E Ragone

Hepatic fibrosis plays a central role in the pathogenesis of thrombocytopenia in patients with chronic viral hepatitis

The pathogenesis of thrombocytopenia in chronic hepatitis is not well known. This study evaluated the relationship between liver injury, serum thrombopoietin, splenomegaly and thrombocytopenia in chronic viral hepatitis. Two hundred and nine patients were enrolled, 85 with splenomegaly and 124 without. Thrombocytopenia was present in 71% and 23% of patients with or without splenomegaly respectively. In subjects with low platelet count, those with splenomegaly showed significantly lower platelet numbers than those without splenomegaly. The spleen size correlated with portal hypertension. An inverse correlation between spleen size and platelet count was observed (r = −0·54; P < 0·0001). In patients without splenomegaly, thrombocytopenia was associated with the grade of fibrosis; platelet counts were the highest in patients with fibrosis 0–2, lower in those with grade 3 (P < 0·008) and lowest in those with grade 4 (P < 0·05). These findings were independent of demographic and biochemical characteristics, hepatic necroinflammatory activity, portal hypertension and splenomegaly. Patients with normal platelet counts showed higher thrombopoietin levels than those with low platelet counts (P < 0·0001). An inverse correlation between thrombopoietin levels and fibrosis grade was observed (r = − 0·50; P < 0·0001). Median thrombopoietin levels were 58 and 27 pg/ml for fibrosis grade 0–1 and grade 4 respectively (P < 0·001). These data indicate that advanced hepatic fibrosis, causing an altered production of thrombopoietin and portal hypertension, plays the central role in the pathogenesis of thrombocytopenia in chronic viral hepatitis.

Streptococcus bovis Endocarditis and Its Association with Chronic Liver Disease: An Underestimated Risk Factor

Clinical and epidemiological characteristics of Streptococcus bovis endocarditis were prospectively studied among 199 patients with definite endocarditis. Thirty patients (15.1%) had S. bovis endocarditis. Compared with patients with non-S. bovis endocarditis, these 30 patients were older (mean age, 58.6+/-12.4 years vs. 46.0+/-17.0 years; P<.001) and had higher rates of bivalvular involvement (43.3% vs. 7.7%; P<.001), embolism (73.3% vs. 40.2%; P=.002), and diskitis (23.3% vs. 0.6% P<.001). In patients with S. bovis biotype I (S. bovis I) endocarditis, advanced liver disease was present in 56.7%, compared with 15.3% of patients with non-S. bovis endocarditis (P<.001), and colonic adenoma was present in 46.7%. The in-hospital mortality rate (16.7%) was correlated with delayed diagnosis and advanced liver diseases. In our city, S. bovis I endocarditis is frequently correlated with liver diseases; diskitis may be the first sign of the disease.

Risk factors for "major" embolic events in hospitalized patients with infective endocarditis.

BACKGROUND Infective endocarditis often is complicated by embolic events after hospital admission. Identifying patients at higher risk may improve the disease outcome. This study was aimed at identifying predictors of embolic risk among the clinical and laboratory data obtained on hospital admission in patients diagnosed as having definite infective endocarditis according to the Duke criteria. METHODS Ninety-four patients were enrolled in a prospective study. The results of hematologic, echocardiographic, and microbiological investigations were analyzed, using statistical methods as appropriate. Multivariate analysis was applied to variables significantly associated with embolism in univariate analysis. RESULTS Forty-six percent of patients had a major embolic complication after admission. No association was found between embolism and sex, site of infection, or microorganism involved. Patients with embolism were significantly younger, had larger vegetation, and showed a significantly higher level of serum C-reactive protein and lower albumin concentrations than those without embolism. Young age, larger vegetation size, and high levels of C-reactive protein were the independent variables associated with an increased incidence of embolic events in the multivariate logistic regression analysis. CONCLUSIONS Our data indicate that patients with infective endocarditis with young age and/or with large vegetation and/or with high serum levels of C-reactive protein are at increased risk of major embolic complications during the in-hospital course of the disease.

HCV RNA levels in serum, liver, and peripheral blood mononuclear cells of chronic hepatitis C patients and their relationship to liver injury

Objective:We sought to evaluate the relationship between HCV RNA levels in serum, liver, and peripheral blood mononuclear cells (PBMC) and the degree of liver injury in chronic hepatitis C (CHC) patients.Methods:Thirty-six consecutive CHC patients were included in the study. The liver damage was evaluated by the histological activity index (HAI) score. The HCV RNA levels in the three compartments studied were assessed by bDNA assay. Nineteen patients were treated with α-interferon 2b (IFN).Results:Serum and liver HCV RNA levels in CHC patients were significantly associated with an increasing HAI score irrespective of the HCV genotypes. Cirrhotic patients showed higher HCV RNA levels than the CHC patients with HAI score 1–4 (p < 0.05), but had lower levels than the group with HAI score > 8 (p < 0.03). Patients with HAI score 1–4 showed the lowest levels of HCV RNA in PBMC. There was a strong relation (r = 0.78; p < 0.001) between serum and liver HCV RNA levels, but not between either serum or liver HCV RNA levels and those of PBMC. Seven patients showed a response to IFN and three of these had a sustained response. Pretreatment levels of HCV RNA in PBMC of the IFN responder patients were lower than those of the nonresponder patients (p < 0.02).Conclusions:The data indicate a relation between serum or liver HCV RNA levels and the degree of liver injury in CHC patients, and show that serum HCV RNA level mirrors the hepatic viral burden.

Comparative activities of isepamicin, amikacin, cefepime, and ciprofloxacin alone or in combination with other antibiotics against Stenotrophomonas maltophilia.

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Hepatic cryptococcosis in a heart transplant recipient

Abstract: Cryptococcosis primarily occurs in patients with impaired immune response. While pulmonary and/or cerebral involvement are more often described, there is limited experience of its presence in other sites. We present a case of hepatic cryptococcosis with possible pulmonary involvement in a 54‐year‐old male heart transplant recipient. Two months after heart transplantation, he developed a persistent, moderate dyspnea with fever and signs of liver damage. Diagnosis was made with liver biopsy for a concurrent reactivation of chronic hepatitis B virus (HBV) infection already present before transplant. Along with a mild chronic HBV hepatitis with fibrosis, we observed sinusoidal dilation and groups of bright, rounded, colorless cells with a central nucleus suggestive of cryptococci. Periodic acid–Schiff stain clearly showed encapsulated yeasts, which supported the diagnosis. Cryptococcal antigen was positive in serum and negative in the cerebrospinal fluid. Computed tomography scan of the chest demonstrated a mild interstitial infiltrate. The patient promptly responded to reduction of immunosuppressive therapy and antifungal treatment with amphotericin B lipid complex and flucytosine followed by maintenance treatment with fluconazole. Cryptococcosis should always be considered in the differential diagnosis in immunocompromised hosts with dyspnea and signs of extrapulmonary involvement. Diagnosis of extrapulmonary and extraneural cryptococcosis is difficult and often fortuitous; a histopathological examination of tissues involved is probably warranted.

First Definite Case of Aortic Valve Endocarditis due to Moraxella phenylpyruvica

Abstract.Described here is the first definite case of endocarditis due to Moraxella phenylpyruvica, which occurred in a 50-year-old male with a bicuspid aortic valve. The diagnosis was delayed because of the confounding positivity of the Widal and Wright tests. The patient was cured with surgical valve replacement and antibiotic treatment.