**2.2 Evolution of the recurrence of HCV in the post-transplant liver**

The histological involvement of the graft and the natural history of the recurrence both vary, with different presenting forms. Post-transplant reinfection with HCV is associated with greater aggressiveness than in immunocompetent patients (Table 1) (Berenguer et al, 2000, Berenguer et al, 2001b).

At around the fifth month after transplantation there is an acute hepatitis, which is generally asymptomatic in some 50% of patients. Its histological findings present characteristics of lobular hepatitis with varying degrees of inflammatory infiltrate in the portal space, mainly of lymphocytes and macrovesicular steatosis, similar to the histological pattern found in acute hepatitis in immunocompetent patients.

Of those patients who experience a relapse of their HCV infection after liver transplantation, 20% have histological lesions compatible with mild chronic hepatitis 5 years posttransplantation. The others experience a more important chronic evolution. The progression to hepatic cirrhosis occurs in 30% of these patients after 5 to 7 years post-transplant, and is much faster than in immunocompetent persons (Forman et al., 2002).

The viral infection recurs in almost all cases and occurs immediately after the graft reperfusion phase. The diagnosis of viral recurrence is purely virological and is established by detection in serum of HCV RNA using polymerase chain reaction (PCR) techniques. The levels of viraemia are generally far higher than those existing before the transplant (García-Retortillo et al, 2002). The diagnosis of relapse of the hepatitis or disease in the graft,

Pathophysiologically, two patterns of recurrence can be distinguished: (1) a pattern of chronic HCV hepatitis similar to that seen in non-transplanted patients but with a faster course, reaching states of advanced fibrosis or cirrhosis in a shorter time (9-12 years versus 20-50 years); (2) a second pattern, called fibrosing cholestatic hepatitis, which is less common (3-5%) but very severe, and generally appears in the context of intense immunosuppression. It can present as an initial manifestation of disease relapse or, less commonly, in the context of recurrent chronic hepatitis, and is characterised by marked jaundice with cholestasis and high titres of viraemia. This form usually progresses rapidly to

Histological confirmation is necessary to establish the diagnosis of HCV recurrence, as well as to assess the degree of activity and perform a periodic follow-up of histological disease progression. This not only provides information about the prognosis, it can also establish the differential diagnosis with other complications such as rejection, biliary disease, or vascular problems (Berenguer et al., 2001a, Berenguer et al., 2003, Roche & Samuel, 2010,

A new non-invasive technique, transient elastography, has recently become available that appears to correlate well with the stage of fibrosis. This technique can detect an important degree of fibrosis (F≥2) with effect from the sixth month after transplantation, and has an

The histological involvement of the graft and the natural history of the recurrence both vary, with different presenting forms. Post-transplant reinfection with HCV is associated with greater aggressiveness than in immunocompetent patients (Table 1) (Berenguer et al, 2000,

At around the fifth month after transplantation there is an acute hepatitis, which is generally asymptomatic in some 50% of patients. Its histological findings present characteristics of lobular hepatitis with varying degrees of inflammatory infiltrate in the portal space, mainly of lymphocytes and macrovesicular steatosis, similar to the histological pattern found in

Of those patients who experience a relapse of their HCV infection after liver transplantation, 20% have histological lesions compatible with mild chronic hepatitis 5 years posttransplantation. The others experience a more important chronic evolution. The progression to hepatic cirrhosis occurs in 30% of these patients after 5 to 7 years post-transplant, and is

excellent diagnostic capacity at 12 months post-transplantation (Carrión et al, 2010a).

**2.2 Evolution of the recurrence of HCV in the post-transplant liver** 

much faster than in immunocompetent persons (Forman et al., 2002).

**2. Natural history of post liver transplant HCV infection** 

**2.1 Recurrence of HCV post transplantation** 

however,is based on histological findings.

acute liver failure, with graft loss soon after.

acute hepatitis in immunocompetent patients.

Samuel et al., 2006).

Berenguer et al, 2001b).

The progression of the fibrosis is much more accelerated in those patients who receive their transplants due to HCV infection and who have a recurrence of the disease, up to five times faster than in immunocompetent persons. Accordingly, the evolution to cirrhosis is also sooner, with the average being 10 years as opposed to 20-30 years for immunocompetent persons with chronic HCV infection (Forman et al., 2002, Firpi et al., 2009).

Once cirrhosis is reached, 40-50% of transplanted patients will experience their first decompensation within one year. Survival after this first episode of decompensation is 50% (Berenguer et al, 2001b, Firpi et al, 2009).

In immunocompetent persons, about 25% experience their first decompensation 10 years after hepatic cirrhosis is diagnosed, and of these 50% survive for five years after the decompensation episode.


Berenguer et al, 2001b.

Table 1. Natural history of hepatitis C before and after transplantation
