Tinh-Hai Collet

Subclinical Thyroid Dysfunction and the Risk of Heart Failure Events An Individual Participant Data Analysis From 6 Prospective Cohorts

Background— American College of Cardiology/American Heart Association guidelines for the diagnosis and management of heart failure recommend investigating exacerbating conditions such as thyroid dysfunction, but without specifying the impact of different thyroid-stimulation hormone (TSH) levels. Limited prospective data exist on the association between subclinical thyroid dysfunction and heart failure events. Methods and Results— We performed a pooled analysis of individual participant data using all available prospective cohorts with thyroid function tests and subsequent follow-up of heart failure events. Individual data on 25 390 participants with 216 248 person-years of follow-up were supplied from 6 prospective cohorts in the United States and Europe. Euthyroidism was defined as TSH of 0.45 to 4.49 mIU/L, subclinical hypothyroidism as TSH of 4.5 to 19.9 mIU/L, and subclinical hyperthyroidism as TSH <0.45 mIU/L, the last two with normal free thyroxine levels. Among 25 390 participants, 2068 (8.1%) had subclinical hypothyroidism and 648 (2.6%) had subclinical hyperthyroidism. In age- and sex-adjusted analyses, risks of heart failure events were increased with both higher and lower TSH levels (P for quadratic pattern <0.01); the hazard ratio was 1.01 (95% confidence interval, 0.81–1.26) for TSH of 4.5 to 6.9 mIU/L, 1.65 (95% confidence interval, 0.84–3.23) for TSH of 7.0 to 9.9 mIU/L, 1.86 (95% confidence interval, 1.27–2.72) for TSH of 10.0 to 19.9 mIU/L (P for trend <0.01) and 1.31 (95% confidence interval, 0.88–1.95) for TSH of 0.10 to 0.44 mIU/L and 1.94 (95% confidence interval, 1.01–3.72) for TSH <0.10 mIU/L (P for trend=0.047). Risks remained similar after adjustment for cardiovascular risk factors. Conclusion— Risks of heart failure events were increased with both higher and lower TSH levels, particularly for TSH ≥10 and <0.10 mIU/L.Background— American College of Cardiology/American Heart Association guidelines for the diagnosis and management of heart failure recommend investigating exacerbating conditions such as thyroid dysfunction, but without specifying the impact of different thyroid-stimulation hormone (TSH) levels. Limited prospective data exist on the association between subclinical thyroid dysfunction and heart failure events. Methods and Results— We performed a pooled analysis of individual participant data using all available prospective cohorts with thyroid function tests and subsequent follow-up of heart failure events. Individual data on 25 390 participants with 216 248 person-years of follow-up were supplied from 6 prospective cohorts in the United States and Europe. Euthyroidism was defined as TSH of 0.45 to 4.49 mIU/L, subclinical hypothyroidism as TSH of 4.5 to 19.9 mIU/L, and subclinical hyperthyroidism as TSH <0.45 mIU/L, the last two with normal free thyroxine levels. Among 25 390 participants, 2068 (8.1%) had subclinical hypothyroidism and 648 (2.6%) had subclinical hyperthyroidism. In age- and sex-adjusted analyses, risks of heart failure events were increased with both higher and lower TSH levels ( P for quadratic pattern <0.01); the hazard ratio was 1.01 (95% confidence interval, 0.81–1.26) for TSH of 4.5 to 6.9 mIU/L, 1.65 (95% confidence interval, 0.84–3.23) for TSH of 7.0 to 9.9 mIU/L, 1.86 (95% confidence interval, 1.27–2.72) for TSH of 10.0 to 19.9 mIU/L ( P for trend <0.01) and 1.31 (95% confidence interval, 0.88–1.95) for TSH of 0.10 to 0.44 mIU/L and 1.94 (95% confidence interval, 1.01–3.72) for TSH <0.10 mIU/L ( P for trend=0.047). Risks remained similar after adjustment for cardiovascular risk factors. Conclusion— Risks of heart failure events were increased with both higher and lower TSH levels, particularly for TSH ≥10 and <0.10 mIU/L. # Clinical Perspective {#article-title-42}

