Hisako Hashimoto

Serological test and chest computed tomography findings in patients with Mycobacterium avium complex lung disease

The present authors have previously reported the usefulness of a serodiagnostic test to detect serum glycopeptidolipid (GPL) core antibody in diagnosing Mycobacterium avium complex (MAC) lung disease in immunocompetent patients. The aim of the present study was to investigate correlations between the levels of antibody against GPL core and chest computed tomography (CCT) findings in patients with MAC lung disease. A total of 47 patients with MAC-positive culture from their sputum and who had radiographic abnormalities were investigated. Thirty-three patients met the American Thoracic Society criteria for MAC disease; 14 did not. All patients underwent both CCT examination and the serodiagnostic test for MAC at the same time. Small nodular shadows were seen on CCT in all 47 patients and bronchiectasis shadows were seen in 39 (83%) of them. There was a significant positive correlation between the extent of the disease and the level of GPL core immunoglobulin (Ig)A antibody. The levels of GPL core IgA antibody were significantly elevated in patients who had nodular shadows (10–30 mm) compared with patients who had small nodular shadows (<10 mm). The present results document that the levels of immunoglobulin A antibody against glycopeptidolipid core correlate with the chest computed tomography findings of Mycobacterium avium complex lung disease.

Acidosis and raised norepinephrine levels are associated with exercise dyspnoea in idiopathic pulmonary fibrosis

Background and objective:  Exertional dyspnoea limits patients with IPF in their activities of daily living. The mechanism, however, has not been elucidated. This study tested the hypothesis in IPF that exertional dyspnoea correlates with cardiopulmonary exercise responses, specifically changes in arterial blood pH and plasma norepinephrine (NE).

Serodiagnosis of Pulmonary Disease Due to Mycobacterium avium Complex Proven by Bronchial Wash Culture

Affi liations: From the Department of Pharmacy (Drs Ogale and Sullivan), University of Washington; the Center for Management of Complex Chronic Care (Dr Lee), Edward Hines Jr VA Hospital; and the Center for Pharmacoeconomic Research, Department of Pharmacy Practice, University of Illinois at Chicago, Chicago, IL. Dr Ogale is currently at Genentech, Inc. Financial nonfi nancial disclosures: The authors have reported to CHEST the following confl icts of interest: Dr Ogale is an employee of Genentech, Inc. Drs Lee and Sullivan have received funding for their contribution to the Burden of Obstructive Lung Disease (BOLD) Initiative, which has been funded in part by unrestricted educational grants to the Operations Center ( www . boldcopd . org ) from ALTANA, Aventis, AstraZeneca, Boehringer Ingelheim, Chiesi, GlaxoSmithKline, Merck, Novartis, Pfi zer, Schering-Plough, Sepracor, and the University of Kentucky. Drs Lee and Sullivan have received past research grants from AstraZeneca, Boehringer Ingelheim, Pfi zer, Novartis, and Glaxo SmithKline. Dr Lee has participated in past advisory boards for AstraZeneca and Novartis. Correspondence to: Todd A. Lee, PharmD, PhD, Edward Hines Jr VA Hospital (151-H), 5000 S 5th Ave, Hines, IL 60141; e-mail: todd.lee@va.gov

The degree of exercise hypoxemia reflects pulmonary artery pressure during early exercise in chronic obstructive pulmonary disease patients

The causes of both exertional pulmonary hypertension and pulmonary hypertension in general in chronic obstructive pulmonary disease (COPD) remain to be elucidated. To further understand the pathophysiology in COPD patients, it may be important to recognize the existence of exertional pulmonary hypertension and to determine the severity of exertional hypoxemia. However, little is known about their relationship. To investigate whether the severity of exertional hypoxemia, as evaluated by the Δartery oxygen tension/Δoxygen consumption (PaO2‐slope) correlates with the mean pulmonary artery pressure (Ppa), cardiopulmonary exercise testing with haemodynamics was done in 10 patients with moderate to very severe COPD. The PaO2‐slope was significantly correlated with the mean Ppa from 25% to 40% of the maximum Watts (Wmax), and was most significant at 30% Wmax (r = −0·904, P<0·0001). In this phase, all parameters, except for the mean Ppa and the mixed venous oxygen tension, were not markedly changed from resting levels. At 30% Wmax, the mean Ppa (mean, 27 mmHg) with no or mild hypoxemia was also significantly correlated with the Δartery oxygen saturation/Δoxygen consumption (SpO2‐slope) (r = −0·789, P = 0·004). On stepwise multiple regression analysis, the PaO2‐slope was the most significant predictor of mean Ppa at 30% Wmax. In conclusion, the PaO2‐slope and the SpO2‐slope reflect Ppa during the early exercise phase. Thus, assessment of these parameters could be useful to evaluate the cardiopulmonary haemodynamic pathophysiology of COPD patients.