Abstract
Background: The mechanisms underlying the increased prevalence of arterial calcification in diabetes are not understood. An association with distal neuropathy has been reported and a particularly high prevalence was found in patients with Charcot’s disease.
Aim: The aim of this study was to confirm this high prevalence and to determine whether it is specific to that disorder by comparing the results to patients with other types of foot disease.
Methods: A retrospective survey was conducted in three groups of patients with X-rays managed by a specialist service for the diabetic foot between 2002 and 2005. Group A (n=34) comprised patients with an acute Charcot foot, Group B (n=53) included patients with osteomyelitis and Group C (n=35) consisted of patients who had neither osteomyelitis nor Charcot’s disease. All X-rays were independently examined by three observers blinded to the underlying diagnosis, with films from each group being mixed.
Results: No differences existed (p> 0.05) in the mean age of the patients (60, 72 and 68 years, respectively), the proportion of men (68%, 64% and 51%) and the prevalence of nephropathy (41%, 30% and 14%). 100% patients in Group A, 94% in Group B and 80% of Group C had evidence of neuropathy. The overall prevalence of calcification in the three groups was 53%, 66% and 54% (p> 0.05). With all three groups combined, the only factor associated with calcification was disease duration (p=0.004). The prevalence of calcification was higher than the 40% previously reported in patients with neuropathy, but lower than that reported in patients with Charcot.
Conclusion: As there was no difference in the prevalence of calcification between the three groups, it is concluded that the increase is not specific to Charcot’s disease. It is possible that the increase in calcification in each group reflects the effect of local inflammation, possibly by activation of the RANKL/OPG signalling system.
The abstracts were prepared by Mr Matt Costa and Mr Ben Ollivere. Correspondence should be addressed to Mr Costa at Clinical Sciences Research Institute, University of Warwick, Clifford Bridge Road, Coventry CV2 2DX, UK.
