Risk factor

C difficile: 10% of Patients Are Carriers at Hospitalization.

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One in 10 (9.7%) patients has asymptomatic Clostridium difficile(CD) colonization at the time of hospitalization, according to a new study. The 3 main risk factors for colonization are recent hospitalization (odds ratio [OR], 2.45; 95% confidence interval [CI], 1.02 – 5.84), chronic dialysis (OR, 8.12; 95% CI, 1.80 – 36.65), and corticosteroid use (OR, 3.09; 95% CI, 1.24 – 7.73).

Surbhi Leekha, MBBS, MPH, from the Division of Infectious Diseases, Mayo Clinic, Rochester, Minnesota, and colleagues present their analysis of adults admitted to a tertiary care hospital in an article published in the May issue of the American Journal of Infection Control. Approximately half of admissions were enrolled in the study, but only 22% of admitted patients provided stool samples (n = 320).

Colonization rates were determined by polymerase chain reaction analysis of formed stool. This approach circumvented the problems associated with anaerobic cultures.

The data are consistent with a previous large, multicenter study in Canada, which demonstrated that recent hospitalization is a risk factor for CD colonization. A previous study has also demonstrated that individuals receiving chronic dialysis are at risk for CD infection. This is the first study, however, to demonstrate that corticosteroid use is a risk factor for CD colonization.

The authors note that although CD epidemiology has changed during the past decades, the risk factors for infection appear to be unchanged.

“We propose that elucidation of risk factors for CD colonization could help identify asymptomatic individuals for targeted surveillance in selected hospital settings such as high endemicity despite the use of other control measures or epidemic situations. Potential infection prevention measures to prevent CD transmission from asymptomatically colonized patients include contact precautions, hand hygiene with soap and water, and environmental cleaning with a sporicidal agent. In our population, by targeting those with identified risk factors, we would need to screen approximately half of those patients with anticipated stays >24 hours, to identify three-fourths of those colonized with C difficile,” the authors write.

Source: medscape.com

 

 

Mental disorders and vulnerability to homicidal death: Swedish nationwide cohort study.

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depressedman

Objective To determine the risk of people with mental disorders being victims of homicide.

Design National cohort study.

Setting Sweden.

Participants Entire adult population (n=7 253 516).

Main outcome measures Homicidal death during eight years of follow-up (2001-08); hazard ratios for the association between mental disorders and homicidal death, with adjustment for sociodemographic confounders; potential modifying effect of comorbid substance use.

Results 615 homicidal deaths occurred in 54.4 million person years of follow-up. Mortality rates due to homicide (per 100 000 person years) were 2.8 among people with mental disorders compared with 1.1 in the general population. After adjustment for sociodemographic confounders, any mental disorder was associated with a 4.9-fold (95% confidence interval 4.0 to 6.0) risk of homicidal death, relative to people without mental disorders. Strong associations were found irrespective of age, sex, or other sociodemographic characteristics. Although the risk of homicidal death was highest among people with substance use disorders (approximately ninefold), the risk was also increased among those with personality disorders (3.2-fold), depression (2.6-fold), anxiety disorders (2.2-fold), or schizophrenia (1.8-fold) and did not seem to be explained by comorbid substance use. Sociodemographic risk factors included male sex, being unmarried, and low socioeconomic status.

Conclusions In this large cohort study, people with mental disorders, including those with substance use disorders, personality disorders, depression, anxiety disorders, or schizophrenia, had greatly increased risks of homicidal death. Interventions to reduce violent death among people with mental disorders should tackle victimisation and homicidal death in addition to suicide and accidents, which share common risk factors.

Source:BMJ

 

 

Cognitive function and other risk factors for mild traumatic brain injury in young men: nationwide cohort study.

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Abstract

Objective To investigate cognitive function and other risk factors for mild traumatic brain injury in young men.

Design Nationwide prospective cohort study.

Setting Sweden.

Participants 305 885 men conscripted for military service from 1989 to 1994.

Main outcome measure mild traumatic brain injuries in relation to cognitive function and other potential risk factors assessed at conscription and follow-up.

