Health care in the United States has seen many great innovations and successes in the past decades. However, to this day, the color of a person’s skin determines—to a considerable degree—his/her prospects of wellness; risk of disease, and death; and the quality of care received. Disparities in cardiovascular disease (CVD)—the leading cause of morbidity and mortality globally—are one of the starkest reminders of social injustices, and racial inequities, which continue to plague our society. People of color—including Black, Hispanic, American Indian, Asian, and others—experience varying degrees of social disadvantage that puts these groups at increased risk of CVD and poor disease outcomes, including mortality. Racial/ethnic disparities in CVD, while documented extensively, have not been examined from a broad, upstream, social determinants of health lens. In this review, we apply a comprehensive social determinants of health framework to better understand how structural racism increases individual and cumulative social determinants of health burden for historically underserved racial and ethnic groups, and increases their risk of CVD. We analyze the link between race, racism, and CVD, including major pathways and structural barriers to cardiovascular health, using 5 distinct social determinants of health domains: economic stability ; neighborhood and physical environment ; education ; community and social context ; and healthcare system . We conclude with a set of research and policy recommendations to inform future work in the field, and move a step closer to health equity.

The worldwide incidence of neuroendocrine tumors (NETs) has been increasing. They are a very diverse group of tumors which are commonly found in the gastrointestinal and bronchopulmonary tracts. These tumors usually express somatostatin receptors. Therefore, somatostatin analogs are used for symptom relief as well as treatment. Of the many therapeutic options available, peptide receptor radionuclide therapy (PRRT) has been shown to be very promising. In January 2018, the Food Drug and Authority (FDA) approved 177 Lu-Dotatate for use in gastroenteropancreatic neuroendocrine tumors (GEP-NETs). Lutetium is a lower energy beta-emitting radionuclide. The therapeutic use of lutetium- 177 ( 177 Lu) has shown better results in advanced gastroenteropancreatic and bronchial neuroendocrine tumors when compared with other therapies available. Adverse effects associated with this therapy include myelotoxicity and nephrotoxicity as the radiopeptides are reabsorbed and accumulate in the renal interstitium. Everolimus is a good and safe option in patients pretreated with 177 Lu-Dotatate. Lutetium, in combination with somatostatin analogs, has proven efficacy to treat gastroenteropancreatic neuroendocrine tumors in candidates with somatostatin receptor-positive advanced tumors and normal renal function. This therapy has great potential as it decreases tumor size, improves symptoms, and improves quality of life.

Objective: This study examined the association between social determinants of health (SDOH) burden and overweight/obesity in a nationally representative sample of adults in the United States. Methods: Data for 161,795 adults aged ≥18 years from the 2013 to 2017 National Health Interview Survey were used. A total of 38 SDOH were aggregated to create a cumulative SDOH score, which was divided into quartiles (Q1-Q4) to denote levels of SDOH burden. Prevalence of overweight and obesity was examined across SDOH quartiles in the total population and by age, sex, and race/ethnicity. Multinomial logistic regression models were used to analyze the association between SDOH quartiles and overweight/obesity, adjusting for relevant covariates.Results: There was a graded increase in obesity prevalence with increasing SDOH burden. At nearly each quartile, overweight and obesity rates were higher for middleaged and non-Hispanic Black adults compared with their counterparts; additional differences were observed by sex. In fully adjusted models, SDOH-Q4 was associated with 15%, 50%, and 70% higher relative prevalence of overweight, obesity class 1 and 2, and obesity class 3, respectively, relative to SDOH-Q1.

Objective Janus kinase (JAK) inhibition effectively treats immune‐mediated inflammatory diseases (IMIDs); however, concern over the risk of major adverse cardiac events (MACE) and venous thromboembolism (VTE) remains. We aimed to evaluate the safety (VTE and MACE outcomes) of JAK inhibitors in the treatment of IMIDs. Methods A search in PubMed, Embase, and http://clinicaltrials.gov databases was conducted for randomized clinical trials (RCTs) of JAK inhibitors across IMIDs. Primary outcomes were VTE and MACE with JAK inhibitors compared with placebo and active comparator arms stratified by follow‐up time. Results Sixty‐six RCTs enrolled 38,574 patients with a mean age of 48.8 years and a mean follow‐up of 10.5 months. JAK inhibitors had a numerically higher rate of VTE when compared with controls (odds ratio [OR] 1.65; 95% confidence interval [CI]: 0.97‐2.79), driven by trials with a follow‐up duration of 12 or more months (OR 2.17; 95% CI: 1.16‐4.05; Pinteraction = 0.05). When compared with active comparators, JAK inhibitors increased VTE in clinical trials with 12 or more months’ versus less than 12 months’ follow‐up time (OR 2.38 [95% CI: 1.24‐4.57] vs 0.30 [95% CI: 0.07‐1.26], respectively; Pinteraction = 0.01). No increased risk of VTE was seen when comparing JAK inhibitors with placebo arms. For the outcome of MACE, the results were largely similar but did not reach statistical significance (OR 1.19; 95% CI: 0.86‐1.64). Conclusion JAK inhibitors when compared with active comparator arms increased the risk of VTE, which was dependent on duration of exposure. Future clinical trials with extended follow‐up are needed to clarify the safety profiles of JAK inhibitors.

Endoscopic retrograde cholangiopancreatography (ERCP) is a minimally invasive procedure that is widely used by endoscopists and has a robust therapeutic profile. It uses endoscopy and imaging for a variety of diagnostic as well as therapeutic purposes. It is used for the management of a lot of pancreaticobiliary diseases such as obstructive jaundice, obstruction related to bile ducts, pancreatic biliary tumors, and traumatic or iatrogenic damage to the bile ducts. Other therapeutic interventions that can be done via ERCP include sphincterotomy, dilation of strictures, removal of biliary stones and placement of stents. Air embolism presents with cardiovascular, pulmonary, and neurologic signs and symptoms. Treatment of air embolism should be started early in suspected cases, and it should be in the differential diagnoses of various complications secondary to high risk of ERCP, especially if a cardiopulmonary compromise is present. Air embolism is rare but a serious complication associated with ERCP. The physicians must keep this in mind while performing ERCP in patients with predisposing risk factors. This review highlights the mechanism, causes, risk factors, pathophysiology, clinical signs, diagnostic modalities, treatment, and preventive measures to deal with this catastrophic complication.

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Disease prevention frameworks and clinical practice guidelines in the United States (US) have traditionally ignored upstream social determinants of health (SDOH), which are critical for reducing disparities in cardiovascular disease (CVD)—the leading cause of death in the US. Existing evidence demonstrates a protective effect of social support, social cohesion, and community engagement on overall health and wellbeing. Increasing community and social support is a major objective of the Healthy People 2030 initiative, with special provisions for vulnerable populations. However, to date, existing evidence of the association between community and social context (CSC)—an integral SDOH domain—and CVD has not been reviewed extensively. In particular, the individual and cumulative impact of CSC on CVD risk and the pathways linking CSC to cardiovascular outcomes are not well understood. In this review, we critically appraise current knowledge of the association between CSC and CVD, describe potential pathways linking CSC to CVD, and identify opportunities for evidence-based policy and practice interventions to improve CVD outcomes.