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Mortality vs Case Fatality in the Assessment of Sarcoidosis LethalityUS Sarcoidosis Mortality FREE TO VIEW

Jerome M. Reich, MD, FCCP
Author and Funding Information

From the Thoracic Oncology Section, Earl A. Chiles Research Institute.

CORRESPONDENCE TO: Jerome M. Reich, MD, FCCP, 7400 SW Barnes Rd A242, Portland, OR 97225-7007; e-mail: Reichje@dnamail.com


FINANCIAL/NONFINANCIAL DISCLOSURES: The author has reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;147(2):e65. doi:10.1378/chest.14-2444
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To the Editor:

In this issue of CHEST (see page 438), the statement by Mirsaeidi and colleagues1 that “The age adjusted mortality rate for African Americans was 12 times higher than for Caucasians” may lead one to mistakenly infer a far greater lethality in African Americans (AA) than Caucasians (CA). Assuming equal case fatality, mortality will reflect the incidence ratio; AA to CA = 12-13:1.2 Multiple series have shown no AA to CA case fatality difference. In a New York City health clinic in which 79% of patients with intrathoracic sarcoidosis were AA, they constituted 66% of those experiencing an adverse course.3 Unadjusted for incidence, mortality rates can lead to absurd conclusions (eg, sickle cell disease is more and Tay Sachs disease less severe in AA than CA).

More frequent suppressive treatment possibly accounts for a secular increase in sarcoidosis mortality. In an ingenious series of experiments using the Kveim suspension to model the genesis of sarcoidosis, Munro inferred that the disorganized early reaction reflected inefficient cell-mediated immunity, leading to the immunologic fallback of a granulomatous response.4 This heterodox conceptual framework furnishes a unifying explanation for absence of an identifiable Kveim immunogen, multiplicity of cellular immune deficiencies associated with sarcoidosis, failure to identify the etiology, assorted identifiable causative agents, and the seeming paradox of favorable outcomes associated with the most intense response.4 Numerous case reports of sarcoidosis following therapy with immunosuppressant monoclonal antibodies support this view. Most importantly in this context, corticosteroid suppression in early disease demonstrated a long-term adverse effect: A systematic review showed stage-corrected fatality of intrathoracic sarcoidosis in tertiary care settings was greater than sevenfold that reported in primary care settings and was highly correlated with the propensity to prescribe corticosteroid therapy in each tertiary care setting.4 Fatality in a case series of conservatively managed sarcoidosis is < 1%.4 Johnston5 reported no fatality among 159 people with intrathoracic sarcoidosis in whom the sole indication for treatment (required in four people) was progressive pulmonary shadowing. To the extent that the authors’ analysis fosters aggressive therapy in AA in the belief that they are at markedly increased risk of death, it may create a self-fulfilling prophecy.

Why was a study (Reference 4 [Rybicki et al] in the article by Mirsaeidi et al1) with anomalous CA incidence data selected for race correction?1 It lacks the distinctive age 20 to 40-year peak (Fig 2 in Rybicki et al6); the age 50 to 69-year ethnic ratio is < 2:1; and 10.9 is twofold to fourfold the US, UK, and Scandinavian CA incidence estimates. Might the high Vermont CA mortality1 (at α, 0.05 in a multistate comparison) be a statistical artifact?

References

Mirsaeidi M, Machado RF, Schraufnagel D, Sweiss NJ, Baughman RP. Racial difference in sarcoidosis mortality in the United States. Chest. 2015;147(2):438-449.
 
Reich JM. A critical analysis of sarcoidosis incidence assessment. Multidiscip Respir Med. 2013;8(1):57. [CrossRef] [PubMed]
 
Reisner D. Observations on the course and prognosis of sarcoidosis; with special consideration of its intrathoracic manifestations. Am Rev Respir Dis. 1967;96(3):361-380. [PubMed]
 
Reich JM. On the nature of sarcoidosis. Eur J Intern Med. 2012;23(2):105-109. [CrossRef] [PubMed]
 
Johnston RN. Pulmonary sarcoidosis after ten to twenty years. Scott Med J. 1986;31(2):72-78. [PubMed]
 
Rybicki BA, Major M, Popovich J Jr, Maliarik M, Iannuzzi MC. Racial differences in sarcoidosis incidence: a 5-year study in a health maintenance organization. Am J Epidemiol. 1997;145(3):234-241. [CrossRef] [PubMed]
 

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References

Mirsaeidi M, Machado RF, Schraufnagel D, Sweiss NJ, Baughman RP. Racial difference in sarcoidosis mortality in the United States. Chest. 2015;147(2):438-449.
 
Reich JM. A critical analysis of sarcoidosis incidence assessment. Multidiscip Respir Med. 2013;8(1):57. [CrossRef] [PubMed]
 
Reisner D. Observations on the course and prognosis of sarcoidosis; with special consideration of its intrathoracic manifestations. Am Rev Respir Dis. 1967;96(3):361-380. [PubMed]
 
Reich JM. On the nature of sarcoidosis. Eur J Intern Med. 2012;23(2):105-109. [CrossRef] [PubMed]
 
Johnston RN. Pulmonary sarcoidosis after ten to twenty years. Scott Med J. 1986;31(2):72-78. [PubMed]
 
Rybicki BA, Major M, Popovich J Jr, Maliarik M, Iannuzzi MC. Racial differences in sarcoidosis incidence: a 5-year study in a health maintenance organization. Am J Epidemiol. 1997;145(3):234-241. [CrossRef] [PubMed]
 
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