Detecção de anticorpos anti-rods and rings (anti-RR) em portadores de Hepatite C crônica submetidos a tratamento

• Ano de defesa: 2017
• Autor(a) principal: Nunes, Eunice Jadriana Soares [UNIFESP]
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• dARK ID: ark:/48912/001300001jdxk
• Idioma: por
• Instituição de defesa: Universidade Federal de São Paulo (UNIFESP)
• Palavras-chave em Português: Hepatitis C; Autoimmunity in hepatitis C; Autoantibodies; Ribavirin; Anti-rods and rings; Hepatite C; Ribavirina; Anti-anéis e bastões; Autoimunidade em hepatite C; Autoanticorpos
• Link de acesso: https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=5359326; http://repositorio.unifesp.br/handle/11600/50084

Background: Patients with chronic hepatitis C often have serum autoantibodies. In 2015, the international consensus for autoantibody research recognized a new pattern of autoantibodies against HEp-2 cells antigens found mostly in patients treated for hepatitis C, which shows rods and rings (RR) structures. The main antigenic target is the enzyme inosine monophosphate dehydrogenase (IMPDH), involved in the synthesis of new guanosine nucleotides that can aggregate in the presence of inhibitory drugs. The objective of this study was to evaluate the occurrence of anti-RR antibodies in patients submitted to one or two treatments with interferon (IFN) and/or ribavirin (RBV) and to correlate positive results to epidemiological, clinical, virological, histological and therapeutic features. Casuistic and Method: Patients with chronic hepatitis C followed at the Hepatitis Division of the Gastroenterology Discipline at UNIFESP were enrolled. Data were retrospectively collected from medical records. Anti-RR was determined by immunofluorescence technique in HEp-2 cells. Results: Of the 112 patients included, none had anti-RR reactivity before first treatment. At the end of the first treatment, anti-RR reactivity was found in 28.5% of the patients (n = 32/112) and all had received double therapy with IFN+RBV (p = 0.003). Due to therapeutic failure, 63 patients underwent a second treatment, of which 12 (19%) already had anti-RR reactivity. From 51 patients who entered the second treatment without anti-RR reactivity, 30/51 (58.8%) developed anti-RR positivity. Positivity increased significantly from the first to the second treatment (p <0.001). By comparing the groups with and without anti-RR reactivity, a higher frequency of anti-RR was observed in the patients who used a full dose of ribavirin (p < 0.001). On the other hand, anti- RR was less frequent in patients with parenteral transmission (p = 0.007) and comorbidities (hemodialysis, renal transplantation and HIV coinfection; p = 0.005). Conclusion: Anti-RR reactivity is induced by dual treatment (interferon + ribavirin) and positivity increases with successive treatments and higher exposure to ribavirin. The absence of a relationship with clinical, virological, histological and response to therapy characteristics suggests that, like other autoantibodies, it is an epiphenomenon associated with the treatment