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Many patients with chronic obstructive pulmonary disease (COPD) continue to experience exacerbations despite receiving standard-of-care treatments. Novel approaches to COPD treatment focus on understanding and targeting molecular mechanisms of airway inflammation, airway obstruction, remodeling and lung destruction. Several identified phenotypes and endotypes of COPD will pave the future path for a more personalized approach to therapy. Although well known to be associated with neutrophilic inflammation, COPD may also be driven by eosinophilic inflammation both at stable states and during exacerbation. Targeting eosinophilic inflammation has been successful in managing severe eosinophilic asthma and may hold promise in certain phenotypes of COPD. The most promising biologic treatments at an advanced stage of development are agents blocking interleukin (IL)-5 or its receptor. This review examines our current understanding of the eosinophilic inflammation in COPD and the rationale for IL-5 targeting agents.

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Bronchoscopy and bronchoalveolar lavage (BAL) are widely accepted diagnostic procedures in various pulmonary etiologies. Complications of bronchoscopy are relatively infrequent and most often minor, namely, bleeding and infection. Pneumothorax is a rare complication of bronchoscopy with transbronchial biopsy. Bilateral pneumothorax developing after BAL without biopsy has been rarely described in the literature. A 51-year-old woman presented with symptoms suggestive of reactive airway syndrome and underwent bronchoscopy with BAL to rule out vocal cord paralysis and to investigate other potential causes of her symptoms. Immediately after BAL, she developed bilateral pneumothorax requiring chest tube placement. The pneumothorax was resolved with the chest tube and the patient recovered. However, the etiology of the pneumothorax remained unclear. We presume that cough-related increase in intrathoracic pressure might have led to interstitial air dissection and bilateral pneumothorax.

Multiple myeloma - a neoplastic proliferation of plasma cell is the second most common blood cancer. Multiple myeloma is characterized by neoplastic proliferation of the plasma cells. These cells infiltrate variety of organs. Infiltration by immature neoplastic cells and overproduction of monoclonal immunoglobulin chain is responsible for clinical manifestations of multiple myeloma. The most common clinical presentation of multiple myeloma is an asymptomatic person having anemia and elevated globulin in laboratory testing. Multiple myeloma is diagnosed by triad of > 10% marrow infiltration by plasma cells, serum/urine monoclonal protein and end organ damages. One of the common end organ damage is lytic bone lesions resulting from imbalance between osteolytic and osteoblastic activities. Lymphadenopathy and osteoblastic lesions are rare presentations of multiple myeloma - lymphadenopathy in 1% of cases with IgA subtype and osteoblastic lesions in IgE myeloma and lambda light chains. Osteoblastic multiple myeloma is a distinct entity from POEMS syndrome. IgG myeloma with kappa chain predominance is not described yet with osteoblastic lesions and lymphadenopathy. We present a rare case of IgG myeloma with kappa chain predominance that had both lymphadenopathy and osteoblastic lesions.