Reply to the letter to the editor ‘Androgen deprivation therapy and risk of rheumatoid arthritis in patients with localized prostate cancer’ by Yang et al. We read with great interest the article by Yang et al. [1] first reporting the association between androgen deprivation therapy (ADT), especially for long-term treatment, and the development of rheumatoid arthritis (RA). Interestingly, considering that autoimmunity is more frequent in female sex, this study addressed the possible immunosuppressive action of testosterone, likely responsible of ADT-related autoimmune diseases due to thymic regeneration with an increase of T cells [2]. RA is a chronic autoimmune-inflammatory disease that primarily affects the joints. It is characterized by a complex etiopathogenesis involving autoantibodies against modified self-proteins, stromal and immune cells, circulating pro-inflammatory cytokines/chemokines, and multiple genetic and no-genetic risk factors. Among mechanisms that might contribute to RA development, abnormalities in TP53 and PTEN genes have been demonstrated. Particularly,

REPLY TO THE LETTER TO THE EDITOR "ANDROGEN DEPRIVATION THERAPY AND RISK OF RHEUMATOID ARTHRITIS IN PATIENTS WITH LOCALIZED PROSTATE CANCER" by YANG et al.

Conteduca V
;
Lauletta G
2018-01-01

Abstract

Reply to the letter to the editor ‘Androgen deprivation therapy and risk of rheumatoid arthritis in patients with localized prostate cancer’ by Yang et al. We read with great interest the article by Yang et al. [1] first reporting the association between androgen deprivation therapy (ADT), especially for long-term treatment, and the development of rheumatoid arthritis (RA). Interestingly, considering that autoimmunity is more frequent in female sex, this study addressed the possible immunosuppressive action of testosterone, likely responsible of ADT-related autoimmune diseases due to thymic regeneration with an increase of T cells [2]. RA is a chronic autoimmune-inflammatory disease that primarily affects the joints. It is characterized by a complex etiopathogenesis involving autoantibodies against modified self-proteins, stromal and immune cells, circulating pro-inflammatory cytokines/chemokines, and multiple genetic and no-genetic risk factors. Among mechanisms that might contribute to RA development, abnormalities in TP53 and PTEN genes have been demonstrated. Particularly,
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11586/225142
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