MEDIAL ARTERIAL CALCIFICATION IN THE FEET OF DIABETIC-PATIENTS AND MATCHED NONDIABETIC CONTROL SUBJECTS

The prevalence and distribution of medial arterial calcification was a ssessed in the feet of four subject groups: 54 neuropathic diabetic pa tients with previous foot ulceration (U), median age 60.5 (50.5-67 int erquartile range) years, duration of diabetes 19.5 (9.9-29.9) years; 4 0 neuropathic diabetic patients without a foot ulcer history (N), age 68 (62-73) years, duration of diabetes 14.0 (8.0-28.0) years; 43 non-n europathic diabetic patients (NN), age 60.5 (52-68.5) years, duration of diabetes 14.0 (8.0-28.0) years and 50 non-diabetic control subjects , age 62.5 (53.7-70) years. A single radiologist graded medial arteria l calcification as absent, mild or severe, at the ankle, hind-foot, mi d-foot, metatarsals and toes on standardised plain lateral and antero- posterior foot radiographs taken by a single radiographer. Diabetes hi story, vibration perception threshold, ankle systolic pressure and ser um creatinine were also assessed. Medial arterial calcification was si gnificantly greater (total score 18 [3-31]) in neuropathic diabetic pa tients with previous ulceration (U vs N p < 0.01, U vs NN p < 0.001). Non-neuropathic diabetic patients did not have significantly higher ar terial calcification scores than age-matched non-diabetic control subj ects. Medial arterial calcification correlated with vibration percepti on threshold (r = 0.35), duration of diabetes (r = 0.32) and serum cre atinine (r = 0.41), (all p < 0.01). Logistic regression models showed vibration perception and duration of diabetes to predict the probabili ty of any calcification. Serum creatinine level was added to predict s evere calcification. Ordered categorical modelling confirmed that medi al arterial calcification was significantly heavier at the ankle than the toes for all groups, odds ratio 4.35 (2.94-6.43, 95 % confidence i ntervals), (p < 0.01). Ankle systolic pressure and ankle-brachial pres sure index were significantly associated with degree of arterial calci fication, r = 0.40 and r = 0.35, respectively, (both p < 0.01) in diab etic patients. However, arterial calcification was present in more tha n one-third of patients with an ankle-brachial pressure index of less than 1.0. In conclusion, although ankle pressures correlate with the d egree of arterial calcification, medial arterial calcification may be present in patients with low ankle systolic pressures, which may be fa lsely elevated even at 'normal' values. This finding may provide a rat ionale for the use of toe rather than ankle pressure measurements in d iabetic patients, particularly those with peripheral neuropathy, and t his hypothesis should be directly tested in future studies.