An analysis of physician reviews in relation to quality and social media presence.

Press Ganey patient engagement survey scores are used among health care facilities throughout the US to evaluate patients' perception of the quality of care provided. The relation of Press Ganey score to primary quality metrics has not been reported before; thus, we studied it in a cohort of Baylor Scott and White Health primary care physicians. Using simple linear regression, we evaluated Press Ganey scores and compared them with primary care quality metrics associated with improved patient outcomes, including cancer screening, depression screening, blood pressure, and glucose control, in addition to well-child visits. We found that overall quality had a very low linear correlation with Press Ganey survey items, and high-quality performance and increased number of practice years had an overall positive correlation with high survey ratings. We also found that social media presence or total website activity was not an important feature in predicting the top 25 quality performers within the health care system.

Kounis syndrome presenting as ST elevation acute myocardial infarction.

Allergic acute coronary syndrome, Kounis syndrome, is a rare cause of ST-segment elevation myocardial infarction triggered by an allergic reaction to a drug or environmental allergen, resulting in atheromatous plaque rupture or coronary artery vasospasm. We report three cases of Kounis syndrome presenting as ST-segment elevation myocardial infarction.

D2HGDH regulates alpha-ketoglutarate levels and dioxygenase function by modulating IDH2.

Isocitrate dehydrogenases (IDH) convert isocitrate to alpha-ketoglutarate (α-KG). In cancer, mutant IDH1/2 reduces α-KG to D2-hydroxyglutarate (D2-HG) disrupting α-KG-dependent dioxygenases. However, the physiological relevance of controlling the interconversion of D2-HG into α-KG, mediated by D2-hydroxyglutarate dehydrogenase (D2HGDH), remains obscure. Here we show that wild-type D2HGDH elevates α-KG levels, influencing histone and DNA methylation, and HIF1α hydroxylation. Conversely, the D2HGDH mutants that we find in diffuse large B-cell lymphoma are enzymatically inert. D2-HG is a low-abundance metabolite, but we show that it can meaningfully elevate α-KG levels by positively modulating mitochondrial IDH activity and inducing IDH2 expression. Accordingly, genetic depletion of IDH2 abrogates D2HGDH effects, whereas ectopic IDH2 rescues D2HGDH-deficient cells. Our data link D2HGDH to cancer and describe an additional role for the enzyme: the regulation of IDH2 activity and α-KG-mediated epigenetic remodelling. These data further expose the intricacies of mitochondrial metabolism and inform on the pathogenesis of D2HGDH-deficient diseases.