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Idiopathic Pulmonary Fibrosis is a progressive and fatal interstitial lung disease (ILD) characterized by a typical radiographic or histologic usual interstitial pneumonia (UIP) pattern. In 2018, diagnostic categories of UIP based on computed tomography patterns were revised by the Fleischner Society. The study aimed to describe differences in comorbidities and spirometry in ILD patients that were characterized by high-resolution computed tomography (HRCT) images as having a typical, probable, indeterminate, and alternative diagnosis of UIP. We retrospectively studied 80 ILD patients from 2017 to 2019. Typical UIP was defined using the Fleischner Society diagnostic criteria for IPF. Atypical UIP was reached by consensus after a multidisciplinary clinical–radiological–pathological review of patient data. Baseline characteristics, comorbidities, and spirometry were compared among the four subgroups. Among 80 patients, 59% were male, 61% had a history of smoking, and the mean age was 67.7 ± 10 years (SD). A typical UIP pattern was more frequently observed among patients with chronic obstructive pulmonary disease (COPD) (p

There is a current paucity of information about the obstetric and perinatal outcomes of pregnant novel coronavirus disease 2019 (COVID-19) patients in North America. Data from China suggest that pregnant women with COVID-19 have favorable maternal and neonatal outcomes, with rare cases of critical illness or respiratory compromise. However, we report two cases of pregnant women diagnosed with COVID-19 in the late preterm period admitted to tertiary care hospitals in New York City for respiratory indications. After presenting with mild symptoms, both quickly developed worsening respiratory distress requiring intubation, and both delivered preterm via caesarean delivery. These cases highlight the potential for rapid respiratory decompensation in pregnant COVID-19 patients and the maternal-fetal considerations in managing these cases.

Progressive fibrosing interstitial lung disease (PF-ILD) has been redefined as a new clinical syndrome that shares similar genetics, pathophysiology, and natural history to idiopathic pulmonary fibrosis (IPF). IPF is the most common form of idiopathic interstitial pneumonias, which is progressive in nature and is associated with significant mortality. Therapies targeting an inflammatory and/or immune response have not been consistently effective or well tolerated in patients with IPF. The two antifibrotic drugs approved for IPF treatment, nintedanib and pirfenidone, have been shown to reduce lung function decline in PF-ILD. Novel uses of antifibrotic therapy are emerging due to a paucity of evidence-based treatments for multiple ILD subtypes. In this review, we describe the current body of knowledge on antifibrotic therapy and immunomodulators in PF-ILD, drawing from experience in IPF where appropriate.

Atypical EEG patterns not consistent with standard sleep staging criteria have been observed in medical intensive care unit (ICU) patients. Our aim was to examine the relationship between sleep architecture and sedation in critically ill mechanically ventilated patients pre‐ and post‐extubation. We performed a prospective observational repeated measures study where 50 mechanically ventilated patients with 31 paired analyses were examined at an academic medical centre. The sleep efficiency was 58.3 ± 25.4% for intubated patients and 45.6 ± 25.4% for extubated patients (p = .02). Intubated patients spent 76.33 ± 3.34% of time in non‐rapid eye movement (NREM) sleep compared to 64.66 ± 4.06% of time for extubated patients (p = .02). REM sleep constituted 1.36 ± 0.67% of total sleep time in intubated patients and 2.06 ± 1.09% in extubated patients (p = .58). Relative sleep atypia was higher in intubated patients compared to extubated patients (3.38 ± 0.87 versus 2.79 ± 0.42; p

Introduction: Deep vein thrombosis (DVT) is a recognized but preventable cause of morbidity and mortality in the medical intensive care unit (MICU). We examined the prevalence and risk factors for DVT in MICU patients who underwent diagnostic venous duplex ultrasonography (DUS) and the potential effect on clinical outcomes. Methods: This is a retrospective study examining prevalence of DVT in 678 consecutive patients admitted to a tertiary care level academic MICU from July 2014 to 2015. Patients who underwent diagnostic DUS were included. Potential conditions of interest were mechanical ventilation, hemodialysis, sepsis, Sequential Organ Failure Assessment (SOFA) scores, central venous catheters, prior DVT, and malignancy. Primary outcomes were pulmonary embolism, ICU length of stay, and mortality. Additionally, means of thromboprophylaxis was compared between the groups. Multivariable logistic regression analysis was utilized to determine predictors of DVT occurrence. Results: Of the 678 patients, 243 (36%) patients underwent DUS to evaluate for DVT. The prevalence of DVT was 16% (38) among tested patients, and a prior history of DVT was associated with DVT prevalence ( P < .01). Between cases and controls, there were no significant differences in central venous catheters, mechanical ventilation, hemodialysis, sepsis, SOFA scores, malignancy, and recent surgery. Patients receiving chemical prophylaxis had fewer DVTs compared to persons with no prophylaxis (14% vs 29%; P = .01) and persons with dual chemical and mechanical prophylaxis ( P = 0.1). Fourteen percent of patients tested had documented DVT while on chemoprophylaxis. There were no significant differences in ICU length of stay ( P = .35) or mortality ( P = .34). Conclusions: Despite the appropriate use of universal thromboprophylaxis, critically ill nonsurgical patients still demonstrated high rates of DVT. A history of DVT was the sole predictor for development of proximal DVT on DUS testing. Dual chemical and mechanical prophylaxis does not appear to be superior to single-chemical prophylaxis in DVT prevention in this population.