Thyroid Hormone Therapy for Older Adults with Subclinical Hypothyroidism

BACKGROUND The use of levothyroxine to treat subclinical hypothyroidism is controversial. We aimed to determine whether levothyroxine provided clinical benefits in older persons with this condition. METHODS We conducted a double‐blind, randomized, placebo‐controlled, parallel‐group trial involving 737 adults who were at least 65 years of age and who had persisting subclinical hypothyroidism (thyrotropin level, 4.60 to 19.99 mIU per liter; free thyroxine level within the reference range). A total of 368 patients were assigned to receive levothyroxine (at a starting dose of 50 μg daily, or 25 μg if the body weight was <50 kg or the patient had coronary heart disease), with dose adjustment according to the thyrotropin level; 369 patients were assigned to receive placebo with mock dose adjustment. The two primary outcomes were the change in the Hypothyroid Symptoms score and Tiredness score on a thyroid‐related quality‐of‐life questionnaire at 1 year (range of each scale is 0 to 100, with higher scores indicating more symptoms or tiredness, respectively; minimum clinically important difference, 9 points). RESULTS The mean age of the patients was 74.4 years, and 396 patients (53.7%) were women. The mean (±SD) thyrotropin level was 6.40±2.01 mIU per liter at baseline; at 1 year, this level had decreased to 5.48 mIU per liter in the placebo group, as compared with 3.63 mIU per liter in the levothyroxine group (P<0.001), at a median dose of 50 μg. We found no differences in the mean change at 1 year in the Hypothyroid Symptoms score (0.2±15.3 in the placebo group and 0.2±14.4 in the levothyroxine group; between‐group difference, 0.0; 95% confidence interval [CI], ‐2.0 to 2.1) or the Tiredness score (3.2±17.7 and 3.8±18.4, respectively; between‐group difference, 0.4; 95% CI, ‐2.1 to 2.9). No beneficial effects of levothyroxine were seen on secondary‐outcome measures. There was no significant excess of serious adverse events prespecified as being of special interest. CONCLUSIONS Levothyroxine provided no apparent benefits in older persons with subclinical hypothyroidism. (Funded by European Union FP7 and others; TRUST ClinicalTrials.gov number, NCT01660126.)

Subclinical Thyroid Dysfunction and the Risk for Fractures: A Systematic Review and Meta-analysis

