Publications by authors named "T Androutsakos"
Introduction: Hepatitis B reactivation and administration of prophylactic antiviral treatment are considered in patients with autoimmune inflammatory rheumatic diseases (AIIRD) undergoing immunosuppressive/immunomodulatory treatment. Data are more robust for rheumatoid arthritis patients receiving bDMARDs but are limited for other AIIRD and drug categories.
Methods: Adult patients with AIIRD (inflammatory arthritis [IA] or connective tissue diseases [CTD]) and documented chronic or resolved HBV infection (defined as serum HBsAg positivity or anti-HBcAb positivity in the case of HBsAg non-detection respectively), followed-up in six rheumatology centers in Greece and Italy, were included.
Background And Aims: A limited number of drugs are used as standard or alternative therapies in autoimmune hepatitis (AIH). No specific recommendations are available for patients failing to respond to these therapies. We analyzed the efficacy and safety of infliximab in patients with AIH.
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- The study investigates the risk of hepatitis B reactivation (HBVr) in patients with autoimmune rheumatic diseases treated with targeted synthetic drugs and anti-interleukin agents, focusing on those with chronic or resolved HBV infections.
- A systematic literature review and meta-analysis found an overall low HBVr risk of less than 6%, but the risk was notably higher (14.4%) for patients with chronic HBV compared to those with resolved infections (5.1%).
- The findings indicate that patients with chronic HBV not receiving antiviral treatment are at the highest risk of HBVr (28%), while those with resolved HBV face a significantly lower risk (4.7%).
Background: Anti-leucine-rich glioma inactivated 1 limbic encephalitis (anti-LGI1 LE) is one of the most frequent autoimmune encephalitis, commonly coexisting with other autoimmune diseases. Rheumatoid arthritis (RA) and monoclonal gammopathy of unknown significance (MGUS) are commonly associated with autoimmune phenomena. However, neither RA nor MGUS have been described in the literature to date as coexisting with anti-LGI1 LE.
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