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Letters to the Editor |
Department of Radiology, Dodoens Ziekenhuis, Zwartzustersvest 47, Mechelen 2800, Belgium. e-mail: pilate.en.blaffart@pandora.be
Editor:
I read with great interest the article by Dr Choi and colleagues in the August 2002 issue of Radiology (1). They demonstrate that paradoxical response (development of new opacities) to treatment for tuberculous pleural effusion should be considered a transient worsening that improves with continuation of medication.
Patients with pulmonary tuberculosis are considered to have a treatment failure if cultures are still positive after 5–6 months of treatment (2). In the case of tuberculous pleuritis, the major indicators of response to therapy are findings from chest radiographs and clinical evaluation (3).
The radiographic improvement of pleural effusion before paradoxical response does not rule out failure of treatment later on. The appearance of new nodular opacities during treatment for tuberculous pleural effusion could be considered as a failure of treatment. Reasons for treatment failure are improper drug prescription, nonadherence to the prescribed therapy, drug resistance, drug malabsorption, and exogenous reinfection with a drug-resistant strain (4).
Resistance of Mycobacterium tuberculosis strains is an increasing problem worldwide; there is marked variation in the incidence of multiple-drug-resistant tuberculosis between different population groups (5). Good data are not available on the relative effectiveness of various regimens and the necessary duration of treatment for patients with multiple-drug resistance (2,4). Could drug susceptibility tests be performed in some of the patients included in the study? Could the paradoxical response seen on chest radiographs in reality be considered as treatment failure caused by multiple-drug resistance?
REFERENCES
Department of Radiology, Hanyang University Hospital, Haengdang-dong 17, Sungdong-ku, Seoul 133–792, South Korea. e-mail: ywchoi@hanyang.ac.kr
I thank Dr Pilate for the interest in our article (1). The major issue raised appears to be if the paradoxical response observed in our study was treatment failure caused by multiple-drug resistance. Treatment failure is defined as continued or recurrent positive cultures after 4 months of treatment in patients in whom medication ingestion was assured (2). Unfortunately, culture and drug susceptibility test results are not available now because all of the tests were performed at least 7 years ago and the results were discarded. I agree with Dr Pilate’s opinion that radiographic improvement of pleural effusion does not rule out failure of treatment later on because tuberculous pleural effusion resolves even without treatment. Despite this and the unavailability of culture data, much other evidence is against the notion that our cases are those of treatment failure caused by multiple-drug resistance.
First, all of the patients were treated with potent first-line bactericidal drugs, including isoniazid, rifampin, ethambutol, and pyrazinamide. The drug regimen was not changed even after the development of new lung lesions, and the paradoxical response subsequently cleared in all cases. If the organisms were resistant to the medication, the patients should not have responded to and improved after the medication.
Second, concomitant postprimary pulmonary tuberculosis detected at diagnosis of pleural effusion displayed radiographic improvement in five patients but no worsening in any patient after administration of antituberculous medication. If the pulmonary lesions were caused by organisms resistant to the medication, they should have worsened.
Third, the paradoxical response in our study was usually observed within 3 months after the start of medication, which coincides well with other types of paradoxical responses that generally occurred weeks or months after the administration of antituberculous therapy (3).
Fourth, new lung lesions that developed as a paradoxical response in our study mostly achieved maximum size before 4 months of treatment and then subsequently disappeared. Because the diagnosis of treatment failure is made after 4 months of treatment (2), it would be difficult to categorize these cases as treatment failures, although culture results are not available.
Fifth, it has been reported that at the time of paradoxical response, there is generally a decline of fever, clinical improvement of a moderate to a marked degree with amelioration of symptoms, and no other signs of treatment failure, such as increasing numbers of acid-fast bacilli on a smear or culture of the sputum or a demonstrated microbial resistance (4). This was the case with our study.
It is important to consider the possibility of treatment failure caused by drug resistance in patients showing worsening of lesions during antituberculous medication. However, I think the features just described indicate that ours are cases of paradoxical response, not treatment failure caused by multiple-drug resistance.
REFERENCES
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