Comment on "Bayesian additional evidence for decision making under small sample uncertainty".

We examine the concept of Bayesian Additional Evidence (BAE) recently proposed by Sondhi et al. We derive simple closed-form expressions for BAE and compare its properties with other methods for assessing findings in the light of new evidence. We find that while BAE is easy to apply, it lacks both a compelling rationale and clarity of use needed for reliable decision-making.

G-protein-independent coupling of MC4R to Kir7.1 in hypothalamic neurons.

The regulated release of anorexigenic α-melanocyte stimulating hormone (α-MSH) and orexigenic Agouti-related protein (AgRP) from discrete hypothalamic arcuate neurons onto common target sites in the central nervous system has a fundamental role in the regulation of energy homeostasis. Both peptides bind with high affinity to the melanocortin-4 receptor (MC4R); existing data show that α-MSH is an agonist that couples the receptor to the Gαs signalling pathway, while AgRP binds competitively to block α-MSH binding and blocks the constitutive activity mediated by the ligand-mimetic amino-terminal domain of the receptor. Here we show that, in mice, regulation of firing activity of neurons from the paraventricular nucleus of the hypothalamus (PVN) by α-MSH and AgRP can be mediated independently of Gαs signalling by ligand-induced coupling of MC4R to closure of inwardly rectifying potassium channel, Kir7.1. Furthermore, AgRP is a biased agonist that hyperpolarizes neurons by binding to MC4R and opening Kir7.1, independently of its inhibition of α-MSH binding. Consequently, Kir7.1 signalling appears to be central to melanocortin-mediated regulation of energy homeostasis within the PVN. Coupling of MC4R to Kir7.1 may explain unusual aspects of the control of energy homeostasis by melanocortin signalling, including the gene dosage effect of MC4R and the sustained effects of AgRP on food intake.

α2A-Adrenergic Receptor Activation Decreases Parabrachial Nucleus Excitatory Drive onto BNST CRF Neurons and Reduces Their Activity In Vivo.

Stress contributes to numerous psychiatric disorders. Corticotropin releasing factor (CRF) signaling and CRF neurons in the bed nucleus of the stria terminalis (BNST) drive negative affective behaviors, thus agents that decrease activity of these cells may be of therapeutic interest. Here, we show that acute restraint stress increases cFos expression in CRF neurons in the mouse dorsal BNST, consistent with a role for these neurons in stress-related behaviors. We find that activation of α2A-adrenergic receptors (ARs) by the agonist guanfacine reduced cFos expression in these neurons both in stressed and unstressed conditions. Further, we find that α- and ß-ARs differentially regulate excitatory drive onto these neurons. Pharmacological and channelrhodopsin-assisted mapping experiments suggest that α2A-ARs specifically reduce excitatory drive from parabrachial nucleus (PBN) afferents onto CRF neurons. Given that the α2A-AR is a Gi-linked GPCR, we assessed the impact of activating the Gi-coupled DREADD hM4Di in the PBN on restraint stress regulation of BNST CRF neurons. CNO activation of PBN hM4Di reduced stress-induced Fos in BNST Crh neurons. Further, using Prkcd as an additional marker of BNST neuronal identity, we uncovered a female-specific upregulation of the coexpression of Prkcd/Crh in BNST neurons following stress, which was prevented by ovariectomy. These findings show that stress activates BNST CRF neurons, and that α2A-AR activation suppresses the in vivo activity of these cells, at least in part by suppressing excitatory drive from PBN inputs onto CRF neurons.SIGNIFICANCE STATEMENT Stress is a major variable contributing to mood disorders. Here, we show that stress increases activation of BNST CRF neurons that drive negative affective behavior. We find that the clinically well tolerated α2A-AR agonist guanfacine reduces activity of these cells in vivo, and reduces excitatory PBN inputs onto these cells ex vivo Additionally, we uncover a novel sex-dependent coexpression of Prkcd with Crh in female BNST neurons after stress, an effect abolished by ovariectomy. These results demonstrate input-specific interactions between norepinephrine and CRF, and point to an action by which guanfacine may reduce negative affective responses.

Duration of Bisphosphonate Drug Holidays and Associated Fracture Risk.

