The novelty and major contribution of the present study is to open the possibility of discriminating the main different aetiologies of cirrhosis according to nutritional and immunological parameters. The patients with alcoholic cirrhosis in the initial compensated form of the disease show already some degree of malnutrition, as revealed by the different nutritional parameters described by various authors [2, 9, 25–27].
On the other hand, the HCV-cirrhotic group has shown better values for nutritional parameters, despite the concomitant and conspicuous biochemical alterations. Therefore, it was not possible to correlate higher levels of aminotransferases and bilirrubin, as well as the lower levels of albumin and platelets, with the observed nutritional alterations.
The CHI is probable the most widely used index for evaluating body muscle mass , as it correlates with oxygen consumption and lean muscle mass . The CHI was more elevated in the HCV group, showing no association with gender and other parameters used for the evaluation of the muscular compartment, similar to the study of Caregaro and collaborators (1996).
Mean values of TSF being significantly lower in the ALC+HCV group can be interpreted as very specific in the estimation of the fat compartment, since this index is not influenced by liquid retention . Contrariwise, in this same group (ALC+HCV), the other index that allegedly evaluates the fat compartment, named arm fat area (AFA) , has not shown a significant alteration in this aetiologic group; as it was also observed by others .
As the presence of ascites and/or edema may interfere in the nutritional evaluation of cirrhosis, a special care was taken in terms of excluding such patients from the study, similarly to what was made by other authors [25, 28, 30].
It is well known that nutritional status does exert an influence in all aspects of immunity, including humoral response, phagocytosis, complement components and, specially, cellular mediated response. As a rule, the effect of caloric and protein depletion in the organism is to suppress or decrease the immune response, although in certain cases malnutrition stimulate immune response. This can be observed, particularly, in the humoral response of patients with alcoholic liver disease or in the response to infections of undernourished patients . The exaggerated humoral response does not mean a higher degree of protection; on the contrary, it is rather a reflex of the dysfunction of the regulatory and stimulatory factors of the immune system .
Similarly to the nutritional evaluation, the immunological parameters in the course of cirrhosis were preferentially evaluated in alcoholic aetiology [2, 12, 32–34]. In our comparative study, the behavior of the lymphocytes mediating the nutritional and immunological alterations was similar in alcoholic and HCV groups. A possible explanation for this similarity in the lymphocyte counting may be due to the fact that the better nutritional state is compensated with the higher immunological alteration and vice-versa in the HCV and alcoholic aetiologies, respectively.
Among the evaluated immunological parameters, there has been observed the decrease in the complement components, fraction 4 in particular, associated with the opsonic and bactericide activity of the cirrhotic sera [35–37]. One could then speculate that lower levels of C4 would lead to higher frequency of infectious processes.
One of the most common immunological alterations in cirrhotic patients is the occurrence of hypergammaglobulinemia , with variable increase in IgG, IgA and IgM in different hepatic disorders . In patients with alcoholic cirrhosis there has been shown elevated levels of IgA and IgG [40–42], and normal IgM . Contrariwise, we have observed equal levels of IgG in the alcoholic-cirrhotic and control groups, and elevated levels of IgG and IgM in the HCV-cirrhotic patients. Since many of the former studies with alcoholic cirrhosis were carried out before the HCV detection, it is difficult to rule out an eventual aetiologic association. The elevated levels of IgM and IgG in HCV cirrhosis, described by Sarin and collaborators (1997), could be due to the dysfunction of the T cells, currently taken as responsible for the virus persistence, as well as the severity of the hepatic disease . The elevated levels of IgM found in the HCV group in our study corroborate with Sarin's et al findings .
The increase in the IgE levels, however, cannot be associated with severity of the chronic liver disease. As others , we observed the elevation of this fraction in the alcoholic aetiology, but its significance is not clear. It is interesting to note, however, that the degree of malnutrition and anergy was higher in this very group, factors that may influence the levels of IgE [44, 45].
The reduction in the number of lymphocytes and the depression in the response to the intradermic tests peculiar to a delayed hypersensitivity seem to be directly related to the severity of liver damage [1, 46–48]. In our study, there was no discrimination among the different aetiologies of cirrhosis according to the lymphocyte subpopulations, CD4+ and CD8+, as seen by others . Even though, the CD4/CD8 ratio has distinguished the cirrhotic group from the control patients, what had been reported for the alcoholic aetiology of cirrhosis .
Intradermic test of delayed hypersensitivity with higher percentages of anergy have been described by many authors in alcoholic cirrhosis [1, 2, 12, 33]. Anergy was found more frequently among alcoholic patients, albeit poor intradermic response was equally frequent in HCV and alcohol groups, differently from other findings . It is important to point out that the immunodeficiency of the HCV group was not associated with higher degrees of malnutrition, except for the lower mean values of the albumin which has been related to the anergy of the intradermic tests .
The most noticeable laboratorial alterations of the HCV group could be related to a deficient cellular immune response. This non-nutritional factor may probably be connected with the severity of the hepatocellular lesion or to immunological alterations triggered by the HCV. These hypotheses demand further investigations to be confirmed.