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Shannon O Armstrong,1 Richard A Little2,31The Medicines Company, Health Economics and Outcomes Research, Parsippany, NJ, USA; 2Consultant Health Economist, Cambridge, UK; 3London School of Hygiene and Tropical Medicines, London, UKIntroduction: Cardiovascular disease (CVD) is the leading cause of death in the United States, and high cholesterol is a leading risk factor for CVD. While statins are effective at reducing cholesterol, they are frequently underused in patients at highest risk of CVD. The objective of this study was to identify interventions which may improve adherence to statins and to assess their cost effectiveness within the US Medicare population.Methods: A literature review was undertaken to identify interventions to improve adherence in patients with CVD at highest risk of a recurrent event and to quantify non-adherence and the consequences of non-adherence to statins in this population. A Markov cost-utility model was developed to assess the cost effectiveness of these interventions.Results: Ten adherence interventions were identified in the literature, with 6 demonstrating statistically significant improvement in adherence. The six interventions were disease management, interactive voice response, nurse counselling, discharge letter, nurse/dietician counselling and electronic pill bottle with feedback. The model found the cost effectiveness of an intervention was highly dependent on its effectiveness and costs. Incremental cost effectiveness ratios ranged from $27,545/QALY for discharge letter with large adherence gain to $130,399/QALY for disease management program with small adherence gain.Conclusion: Some interventions to improve adherence have been shown to be effective, but little attention has been paid to the costs. Further studies on adherence interventions should include economic evaluations.Keywords: cost-effectiveness, adherence, statins, cardiovascular disease

A patient with spontaneous periodic hypothermia who had both a lipoma and agenesis of the corpus callosum is described. Spontaneous periodic hypothermia associated with corpus callosum abnormalities is a distinct entity and although the mechanism underlying the hypothermic episodes is unexplained, the term “diencephalic autonomic epilepsy” does not seem appropriate. [ABSTRACT FROM PUBLISHER]

Abstract Background ADAM33 has been identified as an asthma-associated gene in an out-bred population. Genetic studies suggested that the functional role of this metalloprotease was in airway remodeling. However, the mechanistic roles of the disease-associated SNPs have yet to be elucidated especially in the context of the pathophysiology of asthma. One disease-associated SNP, BC+1, which resides in intron BC toward the 5' end of ADAM33, is highly associated with the disease. Methods The region surrounding this genetic variant was cloned into a model system to determine if there is a regulatory element within this intron that influences transcription. Results The BC+1 protective allele did not impose any affect on the transcription of the reporter gene. However, the at-risk allele enforced such a repressive affect on the promoter that no protein product from the reporter gene was detected. These results indicated that there exists within intron BC a regulatory element that acts as a repressor for gene expression. Moreover, since SNP BC+1 is a common genetic variant, this region may interact with other undefined regulatory elements within ADAM33 to provide a rheostat effect, which modulates pre-mRNA processing. Thus, SNP BC+1 may have an important role in the modulation of ADAM33 gene expression. Conclusion These data provide for the first time a functional role for a disease-associated SNP in ADAM33 and begin to shed light on the deregulation of this gene in the pathophysiology of asthma.