THIS ARTICLE HAS BEEN RETRACTED: Haemodynamic derangement in human immunodeficiency virus-infected patients with hepatitis C virus-related cirrhosis: the role of bacterial translocation

Abstract

Higher intestinal permeability and consequent macrophage activation is observed in patients with cirrhosis; this permeability is even higher in those with portal hypertension. Serum values of IL-6 are associated with the characteristic haemodynamic derangement observed in advanced phases of cirrhosis. HIV/HCV co-infected cirrhotic patients present inflammatory and systemic haemodynamic alterations similar to those observed in HCV mono-infected patients.

Bacterial DNA Translocation and Liver Disease Severity Among HIV-Infected Patients With Chronic Hepatitis C

“…The most likely source of these bacterial products is the gastrointestinal tract, in which mucosal defenses are profoundly disrupted by HIV infection. 5 Our results, and the emerging data from other investigators, 7,11,15,18 indicate that the bacterial products are often circulating in the plasma of HIV-infected and HIV/HCV-coinfected patients. Our finding of an association between lower CD4+ cells and higher bactDNA plasma values support the notion that in HIV-infected patients on cART bactDNA, the plasma levels correlate with CD4+ count, the magnitude of immune CD4+ restoration, and immune activation markers.…”

Enoxaparin Prevents Portal Vein Thrombosis and Liver Decompensation in Patients With Advanced Cirrhosis

“…25 It can lead to ischemic damage of enterocytes, followed by a marked increase in permeability of the intestinal mucosa, a key factor for bacterial translocation, 26 progression of liver damage, 20 and decompensation. 27 Our patients displayed extremely high I-FABP serum levels that correlated positively on ultrasound with the portal vein diameter (a well-known surrogate for PH). The protein I-FABP is made exclusively by enterocytes, and it is released into the circulation upon enterocyte necrosis.…”

Sepsis, the Liver and the Gut

“…Serum levels of interleukin-6 and soluble receptors of tumor necrosis factor were shown to be significantly higher in HIV-HCV co-infected and HCV mono-infected patients with decompensated cirrhosis when compared with those with compensated liver disease. [9] This susceptibility was also demonstrated in non-alcoholic steatohepatitis. [10] In patients with cirrhosis and severe sepsis, high production of proinflammatory cytokines seems to cause a deterioration in liver function and predisposes to the development of shock, renal failure, acute lung injury or acute respiratory distress syndrome, coagulopathy, or hepatic encephalopathy.…”