 

Results Men with one mild traumatic brain injury within two years before (n=1988) or after cognitive testing (n=2214) had about 5.5% lower overall cognitive function scores than did men with no mild traumatic brain injury during follow up (P<0.001 for both). Moreover, men with at least two mild traumatic brain injuries after cognitive testing (n=795) had 15% lower overall cognitive function scores compared with those with no such injury (P<0.001). Independent strong risk factors (P<1×10−10) for at least one mild traumatic brain injury after cognitive testing (n=12 494 events) included low overall cognitive function, a previous mild traumatic brain injury, hospital admission for intoxications, and low education and socioeconomic status. In a sub-cohort of twin pairs in which one twin had a mild traumatic brain injury before cognitive testing (n=63), both twins had lower logical performance and technical performance compared with men in the total cohort with no mild traumatic brain injury (P<0.05 for all).

 

Conclusion Low cognitive function, intoxications, and factors related to low socioeconomic status were strong independent risk factors for mild traumatic brain injuries in men. The low cognitive function in twin pairs discordant for mild traumatic brain injury suggests a genetic component to the low cognitive function associated with such injuries. The study included only men, so inferences to women should be made with caution.

Source:BMJ

 

Selection criteria for lung-cancer screening.

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The National Lung Screening Trial (NLST) used risk factors for lung cancer (e.g., >/=30 pack-years of smoking and <15 years since quitting) as selection criteria for lung-cancer screening. Use of an accurate model that incorporates additional risk factors to select persons for screening may identify more persons who have lung cancer or in whom lung cancer will develop.
METHODS: We modified the 2011 lung-cancer risk-prediction model from our Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial to ensure applicability to NLST data; risk was the probability of a diagnosis of lung cancer during the 6-year study period. We developed and validated the model (PLCO(M2012)) with data from the 80,375 persons in the PLCO control and intervention groups who had ever smoked. Discrimination (area under the receiver-operating-characteristic curve [AUC]) and calibration were assessed. In the validation data set, 14,144 of 37,332 persons (37.9%) met NLST criteria. For comparison, 14,144 highest-risk persons were considered positive (eligible for screening) according to PLCO(M2012) criteria. We compared the accuracy of PLCO(M2012) criteria with NLST criteria to detect lung cancer. Cox models were used to evaluate whether the reduction in mortality among 53,202 persons undergoing low-dose computed tomographic screening in the NLST differed according to risk.
RESULTS: The AUC was 0.803 in the development data set and 0.797 in the validation data set. As compared with NLST criteria, PLCO(M2012) criteria had improved sensitivity (83.0% vs. 71.1%, P<0.001) and positive predictive value (4.0% vs. 3.4%, P=0.01), without loss of specificity (62.9% and. 62.7%, respectively; P=0.54); 41.3% fewer lung cancers were missed. The NLST screening effect did not vary according to PLCO(M2012) risk (P=0.61 for interaction).
CONCLUSIONS: The use of the PLCO(M2012) model was more sensitive than the NLST criteria for lung-cancer detection.

Source:NEJM

Multivitamin Use Does Not Reduce Cardiovascular Risk in Men.

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Taking a daily multivitamin does not reduce the risk for major cardiovascular events in men, according to a JAMA study.

As part of the Physicians’ Health Study II, nearly 15,000 men aged 50 and older were randomized to a daily multivitamin or placebo. After a median follow-up of 11 years, the rate of the primary composite outcome — myocardial infarction, stroke, or cardiovascular mortality — did not differ between the two groups. There were slightly fewer MI deaths among multivitamin users, but the authors speculate that this may have been due to chance. The effect did not differ between men with and without baseline cardiovascular disease.

An editorialist writes that multiple trials “clearly confirm that CVD cannot be prevented or treated with vitamins.” She concludes: “The message needs to remain simple and focused: CVD is largely preventable, and this can be achieved by eating healthy foods, exercising regularly, avoiding tobacco products, and, for those with high risk factor levels or previous CVD events, taking proven, safe, and effective medications.”

Source: JAMA

CRP, Fibrinogen, and Cardiac Risk Stratification.

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Both biomarkers slightly improved prediction when added to a base model, but their comparative clinical value has yet to be determined.

C-reactive protein (CRP) and fibrinogen have both been proposed as predictors of cardiovascular risk in asymptomatic individuals. In this analysis, investigators from the Emerging Risk Factors Collaboration examined data from 52 studies to assess how much the addition of these newer risk factors improve standard risk prediction and to model the likely preventive effect of systematic testing.

