COPD is a clinically heterogeneous syndrome characterized by injury to airways, airspaces, and lung vasculature and usually caused by tobacco smoke and/or air pollution exposure. COPD is also independently associated with nonpulmonary comorbidities (eg, cardiovascular disease) and malignancies (eg, GI, bladder), suggesting a role for systemic injury. Since not all those with exposure develop COPD, there has been a search for plasma and lung biomarkers that confer increased cross-sectional and longitudinal risk. This search typically focuses on clinically relevant COPD outcomes such as FEV1, FEV1 decline, CT measurements of emphysema, or exacerbation frequency. The rapid advances in omics technology and the molecular phenotyping of COPD cohorts now permit large-scale evaluation of genetic, transcriptomic, proteomic, and metabolic biomarkers. This review focuses on protein biomarkers associated with clinically relevant COPD outcomes. The prototypic COPD protein biomarker is alpha-1 antitrypsin; however, this biomarker only accounts for 1% to 5% of COPD. This article reviews and summarizes the evidence for other validated biomarkers for each COPD outcome, and discusses their advantages, weaknesses, and required regulatory steps to move the biomarker from the bench into clinic. Although we highlight the emergence of many novel biomarkers (eg, fibrinogen, soluble receptor for advanced glycation, surfactant protein D, club cell secretory protein), there is increasing evidence that individual biomarkers only explain a fraction of the increased COPD risk and that multiple biomarker panels are needed to completely explain clinical variation and risk in individuals and populations.

The provision of palliative care for severe COPD remains low, resulting in unmet needs in patients and carers.

Historically, β-blockers have been considered to be relatively contraindicated for septic shock because they may cause cardiac suppression. On the other hand, there is an increasing interest in the use of β-blockers for treating patients with sepsis with persistent tachycardia despite initial resuscitation.

Although clinical studies have evaluated dexmedetomidine as a strategy to improve noninvasive ventilation (NIV) comfort and tolerance in patients with acute respiratory failure (ARF), their results have not been summarized.

A 56-year-old man presented to the lung nodule clinic with abnormal chest imaging prompted by a chronic cough and hemoptysis. Approximately 2.5 years earlier, while kneeling beside his car fixing a flat tire, he fell backwards while holding the tire cap in his mouth, causing him to inhale sharply and aspirate the cap. He immediately developed an intractable cough productive of flecks of blood. He presented to an emergency room but left before being seen because of a long wait time and his lack of health-care insurance. He self-medicated for severe cough and chest discomfort with codeine, eventually developing a dependency. Approximately 3 weeks after aspirating the tire cap, his cough became productive, and he developed fever and chills. His symptoms improved transiently with antibiotics and additional narcotics. Ultimately, his chronic cough with intermittent hemoptysis affected his ability to work, and 30 months later he sought medical attention and was diagnosed with pneumonia and reactive airway disease. He was prescribed doxycycline, steroids, inhaled albuterol, and dextromethorphan, with initial improvement, but his symptoms recurred multiple times despite quitting smoking, leading to repeated medication courses.

A 55-year-old woman with COPD, heart failure with preserved ejection fraction (congestive heart failure), diabetes mellitus, and hypertension presented with baseline dyspnea at rest that had worsened over the last week. She reported associated runny nose, congestion, and cough productive of green sputum. She smoked six cigarettes per day and denied alcohol, drugs, or occupational exposure. She was admitted and initiated on treatment for acute exacerbation of COPD; however, her condition did not improve with steroid, ceftriaxone, and nebulized albuterol and budesonide treatments. She had been diagnosed with asthma and COPD without ever undergoing pulmonary function testing. She presented 11 times to the ED with six hospital admissions in the last 1.5 years for worsening dyspnea at rest, wheezing, and lower extremity edema deemed secondary to exacerbation of her COPD or congestive heart failure. She reported medication compliance, which included fluticasone-vilanterol, tiotropium bromide, and furosemide. She repeatedly demonstrated mild vascular congestion on imaging without hyperinflation, a normal to mildly elevated brain natriuretic peptide (<10 to 200 pg/mL), and dyspnea without hypoxia. She was treated normally for both COPD and congestive heart failure exacerbations simultaneously with methylprednisolone, albuterol, and furosemide with rapid improvement over the course of 1 to 2 days. No significant improvement was noted with steroid therapy, despite receiving them as an inpatient and outpatient. At the time of discharge, her symptoms would be at her baseline.

