Published ahead of print on August 14, 2008, doi:10.1164/rccm.200805-686OC
© 2008 American Thoracic Society doi: 10.1164/rccm.200805-686OC
Pulmonary Nontuberculous Mycobacterial DiseaseProspective Study of a Distinct Preexisting Syndrome1 Immunopathogenesis Section, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases; 2 Translational Medicine Branch, National Heart, Lung, and Blood Institute (NHLBI); 3 Department of Laboratory Medicine, Clinical Center; 4 Kidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases; 5 Office of Biostatistics Research, NHLBI; 6 Pulmonary and Vascular Medicine Branch, NHLBI; 7 Molecular Pathology Service, National Cancer Institute; 8 Diagnostic Radiology Department, Clinical Center, National Institutes of Health (NIH); 9 Cardiology Branch, NHLBI; 10 Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases; NIH, U.S. Department of Health and Human Services, Bethesda, Maryland; and 11 Research Technologies Section, Genomics Unit, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, NIH, U.S. Department of Health and Human Services, Hamilton, Montana Correspondence and requests for reprints should be addressed to Steven M. Holland, M.D., Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, NIH, CRC B3-4141, MSC 1684, Bethesda, MD 20892-1684. E-mail: smh{at}nih.gov Rationale: Pulmonary nontuberculous mycobacterial (PNTM) disease is increasing, but predisposing features have been elusive. Objectives: To prospectively determine the morphotype, immunophenotype, and cystic fibrosis transmembrane conductance regulator genotype in a large cohort with PNTM. Methods: We prospectively enrolled 63 patients with PNTM infection, each of whom had computerized tomography, echocardiogram, pulmonary function, and flow cytometry of peripheral blood. In vitro cytokine production in response to mitogen, LPS, and cytokines was performed. Anthropometric measurements were compared with National Health and Nutrition Examination Survey (NHANES) age- and ethnicity-matched female control subjects extracted from the NHANES 2001–2002 dataset.
Measurements and Main Results: Patients were 59.9 (±9.8 yr [SD]) old, and 5.4 (±7.9 yr) from diagnosis to enrollment. Patients were 95% female, 91% white, and 68% lifetime nonsmokers. A total of 46 were infected with Mycobacterium avium complex, M. xenopi, or M. kansasii; 17 were infected with rapidly growing mycobacteria. Female patients were significantly taller (164.7 vs. 161.0 cm; P < 0.001) and thinner (body mass index, 21.1 vs. 28.2; P < 0.001) than matched NHANES control subjects, and thinner (body mass index, 21.1 vs. 26.8; P = 0.002) than patients with disseminated nontuberculous mycobacterial infection. A total of 51% of patients had scoliosis, 11% pectus excavatum, and 9% mitral valve prolapse, all significantly more than reference populations. Stimulated cytokine production was similar to that of healthy control subjects, including the IFN- Conclusions: Patients with PNTM infection are taller and leaner than control subjects, with high rates of scoliosis, pectus excavatum, mitral valve prolapse, and cystic fibrosis transmembrane conductance regulator mutations, but without recognized immune defects.
Key Words: immunodeficiency • IFN-
Related articles in AJRCCM:
This article has been cited by other articles:
|
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
/IL-12 pathway. CD4+, CD8+, B, and natural killer cell numbers were normal. A total of 36% of patients had mutations in the cystic fibrosis transmembrane conductance regulator gene. 
