Comparing of Faecal Calprotectin Levels in Patients With Osteoarthritis Taking Nsaid Treatment and Patients Without Nsaids Therapy

Abstract

Faecal calprotectin (FC) level can be increased in several conditions, which are characterised by neutrophilic inflammation. Some medications, particularly NSAIDs, can elevate its level as well. NSAIDs are taken by patients in many chronic conditions, including osteoarthritis (OA). On the other hand, there is growing evidence that osteoarthritis is not only a degenerative disease, but it has a significant inflammatory component. The role of systemic inflammation is well-known in inflammatory joint diseases, but there is some evidence that it can play an essential role in the OA as well. It can suggest that in the OA, the inflammatory changes could be found in the different organs and systems. The aim of this study was to investigate the FC level in patients with osteoarthritis depending on the NSAIDs intake and to compare it to the FC levels in healthy adults. Materials and methods. In this small observational study, we evaluated the FC levels in patients suffering from OA (36 persons), divided them into two groups depending on their NSAIDs intake, and compared it to FC levels in healthy participants (12 persons). We compared the FC levels depending on the selectivity of the NSAIDs taken by our participants, as well. Results. The median calprotectin level in our patients was 72.57 (IQR 20.55-221.57) mg/kg, 95 %CI 26,18-109.01. OA patients had higher levels than the healthy group (p<0.001). OA patients who took NSAIDs had the highest FC levels – 221.57 (IQR 91.56-448.61) – higher, than those who did not take it – 72.57 (IQR 35.26-164.79) (p=0.03) and than healthy participants, who has normal FC levels (p<0.001); the FC levels of patients who did not take NSAIDs also exceeds healthy subject’s levels (p<0.001). The FC levels in the collective group have a sufficient positive correlation with the duration of NSAIDs intake, VAS score and strong correlation with Lequesne index values. We found that both NSAIDs groups have a significantly greater prevalence of elevated or high FC levels than the control group (p<0.001) and that NSAIDs patients significantly more often have high FC levels than those who do not take NSAIDs (p=0.035). When comparing FC levels in patients depending on the type of NSAIDs they take, we found that those who take non-selective NSAIDs has significantly higher FC levels than those who do not take NSAIDs – 264.1 (IQR 89.72-464.67) to 25.65 (IQR 19.5-75.33) (p=0.0003). The FC levels of who take selective NSAIDs – 98.53 (91.56-105.5) – did not differ significantly to non-selective NSAIDs taker’s group values and non-selective NSAIDs taker’s values (p>0.05). Conclusions. Patients who suffer from OA have higher FC levels than healthy individuals, and patients with OA who take NSAIDs regularly have higher FC levels than those who do not. The intake of non-selective NSAIDs is associated with higher FC levels, than the intake of high-selective NSAIDs. FC levels of those who take high-selective NSAIDs do not differ statistically from those who do not intake NSAIDs. Further research is needed in this area.