Food-borne infection with L. monocytogenes can cause febrile illness with gastroenteritis in immunocompetent persons.

Occult Hepatitis B virus (o-HBVIn liver from patients with acute HBV infection, previous studies have reported that low levels of HBV replicative intermediates [HBV RNA and supercoiled (ccc) DNA] can be detected several years after clinical recovery from acute hepatitis. 4 -6 Moreover, o-HBV has been demonstrated in woodchucks infected with the Woodchuck Hepatitis virus (WHV) 7-10 ; after recovery from acute WHV infection a lifelong occult WHV infection develops with a low level of WHV replication both in liver and in lymphatic tissue.Although low serum levels of HBV DNA are distinctive features of o-HBV, 1,2 all patients remain persistently HBsAg negative without any biochemical or histological evidence of chronic hepatitis.The persistence of the HBV infection in HBsAgnegative carriers without clinical signs of chronic hepatitis appears to be the expression of a particular virushost interaction; it could be due to a strong active longlived CTL response capable of containing HBV expression and replication at very low level. [11][12][13] Latent HBV infection can be frequently detected by surrogate markers of previous HBV exposure (antibodies against surface and/or core antigens). It carries no risk of progression to cirrhosis or hepatocellular carci-

Bleeding time, blood loss and platelet retention by glass beads, measured by standardized techniques, were significantly altered in a group of 30 non-thrombocytopenic patients with chronic renal failure undergoing maintenance haemodialysis. Bleeding time or blood loss did not correlate with platelet retention either before or after haemodialysis. No correlation could be found between the above tests and a number of biochemical parameters characterizing the uraemic condition. Haemodialysis only partially corrected the abnormal bleeding time, blood loss and platelet retention. These tests were still significantly different after haemodialysis from those of 30 normal subjects. It is suggested that some non-dialyzable material could play an important role in the aetiology of uraemic bleeding.

We tested the sera of 67 consecutive patients for hepatitis G virus (HGV) RNA by reverse transcriptase-polymerase chain reaction (RT-PCR). These patients (42 males and 25 females, median age 35 years, range 13-64 years) had liver disease of unknown aetiology and were without markers of hepatitis (A-E) viruses or signs of genetically determined, autoimmune, alcoholic or drug-induced liver disease. The controls in this study were 110 patients (50 females and 60 males, median age 45 years, range 9-65 years) with chronic hepatitis B virus (HBV) infection (19 patients) or hepatitis C virus (HCV) infection (91 patients). Ten of 67 (14.9%) patients with cryptogenic disease were positive for HGV RNA by at least three separate tests; HGV RNA was also detected in one of 19 (5.3%) hepatitis B surface antigen (HBsAg) carriers and in nine of 91 (16.6%) patients with antibody to HCV. These data suggest that HGV occurs as frequently in HCV-infected patients as in those with cryptogenic disease. Elevated serum gamma glutamyl transpeptidase (gamma-GT) (higher than twice the normal value) and alkaline phosphatase levels were found in eight of 10 (80%) HGV RNA positive patients and in six of 57 (10.5%) HGV RNA negative patients (P < 0.0001). Five (50%) HGV RNA positive patients had non-specific inflammatory bile duct lesions. A statistically significant difference was observed between HGV RNA positive and negative patients with chronic HBV or HCV infections (P < 0.029). Therefore, the spectrum of liver disease associated with HGV is wide, but a characteristic lesion of the bile duct leading to elevation of cholestatic enzymes might be specific for this virus.

We conducted a three-arm, randomized trial in 96 patients with chronic hepatitis C who did not respond to interferon alfa to compare treatments. Group 1 (33 patients) received ribavirin alone (1,000 mg/daily for 6 months) followed by interferon alfa n-3 alone (3 MU thrice weekly for 6 months); group 2 (33 patients) received ribavirin plus interferon alfa n-3 for 6 months at the above doses; and group 3 (30 patients) received interferon alfa n-3 alone (3 MU thrice weekly for 6 months). At the end of treatment, 3 patients (10%) in group 1, 13 (41%) in group 2, and 5 (17%) in group 3 had normal alanine transaminase (ALT) levels (group 2 vs. groups 1 and 3, P ‫؍‬ .008). After 6 months of follow-up, only 4 patients (12.5%) in group 2 still had normal ALT values (P ‫؍‬ .03). At the end of therapy, hepatitis C virus (HCV) RNA was no longer detectable by polymerase chain reaction in 4 (13%), 9 (27%), and 2 (7%) patients, respectively, in groups 1, 2, and 3 (P ‫؍‬ NS). Six months posttherapy, only 5 (15%) patients in group 2 were still HCV RNA negative (P ‫؍‬ .02). At the time of follow-up liver biopsy, performed 6 months after the end of treatment, a significant improvement of the necroinflammatory scores was observed among group 2 patients (P ‫؍‬ .01) but not in the other two groups. Side effects reflected the profile of each drug as monotherapy; mild hemolytic anemia was the most frequent side effect caused by ribavirin. In conclusion, concomitant administration of ribavirin and interferon alfa n-3 was significantly superior to the sequential schedule or interferon alfa n-3 monotherapy in inducing a sustained response in patients with chronic hepatitis C who had not responded to interferon alone. However, combination therapy at the dose and duration adopted in this study is capable of modifying the natural course of the disease in only a minority of these patients. (HEPATOLOGY 1998;28:341-346.)Interferon (IFN) monotherapy induces a permanent remission in a minority of treated patients with chronic hepatitis C. 1 Patients in whom IFN monotherapy is not effective do not respond to either initial or repeat IFN therapy. Their alanine transaminase (ALT) levels do not normalize, even during IFN administration. 2,3 Thus, retreatment of nonresponders with IFN alone generally is considered ineffective. 4 Pilot studies 5,6 using ribavirin (a broad-spectrum antiviral drug given by mouth) with IFN have reported sustained responses in approximately 40% of patients who had a relapse or no response to IFN alone. Further studies have shown that the response to combination therapy is significantly different between patients who had no response to IFN and those who had a response while undergoing therapy but then relapsed; with combination therapy a sustained response is observed in most relapsers but in only few nonresponders. 7,8 A recent meta-analysis 9 has shown that the estimated probability of sustained response after IFN-ribavirin combination therapy is approximately 16% for previous IFN nonresponders; the standard schedule curr...