BACKGROUND: Discontinuation of bisphosphonates (BP) or a "drug holiday" after several years of treatment is increasingly common. However, the association of drug holiday duration with future fracture risk is unclear. OBJECTIVES: We evaluated the rate of fracture in relation to various lengths of drug holidays among women receiving long-term BP therapy. RESEARCH DESIGN: Observational cohort study using US Medicare data 2006-2016. Incidence rates (IRs) and Cox proportional hazards models were used to evaluate the rate and adjusted hazard ratios (aHRs) controlling for potential confounders. SUBJECTS: Women aged 65 years and above enrolled in fee-for-service Medicare who had been adherent (≥80%) to alendronate, risedronate, or zoledronate for ≥3 years. MEASURES: Hip, humerus, distal forearm, and clinical vertebral fracture. RESULTS: Among 81,427 eligible women observed for a median (interquartile range) of 4.0 (2.5, 5.3) years, 28% of women underwent a drug holiday. In the alendronate cohort (73% overall), the IR of hip fracture among women who discontinued BP for >2 years was 13.2 per 1000 person-years. Risk was increased (aHR=1.3, 1.1-1.4) versus continuing therapy (IR=8.8, referent). Rates were elevated for humerus fracture with discontinuation >2 years (aHR=1.3, 1.1-1.66) and for clinical vertebral fracture with discontinuation >2 years (aHR=1.2, 1.1-1.4). Results were similar for risedronate, zoledronate, and ibandronate for hip and clinical vertebral fracture. CONCLUSION: Discontinuing alendronate beyond 2 years was associated with increased risk of hip, humerus, and clinical vertebral fractures.

Dorsal BNST α2A-Adrenergic Receptors Produce HCN-Dependent Excitatory Actions That Initiate Anxiogenic Behaviors.

Stress is a precipitating agent in neuropsychiatric disease and initiates relapse to drug-seeking behavior in addicted patients. Targeting the stress system in protracted abstinence from drugs of abuse with anxiolytics may be an effective treatment modality for substance use disorders. α2A-adrenergic receptors (α2A-ARs) in extended amygdala structures play key roles in dampening stress responses. Contrary to early thinking, α2A-ARs are expressed at non-noradrenergic sites in the brain. These non-noradrenergic α2A-ARs play important roles in stress responses, but their cellular mechanisms of action are unclear. In humans, the α2A-AR agonist guanfacine reduces overall craving and uncouples craving from stress, yet minimally affects relapse, potentially due to competing actions in the brain. Here, we show that heteroceptor α2A-ARs postsynaptically enhance dorsal bed nucleus of the stria terminalis (dBNST) neuronal activity in mice of both sexes. This effect is mediated by hyperpolarization-activated cyclic nucleotide-gated cation channels because inhibition of these channels is necessary and sufficient for excitatory actions. Finally, this excitatory action is mimicked by clozapine-N-oxide activation of the Gi-coupled DREADD hM4Di in dBNST neurons and its activation elicits anxiety-like behavior in the elevated plus maze. Together, these data provide a framework for elucidating cell-specific actions of GPCR signaling and provide a potential mechanism whereby competing anxiogenic and anxiolytic actions of guanfacine may affect its clinical utility in the treatment of addiction.SIGNIFICANCE STATEMENT Stress affects the development of neuropsychiatric disorders including anxiety and addiction. Guanfacine is an α2A-adrenergic receptor (α2A-AR) agonist with actions in the bed nucleus of the stria terminalis (BNST) that produces antidepressant actions and uncouples stress from reward-related behaviors. Here, we show that guanfacine increases dorsal BNST neuronal activity through actions at postsynaptic α2A-ARs via a mechanism that involves hyperpolarization-activated cyclic nucleotide gated cation channels. This action is mimicked by activation of the designer receptor hM4Di expressed in the BNST, which also induces anxiety-like behaviors. Together, these data suggest that postsynaptic α2A-ARs in BNST have excitatory actions on BNST neurons and that these actions can be phenocopied by the so-called "inhibitory" DREADDs, suggesting that care must be taken regarding interpretation of data obtained with these tools.

Added Value of Including Entire Brain on Body Imaging With FDG PET/MRI.

