title: Cyclosporine A: good response for patients affected by autoimmune disorders and HCV infection?
abstract: BACKGROUND
  In autoimmune disorders (ADs), if Hepatitis C Virus (HCV) is present, immunosuppressive treatment could increase virus replication. Cyclosporine A (CsA), in standard therapeutic doses, has been proven able to inhibit HCV cyclophilin in vitro. Therefore CsA could improve the therapy of HCV patients with ADs.
  
  
  OBJECTIVE
  In these patients, we started an open pilot study to evaluate the safety of 3 mg/kg CsA and the ability to reduce steroid therapy.
  
  
  METHODS
  Five females and 1 male were recruited; mean age 66 +/- 8 years, mean disease duration 13 +/- 5 years. Three patients are affected by Psoriasic Arthritis, 1 by Rheumatoid Arthritis, 1 by Sjogren Syndrome, and 1 by Myasthenia Gravis. None of them had chronic active hepatitis. HCV genotypes were type 2 (in 3 cases) and type 1 (in 3 cases). Patients were treated with 3 mg/kg of CsA for a period of time ranging from 6 to 12 months. The starting mean dose of prednisone was 12.5 mg/day. Liver function tests were checked monthly and serum HCV-RNA load was checked by RT-PCR before and 2 months into the therapy.
  
  
  RESULTS
  The prednisone dose was reduced from 12.5 mg/day to 7.5 mg/day. The aminotransferases levels were unchanged after 6 months. In patients with low HCV-RNA levels before treatment, no modifications of viral load were observed, whereas patients with increased levels at onset showed mild reduction 2 months into the treatment.
  
  
  CONCLUSIONS
  Immunosuppressive treatment of ADs patients with HCV infection can be safely provided with the integration of CsA.
authors.affiliation: Department of Internal Medicine, Catholic University of the Sacred Heart, Rome, Italy. rmanna@rm.unicatt.it
authors.forename: R
authors.initials: R
authors.lastname: Manna
authors.forename: E
authors.initials: E
authors.lastname: Verrecchia
authors.forename: C
authors.initials: C
authors.lastname: Fonnesu
authors.forename: M
authors.initials: M
authors.lastname: Giovinale
authors.forename: G
authors.initials: G
authors.lastname: De Socio
authors.forename: V
authors.initials: V
authors.lastname: Curigliano
authors.forename: C
authors.initials: C
authors.lastname: Cerquaglia
authors.forename: A
authors.initials: A
authors.lastname: Soriano
authors.forename: M
authors.initials: M
authors.lastname: Granata
authors.forename: A
authors.initials: A
authors.lastname: Migliore
authors.forename: U
authors.initials: U
authors.lastname: Massafra
authors.forename: G
authors.initials: G
authors.lastname: Gasbarrini
mesh_terms: D000368:Aged; D001327:Autoimmune Diseases / Q000150:complications* / Q000188:drug therapy*; D016572:Cyclosporine / Q000008:administration & dosage* / Q000009:adverse effects* / Q000494:pharmacology; D004359:Drug Therapy, Combination; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000187:drug effects* / Q000235:genetics; D006526:Hepatitis C / Q000150:complications* / Q000188:drug therapy*; D006801:Humans; D007166:Immunosuppressive Agents / Q000008:administration & dosage* / Q000009:adverse effects / Q000494:pharmacology; D008297:Male; D010865:Pilot Projects; D011241:Prednisone / Q000008:administration & dosage*; D012333:RNA, Messenger / Q000097:blood; D012367:RNA, Viral / Q000097:blood; D019562:Viral Load
chemical_list: D007166:Immunosuppressive Agents; D012333:RNA, Messenger; D012367:RNA, Viral; D016572:Cyclosporine; D011241:Prednisone