About 10% of women and 3% of men older than 60 years have subclinical hypothyroidism (13), and prevalence increases with age. Subclinical hypothyroidism is defined as elevated thyroid-stimulating hormone (TSH) and normal free thyroxine (FT4) levels (4). Subclinical hyperthyroidism, defined as decreased TSH and normal FT4 and triiodothyronine (T3) levels (4), is less common and affects about 1.5% of women and 1% of men older than 60 years. Subclinical thyroid dysfunction has previously been associated with an increased risk for coronary heart disease and heart failure events (57). Thyroid hormones influence the homeostasis and remodeling of bone (8). Overt hyperthyroidism is a risk factor for fractures (9). A few observational studies have also found an increased risk for fracture in persons with overt hypothyroidism (10, 11). The association between subclinical thyroid dysfunction and fractures remains unclear. A prospective cohort study of 3567 elderly participants found an increased risk for hip fractures in men with endogenous subclinical hyperthyroidism and a similar trend in women, whereas subclinical hypothyroidism was associated with an increased risk for hip fracture in men only (12). Conversely, a casecohort study of 1526 ambulatory men older than 65 years found no significant relationship between subclinical hyperthyroidism and fractures, but low-normal TSH levels were significantly associated with an increased risk for hip fractures (13). Other prospective studies (14) did not adjust for common relevant potential confounders between subclinical thyroid dysfunction and fractures, such as age, sex, body mass index, smoking, and corticosteroid use (1524). Two meta-analyses of postmenopausal women with exogenous subclinical hyperthyroidism due to thyroxine substitution showed a reduction in bone mineral density (BMD), which is a surrogate marker for osteoporosis (25, 26). To our knowledge, no meta-analysis has been done on the risk for fractures related with subclinical thyroid dysfunction. Therefore, we did a meta-analysis to determine whether subclinical thyroid dysfunction and TSH levels were associated with an increased risk for fractures in prospective cohort studies. Methods Data Sources and Searches We followed a standardized protocol to do this meta-analysis. Similar to our previous study (27), we conducted a systematic literature search for articles in any language on the association between subclinical thyroid dysfunction (both subclinical hypothyroidism and hyperthyroidism) and fractures published between 1946 and 16 March 2014 in the MEDLINE and EMBASE databases. In Ovid MEDLINE, we used the following broadly defined Medical Subject Headings: thyroid diseases, hypothyroidism, hyperthyroidism, thyroid hormones, thyrotropin, subclinical hyperthyroidism, subclinical hypothyroidism, subclinical dysthyroidism, subclinical thyroid, and fractures or osteoporosis. These headings were combined with the filter designed by British Medical Journal knowledge information specialists to identify randomized, controlled trials; cohorts; and casecontrol studies without year limitation or exclusion of comments, editorials, meta-analyses, practice guidelines, reviews, letters, journal correspondences, books, conference papers, or animal studies (28). We used a similar procedure in EMBASE. We also searched the bibliographies of key articles in the field and those included in this review, and we contacted authors for unpublished studies. Study Selection Similar to our previous study (27), 2 authors independently screened the abstracts and titles of the search results and retained articles on prospective cohorts studying the association between thyroid dysfunction and osteoporotic fractures. The same reviewers independently assessed the remaining full-text articles for eligibility on the basis of predefined criteria. Any disagreement was resolved by discussion with a third author. Because some prospective studies that measured thyroid function and assessed multiple outcomes may not have reported fracture outcomes in the abstract, we also assessed the full text and tables for reported fracture data in these studies. We included only studies that fulfilled the following a prioridefined criteria: measurement of thyroid function, prospective follow-up of participants, assessment of fracture outcomes, comparison group with euthyroidism, and provision of hazard ratios (HRs) or sufficient data to calculate them. We excluded studies that examined only persons with a history of overt thyroid dysfunction or thyroid cancer. We considered nonspine, hip, and any fractures, but we excluded spine fractures because vertebral fracture age is difficult to assess without serial radiographs and the accuracy of self-report is poor (29). Agreement among reviewers was 97.9% for the first screening of titles and abstracts (= 0.69) and 100% for full-text screening (= 1.0). Data Extraction and Quality Assessment We used a standardized