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Case Presentation A 34-year-old previously healthy man of Korean descent (height, 174 cm; weight, 47.4 kg) demonstrated dyspnea with cough and chest tightness. The patient had no relevant occupational exposures and no history of illicit drug or tobacco use. His medical history was notable for chronic sinus tachycardia of undetermined cause, hypertension, gout, glaucoma of the right eye, and a remote history of an intracranial malignancy 24 years prior treated with unspecified chemotherapy, craniotomy, and ventriculoperitoneal shunt placement. His active medications included diltiazem, candesartan, and colchicine as needed.

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: The ongoing coronavirus disease 2019 (COVID-19) pandemic has resulted in persistent pulmonary complications among survivors. As our understanding of post infectious pulmonary phenomena continues to evolve, it is clear there are multiple difference manifestations of pulmonary lung disease associated with severe acute respiratory syndrome coronavirus 2 (SARS CoV-2). Here we describe a case of bullous lung disease as a complication of COVID-19. CASE PRESENTATION: A 61-year-old gentleman without significant past medical history presented with worsening shortness of breath of two days duration. Three months prior to presentation he was hospitalized for acute hypoxemic respiratory failure due to COVID-19 requiring Bi-level Positive Airway Pressure which was complicated by pneumomediastinum and right-sided pneumothorax that required chemical pleurodesis. On this presentation, he was hypoxemic and CT scan of the chest showed extensive bullous lung disease (BLD) throughout the right lung with mediastinal shift, not noted on prior imaging. He denied family history of lung disease or connective tissue disease. Prior to COVID-19 infection he was an avid marathon-runner, worked as a civil engineer with no occupational exposures, and never smoked tobacco products, vaped electronic cigarettes, or used illicit drugs. Admission vitals were unremarkable and physical exam revealed decreased breath sounds on the right side. His laboratory data including repeat SARS CoV-2 nasal polymerase chain reaction, alpha-1 antitrypsin and angiotensin-converting enzyme levels were unrevealing. Cardiothoracic surgery was consulted and he successfully underwent Video-Assisted Thoracoscopic surgery with wedge resection of the right lower lobe and chemical pleurodesis. Pathology ruled out a loculated pneumothorax and confirmed the presence of bullae localized within the lung parenchyma. DISCUSSION: Bullous lung disease has been described secondary to cocaine, cigarette or marijuana smoking as well as Emphysema, Sarcoidosis, alpha1-antitrypsin deficiency, Marfan's syndrome, Ehlers-Danlos syndrome and inhaled fiberglass exposure. However, our patient did not have any family history of lung disease, occupational exposures or smoking history, and physical exam was not suggestive of either Marfan's or Ehlers-Danlos syndrome. Since there was no underlying lung disease prior to hospitalization, common etiologies of bullous lung disease were ruled out, and given temporal association with COVID-19 infection, we hypothesized that his lung disease was related to his infection. Although the relationship between bullous lung disease and COVID-19 has yet-to-be defined, case reports have described this emerging association. CONCLUSIONS: Further investigation in the development of chronic lung disease following COVID-19 infection is sorely needed given the growing population of COVID-19 survivors. REFERENCE #1: Berhane S, Tabor A, Sahu A, Singh A. Development of bullous lung disease in a patient with severe COVID-19 pneumonitis. BMJ Case Reports. 2020;13(10):e237455. REFERENCE #2: Sun R, Liu H, Wang X. Mediastinal Emphysema, Giant Bulla, and Pneumothorax Developed during the Course of COVID-19 Pneumonia. Korean J Radiol. 2020;21(5):541-544. REFERENCE #3: Goldberg C, Carey KE. Bullous lung disease. West J Emerg Med. 2013;14(5):450-451. doi:10.5811/westjem.2013.3.16276. DISCLOSURES: No relevant relationships by Kwesi Amoah, source=Web Response No relevant relationships by robert homer, source=Web Response No relevant relationships by Denyse Lutchmansingh, source=Web Response No relevant relationships by Prachi Pednekar, source=Web Response No relevant relationships by Changwan Ryu, source=Web Response

