Evaluating the risk of obstructive sleep apnea in type 2 diabetic patients, and its associations

OBJECTIVE: To assess the prevalence of high risk of Obstructive Sleep Apnoea (OSA) in Type 2 diabetics. To identify risk associations of OSA with obesity, sleep quality, daytime sleepiness and Acanthosis Nigricans. DESIGN AND METHODS: A cross sectional study was done in the diabetic wards of health facilities governed by three Regional Health Authorities in Trinidad. OSA risk was assessed by the Snoring, Tiredness, Observed Apnea, high blood Pressure (STOP) – Body mass index, Age, Neck circumference and Gender (BANG) questionnaire. Sleep quality and daytime sleepiness were also assessed by the Pittsburgh Sleep Quality Index and Epworth Sleepiness Scale respectively. Bioimpedance analysis was also done using a stadiometer and standard bioimpedance scale. RESULTS: A total of 281 diabetic patients and 147 non-diabetic patients were interviewed throughout Trinidad. Females made up the majority of the sample, 67% of the diabetics and 66% of the non diabetics. The prevalence of OSA was found to be 73.2% in type 2 diabetics. Non diabetics had an OSA prevalence of 39.5%. Results from a binary regression showed that having diabetes increased the probability of “High Risk of OSA” by 93.1%. CONCLUSION: The prevalence of high risk of OSA in Trinidad was high in type 2 diabetic patients, and has strong correlations with obesity and Acanthosis Nigricans.

Polypharmacy (or polytherapy) in the treatment of heart failure.

There is now conclusive evidence that most patients with heart failure due to left ventricular systolic dysfunction should be treated with angiotensin converting enzyme (ACE) inhibitors and beta-blockers. They will also need diuretics for the control of fluid retention. There is also a powerful case for adding spironolactone to the treatment of patients with more severe symptoms. Many doctors would also use digoxin and, especially if coronary disease is present, aspirin or warfarin. Most patients also have other chronic diseases, such as diabetes, arthritis, depression and dyspepsia, and each of these may provoke the prescription of yet another agent. Many patients will receive prescriptions to treat the side-effects of their therapy. Finding a sure path through the morass of pharmacotherapy is a daunting task. Polypharmacy is having a negative impact on new drug research in an area where there are in fact remarkably few really effective treatments and the therapeutic problem is only partially solved. This paper discusses some of the issues surrounding polypharmacy in heart failure and how to resolve them, using an illustrative case history. It highlights the potential benefits of polypharmacy with effective drugs and the gross over-use of ineffective treatments in heart failure. The major problem with polypharmacy in heart failure is not the heart failure treatment itself, but the drugs for other concomitant conditions, the effectiveness of which is often not supported by an appropriate evidence base and for which alternative, less noxious management strategies often exist. Polypharmacy may be deleterious not only because of the increased potential for side-effects and drug interactions but also because taking unnecessary therapy reduces compliance with effective drugs.

A multistep procedure for the chemical inactivation of human immunodeficiency virus for use as an experimental vaccine.

The kinetics of inactivation of four different strains of HIV-1 (RF, MN, SF2 and IIIB) by beta-propiolactone (BPL) and binary ethylenimine (BEI) were studied under various conditions. The conditions that would be required for the reduction of virus infectivity by at least 10(20) TCID50 ml-1 were estimated on the basis of the experimental rates of inactivation obtained. A multiple step procedure including treatment with 0.2% BPL, 0.05% sodium cholate, 10 mM BEI and 0.02% formaldehyde was designed to inactivate HIV-1 for use as an experimental vaccine. Complete inactivation of virus infectivity was confirmed by prolonged cell culture. The experimental vaccine preparation was analysed for the presence of HIV-1 proviral DNA utilizing the polymerase chain reaction. After treatment with both BPL and BEI proviral DNA was detected in one of four samples using primers encoding a 244 bp segment of the pol region of the viral genome. Proviral DNA could not be detected in any of the four samples using primers encoding segments of > 400 bp in the gag and reverse transcriptase region.