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Inflammatory and bone turnover markers in a cross‐sectional and prospective study of acute Charcot osteoarthropathy
Author(s) -
Petrova N. L.,
Dew T. K.,
Musto R. L.,
Sherwood R. A.,
Bates M.,
Moniz C. F.,
Edmonds M. E.
Publication year - 2015
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/dme.12590
Subject(s) - medicine , osteoprotegerin , n terminal telopeptide , bone remodeling , endocrinology , spinal osteoarthropathy , alkaline phosphatase , diabetes mellitus , gastroenterology , receptor , surgery , activator (genetics) , osteocalcin , biochemistry , chemistry , enzyme
Aims To assess markers of inflammation and bone turnover at presentation and at resolution of Charcot osteoarthropathy. Methods We measured serum inflammatory and bone turnover markers in a cross‐sectional study of 35 people with Charcot osteoarthropathy, together with 34 people with diabetes and 12 people without diabetes. In addition, a prospective study of the subjects with Charcot osteoarthropathy was conducted until clinical resolution. Results At presentation, C‐reactive protein ( P = 0.007), tumour necrosis factor‐α ( P = 0.010) and interleukin‐6 ( P = 0.002), but not interleukin‐1β, ( P = 0.254) were significantly higher in people with Charcot osteoarthropathy than in people with and without diabetes. Serum C‐terminal telopeptide ( P = 0.004), bone alkaline phosphatase ( P = 0.006) and osteoprotegerin ( P < 0.001), but not tartrate‐resistant acid phosphatase ( P = 0.126) and soluble receptor activator of nuclear factor‐κβ ligand ( P = 0.915), were significantly higher in people with Charcot osteoarthropathy than in people with and without diabetes. At follow‐up it was found that tumour necrosis factor‐α ( P = 0.012) and interleukin‐6 ( P = 0.003), but not C‐reactive protein ( P = 0.101), interleukin‐1β ( P = 0.457), C‐terminal telopeptide ( P = 0.743), bone alkaline phosphatase ( P = 0.193), tartrate‐resistant acid phosphatase ( P = 0.856), osteoprotegerin ( P = 0.372) or soluble receptor activator of nuclear factor‐kβ ligand ( P = 0.889), had significantly decreased between presentation and the 3 months of casting therapy time point, and all analytes remained unchanged from 3 months of casting therapy until resolution. In people with Charcot osteoarthropathy, there was a positive correlation between interleukin‐6 and C‐terminal telopeptide ( P = 0.028) and tumour necrosis factor‐α and C‐terminal telopeptide ( P = 0.013) only at presentation. Conclusions At the onset of acute Charcot foot, serum concentrations of tumour necrosis factor‐α and interleukin‐6 were elevated; however, there was a significant reduction in these markers at resolution and these markers may be useful in the assessment of disease activity.