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These data suggest a high prevalence of thyroid papillary cancer in HCV+ patients, overall in presence of thyroid autoimmunity; careful thyroid monitoring is indicated during the follow-up of these patients.

The prevalence of thyroid disorders is increased in patients with HCV-related mixed cryoglobulinaemia. We suggest careful monitoring of thyroid function in these patients.

Oral anticoagulant-associated intracerebral hemorrhage is increasing in incidence and is the most feared complication of therapy with vitamin K1 antagonists. Anticoagulant-associated intracerebral hemorrhage has a high risk of ongoing bleeding, death, or disability. The most important aspect of clinical management of anticoagulant-associated intracerebral hemorrhage is represented by urgent reversal of coagulopathy, decreasing as quickly as possible the international normalized ratio to values ≤1·4, preferably ≤1·2, together with life support and surgical therapy, when indicated. Protocols for anticoagulant-associated intracerebral hemorrhage emphasize the immediate discontinuation of anticoagulant medication and the immediate intravenous administration of vitamin K1 (mean dose: 10-20 mg), and the use of prothrombin complex concentrates (variable doses calculated estimate circulating functional prothrombin complex) or fresh-frozen plasma (15-30 ml/kg) or recombinant activated factor VII (15-120 μg/kg). Because of cost and availability, there is limited randomized evidence comparing different reversal strategies that support a specific treatment regimen. In this paper, we emphasize the growing importance of anticoagulant-associated intracerebral hemorrhage and describe options for acute coagulopathy reversal in this setting. Additionally, emphasis is placed on understanding current consensus-based guidelines for coagulopathy reversal and the challenges of determining best evidence for these treatments. On the basis of the available knowledge, inappropriate adherence to current consensus-based guidelines for coagulopathy reversal may expose the physician to medico-legal implications.

Objective. No single previous study has evaluated serum levels of the proinflammatory cytokines interleukin-1␤ (IL-1␤), IL-6, and tumor necrosis factor ␣ (TNF␣) in patients with hepatitis C virus-associated mixed cryoglobulinemia (HCV-MC). This study was undertaken to evaluate serum levels of these cytokines in patients with HCV-MC.Methods. Serum IL-1␤, IL-6, and TNF␣ were assayed in 43 patients with HCV-MC, in 43 sex-and age-matched patients with chronic HCV without cryoglobulinemia, and in 43 sex-and age-matched controls.Results. HCV-MC patients showed significantly higher mean IL-1␤, IL-6, and TNF␣ levels than did the controls (P < 0.01) or the HCV patients (P < 0.04). Serum levels of IL-6 and TNF␣ were significantly higher in HCV patients than in controls (P < 0.05).Conclusion. Our findings demonstrate elevated serum levels of IL-1␤, IL-6, and TNF␣ in patients with HCV-MC. If the importance of IL-1␤ and IL-6 in the pathogenesis of MC is confirmed, these results will open the way for the evaluation of new therapies for MC.

To evaluate CXCL10 and CCL2 in patients with hepatitis C virus chronic infection in presence/absence of autoimmune thyroiditis (AT). CXCL10 was significantly higher in: (1) patients with AT than controls without AT (control 1) (P < 0.001; ANOVA); (2) patients with hepatitis C infection than control 1 and patients with AT (P < 0.001); (3) patients with hepatitis C virus chronic infection and AT (HCV+AT) than control 1 and patients with AT (P < 0.001) and hepatitis C (P = 0.004). By defining a high CXCL10 level as a value >218 pg/mL, 2% of control 1, 14% of patients with AT, 68% of patients with hepatitis C infection, 81% of HCV+AT had high CXCL10 (P < 0.0001; chi-square). CCL2 was similar in control 1 and patients with AT. CCL2 was significantly higher in: (1) patients with hepatitis C infection than control 1 (P = 0.04; ANOVA); (2) HCV+AT than patients with AT (P = 0.03) and control 1 (P = 0.02); no difference was observed between HCV with or without AT. Our study demonstrates: (1) higher circulating CXCL10 and CCL2 in patients with hepatitis C virus chronic infection than in controls; (2) higher CXCL10 in HCV+AT than in patients with hepatitis C infection, suggesting a stronger Th1 immune response in these patients.

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