Neurological complications of hepatitis C infection.

Though well-known as a cause of liver disease, Hepatitis C virus infection is emerging as a cause of a variety of peripheral and central nervous system disorders. The virus causes chronic persistent infection with complex immune responses in the majority of individuals. Viral infection may have the potential to generate neurological illness through direct infection of neural cells or through immune-mediated mechanisms, including enhancement of autoimmune responses. Moreover, the mainstay of antiviral treatment of hepatitis C infection, interferon-alpha, is itself associated with neurological morbidity. Thus neurologists are increasingly faced with diagnosing or even predicting a wide spectrum of neurological complications of hepatitis C infection and/or its treatment.

Focal segmental glomerulosclerosis secondary to subcutaneous interferon ß-1a treatment in a patient with multiple sclerosis.

Interferon (IFN)-ß is a first line treatment for patients with relapsing remitting multiple sclerosis (RRMS) that has been shown to decrease relapse rates, reduce magnetic resonance imaging (MRI) disease burden and possibly delay onset of disability (Arnason, 2005). There are few reports of nephrotic syndrome related to Minimal Change Disease (MCD) or Focal Segmental Glomerulosclerosis (FSGS) during treatment with IFN-α (Nishimura et al., 2002; Tola et al., 2003; Rettmar et al., 1995). There are fewer reports of nephrotic syndrome induced by IFN-ß (Tola et al., 2003; Auty and Saleh, 2005; Kumasaka et al., 2006). We report a 41 year old African American woman with RRMS that developed FSGS after 3 months of treatment with IFN-ß-1a 3 times weekly and review the previously published cases.