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Correspondence |

Questions About Adenosine Deaminase Testing and Drug Choice in an Unusual Presentation of TB FREE TO VIEW

Alkesh Kumar Khurana, MD, DNB, FCCP; Ujjawal Khurana, MD, DNB
Author and Funding Information

From the Department of Pulmonary Medicine (Dr A. K. Khurana) and the Department of Pathology (Dr U. Khurana), Government Medical College and Hospital.

Correspondence to: Alkesh Kumar Khurana, MD, DNB, FCCP, Department of Pulmonary Medicine, Government Medical College and Hospital, GMCH, Sec 32, Chandigarh, India 160030; e-mail: lungcancer@rediffmail.com


Financial/nonfinancial disclosures: The authors have 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 (www.chestpubs.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;137(5):1252. doi:10.1378/chest.09-2827
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To the Editor:

We read with great interest the case report by Sergew et al (November 2009)1 wherein they reported a case of TB that presented in an unusual fashion as sepsis and ARDS. There are, in our opinion, a couple of issues to be answered.

First, although the authors have mentioned the role of adenosine deaminase (ADA) in ascitic fluid for the diagnosis of TB as the etiology in the discussion of the case report, we wonder why this simple bedside investigation was not done in the case described. ADA levels in ascitic fluid have been suggested as a useful, noninvasive screening test in the diagnosis of peritoneal TB.2 Although not diagnostic, ADA levels in serous fluids, when considered in collaboration with the clinical scenario, can guide the clinician to clinch an early diagnosis and start the required anti-TB therapy in time.

Second, the standard treatment regimen for a fresh case of TB consists of four drugs: isoniazid, rifampicin, pyrazinamide, and ethambutol. Use of potent second-line drugs such as quinolones and an aminoglycoside (amikacin in this case) at the initial phase is not recommended. Inadequate drug regimens promote the selection of drug-resistant strains, which magnify the threat of drug-resistant TB.3 As the incidence of multidrug-resistant TB and extensively drug-resistant TB is steadily increasing throughout the world, judicious use of antitubercular therapy is recommended to keep the drug resistance to a minimum.

Sergew A, Olson AL, Schwarz MI. A 25-year-old woman with diffuse abdominal pain and shock. Chest. 2009;1365:1435-1440. [CrossRef] [PubMed]
 
Fernandez-Rodriguez CM, Perez-Arguelles BS, Ledo L, Garcia-Vila LM, Pereira S, Rodriguez-Martinez D. Ascites adenosine deaminase activity is decreased in tuberculous ascites with low protein content. Am J Gastroenterol. 1991;8610:1500-1503. [PubMed]
 
Raviglione MC, Smith IM. XDR tuberculosis—implications for global public health. N Engl J Med. 2007;3567:656-659. [CrossRef] [PubMed]
 

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References

Sergew A, Olson AL, Schwarz MI. A 25-year-old woman with diffuse abdominal pain and shock. Chest. 2009;1365:1435-1440. [CrossRef] [PubMed]
 
Fernandez-Rodriguez CM, Perez-Arguelles BS, Ledo L, Garcia-Vila LM, Pereira S, Rodriguez-Martinez D. Ascites adenosine deaminase activity is decreased in tuberculous ascites with low protein content. Am J Gastroenterol. 1991;8610:1500-1503. [PubMed]
 
Raviglione MC, Smith IM. XDR tuberculosis—implications for global public health. N Engl J Med. 2007;3567:656-659. [CrossRef] [PubMed]
 
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