data abstraction form to extract information about participant characteristics, the criteria used to define subclinical thyroid dysfunction, and fractures. We evaluated study quality using slightly updated criteria (27, 30), adding inclusion of testing for the assumption of proportional hazards. One physician reviewer extracted data, and another checked data. We assessed key indicators for the quality of the cohort studies (31, 32): the population studied (convenience sample vs. population-based, which was defined as a random sample of the general population) and methods of fracture ascertainment and adjudication (considered adequate if done by an expert panel blinded to thyroid status using a clear outcome definition); assessment of the proportional hazard assumption; completeness of follow-up; and adjustment for potential confounders. We defined age, sex, body mass index, smoking, and corticosteroid use (1524) as common relevant potential confounders for the relationship between subclinical thyroid dysfunction and fractures based on a literature search considering their prevalence and strength of association with fractures and thyroid dysfunction. We required adjustment for most of these risk factors and lack of violation of the proportional hazard assumption for a study to be rated as higher quality. If an article did not clearly mention one of these criteria, we considered that it had not been done. Two reviewers independently rated all studies for quality, and disagreement was resolved with a third reviewer. We contacted the authors of all cohorts to request more detailed data on the association between subclinical thyroid dysfunction and fractures. We used the most adjusted HRs and 95% CIs available. Data Synthesis and Statistical Analysis We used TSH cutoff levels as reported by each cohort. If not otherwise specified by a cohort, we used a common definition of subclinical thyroid disease based on expert reviews (4, 33) and the definition used in the Cardiovascular Health Study (12, 34), as done in previous articles (57). Subclinical hypothyroidism was defined as a TSH level greater than 4.5 to 20.0 mIU/L and an FT4 level in the reference range. Subclinical hyperthyroidism was defined as a TSH level less than 0.45 mIU/L and an FT4 level in the reference range. Euthyroidism was defined as a TSH cutoff level from 0.45 to 4.5 mIU/L. For FT4, we used study-specific cutoff levels because these measurements show greater intermethod variation than TSH. Three studies (14, 35, 36) did not include FT4 in their definition of subclinical thyroid dysfunction. Two of these studies (35, 36) were included in the main analysis of the higher-quality studies, but we did a sensitivity analysis excluding studies without FT4 measurement or with abnormal FT4 because some participants may have overt thyroid dysfunction. Two of these studies differentiated between low and suppressed TSH levels (14, 35). We used data from the group with low but not suppressed TSH levels because, according to unpublished data in our previous individual- participant data analysis (7), about one fourth of persons with a TSH level less than 0.1 mIU/L had overt hyperthyroidism, but only about 5% of those with a TSH level greater than 0.1 mIU/L had overt hyperthyroidism. We qualitatively synthesized data and assessed which participants were included, the definition of thyroid dysfunction, and which types of fractures were studied. First, for the higher-quality studies, we calculated pooled estimates and 95% CIs of the risk for subclinical hyperthyroidism and hypothyroidism on hip and nonspine fractures using random-effects models based on the KnappHartung approach (37) to account for the uncertainty associated with statistical heterogeneity (tau-square estimation) and the small number of studies included (38). Second, we assessed overall pooled estimates for all studies using the same approach. Because the Cardiovascular Health Study only reported estimates stratified by sex, we used fixed effects to combine these estimates before pooling them with other cohorts (12). To assess heterogeneity among studies, we quantified the Q statistic with a conservative P value of 0.10 (39) and used the I 2 statistic, which describes the total variation across studies attributable to heterogeneity rather than chance (I 2> 50%, indicating at least moderate statistical heterogeneity) (40). To explore sources of heterogeneity, we did several predefined sensitivity analyses from all included studies using random-effects models. We also did analyses stratified by age and sex. Stratified analysis were accompanied by interaction tests based on Z scores, which are defined as the difference in effect estimates between strata divided by the SE of the difference. We used an adjusted rank correlation test to assess for publication bias (41). However, graphical and statistical methods may not be reliable because of their limited power due to the small number of studies include

