In March 2020, many elective medical services were canceled in response to the coronavirus disease 2019 (COVID-19) pandemic. The daily case rate is now declining in many states and there is a need ...for guidance about the resumption of elective clinical services for patients with lung disease or sleep conditions.
Volunteers were solicited from the Association of Pulmonary, Critical Care, and Sleep Division Directors and American Thoracic Society. Working groups developed plans by discussion and consensus for resuming elective services in pulmonary and sleep-medicine clinics, pulmonary function testing laboratories, bronchoscopy and procedure suites, polysomnography laboratories, and pulmonary rehabilitation facilities.
The community new case rate should be consistently low or have a downward trajectory for at least 14 days before resuming elective clinical services. In addition, institutions should have an operational strategy that consists of patient prioritization, screening, diagnostic testing, physical distancing, infection control, and follow-up surveillance. The goals are to protect patients and staff from exposure to the virus, account for limitations in staff, equipment, and space that are essential for the care of patients with COVID-19, and provide access to care for patients with acute and chronic conditions.
Transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a dynamic process and, therefore, it is likely that the prevalence of COVID-19 in the community will wax and wane. This will impact an institution's mitigation needs. Operating procedures should be frequently reassessed and modified as needed. The suggestions provided are those of the authors and do not represent official positions of the Association of Pulmonary, Critical Care, and Sleep Division Directors or the American Thoracic Society.
Abstract
The results of previous studies of recreational physical activity and risk of epithelial ovarian cancer are mixed, with some studies supporting an inverse association and others, including ...several prospective studies, observing no association or a suggestive positive association with vigorous activity. Physical activity may decrease ovarian cancer risk by reducing circulating levels of estrogens, decreasing body fat and estrogen synthesis, or reducing the frequency of ovulation. However, plausible mechanisms also exist for a positive association, including possible ovulatory changes with regular vigorous activity, increased pituitary production of gonadotropins, or changes in progesterone or androgen concentrations. In an earlier analysis of the Nurses’ Health Study (NHS) with follow-up through 1996, there was no clear association between physical activity level and ovarian cancer incidence, but there was a suggestion of an increase in risk with frequent vigorous activity. We reanalyzed this association using 10 additional years of follow-up in the NHS and adding data from the younger Nurses’ Health Study II (NHSII) cohort. We calculated current and cumulative average physical activity in hours per week and metabolic equivalent task-hours (MET-hours) per week using data collected every 2-6 years beginning in 1986 (NHS) or 1989 (NHSII). We used Cox proportional hazards regression to model the age- and multivariable-adjusted incidence rate ratios of ovarian cancer for each category of physical activity, compared to the lowest category. Our analysis included 179,443 women with detailed physical activity data and 652 incident, confirmed cases diagnosed through 2006 (NHS) or 2007 (NHSII). There was no clear association between hours per week of current or cumulative average activity and ovarian cancer risk. However, there was evidence of a positive association between cumulative average MET-hours of total activity per week and risk of all epithelial cancers and the serous invasive subtype. The multivariable-adjusted incidence rate ratios and 95% confidence intervals for each MET-hour category, compared to <2.5 MET-hours, were 1.27 (0.90, 1.80) for 2.5-<5 MET-hours, 1.06 (0.77, 1.48) for 5-<10 MET-hours, 1.17 (0.86, 1.60) for 10-<20 MET-hours, 1.56 (1.13, 2.17) for 20-<30 MET-hours, and 1.34 (0.96, 1.87) for ≥30 MET-hours. The corresponding estimates for serous invasive cancers were 1.42 (0.86, 2.35), 1.14 (0.71, 1.84), 1.49 (0.95, 2.32), 1.82 (1.14, 2.92), and 1.48 (0.92, 2.40). Our results do not support an inverse association between physical activity and ovarian cancer risk, and suggest a possible increase in risk with high levels of activity, particularly for the serous invasive subtype. Lagged analyses and analyses of specific types and intensities of activity are ongoing.
