Background It is reported that subclinic intestinal inflammation may occur in Ankylosing spondylitis (AS) patients, besides, using NSAIDs cause peptic and duedenal ulcers. %50–60 of AS patients have asymptomatic ileal and colonic mucosal inflammation. It is reported that inflammatory bowel disease (IBD) is found in 5–10% of AS patients and 4–10% of IBD patients have concomittant findings with AS. These conditions may cause iron deficiency anemia (IDA).
Objectives It is well known that chronic disease anemia is a frequent finding in AS patients. But there is no study in the literature about relationship between AS patients and IDA. In this particular study we aimed to asses frequency of IDA in AS patients and to investigate the etiologies of IDA.
Methods Ninety four consecutive AS patients who meet 2012 ASAS/EULAR criteria, who were followed Çukurova University Romatology Clinic, were icluded. We investigated the etiologies of IDA in anemic patients. Twenty six AS patients were diagnosed as IDA. Twenty six patients without anemia were assigned as a control group. Hepcidin, soluble transferrin receptor1 (sTfR1) and anemia parameters were tested in both groups. Findings were anayzed with SPSS version 23.
Results Twenty six of 94 AS patients were diagnosed as IDA (%27). Frequency of IDA in our AS patients was higher when compared to the IDA prevalence in the society (%1–2). Endoscopy and colonoscopy were performed for searching etiology of IDA. Mucosal inflammation was found in 62% of patients by endoscopy and 11% of patients by colonoscopy. One patient was diagnosed as Crohn's disease and one patient was diagnosed as Coeliac disease histopathologically. Hepcidin was found to be significantly lower in IDA patients (p<0.01). We found sTfR1 levels significantly higher in IDA patients (p<0,01). BASDAI (Bath Ankylosing Spondylitis Disease Activity Index) and sedimentation values were found to be higher in IDA patients statistically (p<0.01and p=0.01 respectively). Although we found C- reactive protein (CRP) values were higher when compared to the non- anemic patients; however it was not statistically significant (p>0.05).
Conclusions We found higher frequency of IDA when compared to the normal population. We found that AS was more active in patients who were diagnosed as IDA. We suggest that AS activitiy may cause mucosal inflammation and subsequently may result as IDA. Also we found that mucosal inflammation in AS patients is not related to NSAIDs because there was no difference about mucosal lesions between NSAID taking and non-NSAID taking group. No study was met in the literature concerning AS and IDA. Our findings should be supported by further studies.
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Disclosure of Interest None declared