ObjectivesPossible association between diabetes mellitus (DM) and Alzheimer’s disease (AD) has been controversial. This study used a nationwide population-based dataset to investigate the relationship between DM and subsequent AD incidence.MethodsData were collected from Taiwan’s National Health Insurance Research Database, which released a cohort dataset of 1,000,000 randomly sampled people and confirmed it to be representative of the Taiwanese population. We identified 71,433 patients newly diagnosed with diabetes (age 58.74±14.02 years) since January 1997. Using propensity score, we matched them with 71,311 non-diabetic subjects by time of enrollment, age, gender, hypertension, hyperlipidemia, and previous stroke history. All the patients were followed up to December 31, 2007. The endpoint of the study was occurrence of AD.ResultsOver a maximum 11 years of follow-up, diabetic patients experienced a higher incidence of AD than non-diabetic subjects (0.48% vs. 0.37%, p<0.001). After Cox proportional hazard regression model analysis, DM (hazard ratio [HR], 1.76; 95% confidence interval [CI], 1.50–2.07, p<0.001), age (HR, 1.11; 95% CI, 1.10–1.12, p<0.001), female gender (HR, 1.24; 95% CI, 1.06–1.46, p = 0.008), hypertension (HR, 1.30; 95% CI, 1.07–1.59, p = 0.01), previous stroke history (HR, 1.79; 95% CI, 1.28–2.50, p<0.001), and urbanization status (metropolis, HR, 1.32; 95% CI, 1.07–1.63, p = 0.009) were independently associated with the increased risk of AD. Neither monotherapy nor combination therapy with oral antidiabetic medications were associated with the risk of AD after adjusting for underlying risk factors and the duration of DM since diagnosis. However, combination therapy with insulin was found to be associated with greater risk of AD (HR, 2.17; 95% CI, 1.04–4.52, p = 0.039).ConclusionNewly diagnosed DM was associated with increased risk of AD. Use of hypoglycemic agents did not ameliorate the risk.

Objective Although the major cause of morbidity and mortality in patients with diabetes mellitus (DM) is cardiovascular disease, DM is also associated with certain site-specific cancers. However, whether DM is associated with an increased risk of cancer of the digestive tract remains undetermined. A nationwide, population-based database in Taiwan was analyzed to explore the relationship between DM and cancer of the digestive organs. Methods From 2000 to 2007, a study cohort consisting of 39,515 patients with newly diagnosed diabetes without a previous diagnosis of gastrointestinal (GI) cancer was identified from the National Health Insurance Research Database in Taiwan. A control cohort of 79,030 age-and sex-matched non-diabetic subjects was selected to compare the occurrence of GI malignancies between the two groups. The association between the incidence of GI cancers and the use of glucose-lowering therapies was also investigated. Results During the 7-year follow-up period, GI cancers developed in 929 diabetic patients (2.35%) and 1,126 subjects (1.42%) in the comparison cohort. DM was associated with a 2.75-fold (95% confidence interval (CI), 2.51-3.02) higher risk of developing GI malignancy. Among GI cancers, the incidences of stomach (adjusted hazard ratio (HR), 1.49; 95% CI, 1.16-1.92), liver (adjusted HR, 2.65; 95% CI, 2.29-3.07), colon (adjusted HR, 1.58; 95% CI, 1.28-1.94) and pancreatic cancers (adjusted HR, 4.35; 95% CI, 2.93-6.47) were significantly increased in the patients with DM. An analysis of the effects of various glucose-lowering therapies in the diabetic patients revealed the use of α-glucosidase inhibitors to be associated with a lower risk of hepatic cancer (adjusted HR, 0.62; 95% CI, 0.4-0.94). Thiazolidinedione (TZD) treatment was associated with lower stomach (adjusted HR, 0.11; 95% CI, 0.02-0.82) and hepatic cancer risks (adjusted HR, 0.46; 95% CI, 0.29-0.73), while sulfonylurea use was associated with a lower colon cancer risk (adjusted HR, 0.74; 95% CI, 0.51-1.09) and a higher pancreatic cancer risk (adjusted HR, 2.36; 95% CI, 1.21-4.61). Conclusion Patients with DM have an increased risk of GI malignancy that may be affected by the use of different categories of glucose-lowering therapies.

Patients with SLE have an increased risk of stroke.

Although the association of hyperuricemia and cardiovascular diseases is well established by previous research studies, the relationship between gout and deep vein thrombosis (DVT) remains unclear. We conducted a nationwide longitudinal cohort study to investigate the relationship between gout and DVT. We used the Taiwan National Health Insurance Research Database to identify patients with gout diagnosed in Taiwan during 2000–2011, and we followed up these patients to determine the incidence of DVT among them. The association between gout and DVT was analyzed by cox proportional hazard model. The study cohort included 35,959 patients with history of gout attack and 35,959 matched controls without gout attack. During the median follow-up of 7.5 ± 3.6 years, the incidence rate of DVT was significantly higher in patients with gout than that in control group (13.48 versus 9.77 per 104 person-years, p < 0.001). Kaplan-Meier analysis revealed a tendency toward DVT development in gout patients (log rank test, p < 0.001). In a Cox model, patients with gout were found to have a 1.38-fold (95% confidence interval [CI], 1.18 to 1.62, p < 0.001) higher risk of developing DVT. Hyperuricemia with gout attack could be a possible risk predictor for DVT, but these findings need to be confirmed in future clinical and experimental studies.

Thiazide diuretics are associated with an increased risk of hyponatremia. The aim of this study was to investigate possible predictors of thiazide-induced hyponatremia.A total of 48 patients admitted to the ward or to the emergency department due to severe thiazide-induced hyponatremia (Na < 125 mmol/L) were enrolled in our study as the case group. Another 211 hypertensive patients with normal sodium levels after treatment with thiazide diuretics were selected as the control group. Twelve tag single nucleotide polymorphism markers were selected from the Potassium Channel, Inwardly Rectifying Subfamily J, Member 1 (KCNJ1) gene: rs1231254, rs2238009, rs1148058, rs675482, rs673614, rs12795437, rs2855800, rs2509585, rs3016774, rs881333, rs4529890, and rs7116606. Clinical and genetic parameters between patients with thiazide-induced hyponatremia and the control group were compared. Logistic regression was used to analyze data.The patients with thiazide-induced hyponatremia were older (P < 0.001), predominantly female (P = 0.008), had a lower mean body mass index (BMI) (P < 0.001), and more commonly used angiotensin II receptor antagonist (P < 0.001) and spironolactone (P = 0.007) compared with the control groups. Analysis with multivariate logistic regression revealed that age (odds ratio [OR], 1.13; 95% confidence interval [CI], 1.08–1.19, P < 0.001), female gender (OR, 4.49; 95% CI, 1.54–13.11, P = 0.006), BMI (OR, 0.80; 95% CI, 0.69–0.93, P = 0.003), and KCNJ1 rs2509585 C/T or T/T polymorphisms (OR, 5.75; 95% CI, 1.25–26.45, P = 0.03) were independent predictors for thiazide-induced hyponatremia.Older female patients with lower BMIs and KCNJ1 rs2509585 C/T or T/T polymorphisms were more likely to develop thiazide-induced hyponatremia.