|Year : 2016 | Volume
| Issue : 3 | Page : 182-184
Pericardial effusion: A paradoxical presentation of tuberculosis treatment
Rahul Kumar Sharma, Arjun Khanna, Harish Kumar
Department of Pulmonary Critical Care and Sleep Medicine, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India
|Date of Web Publication||5-Aug-2016|
Dr. Rahul Kumar Sharma
Department of Pulmonary Critical Care and Sleep Medicine, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi - 110 029
Source of Support: None, Conflict of Interest: None
Paradoxical reactions (PRs) in patients of tuberculosis on antitubercular treatment (ATT) are a well-known entity, but pericardial effusion as a PR to ATT is almost an unheard phenomenon. Here, we report a rare case of pericardial effusion developing after the initiation of ATT in an immunocompetent patient, which resolved after the addition of steroids to his treatment.
Keywords: Antitubercular treatment, paradoxical reaction, pericardial effusion, tuberculosis
|How to cite this article:|
Sharma RK, Khanna A, Kumar H. Pericardial effusion: A paradoxical presentation of tuberculosis treatment. Int J Health Allied Sci 2016;5:182-4
|How to cite this URL:|
Sharma RK, Khanna A, Kumar H. Pericardial effusion: A paradoxical presentation of tuberculosis treatment. Int J Health Allied Sci [serial online] 2016 [cited 2021 Feb 27];5:182-4. Available from: https://www.ijhas.in/text.asp?2016/5/3/182/187833
| Introduction|| |
The phenomenon of "paradoxical reaction" (PR), associated with worsening of existing disease or appearance of new lesions during the treatment of tuberculosis (TB), has been recognized for many years. , This phenomenon, extensively studied in HIV-infected patients (also known as immune reconstitution inflammatory syndrome [IRIS]), is also seen in some immunocompetent patients, especially those with extrapulmonary localization of TB. Most cases of PR have been reported during treatment for lymph node or cerebral tubercular disease, with enlargement of nodes seen in approximately 30% in one large series.  Usually, self-limiting in nature, respiratory failure, and death have been occasionally described. 
On reviewing the literature, only two case reports have shown the appearance of pericardial effusion as part of PR to antitubercular treatment (ATT). , We here report such a case of pericardial effusion as PR in an immunocompetent patient in view of rarity of this presentation.
| Case Report|| |
A 25-year-old male presented with complaints of fever and loss of appetite for 15-20 days. There was no history of cough, weight loss, or any localizing symptoms for fever. On examination, he had stable vitals with unremarkable general and systemic examination. His initial investigations revealed mild anemia (hemoglobin 11.2 g/dl) with normal total and differential white cell count, raised erythrocyte sedimentation rate (ESR) (60 mm), and normal liver and kidney function test. Urine examination and blood tests for malaria, typhoid, HIV, hepatitis B and C were all negative. Mantoux test was positive (18 mm) with two sputum samples negative for acid-fast bacilli (AFB). Chest X-ray showed mediastinal widening suggestive of lymphadenopathy with normal lung parenchyma [Figure 1]. Contrast-enhanced computed tomography chest revealed multiple mediastinal lymphadenopathy involving the right paratracheal and subcarinal nodes with signs of necrosis [Figure 2]. Transbronchial needle aspiration (TBNA) of subcarinal lymph node showed caseating granulomas with AFB stain-positive bacilli confirming TB. The patient was started on four drug ATT as per his weight. The patient showed improvement and fever subsided by day 9 of therapy. Three weeks later, the patient presented with high-grade fever, palpitation, progressive breathlessness, and dry cough. The patient was well compliant to ATT. On examination, there was presence of tachycardia and tachypnea with blood pressure 100/70 mmHg and room air saturation (94%). Jugular venous pressure was raised with no evidence of pedal edema. Cardiovascular system examination revealed muffled heart sounds with no murmur. Rest of systemic examination was within normal limits. Investigations including hemogram, blood and urine culture, sputum examination, malarial serology, and connective tissue workup (antinuclear antibody, rheumatoid factor) were within normal limits except for a highly raised ESR (120 mm). Chest X-ray showed cardiomegaly with loss of heart borders [Figure 3] while electrocardiography revealed sinus tachycardia with low-voltage complexes. An echocardiogram done showed pericardial effusion (thickness 28 mm) [Figure 4]. Aspiration of pericardial fluid was done under echocardiographic guidance, and about 500 ml of straw-colored fluid was drained showing exudative fluid with lymphocytic predominance (total leukocyte count 8000/mm 3 ). Adenosine deaminase (ADA) levels in fluid were 75 IU/dl with negative results for Gram-stain, Ziehl-Neelsen stain, pyogenic, and tubercular bacterial culture. The results of rapid culture from TBNA sample sent initially showed Mycobacterium TB with no resistance to the first-line ATT on drug sensitivity testing.
