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Cryoglobulins are immunogloblulins that persist in the serum, precipitate with cold temperature, and resolubilize when rewarmed. Mixed cryoglobulins, composed of different immunoglobulins, with a monoclonal component in type II and only polyclonal immunoglobulins in type III, are associated with connective tissue, malignant hematologic, or obvious infectious diseases. The syndrome of mixed cryoglobulinemia represents the consequence of an immune complex-type vasculitis. It is characterized by the clinical triad of purpura, arthralgia, and asthenia, and may involve numerous organs, particularly the peripheral nervous system and the kidneys. Mixed cryoglobulinemia frequently is associated with clinical and biologic evidence of liver disease. It seems fairly clear that mixed cryoglobulinemia is often a manifestation of underlying chronic active or persistent hepatitis. In the last 10 years, many studies have demonstrated that infection with hepatitis C virus is involved in the pathogenesis of most mixed cryoglobulinemia vasculitis. This review analyzes the main published data of hepatitis C virus-mixed cryoglobulinemia, the role of liver alterations, the predictive factors associated with mixed cryoglobulin production in hepatitis C virus patients and whether its character is symptomatic, and the different types of vasculitis associated with hepatitis C virus chronic infection and their treatments.

Background: Temporal arteritis (TA) is a inflammatory panarteritis of the elderly, which may diffuse to all large arteries. Five to 10% of the patients present nonclassical signs with respiratory, vascular, cardiologic, neurologic or hepatic manifestations. We reviewed eighteen cases of TA and deafness in the literature and report two new cases., Case Reports: Our two patients developed sudden, bilateral and corticosteroid responsive hearing loss. One patient developed hearing loss before the diagnosis of TA., Conclusion: The mechanism of deafness is probably explained by vertebrobasilar or terminal cochleovestibular arteritis. While the diagnosis of TA is usually easy, it may be difficult in other circumstances. Sensorineural hearing loss may be the first symptom of TA. Prompt recognition and treatment may lead to partial or total improvement of hearing loss in 55% of the cases.

Lymphocytic gastritis is characterized by intense lymphocytic infiltration of gastric epithelium. Excessive gastric protein loss is uncommon. We describe the case of a 49-year-old white woman suffering from generalized edema and abdominal pain. She had severe serum hypoproteinemia, hypoalbuminemia and hypogammaglobulinemia. There was no renal, cardiac or hepatic origin of protein loss, and no protein-losing enteropathy. Endoscopic examination showed diffuse varioliform gastritis and histology confirmed lymphocytic gastritis with > 30% intraepithelial lymphocytes without Helicobacter pylori. The protein loss stopped within two weeks of the beginning of omeprazole and extensive edema disappeared. Four years later, the patient was still free from edema. Inflammatory involvement of the gastric mucosa probably caused protein losing in this patient. Recognition of this exsudative gastropathy is important because long term remission is obtained with omeprazole.