Pulmonary disease remains a primary source of morbidity and mortality in persons living with HIV (PLWH), although the advent of potent combination antiretroviral therapy has resulted in a shift from predominantly infectious to noninfectious pulmonary complications. PLWH are at high risk for COPD, pulmonary hypertension, and lung cancer even in the era of combination antiretroviral therapy. The underlying mechanisms of this are incompletely understood, but recent research in both human and animal models suggests that oxidative stress, expression of matrix metalloproteinases, and genetic instability may result in lung damage, which predisposes PLWH to these conditions. Some of the factors that drive these processes include tobacco and other substance use, direct HIV infection and expression of specific HIV proteins, inflammation, and shifts in the microbiome toward pathogenic and opportunistic organisms. Further studies are needed to understand the relative importance of these factors to the development of lung disease in PLWH.

70-year-old woman with osteoarthritis and a remote history of diverticulitis presented to her primary-care physician with intermittent fevers and dyspnea. These symptoms began 1 day after a recent visit to her family where she reported exposure to grandchildren who were sick with an upper respiratory infection. She was given a diagnosis of a viral infection and advised to take conservative measures. Two days later, the patient presented to the ED with persistent high-grade fevers, diffuse aches, and worsening dyspnea. Physical Examination On presentation, the patient’s vital signs were normal except for tachypnea, with a respiratory rate of 26 breaths/min. Pulse oximetry showed 100% saturation while breathing ambient air. General examination results were normal. Chest auscultation revealed bilateral coarse lung sounds with diffuse rhonchi. Cardiac auscultation revealed normal heart sounds with no murmurs, rubs, or gallops. The abdomen was soft, nontender, and nondistended without organomegaly.

Background Spirometry is recommended for diagnosis and management of obstructive lung disease. While many patients with asthma and COPD are cared for by primary care practices, limited data are available on the use and results associated with spirometry in primary care. Object To assess the technical adequacy, accuracy of interpretation, and impact of office spirometry. Design A before-and-after quasiexperimental design. Setting Three hundred eighty-two patients from 12 family medicine practices across the United States. Participants Patients with asthma and COPD, and staff from the 12 practices. Measurements Technical adequacy of spirometry results, concordance between family physician and pulmonary expert interpretations of spirometry test results, and changes in asthma and COPD management following spirometry testing. Results Of the 368 tests completed over the 6 months, 71% were technically adequate for interpretation. Family physician and pulmonary expert interpretations were concordant in 76% of completed tests. Spirometry was followed by changes in management in 48% of subjects with completed tests, including 107 medication changes (>85% concordant with guideline recommendations) and 102 nonpharmacologic changes. Concordance between family physician and expert interpretations of spirometry results was higher in those patients with asthma compared to those with COPD. Discussion and conclusions US family physicians can perform and interpret spirometry for asthma and COPD patients at rates comparable to those published in the literature for international primary care studies, and the spirometry results modify care.

The lung is a common site of disease in HIV infection. Virus has been detected in BAL fluid (BALF) and saliva. However, the relationship between viral loads detected at different levels of the respiratory tract is unknown.We measured simultaneous HIV viral loads in parotid saliva (PS), bronchial fluid (BF), BALF, and plasma by reverse transcription polymerase chain reaction in 20 HIV-infected individuals.HIV was detected in 53% of BALF samples, 15% of BF samples, 5% of PS samples, and 88% of plasma samples. Viral loads in plasma and BALF samples were positively correlated. There were significantly higher levels of HIV viral load in both plasma and BALF in subjects with CD4 counts of200 cells/ microL compared to those with higher counts. Antiretroviral therapy (ART) was associated with lower BALF and plasma viral loads, and the effect in BALF was independent of the plasma viral load. Interestingly, smoking also was associated with lower levels of both BAL and BF viral loads, independent of the plasma viral load.These data demonstrate that while HIV can be detected in the respiratory tract, the viral load is influenced by both local factors (ie, level of the respiratory tree and cigarette smoking) and systemic factors (ie, ART and peripheral CD4 count).

