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data from Colombia and Mexico) was increased compared to the general population resulting in a standardized risk ratio (SRR) of 1.5 (95% CI 1.0 to 2.1). Many studies have reported a higher prevalence of AHT in AS 8, 9, which may reflect the detrimental effects that chronic inflammation
may have on endothelial function and acceleration of atherosclerosis. The common use of NSAIDS in this cohort of patients may also play a role, even though NSAID-use was associated with less mortality in a study by Bakland et al 10. In addition, the prevalence of tuberculosis (TB) was importantly higher than expected from the general population in LA, resulting in an SRR of 10.3
(95% CI 6.1 to 17.8). Uncontrolled and chronic inflammation may predispose to TB, in addition to the risk that patients receiving immunosuppressive treatments such as corticosteroids 11 and TNF- inhibitors already have 12. The prevalence and risk of malignancies in comparison to the general
population was not significantly increased. Although these findings could not be extrapolated to the whole region (patients came from the three Latin American countries that participated in the ASAS-COMOSPA study), this is one of the first efforts to evaluate comorbidities associated to SpA in Latin America. Our findings described in chapter 4 may have implications for daily clinical practice with regard to rheumatologist’s health assessments, prevention and treatment planning.
While clinical studies have pointed towards a relationship between chronic periodontitis and
rheumatoid arthritis 13, it was unclear if SpA patients have a higher frequency of periodontitis. A case-control study evaluating the clinical, serological and microbiological periodontal condition in a group of patients with SpA is described in chapter 5. We did not find a positive association between SpA and periodontitis and we found even a lower prevalence of periodontitis and less severe periodontitis in comparison to matched-healthy controls. The explanation of these findings is unclear, however, from a physiopathological point of view, it is obvious that the citrullination 14 of proteins is a biochemical process that likely is not relevant in the pathogenesis of SpA.
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