When added to a base model including age, sex, smoking status, history of diabetes, blood pressure, and cholesterol, inclusion of CRP resulted in an improvement of 1.52% in the net reclassification of individuals into low (<10%), intermediate (10% to <20%) and high (20%) 10-year risk for events. Fibrinogen testing was associated with a slightly smaller improvement in net reclassification (0.83%). Based on these data, the authors estimate that assessing CRP in individuals at intermediate risk would help prevent 1 event over 10 years for every 440 people screened; the corresponding estimate for fibrinogen was 1 event for every 490 screened.

Comment: This analysis suggests that both CRP and fibrinogen can improve risk prediction, but the incremental gains are modest. As the authors acknowledge, several important questions remain unanswered, such as how these serum markers compare with other serum markers and with imaging markers such as calcium scoring  with regard to both effectiveness and cost.

Source: Journal Watch Cardiology

Beta-Blockers Might Not Reduce CV Events in Patients with Stable Heart Disease .

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Beta-blockers might not lower the risk for major cardiovascular events in patients with — or at risk for — stable coronary artery disease (CAD), according to a JAMA study.

Investigators compared outcomes with and without beta-blocker therapy in about 22,000 participants in the REACH (Reduction of Atherothrombosis for Continued Health) registry who had prior myocardial infarction, CAD without MI, or CAD risk factors only. Patients were followed for roughly 44 months.

In both cohorts with CAD, risk for the primary outcome — a composite of cardiovascular death, MI, or stroke — did not differ significantly between beta-blocker recipients and nonrecipients. In the risk-factor-only group, the primary outcome occurred more often among beta-blocker recipients (14% vs. 12% among nonrecipients).

The authors note that their findings support recent changes in secondary prevention guidelines, giving class I status only to the short-term use of beta-blockers after MI.

Source:JAMA

 

High cardiovascular risk in severely obese young children and adolescents.

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Abstract

Objective To assess the prevalence of cardiovascular risk factors in severely obese children and adolescents.

Methods A nationwide prospective surveillance study was carried out from July 2005 to July 2007 where paediatricians were asked to report all new cases of severe obesity in 2–18-year-old children to the Dutch Paediatric Surveillance Unit. Severe obesity is defined by gender and age-dependent cut-off points for body mass index based on Dutch National Growth Studies corresponding to the adult cut-off point of 35 kg/m2. Paediatricians were asked to complete a questionnaire for every severely obese child regarding socio-demographic characteristics and cardiovascular risk factors (blood pressure, fasting blood glucose and lipids).

Results In 2005, 2006 and 2007, 94%, 87% and 87%, respectively, of paediatricians in the Netherlands responded to the monthly request from the Dutch Paediatric Surveillance Unit and 500 children with newly diagnosed severe obesity were reported. 72.6% (n=363) of paediatricians responded to a subsequent questionnaire. Cardiovascular risk factor data were available in 255/307 (83%) children who were correctly classified as severely obese. 67% had at least one cardiovascular risk factor (56% hypertension, 14% high blood glucose, 0.7% type 2 diabetes and up to 54% low HDL-cholesterol). Remarkably, 62% of severely obese children aged ≤12 years already had one or more cardiovascular risk factors.

Conclusion A high number (2/3) of severely obese children have cardiovascular risk factors. Internationally accepted criteria for defining severe obesity and guidelines for early detection and treatment of severe obesity and comorbidity are urgently needed.

Source: BMJ.

 

 

Mood disorder as a specific complication of stroke

Appraising the impact of Folstein et al’s1 1977 report on ‘Mood disorder as a specific complication of stroke’ is a challenging task for someone who did not enter medical school until the mid-1980s. Stroke changed in the 1970s, and the view in retrospect appears unrecognisable. This was a dramatic change, from an intellectual backwater too dull for neurologists to even bother seeing, to become a hot topic: a disease to be studied in mega trials and a standard bearer for evidence based medicine. Prior to the 1970s, with the exception of dysphasia, neuropsychiatric complications had been given scant thought—it was a disorder that affected how people walked. It was recognised that some elderly patients became depressed after stroke but the prevailing view appeared to be “so what, they’re old and infirm, what do you expect?” It is against this backdrop that the work of researchers at John Hopkins has to be judged.

