before and after treatment. However, a key strength of our study is the long interval (18 months) between the discontinuation of interferon and ribavirin and the determination of the second portal pressure measurement. Previous studies on the subject addressed the effect of antiviral therapy on HVPG but not that of SVR on HVPG15,16 or they determined changes in portal pressure 6 months after treatment discontinuation11; therefore, the question of whether the reduction of portal pressure after SVR was maintained in the long term remains unresolved. In conclusion, the results of our study support the notion that eradication of HCV is associated with a marked and clinically significant reduction in portal pressure in most—but not all—HIV-infected patients with HCV-related cirrhosis.
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