Focus
Article Outline
- The hepato-protective effect(s) of three cups of a coffee a day: relevance for patients with chronic hepatitis C
- The overlap between hepatitis A and HIV: European patients with acute hepatitis A should be tested for HIV
- Conflict of interest
- References
- Copyright
The hepato-protective effect(s) of three cups of a coffee a day: relevance for patients with chronic hepatitis C
Coffee intake has been reported to exert a number of beneficial effects on health including among others, reducing the risk of type 2 diabetes, reducing inflammatory activity and C reactive protein in various diseases and diminishing oxidative stress. The first observations regarding potential beneficial effects of coffee consumption on alanine aminotransferase and γ-glutamtyl transferase activities in patients with chronic liver disease (CLD) were already reported in the 1990s [1], [2]. Since then, evidence for this association gained significant support in several studies performed in Japan, Europe and the US. Recently Freedman and co-workers have conducted a large prospective study in 766 participants of the HALT-C study who had chronic hepatitis C (CHC) with bridging fibrosis and cirrhosis and who failed to achieve a sustained virologic response to pegylated interferon and ribavirin [3]. In this study coffee consumption at base line was shown to be associated with a number of factors including less severe steatosis and lower alanine aminotransferase levels. Furthermore, regular coffee consumption during the observation period (median follow-up 3.8
years) was associated with lower rates of disease progression. In this study, association of coffee intake with progression of liver disease was independent of alcohol intake and cigarette smoking. One year later, Modi and co-workers reported that caffeine consumption, mainly from regular coffee, at an equivalent of 2–3 cups a day, was associated with less severe fibrosis on liver biopsies, as observed in a cohort of 177 patients, of whom 68% had CHC [4]. Finally, two recent meta-analyses confirmed the protective effect of coffee intake on the development of hepatocellular carcinoma in patients with cirrhosis [5], [6].
In the present issue of the Journal, Costentin and co-workers assessed the impact of caffeine consumption on necroinflammatory disease activity and grade of fibrosis in a relatively homogenous cohort of 238 treatment naïve patients with histologically proven CHC, predominantly with genotype 1. Caffeine intake was established as the sum of mean consumption of coffee, tea and caffeine containing beverages and categorized into four levels according to the calculated daily dose. Multivariate analysis revealed that daily caffeine consumption of 408mg was associated with a lesser risk of necro-inflammatory activity as determined by the Metavir score. However, in contrast to previous observations, the investigators did not find a relationship between the degree of caffeine intake and fibrosis stage. The results in the present study confirm a number of previous observations that caffeine intake has an indirect or direct effect on suppression of necroinflammtory activity as assessed by ALT measurements or by a liver biopsy in CLD in general and in CHC in particular. However, it stands in contrast to a number of previous studies including the recent report of Modi et al. who found a beneficial effect of caffeine on progression of fibrosis in CHC and most probably in CLD of other etiologies. How can these conflicting observations be reconciled? Costentin and co-workers try to provide a hypothesis to explain this difference which suggests that suppression of necroinflammatory liver injury by caffeine directly or indirectly slows down the progression of fibrosis. Although this may be the case, such a hypothesis does not provide a clue to decipher the mechanism involved in the hepato-protective effect(s) of coffee and caffeine in CLD. In their study, Modi et al. could not establish a link between coffee consumption and hepatic inflammation and suggest that caffeine may have an independent anti-fibrogenic effect in the liver, possibly through inhibition of the transforming growth factor β pathway [4]. The impact of such a putative anti-fibrotic effect was not observed in the present study by Costentin et al. Last but not least, in addition to caffeine, coffee contains hundreds of other compounds which may act in concert with caffeine in suppressing the necro-inflammatory activity in patients with CHC and CLD. The lack of a control group of CHC patients consuming decaffeinated coffee in the present study does not enable assessment of the specific hepato-protective effect of caffeine on such activity.
In conclusion, many previous reports as well as the report discussed herewith, suggest that coffee consumption has a beneficial effect on disease progression in CHC and possibly also in CLD of other etiologies as reviewed in the articles by Freedman and Modi et al. [3], [4]. Thus, irrespective of the controversy regarding the mechanism involved and regardless of other potential confounding factors such as alcohol consumption and/or cigarette smoking, the already available evidence suggests that 2–3 cups of coffee a day are beneficial in patients with chronic liver disease in general and in CHC patients with advanced fibrosis in particular.
The overlap between hepatitis A and HIV: European patients with acute hepatitis A should be tested for HIV
The hepatitis A virus (HAV) is transmitted mainly through the fecal-oral route, spreading primarily through close personal contact. Household and sexual contact with another person with hepatitis A has been among the most frequently identified risks in the Western hemisphere. In 2007, this type of contact accounted for 8% of reported cases in the US [7]. Outbreaks of hepatitis A among injection-drug users and men who have sex with men (MSM) who are known to be at an increased risk for HIV infection continue to occur [8], [9], [10]. HAV patients with HIV co-infection develop protracted hepatitis A viremia with slow clinical resolution as compared to non-HIV patients with normal CD4 cell counts [11], [12], [13]. Testing for hepatitis A in patients belonging to these risk groups who present with clinical signs of hepatitis is by now common practice. In contrast, routine testing for HIV among patients with serologically proven acute hepatitis A is far less common.
In the present issue of the Journal, Girardi and co-workers present their retrospective analysis on the prevalence of HIV infection among 473 reported Italian patients (77% males) tested in Rome at the National Institute for Infectious Diseases between 2002 and 2008. Results of serologic tests for HIV were available for 203/368 male and 15/105 female patients. Only 39% of the 203 males reported same gender sex activities in a questionnaire designed to identify risk factors. Overall HIV prevalence was 15.2% in 56/368 male patients with acute hepatitis A. This figure rose to 27.6% for the 203 patients with available test results. Only 1/15 females with acute hepatitis A tested positive for HIV (6.7%). Most importantly, 13/56 HIV positive male patients were unaware of their HIV status until tested positive for both acute HAV and HIV infection. Moreover, 2/13 HIV positive patients with acute hepatitis A, were still in the phase of recent primary acute HIV infection. Since only ∼50% of sera of all patients were available for HIV testing, these data on the prevalence of HIV in this specific cohort, most probably, are underestimated.
The results of this survey deliver a clear message for clinicians as well as public health officials: in the absence of clearly identifiable risk factors such as travel to HAV endemic areas, patients presenting with acute hepatitis in countries with low or very low endemic hepatitis A should also be offered HIV testing. Finally, an obvious consequence of the available information suggests that MEM who are at increased risk for contracting HAV infection should be immunized against hepatitis A.
Conflict of interest
The author declared that he does not have anything to disclose regarding funding or conflict of interest with respect to this manuscript.
References
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PII: S0168-8278(11)00085-7
doi:10.1016/j.jhep.2011.01.017
© 2011 Published by Elsevier Inc.