|Figure 1: X-ray chest showing the right mediastinal widening suggestive of lymphadenopathy (orange arrow)|
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|Figure 2: Contrast-enhanced computed tomography cut sections of chest showing (a and b) right paratracheal lymph node, (c) subcarinal lymph node, (d) heart showing no evidence of pericardial effusion (orange arrows)|
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|Figure 3: X-ray chest showing cardiomegaly with the loss of heart borders suggestive of pericardial effusion|
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|Figure 4: Two-dimensional echocardiogram showing pericardial effusion with thickness of 2.8 mm|
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In view of good initial response to ATT and exudative pericardial effusion with high ADA, diagnosis of PR to ATT was made, and the patient was continued on ATT with the addition of oral steroids to the regimen (prednisolone 40 mg). Fever subsided after 10 days of steroid treatment which were tapered after 2 weeks and stopped after 4 weeks. The patient improved completely on ATT without any new symptoms. Follow-up echocardiogram done 1 month later, and on completion of ATT (6 months) showed no pericardial effusion or thickening.
| Discussion|| |
IRIS or "PR" is an uncommon phenomenon seen as worsening of symptoms after the initiation of therapy. Although conventionally described in HIV, it has been rarely associated with other pathogens including Mycobacterium (Mycobacterium tuberculosis and Mycobacterium avium complex), fungi (Cryptococcus), virus (Cytomegalovirus, hepatitis B or C), bacteria, and some malignancies (Kaposi's sarcoma).  The phenomenon of "PR" can occur anytime from a few days to months after the start of ATT and is unpredictable in its duration and severity. , Various studies have shown about 2-23% of HIV-negative patients infected with TB to experience PR during treatment. , It poses a diagnostic challenge because the apparent clinical deterioration may raise the suspicion of drug-resistant TB, noncompliance to the prescribed regimen, or concomitant disorders unrelated to TB. The most common manifestation of PR is worsening of the original lesion (75%), and occurrence of new lesions commonly seen in the central nervous system, pleural, skin, and lymph node lesions. 
Although the exact mechanisms are not understood, it is most likely that PR is due to an abnormal immune response or reconstitution of the immune system. Rapid killing of bacilli by effective ATT can cause the release of large amounts of tuberculoprotein and other cell wall products. Hypersensitivity to these proteins released from the dying mycobacteria and enhanced focal immune responses recruit lymphocytes and macrophages at the site of previously inactive tuberculous foci which enlarge and then become evident. This immunological explanation is supported by a relatively low mycobacterial culture rate from the paradoxically expanded lesions and significant resolution of the paradoxical response after use of steroids. 
PR is a diagnosis of exclusion. In each case, poor compliance, drug resistance, progression of original disease, and other secondary diagnoses should be ruled out before labeling the patient as PR.  In our patient, the initial clinical improvement after ATT, good compliance with dose reconfirmation, drug sensitivity test results, and radiological improvement without any modification of treatment regimen ruled out drug resistance, treatment failure, or progressive disease. The subsequent subsidence of fever even while ATT was continued ruled out drug fever. Pericardial fluid analysis suggestive of exudative effusion with high ADA, and improvement with steroid treatment excluded other diagnosis. Hence, the diagnosis in our patient was based on temporal correlation, exclusion of other possible etiology of pericardial effusion, and successful treatment with ATT and steroids.
| Conclusion|| |
PR is a common phenomenon during TB treatment regardless of immune status. It often complicates the disease presentation and creates diagnostic dilemma to both patient and physician. Suspicion of paradoxical response in patients who develop clinical symptoms after initial response to ATT avoids unnecessary change or modification of drug regimen. Our case illustrates the varied presentations of PR alerting the clinician to suspect PR in such TB cases with pericardial effusion.
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Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]