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Aim: To assess past suicide attempts in a cohort of adults with Type 2 Diabetes diagnosed within the prior 24 months., Methods: Outpatients were recruited from diabetes education classes or diabetes shared medical appointment. Participants aged 18 or over with a self-reported diagnosis of Type 2 Diabetes (T2DM) in the prior 24 months completed questionnaires about medical (including diabetes), psychiatric, and social history. Participants also completed two screening questionnaires for depression: Patient Health Questionnaire 9 and the Questionnaire Inventory for Depressive Symptoms-Self Report. Those who screened positive for depression had confirmatory testing with a clinician administered Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) checklist., Results: In this convenience sample of 145 patients with Type 2 Diabetes, 9.7% of patients had history of a suicide attempt and 38.2% met diagnosis for major depressive disorder (MDD). Patients with MDD were more likely to have a history of suicide attempts than those without MDD (p=0.0002). Of the patients with prior suicide attempts, 50% screened positive for MDD at the time of the survey., Conclusion: In patients with newly-diagnosed Type 2 Diabetes the rate of past suicide attempts was nearly 10%, which is twice the rate seen in the general population. The rate of past suicide attempts in currently depressed patients with diabetes is 21.8%. These findings suggest the need for monitoring patients with diabetes and depression for future suicide risk., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

The effects of ethanol on cyclic GMP (cGMP) in washed human platelets were studied in the presence and absence of sodium nitroprusside (SNP), nitric oxide donor which stimulates guanylate cyclase. SNP stimulated cGMP accumulation in a dose-dependent fashion. After 1 min exposure to 100 microM SNP, the level of cGMP was approximately four-fold that in vehicle-treated platelets. Alcohol had no effect on basal cGMP, but inhibited SNP-induced cGMP accumulation at 17, 85 and 170 mM. In further experiments, platelets were incubated for 0, 0.5, 1 2 or 5 min with 10 microM SNP, with or without 100 microM zaprinast, a selective cGMP-phosphodiesterase (PDE) inhibitor and 85 mM ethanol. In the presence of zaprinast but not alcohol, cGMP levels rose continuously, to 10-fold the basal level at 5 min. Without zaprinast, cGMP levels were lower and reached a plateau by 2 min. Accumulation of cGMP was attenuated by alcohol 2 and 5 min after SNP addition, both in zaprinast-treated platelets and those without zaprinast. Thus, alcohol inhibits platelet cGMP accumulation stimulated by nitric oxide donor. Its mechanism probably does not involve a major effect on PDE, because the inhibition was observed in the presence or absence of zaprinast. We hypothesize that alcohol inhibits guanylate cyclase, contributing to its complex functional effects in platelets.

Our previous studies have demonstrated that addition of moderate volumes of absolute alcohol (34-170 mM final concentration) to whole blood produces concentration-dependent platelet aggregation, due to release of adenosine diphosphate (ADP) from erythrocytes. We have now investigated the effects of exposure of blood to ethanol by a more "physiologic" protocol, in which 7.8% (w/v) alcohol is added to achieve a final concentration of 1 to 85 mM in human and rat blood or platelet rich plasma (PRP). The effects of short incubation with alcohol on platelet aggregation induced by ADP, collagen and arachidonic acid were examined by the impedance method of aggregometry. Aggregation induced by collagen in PRP of either species was significantly inhibited by 85 mM ethanol, with concentrations as low as 4.25 mM inhibiting the response to collagen in rat whole blood. ADP stimulated only primary, reversible aggregation in rat PRP and whole blood, and these responses were unaffected by alcohol. Human platelets responded to ADP with irreversible aggregation, which was significantly attenuated by 85 mM ethanol in whole blood but not PRP. Arachidonic acid evoked irreversible platelet aggregation in all four preparations; this was significantly inhibited by the high dose ethanol in human and rat PRP, but not whole blood. In contrast to our earlier studies with absolute ethanol, there was no evidence of hemolysis (and therefore, ADP release from red blood cells) using the current protocol. The results of these experiments show that alcohol, at physiologically relevant concentrations, has an inhibitory effect on secondary platelet aggregation responses to some agonists in whole blood as well as PRP, possibly by its previously demonstrated effects on arachidonic acid release by phospholipases. The possibility remains to be considered that other blood cells might contribute to the effects of alcohol on platelet aggregation in whole blood.

Effects of ethanol on blood clotting and platelet aggregation have been reported in many models, but its in vitro actions in whole blood, impedance aggregometry have not been reported. We investigated the effect of ethanol in vitro in whole blood and platelet rich plasma of humans and rats, as measured by impedance aggregometry. Ethanol (34 to 170 mM) induced concentration-dependent aggregation in whole blood but not platelet rich plasma. In further studies in rats, aggregation was inhibited by pretreatment of whole blood with the prostacyclin analog iloprost or the enzyme apyrase, which degrades ADP to AMP. Levels of ethanol which produced aggregation in whole blood were also associated with concentration-dependent hemolysis. Based on the requirement for whole blood for ethanol-induced aggregation, the inhibitory effect of apyrase and our observation of hemolysis, and previous studies which have demonstrated the potential contribution of ADP from lysed red blood cells to platelet aggregation, we conclude that ethanol-induced aggregation in whole blood is mediated by erythrocyte lysis and the ADP released from these cells.