The importance of the paper was perhaps not the findings but the very fact that they published the study at all. Two years earlier their John Hopkins colleague Robert Robinson published a fascinating study demonstrating that experimentally induced strokes in rats led to alteration in cerebral metabolism of catecholamines that correlated with behavioural changes in the rats that mimicked depression.2 Folstein’s data appeared to be an early example of translational research and were widely disseminated as they appeared to link laboratory based neurobiology with clinical practice. Tantalisingly it seemed to offer a human model for studying the anatomy of depression. Appearing, as it did, contemporaneously with the development of cerebral imaging techniques, this was the impetus researchers had needed. Over the next 2 decades, 143 reports were made on this topic. Sadly, the theory of anatomical location of brain lesions as a simplistic explanation for mood disorder did not stand up to scrutiny.3 It was perhaps too good to be true; a salient reminder of the need for confirmation in humans of findings from animal models.

In critical analysis the paper itself has suffered with the passage of time. Epidemiological techniques have advanced, as has expectation of sample sizes and analysis strategies. Future investigators submitting to the journal are unlikely to get a case control study past peer review without any statistical comparisons! But for all that, it is a well written report that gets its key messages across clearly and succinctly, perhaps because the manuscript was not cluttered with t tests and hazard ratios, and that is something editors welcome in any era.

And the key messages were important—the realisation that depression after stroke was not simply an understandable reaction to disability has stood the test of time. We now know that 33% of stroke patients suffer from depression (95% CI 29% to 36%).4 We now know that this depression leads to increased disability5 and probably increased mortality.6 Most importantly, we now know that antidepressants are effective in treating it.7 Countless patients round the world are benefiting from this knowledge and that is an impact that any researcher can be proud of.

Footnotes

  • Competing interests None.
  • Provenance and peer review Commissioned; not externally peer reviewed.

References

  1. ↵
    1. Folstein MF,
    2. Maiberger R,
    3. McHugh PR

. Mood disorder as a specific complication of stroke. J Neurol Neurosurg Psychiatry 1977;40:1018–20.

[Abstract/FREE Full text]

  1. ↵
    1. Robinson RG,
    2. Shoemaker WJ,
    3. Schlumpf M,
    4. et al

. Effect of experimental cerebral infarction in rat brain on catecholamines and behaviour. Nature 1975;255:332–4.

[CrossRef][Medline]

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    1. Carson AJ,
    2. Machale S,
    3. Allen K,
    4. et al

. Depression after stroke and lesion location: a systematic review. Lancet 2000;356:122–6.

[CrossRef][Medline][Web of Science]

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    1. Hackett ML,
    2. Yapa C,
    3. Parag V,
    4. et al

. Frequency of depression after stroke: a systematic review of observational studies. Stroke 2005;36:1330–40.

[Abstract/FREE Full text]

  1. ↵
    1. Pohjasvaara T,
    2. Vataja R,
    3. Leppavuori A,
    4. et al

. Depression is an independent predictor of poor long-term functional outcome poststroke. Eur J Neurol 2001;8:315–19.

[CrossRef][Medline][Web of Science]

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    1. House A,
    2. Knapp P,
    3. Bamford J,
    4. et al

. Mortality at 12 and 24 months after stroke may be associated with depressive symptoms at 1 month. Stroke 2001;32:696–701.

[Abstract/FREE Full text]

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    1. Hackett ML,
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    4. et al

. Interventions for treating depression after stroke. Cochrane Database Syst Rev 2008;4:CD003437.

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Source:BMJ

 

 

High Breast Density Does Not Predict Death among Breast Cancer Patients.

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High breast density is a strong risk factor for developing breast cancer, but it does not affect a breast cancer patient’s risk of death, according to a study recently published in the Journal of the National Cancer Institute.

Denser breasts have more glandular tissue (cells that produce milk during lactation) and supportive connective tissue than fatty tissue. Doctors use a scale called the Breast Imaging Reporting and Data System (BI-RADS) to classify breast density as observed on mammograms on a scale from 1 to 4, with 1 being the least dense and 4 the most dense.