Thyroid Antibody Status, Subclinical Hypothyroidism, and the Risk of Coronary Heart Disease: An Individual Participant Data Analysis

CONTEXT Subclinical hypothyroidism has been associated with increased risk of coronary heart disease (CHD), particularly with thyrotropin levels of 10.0 mIU/L or greater. The measurement of thyroid antibodies helps predict the progression to overt hypothyroidism, but it is unclear whether thyroid autoimmunity independently affects CHD risk. OBJECTIVE The objective of the study was to compare the CHD risk of subclinical hypothyroidism with and without thyroid peroxidase antibodies (TPOAbs). DATA SOURCES AND STUDY SELECTION A MEDLINE and EMBASE search from 1950 to 2011 was conducted for prospective cohorts, reporting baseline thyroid function, antibodies, and CHD outcomes. DATA EXTRACTION Individual data of 38 274 participants from six cohorts for CHD mortality followed up for 460 333 person-years and 33 394 participants from four cohorts for CHD events. DATA SYNTHESIS Among 38 274 adults (median age 55 y, 63% women), 1691 (4.4%) had subclinical hypothyroidism, of whom 775 (45.8%) had positive TPOAbs. During follow-up, 1436 participants died of CHD and 3285 had CHD events. Compared with euthyroid individuals, age- and gender-adjusted risks of CHD mortality in subclinical hypothyroidism were similar among individuals with and without TPOAbs [hazard ratio (HR) 1.15, 95% confidence interval (CI) 0.87-1.53 vs HR 1.26, CI 1.01-1.58, P for interaction = .62], as were risks of CHD events (HR 1.16, CI 0.87-1.56 vs HR 1.26, CI 1.02-1.56, P for interaction = .65). Risks of CHD mortality and events increased with higher thyrotropin, but within each stratum, risks did not differ by TPOAb status. CONCLUSIONS CHD risk associated with subclinical hypothyroidism did not differ by TPOAb status, suggesting that biomarkers of thyroid autoimmunity do not add independent prognostic information for CHD outcomes.

Subclinical thyroid dysfunction and cardiovascular diseases: 2016 update.

Subclinical thyroid dysfunction comprises subclinical hypothyroidism (SHypo), defined as elevated thyroid-stimulating hormone (TSH) by normal free thyroxine (FT4), and subclinical hyperthyroidism (SHyper) with decreased or undetectable TSH and normal FT4. Up to 10% of the elderly have SHypo, which is usually asymptomatic. Individual participant data (IPD) analyses of prospective cohort studies from the international Thyroid Studies Collaboration show that SHypo is associated with increased coronary heart disease (CHD) mortality [hazard ratio (HR) 1,58 for TSH ≥ 10 mIU/L, 95% CI 1.10-2.27), as well as increased risk of stroke, and heart failure (HF) for both higher and lower TSH. Small studies found that SHypo affects carotid intima media thickness (CIMT), diastolic function, peripheral vascular resistance, endothelial function, and lipid profile. SHyper is associated with increased risk of atrial fibrillation (AF) (HR 1.68, 95% CI 1.16-2.43) and CHD events (HR 1.21, 95% CI 0.99-1.46). The TSH threshold for initiating treatment is unclear. In the absence of large randomized controlled trials, the best evidence suggests SHypo therapy should be started at TSH ≥ 10 mIU/L, and SHyper therapy at TSH < 0.1 mIU/L. Recommendations on screening are discordant, but most guidelines advocate that thyroid function should be checked in those at risk for hypothyroidism, those over 60, and those with known CHD and HF. This review updates current evidence on the association between thyroid dysfunction and cardiovascular disease, as well as on screening and treatment of subclinical thyroid dysfunction.

Reversal of Primary Male Infertility and Testicular Adrenal Rest Tumors in Salt-Wasting Congenital Adrenal Hyperplasia

A26-yr old male with a salt-wasting form of congenital adrenal hyperplasia presented with a 4-yr history of primary infertility. He had done well on deflazacort (range 6–18 mg/d) and fludrocortisone [0.05 mg twice a day (bid)] until late adolescence when he had several Addison’s crises due to decreased therapeutic adherence. He was lost to follow-up for several years before infertility work-up. LH and FSH were undetectable, whereas serum testosterone level was 37.4 nmol/liter normal (N): 8–26 , ACTH 501 ng/liter (N: 10 – 60), and 17-hydroxyprogesterone 1047 nmol/liter (N: 1.8 –9.2). Computed tomography scan showed massive bilateral adrenal hyperplasia (Fig. 1), and testicular ultrasonography multiple bilateral testicular adrenal rest tumors (TARTs). Semen analysis showed azoospermia. Congenital adrenal hyperplasia was shown to be due to a missense mutation in exon 8 of the 21hydroxylase gene. In response to dexamethasone (0.5 mg bid) and fludrocortisone (0.05 mg bid), ACTH and 17-hydroxyprogesterone levels fell (8 ng/liter and 2.5nmol/liter, respectively), whereas LH (4.2 U/liter) and FSH (9.3 U/liter) rose, followed by spontaneous conception. The patient’s wife delivered a healthy term male baby 12 months after the change of replacement therapy. However, repeat semen analysis and paternity confirmation were not performed. Repeat imaging studies after 13 months of treatment disclosed dramatic reduction of adrenal hyperplasia and the disappearance of TARTs. These data demonstrate the rapid reversibility of TARTs using dexamethasone as first described by Cunnah et al. (1) without side effects in contrast to previous reports (2). The chronological association of TART disappearance with pregnancy suggests that mechanical obstruction on seminal tubules might have caused this patient’s infertility, although gonadal axis suppression may also have contributed to infertility, as discussed recently (3, 4).