OBJECTIVE: FDG PET/MRI examination of the body is routinely performed from the skull base to the mid thigh. Many types of brain abnormalities potentially could be detected on PET/MRI if the head was included. The objective of this study was therefore to identify and characterize brain findings incidentally detected on PET/MRI of the body with the head included. MATERIALS AND METHODS: We retrospectively identified 269 patients with FDG PET/MRI whole-body scans that included the head. PET/MR images of the brain were reviewed by a nuclear medicine physician and neuroradiologist, first individually and then concurrently. Both PET and MRI findings were identified, including abnormal FDG uptake, standardized uptake value, lesion size, and MRI signal characteristics. For each patient, relevant medical history and prior imaging were reviewed. RESULTS: Of the 269 subjects, 173 were women and 96 were men (mean age, 57.4 years). Only the initial PET/MR image of each patient was reviewed. A total of 37 of the 269 patients (13.8%) had abnormal brain findings noted on the PET/MRI whole-body scan. Sixteen patients (5.9%) had vascular disease, nine patients (3.3%) had posttherapy changes, and two (0.7%) had benign cystic lesions in the brain. Twelve patients (4.5%) had serious nonvascular brain abnormalities, including cerebral metastasis in five patients and pituitary adenomas in two patients. Only nine subjects (3.3%) had a new neurologic or cognitive symptom suggestive of a brain abnormality. CONCLUSION: Routine body imaging with FDG PET/MRI of the area from the skull base to the mid thigh may miss important brain abnormalities when the head is not included. The additional brain abnormalities identified on whole-body imaging may provide added clinical value to the management of oncology patients.

α(2A)-adrenergic receptors filter parabrachial inputs to the bed nucleus of the stria terminalis.

α2-adrenergic receptors (AR) within the bed nucleus of the stria terminalis (BNST) reduce stress-reward interactions in rodent models. In addition to their roles as autoreceptors, BNST α(2A)-ARs suppress glutamatergic transmission. One prominent glutamatergic input to the BNST originates from the parabrachial nucleus (PBN) and consists of asymmetric axosomatic synapses containing calcitonin gene-related peptide (CGRP) and vGluT2. Here we provide immunoelectron microscopic data showing that many asymmetric axosomatic synapses in the BNST contain α(2A)-ARs. Further, we examined optically evoked glutamate release ex vivo in BNST from mice with virally delivered channelrhodopsin2 (ChR2) expression in PBN. In BNST from these animals, ChR2 partially colocalized with CGRP, and activation generated EPSCs in dorsal anterolateral BNST neurons that elicited two cell-type-specific outcomes: (1) feedforward inhibition or (2) an EPSP that elicited firing. We found that the α(2A)-AR agonist guanfacine selectively inhibited this PBN input to the BNST, preferentially reducing the excitatory response in ex vivo mouse brain slices. To begin to assess the overall impact of α(2A)-AR control of this PBN input on BNST excitatory transmission, we used a Thy1-COP4 mouse line with little postsynaptic ChR2 expression nor colocalization of ChR2 with CGRP in the BNST. In slices from these mice, we found that guanfacine enhanced, rather than suppressed, optogenetically initiated excitatory drive in BNST. Thus, our study reveals distinct actions of PBN afferents within the BNST and suggests that α(2A)-AR agonists may filter excitatory transmission in the BNST by inhibiting a component of the PBN input while enhancing the actions of other inputs.

Fractures and mortality in relation to different osteoporosis treatments.

OBJECTIVES: Few studies have assessed the effectiveness of different drugs for osteoporosis (OP). We aimed to determine if fracture and mortality rates vary among patients initiating different OP medications. METHODS: We used the Medicare 5% sample to identify new users of intravenous (IV) zoledronic acid (n=1.674), oral bisphosphonates (n=32.626), IV ibandronate (n=492), calcitonin (n=2.606), raloxifene (n=1.950), or parathyroid hormone (n=549). We included beneficiaries who were ≥65 years of age, were continuously enrolled in fee-for-service Medicare and initiated therapy during 2007-2009. Outcomes were hip fracture, clinical vertebral fracture, and all-cause mortality, identified using inpatient and physician diagnosis codes for fracture, procedure codes for fracture repair, and vital status information. Cox regression models compared users of each medication to users of IV zoledronic acid, adjusting for multiple confounders. RESULTS: During follow-up (median, 0.8-1.5 years depending on the drug), 787 subjects had hip fractures, 986 had clinical vertebral fractures, and 2.999 died. Positive associations included IV ibandronate with hip fracture (adjusted hazard ratio (HR), 2.37; 95% confidence interval (CI) 1.25-4.51), calcitonin with vertebral fracture (HR=1.59, 95%CI 1.04-2.43), and calcitonin with mortality (HR=1.31; 95%CI 1.02-1.68). Adjusted HRs for other drug-outcome comparisons were not statistically significant. CONCLUSIONS: IV ibandronate and calcitonin were associated with higher rates of some types of fracture when compared to IV zolendronic acid. The relatively high mortality associated with use of calcitonin may reflect the poorer health of users of this agent.

