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The aims of this study were to assess adherence to oral hypoglycaemic/cardiovascular drugs and determine non-adherence predictors in type 2 diabetes patients. It was designed as a population-based cross-sectional study in which 90 patients from a primary care setting were studied. Pill count and self-report methods were used to measure adherence. Logistic regression analysis was performed to predict factors related to non-adherence. Adequate adherence to all drugs was found in 29 patients (35.4%; 95% confidence interval (CI) 25.0-45.7). Variables associated with non-adherence were HbA1c odds ratio (OR) 2.32 (95% CI: 1.09-4.95), systolic blood pressure OR 1.68 (95% CI: 1.08-2.62), total cholesterol OR 1.34 (95% CI: 1.08-1.66), number of pills OR 1.80 (95% CI: 1.26-2.55) and duration of disease OR 0.44 (CI 95%: 0.24-0.83). In conclusion, one in three patients had adequate adherence. Factors associated with non-adherence were duration of disease, complexity of drug regimen and inadequate control of cardiovascular risk factors.

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Pancreastatin is a regulatory peptide known to inhibit insulin secretion and insulin action with a glycogenolytic effect in the liver. This peptide is present in and secreted by many endocrine and chromaffin cells. Abnormalities of glucose, insulin and lipoprotein metabolism are common in patients with hypertension, as well as their first-degree relatives. We have recently studied a group of non-obese hypertensive subjects in which pancreastatin-like levels were increased compared with controls, and correlated with norepinephrine levels. We hypothesized that pancreastatin alongside the sympathoadrenal system might have a part in the insulin resistance of these patients, and this metabolic syndrome could play a role in the pathogenesis and complications of hypertension. In this article, we studied the normotensive offspring of these nonobese hypertensive patients and looked for metabolic abnormalities as well as plasma pancreastatin, glucagon and catecholamine levels. The subjects were separated into two groups: (1) offspring from non-insulin-resistant patients and (2) offspring from insulin-resistant patients. We found that after an intravenous glucose load, offspring from insulin-resistant patients were already hyperinsulinemic, although glucose clearance was normal, suggesting an early alteration in insulin sensitivity, whereas pancreastatin and catecholamine levels were normal compared with matched controls. However, offspring from non-insulin-resistant patients had no differences with controls. These results suggest that pancreastatin and catecholamines may not play an important role in triggering insulin resistance, although they may be important once the syndrome is established.

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