Presence of tophi is a predictive factor of arterial stiffness in patients with gout.

The objective of this study is to determine whether the presence of tophi could predict an increase in arterial stiffness. Between June 2017 and June 2018, the augmentation index (AI) was measured using SphygmoCor® for patients with gout who visited the Jeju National University Hospital in South Korea. Patients were divided into the following groups: group with tophi and group without tophi. Medical records, laboratory data, and AI were retrospectively analyzed. One hundred and twenty patients with gout or participated in the study, with most (96.7%) of the patients being male. The mean duration of the disease was 7.0 years. At the time of the examination, 99 patients (82.5%) were treated with a uric acid-lowering agent. Of the total patients, 24 (19.7%) had tophi. Patients with tophi were significantly older (60.2 ± 11.6 years vs. 53.8 ± 13.0 years, p = 0.031), had longer disease duration (13.0 ± 6.5 years vs 5.5 ± 5.4 years, p < 0.001), and higher AI@75 (28.7 ± 7.8 vs 20.9 ± 10.0, p = 0.001) than those without tophi. In the multiple linear regression analysis, tophi was shown to be a significant predictor of high AI (p = 0.040). The presence of tophi is a predictor of increased arterial stiffness in patients with gout. Therefore, more strict control of cardiovascular disease risk factors is needed in the treatment of patients with tophi.

Changes in Adenosine Deaminase Activity in Patients with Type 2 Diabetes Mellitus and Effect of DPP-4 Inhibitor Treatment on ADA Activity.

BACKGROUND: Dipeptidyl peptidase 4 (DPP-4, also known as CD26) binds with adenosine deaminase (ADA) to activate T lymphocytes. Here, we investigated whether ADA activity is specifically affected by treatment with DPP-4 inhibitor (DPP4I) compared with other anti-diabetic agents. METHODS: Fasting ADA activity, in addition to various metabolic and biochemical parameters, were measured in 262 type 2 diabetes mellitus (T2DM) patients taking various anti-diabetic agents and in 46 non-diabetic control subjects. RESULTS: ADA activity was increased in T2DM patients compared with that in non-diabetic control subjects (mean±standard error, 23.1±0.6 U/L vs. 18.6±0.8 U/L; P<0.05). ADA activity was correlated with fasting plasma glucose (r=0.258, P<0.05), HbA1c (r=0.208, P<0.05), aspartate aminotransferase (r=0.325, P<0.05), and alanine aminotransferase (r=0.248, P<0.05). Compared with the well-controlled T2DM patients (HbA1c<7%), the poorly controlled group (HbA1c>9%) showed significantly increased ADA activity (21.1±0.8 U/L vs. 25.4±1.6 U/L; P<0.05). The effect of DPP4I on ADA activity in T2DM patients did not differ from those of other oral anti-diabetic agents or insulin. T2DM patients on metformin monotherapy showed a lower ADA activity (20.9±1.0 U/L vs. 28.1±2.8 U/L; P<0.05) compared with that of those on sulfonylurea monotherapy. CONCLUSION: Our results show that ADA activity is increased in T2DM patients compared to that in non-diabetic patients, is positively correlated with blood glucose level, and that DPP4I has no additional specific effect on ADA activity, except for a glycemic control- or HbA1c-dependent effect.