A 2-year-old boy was referred to the Ankara University School of Medicine Children's Hospital with a history of recurrent respiratory distress and cyanosis since birth. His medical history was significant for premature birth at 31 weeks via cesarean section, as an infant of a diabetic mother. There was no parental consanguinity. He was hospitalized in the neonatal ICU after birth because of respiratory distress. After receiving invasive mechanical ventilation for 4 days, noninvasive mechanical ventilation and oxygen therapy were given gradually. As a result of further investigations, he received a diagnosis of situs inversus totalis and pulmonary hypertension. He was discharged on postnatal day 53 without supplemental oxygen therapy or treatment for pulmonary hypertension. Up to the age of 2 years, the patient had a history of multiple admissions to hospital for respiratory distress, lower respiratory tract infection, and cyanosis as an inpatient and outpatient. After starting to walk, shortness of breath and coughing occurred with effort.

A 33-year-old white man presented to the ED with 1-month history of worsening dyspnea. He experienced gradual onset of right-sided scapular pain and shortness of breath on exertion that progressively worsened over the course of 1 month. He had a mild nonproductive cough and intermittent subjective fevers and reported weight loss of approximately 2 kg over 1 month. He had a history of two episodes of acute pancreatitis that was thought to be autoimmune in origin. He was a never smoker; he denied illicit drug use or recent alcohol consumption. He had no known TB exposure, but his mother had a history of sarcoidosis.

A 28-year-old man presented with shortness of breath, chest pain, and scant hemoptysis. Three weeks previously, he was admitted for coronavirus disease 2019 pneumonia that had been diagnosed by nasal swab polymerase chain reaction. Chest CT imaging demonstrated bilateral ground-glass opacities without evidence of VTE. He was treated with hydroxychloroquine, up to 7 L/min oxygen, and self-proning. After 8 days of hospitalization, he was discharged on 4 L/min oxygen. After discharge, his symptoms and hypoxia resolved.

A 65-year-old woman with a history of chronic persistent atrial fibrillation, tobacco use, and COPD was admitted to the hospital 2 months after catheter ablation for persistent atrial fibrillation and dyspnea. Her dyspnea was present at rest and worsened by exertion with limitation to ambulating less than two blocks. She also endorsed a 1-month history of cough with minimally productive whitish sputum with frequent nocturnal exacerbations and orthopnea. She denied any fevers, chest pain, or hemoptysis.

A 49-year-old man presented with 3 months of persistent fever, cough, shortness of breath, and chest tightness. He had no response to treatment with antibiotics. He had been treated with an empiric 2-week course of steroids approximately 2 months before presentation, with mild and transient improvement. He did not use tobacco and had not experienced any weight loss, hemoptysis, arthralgia, or myalgia, and was otherwise in good health. He denied contact with anyone with pulmonary TB or other respiratory illnesses.

A 17-year-old male patient who was diagnosed with Becker muscular dystrophy (nonsense mutation [c.3822C>A] within exon 28 of the DMD gene) at 6 years of age was evaluated in the multidisciplinary neuromuscular clinic for loss of ambulation for 1 year. From a pulmonary perspective, there were no acute or chronic respiratory symptoms, and no history of pneumonia or aspiration. Clinical examination revealed a nonambulant teenager, with normal oxygen saturation and end-tidal CO2 when awake, no respiratory distress, and symmetrically diminished aeration due to obesity (BMI 40 kg/m2). Results of pulmonary function testing revealed FVC of 83% predicted with actual volume of 3.5 L and peak cough flow of 445 L/min (all within normal limits).

A 21-year-old man was admitted to our hospital with recurrent bilateral pneumothorax and hemoptysis. Three years earlier, he underwent coil embolization due to a subarachnoid hemorrhage caused by an intracerebral aneurysm rupture. Two months after the coil embolization, he underwent an emergent total colectomy due to a massive infarction of the colon. One year after the colectomy, he started to have recurrent hemoptysis, and a few months later, multiple episodes of bilateral pneumothorax that required a chest tube placement began to occur. Notably, he had a history of easy bruising. He was taking Depakote and aspirin to prevent seizure and thromboembolic complications, respectively, both of which he began taking after the coil embolization. He denied the use of any illicit drugs. The histories of his parents and sister were not remarkable.

Sclerosing pneumocytoma (SP) is a rare primary lung tumor. Typical carcinoids (TCs) count for 2% of lung malignancies. A description of a combined neoplasm of SP with a nodal and pleural metastasized TC has, to our knowledge, never been published. A 57-year-old actively smoking woman received a diagnosis of a lesion in the left lower lobe via a screening CT scan for rheumatoid arthritis. A fluorodeoxyglucose-PET scan confirmed a 21 × 26 × 16 mm (standardized uptake maximum value, 3.0), well-circumscribed round lesion with calcification, which was thought to be most probably benign. No mediastinal lymph node enlargement or fluorodeoxyglucose uptake was detected. The results of routine laboratory tests, respiratory function tests, and physical examination were unremarkable. In diagnostic thoracoscopy pleural, diaphragmatic, and pericardial lesions were discovered and biopsied in addition to a wedge resection. After diagnosis of a pleural metastasized TC mixed with SP, radical resection and systemic lymph node dissection were performed. The patient is in remission after 36 months of follow-up.