Although obstructive sleep apnea (OSA) is common and pneumonia is a frequent cause of acute respiratory failure requiring admission to the intensive care unit, little is known about the effect of OSA on this patient population. This study examined outcomes associated with OSA in patients with pneumonia requiring invasive mechanical ventilation.The Nationwide Inpatient Sample was investigated for discharges with a primary diagnosis of pneumonia requiring invasive mechanical ventilation between 2009 and 2011. Persons aged 18 to 75 years with OSA were compared with patients without OSA. Outcomes included in-hospital mortality and nonroutine discharges.Among 74032 hospitalizations, 13.8% (10227) were obese, and 10.3% (7610) had OSA. Obstructive sleep apnea patients had decreased in-hospital mortality (17.0% vs 25.8%; P.01) and nonroutine discharge (74.4% vs 79.4%; P.01) when compared with non-OSA patients. In adjusted logistic models, OSA was associated with a 27% decreased risk of in-hospital mortality (odds ratio, 0.73; 95% confidence interval, 0.68-0.79; P.01) and a 21% decreased risk of nonroutine discharge (odds ratio, 0.79; 95% confidence interval, 0.74-0.84; P.01).In mechanically ventilated patients with pneumonia, OSA was associated decreased in-hospital mortality and nonroutine discharge. It is possible that differences in treatment pattern may partially explain improved survival.

Background:Exercise improves sleep quality, yet people with untreated obstructive sleep apnea (OSA) may engage in less physical activity (PA) due to fatigue and daytime sleepiness. We examined changes in PA and sleep quality before and after treatment with continuous positive airway pressure (CPAP) in OSA patients.Methods:In this prospective longitudinal study, persons with a primary diagnosis of OSA were enrolled at a community-based hospital in New York City. At 3 time intervals pre- and post-CPAP (3–8 months), we measured sleep quality using validated questionnaires, perceived PA using the International Physical Activity Questionnaire (IPAQ), and actual PA using pedometer steps per day. We sought to investigate how CPAP use and changes in sleep quality impacted the number of steps taken, as recorded in pedometer steps.Results:In total, 62 patients were enrolled in the study from March 2012 to July 2014. In all, patients averaged 53 years of age, and 26 patients (42%) were female. Among all participants, 86% of persons had moderate to severe sleep apnea (AHI ≥15). Approximately 73% of participants were compliant with CPAP use. Poor sleep quality correlated with lower actual PA (P = .004) at baseline. At 3 and 7 months, there was significant improvement in sleep quality (Δ –2.63 ± 3.4 and Δ –3.5 ± 3.8; P < .001) and actual PA (Δ 840 ± 1313 and Δ 1431 ± 1419 steps/day, P < .001) compared with baseline. On multivariate analyses, participants with a higher waist circumference had a significantly greater increase in actual PA (P = .018).Conclusion:Treatment of OSA with CPAP had a progressive incremental improvement in sleep quality and actual PA.

There is growing evidence supporting a multifactorial etiology that includes genetic, neurochemical, and physiological components for eating disorders above and beyond the more conventional theories based on psychological and sociocultural factors. Ghrelin is one of the key gut signals associated with appetite, and the only known circulating hormone that triggers a positive energy balance by stimulating food intake. This review summarizes recent findings and several conflicting reports on ghrelin in eating disorders. Understanding these findings and inconsistencies may help in developing new methods to prevent and treat patients with these disorders.