A corticotropin releasing factor pathway for ethanol regulation of the ventral tegmental area in the bed nucleus of the stria terminalis.

A growing literature suggests that catecholamines and corticotropin-releasing factor (CRF) interact in a serial manner to activate the bed nucleus of the stria terminalis (BNST) to drive stress- or cue-induced drug- and alcohol-seeking behaviors. Data suggest that these behaviors are driven in part by BNST projections to the ventral tegmental area (VTA). Together, these findings suggest the existence of a CRF-signaling pathway within the BNST that is engaged by catecholamines and regulates the activity of BNST neurons projecting to the VTA. Here we test three aspects of this model to determine: (1) whether catecholamines modify CRF neuron activity in the BNST; (2) whether CRF regulates excitatory drive onto VTA-projecting BNST neurons; and (3) whether this system is altered by ethanol exposure and withdrawal. A CRF neuron fluorescent reporter strategy was used to identify BNST CRF neurons for whole-cell patch-clamp analysis in acutely prepared slices. Using this approach, we found that both dopamine and isoproterenol significantly depolarized BNST CRF neurons. Furthermore, using a fluorescent microsphere-based identification strategy we found that CRF enhances the frequency of spontaneous EPSCs onto VTA-projecting BNST neurons in naive mice. This action of CRF was occluded during acute withdrawal from chronic intermittent ethanol exposure. These findings suggest that dopamine and isoproterenol may enhance CRF release from local BNST sources, leading to enhancement of excitatory neurotransmission on VTA-projecting neurons, and that this pathway is engaged by patterns of alcohol exposure and withdrawal known to drive excessive alcohol intake.

Synthesis and application of resorufin ß-D-glucuronide, a low-cost chromogenic substrate for detecting Escherichia coli in drinking water.

The development of low-cost tests for Escherichia coli is hampered by the expense and limited choice of enzyme substrates. Most chromogenic substrates are required in costly amounts, while fluorogenic substrates require an additional apparatus (e.g., an ultraviolet lamp) to be detected. Herein, we propose an alternative chromogenic substrate, resorufin ß-d-glucuronide (REG), which is exceptionally sensitive and may be employed in very small amounts. We show that REG can be produced similarly to other simple glucuronides and should therefore be no more expensive. The compound is used by both healthy and injured E. coli, resulting in a pronounced color change from orange to a bright pink. Because the released dye (resorufin) has a high extinction coefficient, substantially lower amounts are needed than for commercially available substrates. The potential of this substrate is demonstrated by a presence/absence test requiring just 0.1 mg of REG/100 mL of water sample, one hundredth of the quantity needed for common chromogenic substrates, with an estimated bulk cost of ≤0.1 U.S. cents/test. REG shows promise as a chromogenic substrate for E. coli detection and should be considered in the development of new water tests, especially for low-income settings.

Broader incubation temperature tolerances for microbial drinking water testing with enzyme substrate tests.

Microbiological testing is an integral part of measures to ensure safe drinking water. However, testing can be restricted in low-resource settings by the requirement for specialized laboratory facilities and testing procedures. Precisely controlled incubation temperature is one example. The effect of varied incubation temperatures on the performance of two enzyme substrate tests for the detection of Escherichia coli and total coliforms has been examined. The aim was to determine whether these tests would provide consistent and comparable enumeration over a broader temperature range than currently specified. Recovery of chlorine-injured and wild type E. coli was examined over a range of non-standard incubation temperatures in comparison to 37 °C ± 1. Colilert(®) and Aquatest, a new E. coli-specific detection medium, served as the two representative enzyme substrate media. Recovery of chlorine-injured E. coli in Colilert was not impaired within the range 33-39 °C; the equivalent range in Aquatest medium was 31-43 °C. Both these tests recovered E. coli without significant loss of performance over a wider range of temperatures than currently specified.

Patterns and predictors of osteoporosis medication discontinuation and switching among Medicare beneficiaries.

