Eun-Kyoung Park1, Seung-Geun Lee2, Bo-Hyun Kim3, Ji-Heh Park1, Shinwon Lee4, Geun-Tae Kim5. 1. Divsion of Rheumatology, Department of Internal Medicine, Pusan National University School of Medicine, Pusan National University Hospital, Busan, South Korea. 2. Division of Rheumatology, Department of Internal Medicine, Pusan National University School of Medicine, Pusan National University Hospital, Busan, South Korea. sglee@pusan.ac.kr. 3. Divsion of Endocrinology and Metabolism, Department of Internal Medicine, Pusan National University School of Medicine, Pusan National University Hospital, Busan, South Korea. 4. Department of Internal Medicine, Pusan National University School of Medicine, Medical Research Institute, Pusan National University Hospital, Busan, South Korea. 5. Division of Rheumatology, Department of Internal Medicine, Kosin University College of Medicine, Busan, South Korea.
Abstract
OBJECTIVES: To investigate the relationship between insulin resistance and digital ulcers (DUs) in patients with systemic sclerosis (SSc). METHODS: Using a cross-sectional design, we recruited 73 consecutive female patients with SSc and 109 sex- and age-matched healthy controls in South Korea from July 2014 to June 2015. The magnitude of insulin resistance was measured using the homeostatic model assessment of insulin resistance (HOMA-IR). DUs ever included active and healed DUs and the extent of skin fibrosis was evaluated using the modified Rodnan skin score (MRSS). RESULTS: The HOMA-IR in patients with SSc was significantly higher than that in healthy controls (median 1.18 vs. 0.71, p<0.001). In SSc patients, 7 (9.6%) had active DUs and 14 subjects (19.2%) had healed DUs; thus, DUs ever were observed in 21 cases (28.8%). SSc patients with DUs ever had significantly higher HOMA-IR and MRSS compared with those without this feature (median, 2.05 vs. 0.99, p=0.001 and 14 vs. 9.5, p=0.011, respectively). After adjustment for confounding factors using multivariable logistic regression analyses, the HOMA-IR showed a significant positive association with the presence of DUs ever in patients with SSc (OR=1.43, 95% CI=1.01-2.05, p=0.048). In addition, higher MRSS was significantly correlated with DUs ever (OR=1.11, 95% CI=1.02-1.21, p=0.015). CONCLUSIONS: Insulin resistance was independently associated with the presence of DUs in patients with SSc and may be a potential biomarker for SSc micro-vasculopathy. Moreover, our data also suggest a potential contribution of insulin resistance to the pathogenesis of DUs.
OBJECTIVES: To investigate the relationship between insulin resistance and digital ulcers (DUs) in patients with systemic sclerosis (SSc). METHODS: Using a cross-sectional design, we recruited 73 consecutive female patients with SSc and 109 sex- and age-matched healthy controls in South Korea from July 2014 to June 2015. The magnitude of insulin resistance was measured using the homeostatic model assessment of insulin resistance (HOMA-IR). DUs ever included active and healed DUs and the extent of skin fibrosis was evaluated using the modified Rodnan skin score (MRSS). RESULTS: The HOMA-IR in patients with SSc was significantly higher than that in healthy controls (median 1.18 vs. 0.71, p<0.001). In SSc patients, 7 (9.6%) had active DUs and 14 subjects (19.2%) had healed DUs; thus, DUs ever were observed in 21 cases (28.8%). SSc patients with DUs ever had significantly higher HOMA-IR and MRSS compared with those without this feature (median, 2.05 vs. 0.99, p=0.001 and 14 vs. 9.5, p=0.011, respectively). After adjustment for confounding factors using multivariable logistic regression analyses, the HOMA-IR showed a significant positive association with the presence of DUs ever in patients with SSc (OR=1.43, 95% CI=1.01-2.05, p=0.048). In addition, higher MRSS was significantly correlated with DUs ever (OR=1.11, 95% CI=1.02-1.21, p=0.015). CONCLUSIONS:Insulin resistance was independently associated with the presence of DUs in patients with SSc and may be a potential biomarker for SSc micro-vasculopathy. Moreover, our data also suggest a potential contribution of insulin resistance to the pathogenesis of DUs.