Citation Format: {Authors}. {Abstract title} abstract. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1830.
Abstract
The use of common analgesics, such as aspirin, non-aspirin NSAIDs and acetaminophen, may be associated with the risk of several hormone-related cancers, possibly via effects on sex hormone ...and prolactin concentrations. Therefore, we assessed the cross-sectional relationship between analgesic (aspirin, non-aspirin NSAIDS, and acetaminophen) use and sex hormone and prolactin concentrations among 2,034 premenopausal women, 32 to 54 years old, from the Nurses' Health Study II. Approximately 84% of women provided timed luteal and follicular blood samples; the remainder provided a single untimed sample. After adjustment for age, BMI, parity, and other potential confounders, acetaminophen use was inversely associated with prolactin levels (ptrend= 0.04). Compared to non-users, prolactin concentrations were 11.8% lower among women who reported using acetaminophen at least 2 times per week (p<0.01). Similarly, acetaminophen was inversely associated with free testosterone, when comparing use at least 2 times per week to non-users (7.1% lower, p = 0.04; ptrend= 0.04). Use of non-aspirin NSAIDs was positively associated with follicular free estradiol, with 13.5% higher levels in women who reported use 4 or more days per week as compared to non-users (p = 0.04; ptrend= 0.11); results for free follicular estradiol were similar (13.2% higher, p = 0.06; ptrend= 0.11) though not statistically significant. There were no clear associations observed between analgesic use and luteal estradiol, estrone, estrone sulfate, DHEA, DHEAS, androstenedione, and estrogen/androgen ratios. After adjustment for multiple comparisons, none of the associations were statistically significant. In conclusion, our study provides modest evidence for an association of acetaminophen use with prolactin and free testosterone concentrations in premenopausal women, and the suggestion of an association between non-aspirin NSAIDs and follicular free estradiol among those with frequent use.
Citation Format: Scott R. Bauer, Renee T. Fortner, Margaret A. Gates, Heather Eliassen, Susan E. Hankinson, Shelley S. Tworoger. Analgesic use in relation to sex hormone and prolactin concentrations in premenopausal women. abstract. In: Proceedings of the AACR Special Conference on Post-GWAS Horizons in Molecular Epidemiology: Digging Deeper into the Environment; 2012 Nov 11-14; Hollywood, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2012;21(11 Suppl):Abstract nr 77.
The presence of multiple (5-100) colorectal adenomas suggests an inherited predisposition, but the genetic aetiology of this phenotype is undetermined if patients test negative for Mendelian ...polyposis syndromes such as familial adenomatous polyposis (FAP) and MUTYH-associated polyposis (MAP). We investigated whether 18 common colorectal cancer (CRC) predisposition single-nucleotide polymorphisms (SNPs) could help to explain some cases with multiple adenomas who phenocopied FAP or MAP, but had no pathogenic APC or MUTYH variant. No multiple adenoma case had an outlying number of CRC SNP risk alleles, but multiple adenoma patients did have a significantly higher number of risk alleles than population controls (P=5.7 × 10(-7)). The association was stronger in those with ≥10 adenomas. The CRC SNPs accounted for 4.3% of the variation in multiple adenoma risk, with three SNPs (rs6983267, rs10795668, rs3802842) explaining 3.0% of the variation. In FAP patients, the CRC risk score did not differ significantly from the controls, as we expected given the overwhelming effect of pathogenic germline APC variants on the phenotype of these cases. More unexpectedly, we found no evidence that the CRC SNPs act as modifier genes for the number of colorectal adenomas in FAP patients. In conclusion, common colorectal tumour risk alleles contribute to the development of multiple adenomas in patients without pathogenic germline APC or MUTYH variants. This phenotype may have 'polygenic' or monogenic origins. The risk of CRC in relatives of multiple adenoma cases is probably much lower for cases with polygenic disease, and this should be taken into account when counselling such patients.
PDF