Study objectives To determine if persistent airway tissue mast cells are associated with treatment failure when patients discontinue inhaled corticosteroids (ICS). Design Double-blind, randomized, placebo-controlled trial. Setting Multicenter, tertiary referral centers. Patients or participants Forty-five subjects with asthma recruited from six medical centers in the United States. Interventions The Asthma Clinical Research Network undertook a 28-week, randomized, multicenter, double-blind, placebo-controlled trial of 164 subjects with clinically stable, persistent asthma. A subset of subjects (n = 45) underwent bronchoscopy with endobronchial biopsy and BAL at the end of a 6-week run-in period, during which all subjects received triamcinolone acetonide (TAA), 400 μg bid. Airway tissue mast cells, eosinophils, neutrophils, macrophages, and T cells were quantified morphometrically along with determination of BAL tryptase. At the end of the run-in period, subjects were then randomized to receive salmeterol (42 μg bid), placebo, or continue TAA for 16 weeks followed by a second bronchoscopy. Measurements and results Outcome variables included airway tissue mast cells, eosinophils, neutrophils, macrophages, and T cells that were quantified morphometrically and BAL tryptase. Thirty-five subjects completed the treatment phase; an additional 10 subjects, who were randomized to either salmeterol or placebo after the run-in, had treatment failure. When the bronchoscopy results performed at the end of the run-in, prior to randomization, were analyzed, the treatment failure group demonstrated significantly more tissue mast cells as compared to the nontreatment failure group despite 6 weeks of therapy with TAA (p = 0.04). BAL tryptase was also significantly higher in the treatment failure group (p 0.05). Conclusions Persistent elevations in airway tissue mast cells and BAL tryptase after treatment with TAA predict treatment failure in patients for whom discontinuation of ICS is being considered.

Interleukin (IL)-13 is a key cytokine in asthma pathogenesis. We used constitutive and inducible overexpression transgenic mice to characterize the mechanisms by which IL-13 causes phenotypic alterations in the lung. These studies demonstrated that chemokine receptor-2, transforming growth factor-beta(1), and IL-11 play an important role in the regulation of inflammation and remodeling in the IL-13-treated lung. The study results also demonstrated that IL-13 induces vascular endothelial growth factor, which causes bronchial circulation neovascularization in the murine airway. Last, it was demonstrated that IL-13 induces adenosine accumulation and that adenosine in turn stimulates IL-13 elaboration. These approaches validated in vivo genetic targets against which therapies can be directed to selectively regulate aspects of the IL-13 phenotype.

Increasing morbidity due to asthma and antimicrobial resistance among human pathogens are both major public-health concerns. Numerous studies describe the overuse of antibiotics in general populations and underuse of anti-inflammatory medications by asthmatic patients. However, little is known about the relationship between asthma medication and antibiotic use in asthmatics. Specifically, we tested the hypothesis that higher use of bronchodilator and anti-inflammatory medication by asthmatics, as a marker of problematic asthma, is associated with greater antibiotic use. We also test the hypothesis that physicians who are low prescribers of anti-inflammatory medications are high prescribers of antibiotics.We conducted a retrospective cohort study evaluating asthma medication and antibiotic use by children and adults with asthma and the prescribing of these medications by primary-care physicians.Subjects were continuously enrolled asthma patients aged 6 to 55 years receiving care in an urban, group-model, health maintenance organization.None.Main outcome measures were (1) antibiotic use by asthmatics stratified by low, moderate, and high bronchodilator use; (2) antibiotic use by asthmatics stratified by no, intermittent, and long-term anti-inflammatory use; and (3) correlation between physician-level anti-inflammatory agent to bronchodilator ratio (AIF:BD) and their rate of antibiotic prescribing. We found that (1) high bronchodilator users received 1.72 antibiotics per person-year (95% confidence interval [CI], 1.62 to 1.83), whereas low bronchodilator users received 1.23 antibiotics per person-year (95% CI, 1.19 to 1.27; p0.0001); (2) long-term users of anti-inflammatory agents received 1.85 antibiotics per person-year (95% CI, 1.76 to 1.95), whereas those not receiving an anti-inflammatory agent received 0.95 antibiotics per person-year (95% CI, 0.90 to 1.00; p0.0001); and (3) despite variations in physician AIF:BDs and antibiotic prescribing, respectively, these measures were not correlated.Antibiotic use and asthma medication use are positively associated in a cohort of asthma patients. Greater effort is needed to define the appropriate role of antibiotics in asthma management.