Energy expenditure in frontotemporal dementia: a behavioural and imaging study

See Finger (doi:10.1093/aww312) for a scientific commentary on this article. Abnormal eating behaviour and metabolic parameters including insulin resistance, dyslipidaemia and body mass index are increasingly recognized as important components of neurodegenerative disease and may contribute to survival. It has previously been established that behavioural variant frontotemporal dementia is associated with abnormal eating behaviour characterized by increased sweet preference. In this study, it was hypothesized that behavioural variant frontotemporal dementia might also be associated with altered energy expenditure. A cohort of 19 patients with behavioural variant frontotemporal dementia, 13 with Alzheimer’s disease and 16 (age- and sex-matched) healthy control subjects were studied using Actiheart devices (CamNtech) to assess resting and stressed heart rate. Actiheart devices were fitted for 7 days to measure sleeping heart rate, activity levels, and resting, active and total energy expenditure. Using high resolution structural magnetic resonance imaging the neural correlates of increased resting heart rate were investigated including cortical thickness and region of interest analyses. In behavioural variant frontotemporal dementia, resting (P = 0.001), stressed (P = 0.037) and sleeping heart rate (P = 0.038) were increased compared to control subjects, and resting heart rate (P = 0.020) compared to Alzheimer disease patients. Behavioural variant frontotemporal dementia was associated with decreased activity levels compared to controls (P = 0.002) and increased resting energy expenditure (P = 0.045) and total energy expenditure (P = 0.035). Increased resting heart rate correlated with behavioural (Cambridge Behavioural Inventory) and cognitive measures (Addenbrooke’s Cognitive Examination). Increased resting heart rate in behavioural variant frontotemporal dementia correlated with atrophy involving the mesial temporal cortex, insula, and amygdala, regions previously suggested to be involved exclusively in social and emotion processing in frontotemporal dementia. These neural correlates overlap the network involved in eating behaviour in frontotemporal dementia, suggesting a complex interaction between eating behaviour, autonomic function and energy homeostasis. As such the present study suggests that increased heart rate and autonomic changes are prevalent in behavioural variant frontotemporal dementia, and are associated with changes in energy expenditure. An understanding of these changes and neural correlates may have potential relevance to disease progression and prognosis.

Polypharmacy and specific comorbidities in university primary care settings.

