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Correspondence |

The Lady Windermere Syndrome: Is There a Racial as Well as a Gender Bias? FREE TO VIEW

Henry Yeager, MD, FCCP
Author and Funding Information

Georgetown University Medical Center Washington, DC

Correspondence to: Henry Yeager, MD, FCCP, Georgetown University Medical Center, 4 N Main, 3800 Reservoir Rd NW, Washington, DC 20007; e-mail: yeagerh@georgetown.edu


The author has no conflict of interest to disclose.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).


Chest. 2008;134(4):889-890. doi:10.1378/chest.08-1428
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To the Editor:

Jeffrey Glassroth1 wrote a fine review of nontuberculous mycobacterial pulmonary disease in CHEST (January 2008). Judging from a number of reports, as summarized in the 2007 American Thoracic Society/Infectious Diseases Society of America Nontuberculous Mycobacterial Disease Statement,2 the Lady Windermere syndrome has been said to more common in white women than in women of African or African-American background. It may be more common in Asian women as well.3 However, since these observations have come from case series, the apparent racial bias may not be genuine. The strongest data pertaining to this topic this writer have discovered are in a doctoral thesis published in 2004.4

In 2000, according to the US Census Bureau, Harris County, TX, had a population of approximately 3,400,000, and a rough white-to-black ratio of about 3:1. The actual figures on race were listed as follows: 58.7% white; 18.5% black or African American; 0.4% American Indian and Alaska Native; 5.1% Asian; 0.1% Native Hawaiian and other Pacific Islander; 14.2% some other race; and 3.0% two or more races.5 It was noted that some persons declared two races, making the total exceed 100% by a small percentage.

A study was done of HIV-negative women aged ≥ 50 years in Harris County between January 1998 and December 2000 who had at least one positive Mycobacterium avium complex (MAC) culture from a pulmonary source, as obtained from the records of hospitals and clinics in the county. Only women with incident cultures positive for MAC for the 3-year collection period were included. Cultures were identified as positive for MAC by growth on solid media or broth methods (BACTEC; Becton Dickinson; Sparks, MD), and results confirmed using a DNA probe technique. A laboratory and population-based surveillance program for Mycobacterium tuberculosis and MAC had been in place since 1997 in Harris County through cooperative efforts between the Baylor College of Medicine, the University of Texas Health Science Center, about 40 Houston-area hospitals, and the Centers for Disease Control and Prevention in Atlanta, GA. This was done as part of the Houston Tuberculosis Initiative, which tracks tuberculosis in the Houston metropolitan area. A comparison population was selected from tuberculosis suspects found throughout Harris County. A hybrid study design using both cross-sectional and case-control methodologies was used. There were 136 subjects with positive MAC culture findings identified and included in the study, and 136 control subjects who had been tuberculosis suspects. The self-declared race of the MAC culture-positive women was “white” in 125, “black” or “African American” in 7, and “Hispanic” in 11. After various risk factors were controlled for, subjects with positive MAC cultures were more likely to be white (odds ratio, 4.6; 95% confidence interval, 2.3 to 9.2). In addition, they were more likely to have bronchiectasis, scoliosis, and pleural disease and lung cavitation on radiography than the control subjects. Cavitation was especially interesting because that traditionally had not been part of the Lady Windermere syndrome. Whether this represented a true genetic difference in susceptibility, and/or differing environmental exposures, or some combination remains unknown at the present time, although it would seem likely that genetics might have had a considerable role.

Glassroth J. Pulmonary disease due to nontuberculous mycobacteria. Chest. 2008;133:243-251. [PubMed] [CrossRef]
 
Griffith DE, Aksamit T, Brown-Elliott BA, et al. An official ATS/IDSA statement: diagnosis, treatment, and prevention of nontuberculous mycobacterial diseases. Am J Respir Crit Care Med. 2007;175:367-416. [PubMed]
 
Kitada S, Kobayashi K, Ichiyama S, et al. Serodiagnosis ofMycobacterium avium-complex pulmonary disease using an enzyme immunoassay kit. Am J Respir Crit Care Med. 2008;177:793-797. [PubMed]
 
Gardner TG. Evaluation ofMycobacterium avium-complex lung disease in women. 2004; Houston, TX EDT Collection for Houston Academy of Medicine-Texas Medical Center paperAAI3143616.
 
US Census Bureau Census 2000 demographic profile highlights.Accessed September 16, 2008 Available at:http://factfinder.census.gov/servlet/SAFFFacts.
 

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References

Glassroth J. Pulmonary disease due to nontuberculous mycobacteria. Chest. 2008;133:243-251. [PubMed] [CrossRef]
 
Griffith DE, Aksamit T, Brown-Elliott BA, et al. An official ATS/IDSA statement: diagnosis, treatment, and prevention of nontuberculous mycobacterial diseases. Am J Respir Crit Care Med. 2007;175:367-416. [PubMed]
 
Kitada S, Kobayashi K, Ichiyama S, et al. Serodiagnosis ofMycobacterium avium-complex pulmonary disease using an enzyme immunoassay kit. Am J Respir Crit Care Med. 2008;177:793-797. [PubMed]
 
Gardner TG. Evaluation ofMycobacterium avium-complex lung disease in women. 2004; Houston, TX EDT Collection for Houston Academy of Medicine-Texas Medical Center paperAAI3143616.
 
US Census Bureau Census 2000 demographic profile highlights.Accessed September 16, 2008 Available at:http://factfinder.census.gov/servlet/SAFFFacts.
 
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