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THE ENDOCRINE PANCREAS OF LACERTIDS - AN IMMUNOCYTOCHEMICAL STUDY OF THE GENERA PEDIOPLANIS AND MEROLES
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Hyperviscosity syndrome in cryoglobulinemia: clinical aspects and therapeutic considerations.
No full textThe term cryoglobulinemia refers to the presence in the serum of proteins that precipitate at temperatures below 37 degrees C and redissolve on rewarming. The cryoglobulins can be divided into three categories: monoclonal, mixed, and polyclonal. Hyperviscosity syndrome is much more common in monoclonal than in mixed or polyclonal cryoglobulinemia. The clinical manifestations of cryoglobulinemia depend on the underlying disease and may involve various organs or systems. Mixed cryoglobulinemia (MC) is dominated by a vasculitic process, and the clinical manifestations can range from mild to life threatening in their severity. Another common feature of this disorder is the presence of a benign smoldering lymphoproliferative process that can evolve (in a limited number of cases) into non-Hodgkin's lymphoma. The elective treatment for hyperviscosity syndrome, whether associated with monoclonal, mixed, or polyclonal cryoglobulinemia, is plasma exchange. In monoclonal cryoglobulinemia, this procedure seems to act by removing large amounts of abnormal proteins, but its mechanism in MC is far from clear. Here it is possible that qualitative and quantitative variations in the circulating cryoglobulins, as well as hemodynamic changes, are at play. This article will focus on the hyperviscosity syndrome in cryoglobulinemia, beginning with a discussion of its clinical features and then examining the role of hemorheological parameters in the condition
From essential mixed cryoglobulinemia to virus-induced autoimmunity: ten years of research on mixed cryoglobulinemia.
No full textthe chapter illustrates the history of clinical and laboratoristic research about the etiopathogenesis of mixed cryoglobulinemia, firstly considered "essential", that is idiopathic, and than related to infection of HCV
How HCV has changed the approach to mixed cryoglobulinemia
No full textMixed cryoglobulinemia is a systemic disease due to a small vessel immune-complex mediated vasculitis. The discovery of a viral origin of the disease has launched a great expectancy among researchers and the years after this finding have been characterized by the effort to reach viral eradication in the hope of obtaining disease remission. Moreover, the use of immunosuppressives has been discouraged for many years as they could favour viral replication, and HCV infection has represented a contraindication to the more recent biological drugs directed against cytokines. The trials with antiviral agents in this disorder, however, has not met the expectations, especially when challenged with some of the most severe complications of the disease; moreover, these medications were not devoid of unexpected side effects, such as the occurrence of peripheral neuropathies. Since lymphoproliferation is one of the features of the disease, this has focused the attention of investigators on the potential benefit of newly targeted therapies specifically directed against B-lymphocytes (such as rituximab). Preliminary results on the use of these medications are promising. Furthermore, the use of biological agents in small open trials in HCV positive arthritis patients has demonstrated an acceptable safety profile. All these empirical observations should probably induce the scientific community to reconsider the therapeutical approach to HCV-related mixed cryoglobulinemia. Indeed, the use of aggressive chemotherapy treatments in the era preceding HCV discovery has not been associated with significant liver toxicities and standard chemotherapy during HCV-related lymphoma carried out a unexpected low rate of severe liver damage. Future efforts should probably focus on the potential benefit of a multi-step, combined anti-viral and cytotoxic therapy (both with standard regimens and new medications
Treatment of chronic hepatitis C infection with cryoglobulinemia.
No full textMixed cryoglobulinemia is characterized by a wide spectrum of manifestations that may vary from mild symptoms (such as purpura, arthralgias, and Raynaud phenomenon) to life-threatening conditions (such as acute abdomen, hyperviscosity syndrome, and renal involvement). Hepatitis C virus infection is considered the principal trigger of the disease. Therefore, the treatment not only should be tailored to the prevailing symptom but also take into account the presence of a chronic, often smoldering infection. Symptomatic therapies are to be used in cases of minor clinical manifestations and aggressive modalities in cases of life-threatening conditions. The use of aggressive cytotoxic regimens should actually be stopped and every potentially immunosuppressive drug should be used with caution. Antiviral medications are used with growing frequency. To date, a few small trials with interferon-alpha alone or in combination with ribavirin in mixed cryoglobulinemia have been conducted. This overview deals with the current approach to the management of mixed cryoglobulinemia, focusing in particular on antiviral treatment in hepatitis C virus infection with or without mixed cryoglobulinemia
Mixed cryoglobulinemia and hepatitis C virus association: ten years later.
No full textMixed cryoglobulinemia is a systemic vasculitis described as a triad characterized by purpura, weakness and arthralgias. Since the first description of the disease in 1964 by Meltzer and Franklin our understanding of its pathogenesis has increased considerably. The striking association of the disease with hepatitis C virus infection was initially noted in 1990. Since then, the disease has gained growing attention among investigators involved in the study of autoimmune systemic disorders because it represents one of the most intriguing models of autoimmunity triggered by a virus. Nonetheless, a number of answered questions still remain to be resolved and are reviewed in this article
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