AIMS Polypharmacy is associated with adverse events and multimorbidity, but data are limited on its association with specific comorbidities in primary care settings. We measured the prevalence of polypharmacy and inappropriate prescribing, and assessed the association of polypharmacy with specific comorbidities. METHODS We did a cross-sectional analysis of 1002 patients aged 50-80years followed in Swiss university primary care settings. We defined polypharmacy as ≥5 long-term prescribed drugs and multimorbidity as ≥2 comorbidities. We used logistic mixed-effects regression to assess the association of polypharmacy with the number of comorbidities, multimorbidity, specific sets of comorbidities, potentially inappropriate prescribing (PIP) and potential prescribing omission (PPO). We used multilevel mixed-effects Poisson regression to assess the association of the number of drugs with the same parameters. RESULTS Patients (mean age 63.5years, 67.5% ≥2 comorbidities, 37.0% ≥5 drugs) had a mean of 3.9 (range 0-17) drugs. Age, BMI, multimorbidity, hypertension, diabetes mellitus, chronic kidney disease, and cardiovascular diseases were independently associated with polypharmacy. The association was particularly strong for hypertension (OR 8.49, 95%CI 5.25-13.73), multimorbidity (OR 6.14, 95%CI 4.16-9.08), and oldest age (75-80years: OR 4.73, 95%CI 2.46-9.10 vs.50-54years). The prevalence of PPO was 32.2% and PIP was more frequent among participants with polypharmacy (9.3% vs. 3.2%, p<0.006). CONCLUSIONS Polypharmacy is common in university primary care settings, is strongly associated with hypertension, diabetes mellitus, chronic kidney disease and cardiovascular diseases, and increases potentially inappropriate prescribing. Multimorbid patients should be included in further trials for developing adapted guidelines and avoiding inappropriate prescribing.

Obesity and overweight associated with lower rates of colorectal cancer screening in Switzerland

Screening for colorectal cancer (CRC) is associated with reduced CRC mortality, but low screening rates have been reported in several settings. The aim of the study was to assess predictors of low CRC screening in Switzerland. A retrospective cohort of a random sample of 940 patients aged 50–80 years followed for 2 years from four Swiss University primary care settings was used. Patients with illegal residency status and a history of CRC or colorectal polyps were excluded. We abstracted sociodemographic data of patients and physicians, patient health status, and indicators derived from RAND’s Quality Assessment Tools from medical charts. We defined CRC screening as colonoscopy in the last 10 years, flexible sigmoidoscopy in the last 5 years, or fecal occult blood testing in the last 2 years. We used bivariate and multivariate logistic regression analyses. Of 940 patients (mean age 63.9 years, 42.7% women), 316 (33.6%) had undergone CRC screening. In multivariate analysis, birthplace in a country outside of Western Europe and North America [odds ratio (OR) 0.65, 95% confidence interval (CI) 0.45–0.97], male sex of the physician in charge (OR 0.67, 95% CI 0.50–0.91), BMI 25.0–29.9 kg/m2 (OR 0.66, CI 0.46–0.96) and at least 30.0 kg/m2 (OR 0.61, CI 0.40–0.90) were associated with lower CRC screening rates. Obesity, overweight, birthplace outside of Western Europe and North America, and male sex of the physician in charge were associated with lower CRC screening rates in Swiss University primary care settings. Physician perception of obesity and its impact on their recommendation for CRC screening might be a target for further research.

Community-based pharmacies: an opportunity to recruit patients?

Recruiting representative population groups with a specific disease is a challenge. In jurisdictions with no existing or no access to a database including individual disease diagnoses (e.g., electronic medical records), there are few satisfying strategies. Usually, population health surveys do not provide enough diagnostic information and may not allow recruiting large enough samples to study a specific disease. Registries or clinical cohorts may exist for specific diseases, but are often not truly population-based. Recruitment from patients’ associations and physicians’ practices may also be selective. In addition, the latter is difficult to run in busy primary care clinics. Finally, the type of information and the possibility to access health insurances’ databases may preclude their use. For diseases that require treatment involving pharmacies regularly, we propose to recruit patients in community pharmacies; this has been seldom described (Knoester et al. 2005; Van Wieren-de Wijer et al. 2009). In the canton of Vaud, Switzerland (*700,000 residents), we have applied such an approach to conduct a survey designed to describe the current population of diabetic patients and to assess the quality of their care. This survey was developed within the framework of a regional diabetes program that started in the summer of 2010 (Hagon-Traub et al. 2010), as one of many such programs implemented to tackle the chronic diseases epidemic (Nolte et al. 2008). The aim of this Hints and Kinks is to present a pharmacy-based approach of recruiting diabetic patients.