Neuroimaging is becoming increasingly common in obesity research as investigators try to understand the neurological underpinnings of appetite and body weight in humans. Positron emission tomography (PET), functional magnetic resonance imaging (fMRI) and magnetic resonance imaging (MRI) studies examining responses to food intake and food cues, dopamine function and brain volume in lean vs. obese individuals are now beginning to coalesce in identifying irregularities in a range of regions implicated in reward (e.g. striatum, orbitofrontal cortex, insula), emotion and memory (e.g. amygdala, hippocampus), homeostatic regulation of intake (e.g. hypothalamus), sensory and motor processing (e.g. insula, precentral gyrus), and cognitive control and attention (e.g. prefrontal cortex, cingulate). Studies of weight change in children and adolescents, and those at high genetic risk for obesity, promise to illuminate causal processes. Studies examining specific eating behaviours (e.g. external eating, emotional eating, dietary restraint) are teaching us about the distinct neural networks that drive components of appetite, and contribute to the phenotype of body weight. Finally, innovative investigations of appetite-related hormones, including studies of abnormalities (e.g. leptin deficiency) and interventions (e.g. leptin replacement, bariatric surgery), are shedding light on the interactive relationship between gut and brain. The dynamic distributed vulnerability model of eating behaviour in obesity that we propose has scientific and practical implications.

The rising prevalence of obesity has reached pandemic proportions, with an associated cost estimated at up to 7% of health expenditures worldwide. Bariatric surgery is currently the only effective long-term treatment for obesity and obesity-related co-morbidities in clinically severely obese patients. However, the precise physiological mechanisms underlying the postsurgical reductions in caloric intake and body weight are poorly comprehended. It has been suggested that changes in hormones involved in hunger, food intake and satiety via the neurohormonal network may contribute to the efficacy of bariatric procedures. In this review, we consider how gastrointestinal hormone concentrations, involved in appetite and body weight regulation via the gut–brain axis, are altered by different bariatric procedures. Special emphasis is placed on neurohormonal changes following Roux-en-Y gastric bypass surgery, which is the most common and effective procedure used today.

Obesity has reached pandemic proportions, with bariatric surgery representing the only currently available treatment demonstrating long-term effectiveness. Over 200,000 bariatric procedures are performed each year in the US alone. Given the reliable and singular success of bariatric procedures, increased attention is being paid to identifying the accompanying neurohormonal changes that may contribute to the resulting decrease in energy intake. Numerous investigations of postsurgical changes in gut peptides have been conducted, suggesting greater alterations in endocrine function in combination restrictive and malabsorptive procedures (e.g., Roux-en-Y gastric bypass) as compared to purely restrictive procedures (e.g., gastric banding), which may contribute to the increased effectiveness of combination procedures. However, very few studies have been performed and relatively little is known about changes in neural activation that may result from bariatric procedures, which likely interact with changes in gut peptides to influence postsurgical caloric intake. This review provides a background in the neurohormonal regulation of energy intake and discusses how differing forms of bariatric surgery may affect the neurohormonal network, with emphasis on Roux-en-Y gastric bypass, the most commonly performed procedure worldwide. The paper represents an invited review by a symposium, award winner or keynote speaker at the Society for the Study of Ingestive Behavior [SSIB] Annual Meeting in Portland, July 2009.

Obesity has increasingly become a major medical and public health burden in both developed and developing countries. Numerous hormones are involved in controlling appetite and food intake via the neuro-humoral gut-brain axis and several peptides that are synthesized and secreted from the gut have been recently investigated in order to determine their effects on food intake and satiety. Ghrelin is an appetite-stimulating peptide that rises in the fasted state causing in- creases in food intake. Obestatin is a newly discovered hormone encoded by the same gene as ghrelin, and its putative role in the regulation of appetite and metabolism is unclear. A number of studies using animal models have shown that obes- tatin opposes the effects of ghrelin on food intake whilst others found that obestatin has little if any affect on gastrointesti- nal motility, or on food intake. There are also controversies to the receptor mediating obestatin effects with the previously orphan G protein coupled receptor GPR39 suggested to be the main candidate. Investigating the molecular mechanism underlying obestatin and other gut hormones involved in appetite regulation may prove to be useful in finding new strate- gies to treat obesity.

Sexually-dimorphic behavioral and biological aspects of human eating have been described. Using psychophysiological interactions (PPI) analysis, we investigated sex-based differences in functional connectivity with a key emotion-processing region (amygdala, AMG) and a key reward-processing area (ventral striatum, VS) in response to high vs. low energy-dense (ED) food images using blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI) in obese persons in fasted and fed states. When fed, in response to high vs. low-ED food cues, obese men (vs. women) had greater functional connectivity with AMG in right subgenual anterior cingulate, whereas obese women had greater functional connectivity with AMG in left angular gyrus and right primary motor areas. In addition, when fed, AMG functional connectivity with pre/post-central gyrus was more associated with BMI in women (vs. men). When fasted, obese men (vs. women) had greater functional connectivity with AMG in bilateral supplementary frontal and primary motor areas, left precuneus, and right cuneus, whereas obese women had greater functional connectivity with AMG in left inferior frontal gyrus, right thalamus, and dorsomedial prefrontal cortex. When fed, greater functional connectivity with VS was observed in men in bilateral supplementary and primary motor areas, left postcentral gyrus, and left precuneus. These sex-based differences in functional connectivity in response to visual food cues may help partly explain differential eating behavior, pathology prevalence, and outcomes in men and women.