Study objectives Several methods of utilizing peak expiratory flow (PEF) and other markers of disease activity have been suggested as useful in the management of asthma. It remains unclear, however, as to which surrogate markers of disease status are discriminative indicators of treatment failure, suitable for use in clinical trials. Design We analyzed the operating characteristics of 66 surrogate markers of treatment failure using a receiver operating characteristic (ROC) curve analysis. Participants Information regarding FEV 1 , symptoms, ββ 2 -agonist use, and PEF was available from 313 subjects previously enrolled in two Asthma Clinical Research Network trials, in which 71 treatment failures occurred (defined by a 20% fall in FEV 1 from baseline). Interventions None. Measurements and results None of the measures had an acceptable ability to discriminate subjects with a ≥≥ 20% fall in FEV 1 from those without, regardless of the duration of the period of analysis or the criteria for test positivity employed. Areas under the ROC curves generated ranged from 0.51 to 0.79, but none were statistically superior. Sensitivity and specificity combinations were generally poor at all cutoff values; true-positive rates could not be raised without unacceptably elevating false-positive rates concurrently. Conclusions Studies that seek to detect treatment failure defined by a significant fall in FEV 1 should not use such individual surrogate measures to estimate disease severity.

Study objectives To determine if African-American and white patients with asthma (1) differ in the words they use to describe their breathlessness, and (2) differ in their perception of breathlessness. Design Descriptive cross-sectional design. Setting and participants The study setting was located in Northern California, an ethnically and economically diverse area. A total of 32 subjects, 16 per group, completed the study. Measurements All had a provocation concentration of methacholine chloride causing a 30% fall in FEV 1 (PC 30 ) of ≤ 8 mg/mL. Serial pulmonary function testing was performed. Breathlessness was measured using the Borg scale and the visual analog scale. Word descriptors were measured by an open-ended word descriptor questionnaire. Results Significant ethnic differences in the words used to describe the sensation of breathlessness were present at PC 30 . African Americans used upper airway word descriptors: tight throat (p scared-agitated (p voice tight (p itchy throat (p tough breath (p deep breath (p lightheaded (p out of air (p aware of breathing (p hurts to breathe (p 30 (p Conclusion This study provides valuable new information about ethnicity and the words used to describe breathlessness during airflow obstruction. Asthmatic African Americans used primarily upper airway word descriptors; whites used lower airway or chest-wall word descriptors. Effective symptom monitoring requires asking the correct question and awareness that ethnic differences in the words used to describe breathlessness may exist.

Lenalidomide is an immunomodulatory agent approved for use in patients with myelodysplastic syndrome, and in combination with dexamethasone for refractory or relapsed multiple myeloma. Pulmonary toxicity is believed to be uncommon. In this report, we describe a patient receiving lenalidomide in whom dyspnea, fever, hypoxia, and diffuse pulmonary infiltrates developed. BAL demonstrated a significant lymphocytic alveolitis typical for hypersensitivity pneumonitis. Extensive workup for other causes, including infections, was negative. Finally, the patient had improvement in symptoms and oxygenation after withdrawing lenalidomide and recurrence of symptoms when the drug was restarted. Thus, the patient's clinical course and workup strongly support a diagnosis of lenalidomide-induced hypersensitivity pneumonitis-like syndrome. Physicians should be cognizant of this potential complication in patients receiving thalidomide or thalidomide-like drugs who present with fever and pulmonary infiltrates and fail to improve despite treatment with broad-spectrum antibiotics.

Examining case studies from patients with interstitial lung diseases (ILDs) is important in order to evaluate current diagnosis and treatment options. Two cases will be discussed; the first case examines a patient with usual interstitial pneumonia, and the second case examines a patient with subacute ILD and elements to suggest a forme fruste presentation of an unclassifiable connective tissue disease. Each case highlights components of the differential diagnosis, as well as reviews the treatments and prognoses of these patients. The cases provide clinical pearls that are designed to enhance the reader's understanding of ILDs.