To examine the relationship between breast density and risk of death from breast cancer, Dr. Gretchen Gierach and her colleagues from NCI’s Division of Cancer Epidemiology and ­­­Genetics and the NCI-sponsored Breast Cancer Surveillance Consortium (BCSC) examined medical records from more than 9,000 breast cancer patients collected by the BCSC.

After accounting for age, body mass, treatment, and other factors that could influence the risk of death, the researchers found that among women diagnosed with breast cancer, women with dense breasts were not more likely to die of the disease or of other causes than women with less-dense breasts during nearly 7 years of follow-up, on average.

Unexpectedly, the researchers observed that breast cancer patients with the least-dense breasts had an increased risk of death from breast cancer if they had large tumors or were obese. However, given that this result was based on relatively small numbers of women and has not been previously suggested by other studies, “these findings need to be replicated in larger studies,” said Dr. Gierach.

Obesity is a risk factor for death from breast cancer and is also inversely related to breast density. (That is, obese women are less likely to have dense breasts.) Therefore, obesity could affect associations between breast density and breast cancer death.

“We already know that obesity is a poor prognostic factor for breast cancer in general, but this particular analysis showed that the subgroup of women who were obese and had less-dense, fatty breasts were at greatest risk,” she explained. “Our hypothesis is that the fat content in the breast might be enhancing obesity-related mechanisms that heighten tumor aggressiveness in breast cancer. We are conducting studies to better understand the biology of breast density.”

Source: NCI

Erectile dysfunction: A sign of heart disease?

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The same process that creates heart disease may also cause erectile dysfunction, only earlier.

Erectile dysfunction — difficulty maintaining an erection sufficient for sex — can be an early warning sign of heart problems. Understanding the connections between the two may help you get treatment before heart problems become serious. Likewise, if you have heart disease, getting the right treatment may help with erectile dysfunction.

Clogged arteries: Where erectile dysfunction and heart disease meet

Atherosclerosis (ath-ur-o-skluh-ROE-sis) — sometimes called hardening of the arteries — is the buildup of plaques in the arteries of your body. The smaller arteries in the body, such as in the penis, are the first to get plugged up. The plaque reduces blood flow in the penis, making an erection difficult. Erectile dysfunction is an alert to look for atherosclerosis in larger arteries supplying your heart and other organs and to take steps to treat it. Atherosclerosis also increases your risk of other problems, including aneurysm, stroke and peripheral artery disease.

Certain men are at increased risk

Besides sharing a common disease process, erectile dysfunction and heart disease also share many risk factors. These risk factors increase the likelihood that your erectile dysfunction could be a sign of underlying atherosclerosis and heart disease:

  • Having diabetes. Men who have diabetes are at especially high risk of erectile dysfunction, heart disease and other problems caused by restricted blood flow.
  • Having high cholesterol. A high level of low-density lipoprotein (LDL, or “bad”) cholesterol can lead to atherosclerosis.
  • Being a smoker. Smoking cigarettes raises your risk of developing atherosclerosis. It also directly affects your ability to get an erection.
  • Having high blood pressure. Over time, high blood pressure damages the lining of your arteries and accelerates the process of atherosclerosis.
  • Having a family member with heart disease. It’s more likely your erectile dysfunction could be linked to heart disease if you have a first-degree relative such as a sibling or parent who had heart disease at a young age.
  • Your age. The younger you are, the more likely that erectile dysfunction signals a risk of heart disease. Men younger than 50 are at especially high risk. In men older than 70, erectile dysfunction is much less likely to be a sign of heart disease.
  • Being overweight. Being overweight or obese increases your risk of both heart disease and erectile dysfunction due to atherosclerosis and other reasons.
  • Being depressed. There’s some evidence that depression is associated with an increased chance of having heart problems — and erectile dysfunction.

Treatment for erectile dysfunction caused by heart disease

If your doctor thinks you may be at risk of heart disease, making lifestyle changes such as exercising, changing your diet or losing weight may be enough to help keep your heart healthy — and improve your ability to have an erection. If you have more-serious signs and symptoms of heart disease, you may need further tests or treatment. If you have both erectile dysfunction and heart disease, talk to your doctor about treatment options for erectile dysfunction. If you take certain heart medications, especially nitrates, it is not safe to use many of the medications used to treat erectile dysfunction.

Source: Mayo Clinic.