A Comparison of Preoperative Telephone Call Versus Mailed Educational Materials on Patient-Reported Outcomes in Mohs Micrographic Surgery.

BACKGROUND: Preoperative education has uncertain benefits on the preparedness and satisfaction of patients undergoing Mohs micrographic surgery (MMS). OBJECTIVE: We sought to determine the effect of a preoperative telephone call on preparedness and satisfaction in patients undergoing same-day office consultation and MMS. MATERIALS AND METHODS: All new patients ( N = 208) scheduled for same-day office consultation and MMS were mailed a standardized preoperative packet. Approximately half of those patients were randomly selected to also receive a preoperative phone call. On the day of the surgery, patients completed an anonymous preoperative and postoperative survey assessing their preparedness and satisfaction with the preoperative education received. RESULTS: There was no significant difference in patient preparedness between the letter only (LO) and phone call and letter study groups. There was a significant difference in preoperative satisfaction-a higher percentage of LO patients were "somewhat satisfied" or "not satisfied" with the preoperative education received ( p = .013). CONCLUSION: Preoperative phone consultation, in addition to mailed educational materials, did not have a statistically significant effect on patient preparedness in patients undergoing MMS; however, there was a trend toward increased satisfaction with the preoperative education provided in patients who received a preoperative phone call.

Byproducts of inflammatory radical metabolism provide transient nutrient niches for microbes in the inflamed gut.

Louis Pasteur's experiments on tartaric acid laid the foundation for our understanding of molecular chirality, but major questions remain. By comparing the optical activity of naturally-occurring tartaric acid with chemically-synthesized paratartaric acid, Pasteur realized that naturally-occurring tartaric acid contained only L-tartaric acid while paratartaric acid consisted of a racemic mixture of D- and L-tartaric acid. Curiously, D-tartaric acid has no known natural source, yet several gut bacteria specifically degrade D-tartaric acid. Here, we investigated the oxidation of monosaccharides by inflammatory reactive oxygen and nitrogen species. We found that this reaction yields an array of alpha hydroxy carboxylic acids, including tartaric acid isomers. Utilization of inflammation- derived D- and L-tartaric acid enhanced colonization by Salmonella Typhimurium and E. coli in murine models of gut inflammation. Our findings suggest that byproducts of inflammatory radical metabolism, such as tartrate and other alpha hydroxy carboxylic acids, create transient nutrient niches for enteric pathogens and other potentially harmful bacteria. Furthermore, this work illustrates that inflammatory radicals generate a zoo of molecules, some of which may erroneously presumed to be xenobiotics.

Colonocyte-derived lactate promotes E. coli fitness in the context of inflammation-associated gut microbiota dysbiosis.

BACKGROUND: Intestinal inflammation disrupts the microbiota composition leading to an expansion of Enterobacteriaceae family members (dysbiosis). Associated with this shift in microbiota composition is a profound change in the metabolic landscape of the intestine. It is unclear how changes in metabolite availability during gut inflammation impact microbial and host physiology. RESULTS: We investigated microbial and host lactate metabolism in murine models of infectious and non-infectious colitis. During inflammation-associated dysbiosis, lactate levels in the gut lumen increased. The disease-associated spike in lactate availability was significantly reduced in mice lacking the lactate dehydrogenase A subunit in intestinal epithelial cells. Commensal E. coli and pathogenic Salmonella, representative Enterobacteriaceae family members, utilized lactate via the respiratory L-lactate dehydrogenase LldD to increase fitness. Furthermore, mice lacking the lactate dehydrogenase A subunit in intestinal epithelial cells exhibited lower levels of inflammation in a model of non-infectious colitis. CONCLUSIONS: The release of lactate by intestinal epithelial cells during gut inflammation impacts the metabolism of gut-associated microbial communities. These findings suggest that during intestinal inflammation and dysbiosis, changes in metabolite availability can perpetuate colitis-associated disturbances of microbiota composition. Video Abstract.

Postoperative Pain After Mohs Surgery: Physician Perceptions and How Those Perceptions Influence Opioid Prescribing Practices.

BACKGROUND: Little is known about dermatologists' perceptions of postoperative pain and how those perceptions correlate with patient-reported pain and opioid prescribing. OBJECTIVE: To determine dermatologists' accuracy in predicting postoperative pain compared with patient-reported pain and how physicians' perceptions affect opioid prescribing practices. METHODS AND MATERIALS: A prospective observational study in which patients undergoing Mohs surgery rated pain on the Numerical Rating Scale (0-10). Using the same scale, the physician predicted how much pain the patient would experience postoperatively on the evening of surgery. All analgesic medications taken in postoperative period were recorded. RESULTS: A total of 316 patients completed the study (70% completion rate). Physician predictions were correlated with patient-reported pain (p < .001; r = 0.29) and were within 2 points of patient-reported pain in 70% of cases. When physicians overestimated patient-reported by ≥3 points, they were not more likely to prescribe opioids (p = .8094). Physicians predicted higher pain for patients who were prescribed opioids (p = .0002). CONCLUSION: Dermatologists were fairly accurate at predicting postoperative pain. Dermatologists were not more likely to prescribe opioids when pain was overpredicted.

Epithelial-Derived Reactive Oxygen Species Enable AppBCX-Mediated Aerobic Respiration of Escherichia coli during Intestinal Inflammation.

The intestinal epithelium separates host tissue and gut-associated microbial communities. During inflammation, the host releases reactive oxygen and nitrogen species as an antimicrobial response. The impact of these radicals on gut microbes is incompletely understood. We discovered that the cryptic appBCX genes, predicted to encode a cytochrome bd-II oxidase, conferred a fitness advantage for E. coli in chemical and genetic models of non-infectious colitis. This fitness advantage was absent in mice that lacked epithelial NADPH oxidase 1 (NOX1) activity. In laboratory growth experiments, supplementation with exogenous hydrogen peroxide enhanced E. coli growth through AppBCX-mediated respiration in a catalase-dependent manner. We conclude that epithelial-derived reactive oxygen species are degraded in the gut lumen, which gives rise to molecular oxygen that supports the aerobic respiration of E. coli. This work illustrates how epithelial host responses intersect with gut microbial metabolism in the context of gut inflammation.