Polyneuropathy with demyelinating features in mixed cryoglobulinemia with hepatitis C virus infection.

Saved in:

Bibliographic Details
Title:	Polyneuropathy with demyelinating features in mixed cryoglobulinemia with hepatitis C virus infection.
Authors:	Boukhris, S., Magy, L., Senga-mokono, U., Loustaud-ratti, V., Vallat, J.-M.
Source:	European Journal of Neurology. Sep2006, Vol. 13 Issue 9, p937-941. 5p. 3 Black and White Photographs, 3 Charts.
Subjects:	Cryoglobulinemia, Polyneuropathies, Demyelination, Hepatitis C, Biopsy
Abstract:	Peripheral neuropathy can arise from various mechanisms during hepatitis C virus (HCV) infection, mainly involving associated mixed cryoglobulinemia. The frequency of demyelinating polyneuropathy is probably underestimated in these patients. We report two cases of demyelinating polyneuropathy in HCV-infected patients. The first case concerned a 76-year-old woman followed for hepatitis C associated with a mixed cryoglobulinemia (type II), who developed a chronic progressive distal motor weakness and sensory disturbances concomitant with a raise in serum aspartate aminotransferase (GOT/AST) and alanine aminotransferase (GPT/ALT) levels. Other laboratory studies were normal except for a decrease in the hemolytic fraction of complement to 75 IU ( n = 400–520). The second case was a 68-year-old woman followed for hepatitis C associated with a mixed cryoglobulinemia (type II), who had sensory disturbances in the lower limbs. Laboratory studies were otherwise unremarkable. Cerebrospinal fluid studies showed a normal protein content without pleocytosis in both patients. In both cases nerve conduction studies were suggestive of a mixed axonal and demyelinating sensorimotor neuropathy. Sural nerve biopsy showed segmental demyelination and severe loss of large myelinated fibers as well as some onion bulb formation in both cases. The two patients subsequently improved, the first with an antiviral treatment and the second with oral steroids. [ABSTRACT FROM AUTHOR]
	Copyright of European Journal of Neurology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database:	Psychology and Behavioral Sciences Collection

Description
Abstract:	Peripheral neuropathy can arise from various mechanisms during hepatitis C virus (HCV) infection, mainly involving associated mixed cryoglobulinemia. The frequency of demyelinating polyneuropathy is probably underestimated in these patients. We report two cases of demyelinating polyneuropathy in HCV-infected patients. The first case concerned a 76-year-old woman followed for hepatitis C associated with a mixed cryoglobulinemia (type II), who developed a chronic progressive distal motor weakness and sensory disturbances concomitant with a raise in serum aspartate aminotransferase (GOT/AST) and alanine aminotransferase (GPT/ALT) levels. Other laboratory studies were normal except for a decrease in the hemolytic fraction of complement to 75 IU ( n = 400–520). The second case was a 68-year-old woman followed for hepatitis C associated with a mixed cryoglobulinemia (type II), who had sensory disturbances in the lower limbs. Laboratory studies were otherwise unremarkable. Cerebrospinal fluid studies showed a normal protein content without pleocytosis in both patients. In both cases nerve conduction studies were suggestive of a mixed axonal and demyelinating sensorimotor neuropathy. Sural nerve biopsy showed segmental demyelination and severe loss of large myelinated fibers as well as some onion bulb formation in both cases. The two patients subsequently improved, the first with an antiviral treatment and the second with oral steroids. [ABSTRACT FROM AUTHOR]
ISSN:	13515101
DOI:	10.1111/j.1468-1331.2006.01416.x