IMPORTANCE

New dissemination methods are needed to engage physicians in evidence-based continuing medical education (CME).

OBJECTIVE

To examine the effectiveness of social media in engaging physicians in non-industry-sponsored CME.

DESIGN

We tested the effect of different media platforms (e-mail, Facebook, paid Facebook and Twitter), CME topics, and different "hooks" (e.g., Q&A, clinical pearl and best evidence) on driving clicks to a landing site featuring non-industry sponsored CME. We modelled the effects of social media platform, CME topic, and hook using negative binomial regression on clicks to a single landing site. We used clicks to landing site adjusted for exposure and message number to calculate rate ratios. To understand how physicians interact with CME content on social media, we also conducted interviews with 10 physicians.

SETTING

The National Physicians Alliance (NPA) membership.

PARTICIPANTS

NPA e-mail recipients, Facebook followers and friends, and Twitter followers.

MAIN OUTCOMES AND MEASURES

Clicks to the NPA's CME landing site.

RESULTS

On average, 4,544 recipients received each message. Messages generated a total of 592 clicks to the landing site, for a rate of 5.4 clicks per 1000 recipients exposed. There were 5.4 clicks from e-mail, 11.9 clicks from Facebook, 5.5 clicks from paid Facebook, and 6.9 clicks from Twitter to the landing site for 1000 physicians exposed to each of 4 selected CME modules. A Facebook post generated 2.3x as many clicks to the landing site as did an e-mail after controlling for participant exposure, hook type and CME topic (p<0.001). Twitter posts (p = 0.13) and paid Facebook posts (p = 0.06) were not statistically different from e-mail in generating clicks to the landing site. Use of different hooks to engage physicians had no impact on clicks to the landing site. Interviews with physicians suggested that social media might not be a preferred vehicle for disseminating CME.

CONCLUSIONS

Social media has a modest impact on driving traffic to evidence-based CME options. Facebook had a superior effect on driving physician web traffic to evidence-based CME compared to other social media platforms and email.

The statins have been used for 30 years to prevent coronary artery disease and stroke. Their primary mechanism of action is the lowering of serum cholesterol through inhibiting hepatic cholesterol biosynthesis thereby upregulating the hepatic low-density lipoprotein (LDL) receptors and increasing the clearance of LDL-cholesterol. Statins may exert cardiovascular protective effects that are independent of LDL-cholesterol lowering called pleiotropic effects. Because statins inhibit the production of isoprenoid intermediates in the cholesterol biosynthetic pathway, the post-translational prenylation of small GTP-binding proteins such as Rho and Rac, and their downstream effectors such as Rho kinase and nicotinamide adenine dinucleotide phosphate oxidases are also inhibited. In cell culture and animal studies, these effects alter the expression of endothelial nitric oxide synthase, the stability of atherosclerotic plaques, the production of proinflammatory cytokines and reactive oxygen species, the reactivity of platelets, and the development of cardiac hypertrophy and fibrosis. The relative contributions of statin pleiotropy to clinical outcomes, however, remain a matter of debate and are hard to quantify because the degree of isoprenoid inhibition by statins correlates to some extent with the amount of LDL-cholesterol reduction. This review examines some of the currently proposed molecular mechanisms for statin pleiotropy and discusses whether they could have any clinical relevance in cardiovascular disease.

BACKGROUND

Chronic kidney disease (CKD) is common among HIV-infected individuals but serum creatinine is insensitive for detecting kidney damage at early stages. We hypothesized that HIV infection would be associated with elevations in subclinical markers of kidney injury and fibrosis in a contemporary cohort of men.

METHODS

In this cross-sectional study, we measured urine levels of interleukin-18 (IL-18), kidney injury molecule-1 (KIM-1), pro-collagen type III N-terminal pro-peptide (PIIINP) and albumin-creatinine ratio (ACR) in 813 HIV-infected and 331 uninfected men enrolled in the Multicenter AIDS Cohort Study.

RESULTS

Median eGFR was 95 ml/min/1.73 m among African-Americans (n=376) and 87 ml/min/1.73 m among Caucasians (n=768). Among HIV-infected men, the median CD4 lymphocyte count was 572 cells/mm and 76% of men had undetectable HIV RNA levels. After multivariable adjustment for traditional CKD risk factors including eGFR, HIV infection was associated with 52% higher urine IL-18 (95% CI, 33%, 73%), 44% higher KIM-1 (27%, 64%), 30% higher PIIINP (15%, 47%) and 84% higher ACR (54%, 120%), with similar effect sizes among African-Americans and Caucasians (P>0.2 for tests of interaction by race). These associations remained statistically significant in analyses that excluded persons with detectable HIV RNA levels and in models that adjusted for cumulative exposure to tenofovir disoproxil fumarate.

CONCLUSIONS

Compared with uninfected men, HIV-infected men had more extensive glomerular and tubulointerstitial damage, as assessed by urine biomarkers. Future studies should evaluate whether combinations of biomarkers can be used to monitor stages of kidney injury and to predict CKD risk in HIV-infected individuals.