BACKGROUND: Low adherence to bisphosphonate therapy is associated with increased fracture risk. Factors associated with discontinuation of osteoporosis medications have not been studied in-depth. This study assessed medication discontinuation and switching patterns among Medicare beneficiaries who were new users of bisphosphonates and evaluated factors possibly associated with discontinuation. METHODS: We identified patients initiating bisphosphonate treatment using a 5% random sample of Medicare beneficiaries with at least 24 months of traditional fee-for-service and part D drug coverage from 2006 through 2009. We classified medication status at the end of follow-up as: continued original bisphosphonate, discontinued without switching or restarting, restarted the same drug after a treatment gap (≥ 90 days), or switched to another anti-osteoporosis medication. We conducted logistic regression analyses to identify baseline characteristics associated with discontinuation and a case-crossover analysis to identify factors that precipitate discontinuation. RESULTS: Of 21,452 new users followed respectively for 12 months, 44% continued their original therapy, 36% discontinued without switching or restarting, 8% restarted the same drug after a gap greater than 90 days, and 11% switched to another anti-osteoporosis medication. Factors assessed during the 12-month period before initiation were weakly associated with discontinuation. Several Factors measured during follow-up were associated with discontinuation, including more physician visits, hospitalization, having a dual-energy X-ray absorptiometry test, higher Charlson comorbidity index scores, higher out-of-pocket drug payments, and upper gastrointestinal problems. Patterns were similar for 4,738 new users followed for 30 months. CONCLUSIONS: Among new bisphosphonates users, switching within and across drug classes and extended treatment gaps are common. Robust definitions and time-varying considerations should be considered to characterize medication discontinuation more accurately.

Generic alendronate use among Medicare beneficiaries: are Part D data complete?

BACKGROUND: Generic alendronate was approved in the United States on February 6, 2008. Medicare beneficiaries might pay for generic alendronate out-of-pocket without having claims submitted, resulting in misclassification of generic alendronate use in Medicare data. OBJECTIVES: To estimate the completeness of generic alendronate use in 2008 Medicare Part D data; to identify factors associated with staying on branded alendronate versus switching to a generic product. METHODS: We identified Medicare beneficiaries highly adherent (medication possession ratio ≥80%) with branded alendronate during 1/1/06-2/6/07 ("2007 cohort") and during 1/1/07-2/6/08 ("2008 cohort"). The outcome was medication status at the end of follow-up (12/31/2007 or 12/31/2008), classified as continued branded alendronate, switched to generic alendronate, switched to another bisphosphonate or presumed discontinued bisphosphonate therapy. Cox regression estimated the hazard ratio (HR) for discontinuation in 2008 compared to 2007. Multinomial logistic regression identified factors associated with medication status for the 2008 cohort. RESULTS: Among 15,310 subjects using branded alendronate in the 2008 cohort, 81% switched to generic alendronate. The proportion presumably discontinuing bisphosphonate therapy was 8.9% in 2008 compared to 7.7% in the 2007 cohort (adjusted HR, 1.15; 95% confidence interval, 1.05, 1.26). Factors associated with staying on branded alendronate in 2008 were higher income, eligibility for a low income subsidy and use of Fosamax® plus vitamin D. CONCLUSION: Evaluation of Medicare prescription drug data suggests that the amount of missing claims for generic alendronate in 2008 was not substantial, and misclassification of exposure in studies examining alendronate use post-generic product availability should be minimal.

Driving performance and turning reaction time following hip arthroscopy for FAIS: does capsular repair matter?

PURPOSE: (1) To compare the pre- and postoperative driving performance in patients undergoing hip arthroscopy for femoroacetabular impingement syndrome (FAIS); (2) to examine the differences in driving performance between patients with versus without capsular repair. METHODS: Patients who underwent arthroscopic hip surgery for FAIS were included. Driving performance of participating patients was collected using a driving simulator preoperatively and at 2 weeks, 4-6 weeks and 8-12 weeks postoperatively. Data collected included demographics, surgery laterality, intraoperative procedures, left and right turn reaction time, total turn reaction time, gas off time (GOF), and break reaction time (BRT). Repeated measures analysis of variance (ANOVA) was used for statistical analysis. RESULTS: 21 subjects (9 males, 12 females) with a mean age of 30 ± 9 years were included and 57.1% of the subjects had right-sided surgery. There was no difference between the mean preoperative and the 2-week postoperative left (0.72 seconds and 0.75 seconds, respectively) right (0.77 seconds and 0.75 seconds, respectively), and total (0.74 seconds and 0.75 seconds, respectively) turn reaction times as well as GOF (0.62 seconds and 0.60 seconds, respectively) and BRT (0.92 seconds and 0.93 seconds, respectively), indicating that the patients' driving performance returned to the preoperative level as early as 2 weeks following hip arthroscopy for FAIS. There was no significant difference amongst any of the driving variables between patients who underwent capsular repair (50%) and those who did not. There was no significant difference amongst any of the driving variable s between patients who underwent left versus right hip arthroscopy. CONCLUSIONS: Patients' driving performance returns to the preoperative level as early as 2 weeks after hip arthroscopy for FAIS. Surgery laterality nor capsular repair make any significant difference in the time for driving abilities to return to baseline. The impact of intraoperative procedures performed, and the analgesic medications used postoperatively on the driving ability of patients undergoing hip arthroscopy warrants further investigation in larger patient populations.

