Suboptimal use of gastroprotective medication in elderly antiplatelet users.

BACKGROUND: Use of acetylsalicylic acid (ASA) or thienopyridines in monotherapy or combination of both drugs is associated with increased risk of gastrointestinal (GI) bleeding. The administration of drugs inhibiting gastric acid production represents an effective way to avoid GI disorders associated with antiplatelet therapy. OBJECTIVES: The aim of our study was to evaluate the use of gastroprotective medication in elderly antiplatelet users in relation to risk factors for GI bleeding. METHODS: Patients (n = 428) aged ≥ 65 years who were prescribed low dose ASA or clopidogrel in monotherapy or combination at hospital discharge were enrolled in the study. RESULTS: Only 39.7 % of patients with 2 or more risk factors for GI bleeding were prescribed gastroprotective medication at hospital discharge. The probability of elderly antiplatelet drug user for prescription of gastroprotective medication was improved with following risk factors: age ≥ 85 years (OR = 2.99); history of peptic ulcer disease/ GI bleeding (OR = 15.79); other GI disorders (OR = 15.48); concomitant therapy with drugs increasing the risk of GI bleeding - systemic corticosteroids (OR = 29.03) and NSAIDs (OR = 4.79). CONCLUSION: Results of our study indicate the necessity to increase the awareness of GI bleeding risk in long-term antiplatelet users among prescribing physicians.

Pycnogenol efficiency on glycaemia, motor nerve conduction velocity and markers of oxidative stress in mild type diabetes in rats.

The aim of this study was to describe the effects of Pycnogenol at various doses on preprandial and postprandial glucose levels, the levels of thiobarbituric acid reactive substances (TBARs) and N-acetyl-beta-d-glucosaminidase (NAGA) and on motor nerve conduction velocity (MNCV) in streptozotocin (STZ)-induced diabetic rats. Pycnogenol treatment (10, 20, 50 mg/kg body weight (b.w.)/day) lasted for 8 weeks after induction of diabetes. Pycnogenol significantly decreased elevated levels of preprandial glycaemia in treated animals at all doses. At doses of 10 mg/kg b.w./day and 20 mg/kg b.w./day it significantly decreased elevated levels of postprandial glycaemia compared with diabetic non-treated animals. Pycnogenol failed to induce a significant decrease of postprandial glycaemia at a dose of 50 mg/kg b.w./day. Pycnogenol improved significantly the impaired MNCV at doses of 10 and 20 mg/kg b.w./day compared with non-treated animals. The levels of TBARs were elevated in diabetic rats. The levels of NAGA increased gradually despite the treatment. Pycnogenol failed to affect the increased levels of TBARs and NAGA. Pycnogenollowered the elevated levels of glycaemia and reduced the decline in motor nerve conduction velocity in STZ-induced diabetic rats. The effect of Pycnogenol on postprandial glycaemic levels and MNCV was not dose-dependent.