Purpose of Review Hypertriglyceridemia (HTG) is common and is a significant contributor to atherosclerosis and pancreatitis risk. Specific HTG treatments have had variable success in reducing atherosclerosis risk. Novel therapies for severe HTG treatment and pancreatitis risk reduction are likely to be available soon. These novel therapies are expected to have broader applications for more moderate HTG and atherosclerosis risk reduction as well. Recent Findings NHANES 2012 data has confirmed a reduction in average triglyceride (TG) levels in the US population. Dietary modification and weight reduction when needed remain the core treatment elements for all individuals with HTG, while statin therapy is a foundational pharmacologic care for atherosclerotic cardiovascular disease (ASCVD) event risk reduction. In addition, the REDUCE-IT study provides evidence for additional benefit from the use of high-dose icosapent ethyl (IPE) on top of background medical therapy in adults with moderate HTG and ASCVD or type 2 diabetes mellitus (T2D) and additional ASCVD risk factors. However, treatment with eicosapentaenoic acid (EPA) combined with docosahexanoic acid (DHA) did not reduce ASCVD in a similar population studied in the STRENGTH trial. Furthermore, novel therapeutics targeting PPAR-ɑ, as well as ApoC-III and AngPTL3, effectively lower TG levels in individuals with moderate and severe HTG, respectively. These treatments may have applicability for reducing risk from ASCVD among individuals with chylomicronemia; in addition, ApoC-III and AngPTL3 treatments may have a role in treating individuals with the rare monogenic familial chylomicronemia syndrome (FCS) at risk for acute pancreatitis (AP) . Summary Residual ASCVD risk in individuals treated with contemporary care may be due in part to non-LDL lipid abnormalities including HTG. The findings from REDUCE-IT, but not STRENGTH, confirm that consumption of high-dose EPA may reduce ASCVD risk, while combination therapy of EPA plus DHA does not reduce ASCVD in a similar population. TG lowering likely reduces ASCVD risk in individuals with HTG, but ASCVD risk is multifactorial; the added benefit of IPE to contemporary preventive therapy is the consequence of differential non-TG biologic properties between the two fatty acids. Acute pancreatitis is more difficult to study prospectively since it is less common; however, TG lowering is likely critical for the care of at-risk individuals. Additional benefit from novel therapy that has an impact on this otherwise refractory condition is anticipated.

The rapid resolution of hypercalcemia after termination of pregnancy, despite persistent gigantomastia, provides evidence for a pathologic role of the placenta in the excess production of PTHrP, possibly through an as yet uncharacterized placenta-breast hormonal axis.

Infantile hypertrophic pyloric stenosis is a concerning cause of nonbilious vomiting in the neonatal population. Although a number of etiological theories exist, its exact cause remains nebulous. The question of an infectious etiology (or contribution) has been previously examined in case reports and case series, with recent support through suggestions of seasonality and familial aggregation with unclear inheritance patterns. The present review discusses the published literature regarding infectious etiologies of infantile hypertrophic pyloric stenosis. Furthermore, it attempts to demonstrate that newer research regarding an NOS1 genetic etiology does not exclude, but rather can be consistent with, an infectious etiology.

To the Editor: The article by Nagaraja and Lincoff 1 is an excellent review of the International Study of Comparative Health Effectiveness With Medical and Invasive Approaches trial. It highlights the continuing evolution of patient-centered approaches in the management of stable coronary artery disease. Their algorithm contains the phrase "cardiac computed tomography to assess calcium score and exclude left main disease." Are the authors referring to the coronary artery calcium score (CACS) or coronary computed tomography angiography (CCTA)? I believe they mean the latter, but as both are computed tomographic modalities of the heart and the difference may not be readily appreciated by a general medicine audience, it may be helpful to clarify.The CACS is most useful in risk assessment in primary prevention, particularly to improve specifi city in older adults and allow for a personalized and risk-driven decision in use of lipid-lowering medications. For patients with established coronary artery disease and an abnormal stress test, it seems unlikely that the CACS will add any clinically useful information and may provide false reassurance, particularly in exclusion of disease. Noncalcifi ed plaque, including that in the left main, would not be visible on CACS.Further, it is noncalcifi ed plaque that is