Heightened cortisol response to stress due to hyperactivation of the hypothalamic–pituitary–adrenal (HPA) axis may stimulate appetite and food intake. In this study, we assessed cortisol responsivity to a cold pressor test (CPT) as well as appetite ratings and subsequent test meal intake (TMI) in obese women. Following an overnight fast on two counterbalanced days, 20 obese women immersed their non-dominant hand for 2 min in ice water (CPT) or warm water (WW) as a control. Plasma cortisol (ng/ml), heart rate, and blood pressure, as well as ratings of stress, pain, and appetite, were serially acquired. An ad libitum liquid meal was offered at 45 min and intake measured covertly. Fasting cortisol was higher at 15 min (mean peak cortisol) following the CPT compared to WW. Higher stress was reported at 2 and 15 min for the CPT compared to WW. Pain, an indirect marker of the acute stress, systolic and diastolic blood pressure increased following the CPT at 2 min compared to WW. Hunger decreased after the CPT at 2 and 15 min, and desire to eat ratings were lower following CPT compared to WW. Subjects did not have greater test meal intake (TMI) following CPT compared to WW. There was also no significant relationship between cortisol levels following stress and TMI, indicating that cortisol did not predict subsequent intake in obese women.

Body Adiposity Index (BAI), a new surrogate measure of body fat (hip circumference/[height1.5 -18]), has been proposed as an alternative to BMI. We compared BAI with BMI, and each of them with laboratory measures of body fat-derived from bioimpedance analysis (BIA), air displacement (ADP), and dual-energy x-ray absorptiometry (DXA) in clinically severe obese (CSO) participants. Nineteen pre-bariatric surgery CSO, non-diabetic women were recruited (age=32.6±7.7 SD; BMI=46.5±9.0 kg/m2). Anthropometrics and body fat percentage (% fat) were determined from BIA, ADP, and DXA. Scatter plots with lines of equality and Bland-Altman plots were used to compare BAI and BMI with % fat derived from BIA, ADP, and DXA. BAI and BMI correlated highly with each other (r=0.90, p

Dopaminergic hypofunction and hyperprolactinaemia have been implicated in the pathogenesis of obesity and glucose intolerance. The aim of this pilot study was to determine the efficacy of cabergoline, a dopamine receptor agonist, on body weight and glucose tolerance in obese non-diabetic persons with normal plasma prolactin levels.This 16-week double blind, placebo-controlled pilot study randomized non-diabetic obese adults (body mass index 30-42 kg/m(2) ) to placebo or cabergoline (0.25 mg twice weekly for 4 weeks followed by 0.5 mg twice weekly for the next 12 weeks). Of 40 subjects enrolled, 29 completed 16 weeks: 16 randomized to placebo and 13 to cabergoline. All subjects were counselled on a 500 kcal/day calorie deficit diet. A 75-g oral glucose tolerance test was performed at baseline and at 16 weeks.As expected, prolactin levels decreased after cabergoline (p0.001). Weight loss was similar after placebo compared with cabergoline treatment: 1.0 vs. 1.2% body weight, respectively. Fasting glucose levels did not differ between groups after treatment, however, 90-min postprandial glucose and insulin decreased in the cabergoline group only (p = 0.029). HOMA-IR (homeostasis model of assessment) increased by 40% after placebo and 1.5% after cabergoline treatment.This pilot study suggests that cabergoline therapy may improve glucose tolerance independent of weight loss, however, a larger, longer term study of dopamine receptor agonist therapy in obese individuals is warranted to confirm this finding.

Two major biological players in the regulation of body weight are the gut and the brain. Peptides released from the gut convey information about energy needs to areas of the brain involved in homeostatic control of food intake. There is emerging evidence that human food intake is also under the control of cortical and subcortical areas related to reward and cognition. The extent to which gut hormones influence these brain areas is not fully understood. Novel methods combining the study of neural activity and hormonal signalling promise to advance our understanding of gut-brain interactions. Here, we review a growing number of animal and human studies using neuroimaging methods (functional magnetic resonance imaging, positron emission tomography) to measure brain activation in relation to nutrient loads and infusion of gut peptides. Implications for current and future pharmacological treatments for obesity are discussed.