Prior research has shown that individuals with obstructive lung disease are at risk for sleep fragmentation and poor sleep quality. We postulated that patients with chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (known as overlap syndrome) who have more severe lung disease, as measured by lung hyperinflation (inspiratory capacity/total lung capacity), would have greater sleep disturbances independent of traditional measures of sleep apnea. We performed a retrospective chart review of consecutive patients evaluated and treated in an academic pulmonary clinic for overlap syndrome. Pulmonary function tests and polysomnogram data were collected. Thirty patients with overlap syndrome were included in the analysis. We found significant univariable associations between sleep efficiency and apnea/hypopnea index (beta = -0.285, p = 0.01) and between sleep efficiency and lung hyperinflation (beta = 0.654, p = 0.03). Using multivariable linear regression, the relationship between sleep efficiency and lung hyperinflation remained significant (beta = 1.13, p = 0.02) after adjusting for age, sex, body mass index, apnea/hypopnea index, FEV(1)% predicted, oxygen saturation nadir, medications, and cardiac disease. We conclude that increased severity of hyperinflation is associated with worse sleep efficiency, independent of apnea and nocturnal hypoxemia. The mechanisms underlying this observation are uncertain. We speculate that therapies aimed at reducing lung hyperinflation may improve sleep quality in patients with overlap syndrome.
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A 51-year-old female presented to the emergency department complaining of left-sided, nonpleuritic chest pain and a 10-lb. weight loss over the previous 2 months. She was a current smoker with a 20 pack-year history. A PA/lateral chest radiograph and chest computed tomogram (CT) demonstrated a large loculated effusion with pleural thickening (Fig. 1). There were no lung nodules or pathologic mediastinal or hilar lymphadenopathy.A diagnostic thoracentesis was performed, and serosanguineous pleural fluid was obtained. Cytology was negative. For further diagnostic sampling, she underwent a thoracotomy with pleural fluid drainage and pleural biopsy, which demonstrated sheets of atypical epithelioid cells displaying prominent intra-alveolar growth (Fig. 2). The cells stained positive for CD31 and CD34. Stains for pan-cytokeratin, CK5-6, p63, calretinin, S-100, Melan-A, TTF-1, CD68, and EMA were negative. She was given a diagnosis of pleural epithelioid hemangioendothelioma.In the multidisciplinary oncology conference, it was felt she was not a candidate for surgical resection given the extensive nature of the tumor. She was offered chemotherapy with doxorubicin. Less than 4 months after her initial presentation, the patient was admitted to the hospital with a bowel obstruction. Repeat imaging demonstrated further extension of tumor in the left hemithorax with associated volume loss, an enlarging right-sided pleural effusion, evidence of liver and spleen metastasis, and new-onset ascites. Her condition continued to deteriorate with the onset of respiratory failure and she died several days later. DiscussionEpithelioid hemangioendothelioma (EHE) is a malignancy of vascular endothelial origin often involving bone, liver, soft tissues, and lung. Pleural EHE is rare, usually affects males, and is associated with a grim prognosis with disseminated disease [1][2][3]. Pleural involvement in females is even more unusual. In a recent review of 22 patients with pleural EHE, 82% were men and the average survival was only 10 months [1]. Radiographically, pleural EHE is nonspecific and can be easily mistaken for pleural infections or malignant mesothelioma. Chest CT usually demonstrates a pleural effusion with localized or diffuse nodular pleural thickening similar to our case [3][4][5].Diagnosis is confirmed by pathologic examination of specimen obtained by surgical lung biopsy. On immunohistochemistry, EHEs show the typical phenotype of endothelial cells with reactivity to vascular-specific markers, including Factor VIII-related antigen, CD31, CD34, and Fli-1 [5]. The identification of Weibel-Palade bodies and pinocytotic vesicles on electron microscopy can also be useful in the diagnosis of EHE but is
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