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Reducing immunosuppression not only reduces complications but also may lessen recurrent hepatitis C virus (HCV) infection after liver transplantation. Patients/Methods. HCV-infected cirrhotic patients randomised to tacrolimus monotherapy (MT) or triple therapy (TT) using tacrolimus 0.1 mg/kg/day, azathioprine 1 mg/kg/day, and prednisolone 20 mg/day, tapering over 3 months. Results. Twenty-seven patients (MT) and 29 (TT) – median follow up 661 days (range, 1–1603). Rejection episodes (protocol/further biopsies) within first 3 months and use of empirical treatment were evaluated. New rejection was diagnosed if repeat biopsy (5-day interval) did not show improvement. Treated rejection episodes: 20 MT (15 biopsy-proven) vs. 24 TT (21 biopsy-proven), with 19 (MT) vs. 24 (TT) methylprednisolone boluses. Overall: 35 episodes (MT) and 46 (TT). Fewer MT patients had histological rejection (70%) than TT patients (86%), with fewer episodes of rejection (18.5% vs. 10%), and more moderate rejection (22% vs. 41%). The MT group had higher early tacrolimus levels. Rates of renal dysfunction, retransplantation, and death were not significantly different. Conclusion. Tacrolimus monotherapy is a viable immunosuppressive strategy in HCV-infected liver transplant recipients. [ABSTRACT FROM AUTHOR]

Bacterial infections in cirrhotic patients are common. There is a predisposition to intestinal bacterial overgrowth, intestinal dysmotility, and increased intestinal permeability, all leading to an increase in bacterial translocation. Bacterial translocation is the probable mechanism for some of the most common infections in cirrhosis, such as spontaneous bacterial peritonitis, but is also the source of bacterial byproducts such as endotoxin which can cause an increase in portal pressure, impairment of liver function, and worsening of haemostasis. The effects of bacterial infection and bacterial products on portal and systemic haemodynamics in cirrhosis and clinical data on infection, from both retrospective and prospective studies of variceal bleeding and other settings, demonstrate the importance of infection in pathophysiological mechanisms in cirrhosis. This has been followed by recent clinical evidence that antibiotic therapy reverses systemic vasodilation and prevents early variceal rebleeding. [ABSTRACT FROM AUTHOR]

Background: Bacterial infections have been proposed as a trigger for portal hypertensive bleeding in cirrhotic patients. Endogenous low molecular weight heparinoids have been previously detected in vitro by heparinase-modified thromboelastography, but it is not known what type of heparinoids they are. The aim of this study was to assay anti-Xa concentrations to detect heparin activity in infected cirrhotics in vivo. Methods: We evaluated 30 cirrhotic patients (15 with bacterial infection, 15 not infected) and 9 non-cirrhotic patients with bacterial infection. The anti-Xa assay was performed at the start of infection in all patients and after resolution of infection in 8 cirrhotics (5 to 10 days after starting antibiotics); thromboelastography (native and heparinase I-modified TEG) was performed in a subgroup of 11 cirrhotic patients with infection, 8 cirrhotics without infection and 8 non-cirrhotics with infection. Results: Anti-Xa activity was detected in 9 of the 15 infected cirrhotics (60%) and only in 1 of 15 non-infected cirrhotics (6.7%) ( P < 0.01). In the infected cirrhotic patients, a heparinase effect was shown in the heparinase I-modified TEG: k time ( P < 0.01), α-angle ( P < 0.01) and r time ( P = 0.05), with no effect in the non-infected cirrhotics. Four of 9 (44%) infected non-cirrhotics were positive with the anti-Xa assay. Conclusion: In cirrhotic patients, bacterial infections modify haemostasis by producing endogenous heparin-like substances which can inhibit the activated clotting factor X (factor Xa). In infected non-cirrhotics, anti-Xa activity can also be found. [ABSTRACT FROM AUTHOR]

Recurrent variceal bleeding is very frequent after variceal haemorrhage and pharmacological therapy is the first choice treatment. Recently, baseline and repeat measurements of hepatic venous pressure gradient (HVPG) have been considered necessary to optimally manage patients receiving pharmacological therapy so as to reduce the frequency of rebleeding. However, the clinical validity and applicability of monitoring for target HVPG reductions is not sufficiently proven and needs to be specifically evaluated in a prospective trial. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented about the association of Gitelman's syndrome (GS) with calcium pyrophosphate dihydrate (CPPD-CDD).

The article describes the case of a 44-year-old women presented with gastroesophageal reflux and was diagnosed with sebaceous glands in the esophagus.

Presents a response to a letter on the influence of bacterial infection on the pathophysiology of cirrhosis.