Anaemia as an inflammation-mediated condition during chronic heart failure. Possible role of fibrinogen.

BACKGROUND: In patients with chronic heart failure (CHF) anaemia is a common finding and may worsen clinical conditions. Moreover, CHF itself could be involved in the pathogenesis of anaemia. Early studies suggested a pathogenic role of inflammation mediators. OBJECTIVES: The objectives of the study were to assess the relationship between CHF and haemoglobin (Hgb) plasma levels, and to investigate a possible link between fibrinogen plasma levels and anaemia. METHODS: This retrospective study included consecutively hospitalized patients with CHF and left ventricular ejection fraction (LVEF) < 50%. Patients without signs or symptoms of CHF and with LVEF > or = 50% were selected as controls. Patients with secondary anaemia were excluded. RESULTS: 257 patients (72% men) with CHF and 224 controls (65% men) were studied.The average +/- SD of Hgb in CHF patients was 12.38 +/- 1.98 g/dl vs. 13.43 +/- 1.64 g/dl in controls (P < 0.0001). A total of 69 patients (26.7%) had both CHF and anaemia. Plasma fibrinogen concentration was higher in the patients compared with the control subjects (364.83 +/- 123.76 mg/dl vs. 343.44 +/- 135.43 mg/dl; respectively; P = 0.013). Patients with anaemia showed a significantly higher plasma fibrinogen concentration compared to those without anaemia (400.57 +/- 132.36 mg/dl vs. 351.72 +/- 118.13 mg/dl; P = 0.0059). Stepwise logistic regression analysis showed that female gender, creatinine plasma levels, and fibrinogen plasma levels were independently associated with anaemia. No significant relationship between fibrinogen and creatinine plasma concentration was found. CONCLUSION: Anaemia is common in CHF patients and it is associated with heart failure severity.The increase of fibrinogen plasma levels in CHF patients seems to confirm that chronic inflammation is involved in the pathogenesis of anaemia.

Hepatitis C flare due to superinfection by genotype 4 in an HCV genotype 1b chronic carrier.

We report here on a patient affected by chronic hepatitis C who developed acute hepatitis C virus (HCV) superinfection with replacement of genotype 1b by genotype 4. The history revealed no risk factors for a new exposure to HCV, with the exception of colonoscopy with mucosal biopsy performed about 3 months before. This report underlines the absence of an effective immune-mediated cross-protection against different HCV genotypes. Moreover, the possible relationship between HCV infection and colonoscopy points out the importance of strict adherence to international guidelines for disinfection and cleaning of invasive diagnostic tools for all subjects examined, including HCV chronic carriers.