Publications

AIM

To compare thromboembolism rates between hospitalized patients with a diagnosis of ulcerative colitis and other hospitalized patients at high risk for thromboembolism. To compare thromboembolism rates between patients with ulcerative colitis undergoing a colorectal operation and other patients undergoing colorectal operations.

METHODS

Data from the National Hospital Discharge Survey was used to compare thromboembolism rates between (1) hospitalized patients with a discharge diagnosis of ulcerative colitis and those with diverticulitis or acute respiratory failure, and (2) hospitalized patients with a discharge diagnosis of ulcerative colitis who underwent colectomy and those with diverticulitis or colorectal cancer who underwent colorectal operations.

RESULTS

Patients diagnosed with ulcerative colitis had similar or higher rates of combined venous thromboembolism (2.03%) than their counterparts with diverticulitis (0.76%) or respiratory failure (1.99%), despite the overall greater prevalence of thromboembolic risk factors in the latter groups. Discharged patients with colitis that were treated surgically did not have significantly different rates of venous or arterial thromboembolism than those with surgery for diverticulitis or colorectal cancer.

CONCLUSION

Patients with ulcerative colitis who do not undergo an operation during their hospitalization have similar or higher rates of thromboembolism than other medical patients who are considered to be high risk for thromboembolism.

OBJECTIVE

To evaluate if anger expression affects sleep quality in patients with coronary heart disease (CHD). Research has indicated that poor sleep quality independently predicts adverse outcomes in patients with CHD. Risk factors for poor sleep quality include older age, socioeconomic factors, medical comorbidities, lack of exercise, and depression.

METHODS

We sought to examine the association of anger expression with sleep quality in 1020 outpatients with CHD from the Heart and Soul Study. We assessed anger-in, anger-out, and anger temperament, using the Spielberger State-Trait Anger Expression Inventory 2, and measured sleep quality, using items from the Cardiovascular Health Study and Pittsburgh Sleep Quality Index. We used multivariate analysis of variance to examine the association between anger expression and sleep quality, adjusting for potential confounding variables.

RESULTS

Each standard deviation (SD) increase in anger-in was associated with an 80% greater odds of poor sleep quality (odds ratio (OR) = 1.8, 95% Confidence Interval (CI) = 1.6-2.1; p < .0001). This association remained strong after adjusting for demographics, comorbidities, lifestyle factors, medications, cardiac function, depressive symptoms, anger-out, and anger temperament (adjusted OR = 1.4, 95% CI = 1.5-1.7; p = .001). In the same model, each SD increase in anger-out was associated with a 21% decreased odds of poor sleep quality (OR = 0.79, 95% CI = 0.64-0.98; p = .03). Anger temperament was not independently associated with sleep quality.

CONCLUSIONS

Anger suppression is associated with poor sleep quality in patients with CHD. Whether modifying anger expression can improve sleep quality or reduce cardiovascular morbidity and mortality deserves further study.

BACKGROUND

Understanding the progression from beryllium exposure (BeE) to chronic beryllium disease (CBD) is essential for optimizing screening and early intervention to prevent CBD.

METHODS

We developed an analytic markov model of progression to cbd that assigns annual probabilities for progression through three states: from BeE to beryllium sensitization and then to CBD. We used calculations of the number in each state over time to assess which of several alternative progression models are most consistent with the limited available empirical data on prevalence and incidence. We estimated cost-effectiveness of screening considering both incremental (cost/case) and cumulative program costs.

RESULTS

No combination of parameters for a simple model in which risk of progression remains constant over time can meet the empirical constraints of relatively frequent early cases and continuing development of new cases with long latencies. Modeling shows that the risk of progression is initially high and then declines over time. Also, it is likely that there are at least two populations that differ significantly in risk. The cost-effectiveness of repetitive screening declines over time, although new cases will still be found with long latencies. However, screening will be particularly cost-effective when applied to persons with long latencies who have not been previously screened.

CONCLUSIONS

To optimize use of resources, the intensity of screening should decrease over time. Estimation of lifetime cumulative CBD risk should consider the declining risk of progression over time.

Interleukin-6 (IL-6) is an inflammatory cytokine that influences the development of inflammatory and aging-related disorders and ultimately longevity. In order to study the influence of variants in genes that regulate inflammatory response on IL-6 levels and longevity, we screened a panel of 477 tag SNPs across 87 candidate genes in >5000 older participants from the population-based Cardiovascular Health Study (CHS). Baseline plasma IL-6 concentration was first confirmed as a strong predictor of all-cause mortality. Functional alleles of the IL6R and PARP1 genes were significantly associated with 15%-20% higher baseline IL-6 concentration per copy among CHS European-American (EA) participants (all p<10(-4)). In a case/control analysis nested within this EA cohort, the minor allele of PARP1 rs1805415 was nominally associated with decreased longevity (p=0.001), but there was no evidence of association between IL6R genotype and longevity. The PARP1 rs1805415--longevity association was subsequently replicated in one of two independent case/control studies. In a pooled analysis of all three studies, the "risk" of longevity associated with the minor allele of PARP1 rs1805415 was 0.79 (95%CI 0.62-1.02; p=0.07). These findings warrant further study of the potential role of PARP1 genotype in inflammatory and aging-related phenotypes.