The Cost of Mental Health Comorbid Conditions in Burn Patients: A Single-site Experience.

Many burn survivors suffer from psychiatric sequelae long after their physical injuries have healed. This may even be more pronounced in individuals who have a history of mental health disorders prior to admission. The aim of this study was to explore the clinical outcomes of patients with previously diagnosed mental health disorders who were admitted to our Burn Center. This was a single-site, retrospective review using our institutional Burn Center registry. All adult patients (18 years or older) admitted to our Burn Center between January 1, 2014 and June 30, 2021 with burn injury or inhalation injury were included in this study. Variables of interest included demographics and burn mechanism. Outcomes of interests were length of stay, cost of hospitalization, and mortality. A P-value of < .05 was considered statistically significant for all analyses. There were 4958 patients included in this study, with 35% of these patients having a previous diagnosis of mental health disorders. Patients with mental health disorders were younger, with larger burns, P < .05. They had significantly longer lengths of stay and significantly higher costs (P < .00001). Mortality for those with a mental health disorder history was 2% and 3% for those without (P = .04). Patients with pre-existing mental health disorders had decreased odds of mortality. However, they do have extended lengths of stay, which may exhaust current sparse staff and burn bed resources.

Does A History of Malignancy Lead to Worse Outcomes in a Single-center Burn Unit?

A history of malignancy is associated with worse outcomes in cardiac disease and trauma. Our objective was to determine if a past medical history or comorbid condition of cancer portends an increased morbidity or mortality in burns or skin-sloughing disorders at our institution. Patients were identified using our Institutional Burn Center registry and linked to the clinical and administrative data. All patients admitted between January 1, 2014 and June 30, 2021 were eligible for inclusion. Demographics, length of stay, comorbid conditions and mortality were evaluated. Statistical analysis was performed with Kruskal-Wallis, chi-square, and Fisher's exact tests. Seven thousand three hundred seventy-two patients were admitted during this time period. Three hundred eighty-six patients had a history of cancer (5%). Patients with a history of cancer were older (56 vs 44 years, P < .0001). They had a significantly longer length of stay (16 vs 10 days, P < .0001). They also had larger burns and higher hospital costs ($147,021 versus $83,788, P < .0001), were more likely to be male and more likely to have a skin-sloughing disorder. A history of cancer was not associated with increased odds of burn mortality. Thus, a history of cancer is associated with increased lengths of stay and costs in patients admitted for burn injury or skin-sloughing disorders, but not associated with increased mortality. Further study is warranted to investigate and mitigate what aspects of their care could be adjusted to improve outcomes.

Outcomes of COPD Patients with Flame Burn and Inhalation Injuries at a Single Institution.

The presence of any comorbid condition may lead to worse outcomes after burn injury. Chronic obstructive pulmonary disease (COPD) is a condition with significant morbidity and mortality. In 2018, about 16 million adults in the United States reported a diagnosis of COPD based on data from the American Lung Association. The objective of this study was to explore the outcomes of patients with COPD admitted to our Burn Center with flame burns and/or inhalation injury. Patients were identified using our Institutional Burn Center registry and linked to the clinical and administrative data. All adult flame-injured and/or inhalation injury-only patients admitted to our burn center between July 1, 2011 and June 30, 2020 were included. Demographics, length of stay, burn, and patient characteristics and outcomes, including mortality, were evaluated. Four thousand three hundred ninety-seven patients were included in the study. Patients were divided into two populations, those with COPD (n = 515) and those without a diagnosis of COPD (n = 3882). Patients with COPD were older, more likely to be white and male, and had smaller sized burns, p < .001. Patients with COPD were more likely to be smokers and have comorbid conditions. There was no statistically significant difference between the incidence of inhalation injury, lengths of stay, or number of ventilator days. Burn size and inhalation injury increased mortality risk regardless of COPD severity, as did age among those not on home oxygen. More studies are needed to determine the genomic or proteomic changes in patients with COPD that lead to worse outcomes after flame injury, and/or inhalation injury alone.