Ann Nucl Med (2010) 24:421–425 DOI 10.1007/s12149-010-0365-y
CASE REPORT
Constrictive tuberculous pericarditis diagnosed using 18F-fluorodeoxyglucose positron emission tomography: a report of two cases Eleni Testempassi • Kazuo Kubota • Miyako Morooka • Kimiteru Ito • Yoko Masuda-Miyata • Hiroyuki Yamashita • Kenji Ito • Akio Mimori Hirofumi Kuroki
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Received: 27 September 2009 / Accepted: 10 February 2010 / Published online: 14 April 2010 Ó The Japanese Society of Nuclear Medicine 2010
Abstract We present two cases of tuberculous pericarditis that were diagnosed using 18F-fluorodeoxyglycose (18F-FDG) positron emission tomography (PET). Here, we highlight the value of 18F-FDG-PET for demonstrating tuberculous pericardial involvement as well as disease dissemination and activity. The patients received antitubercular treatment, and their symptoms and findings resolved accordingly. Keywords
FDG PET-CT Tuberculosis Pericarditis
E. Testempassi Division of CT and MRI, Department of Radiology, General Hospital Evangelismos, Athens, Greece K. Kubota (&) M. Morooka Division of Nuclear Medicine, Department of Radiology, National Center for Global Health and Medicine, 1-21-1 Toyama, Shinjuku-ku, Tokyo 162-8655, Japan e-mail:
[email protected] K. Ito Department of Nuclear Medicine, Saitama Medical University International Medical Center, Saitama, Japan Y. Masuda-Miyata Medicheck Imaging Center, Iwai Medical Foundation, Tokyo, Japan H. Yamashita K. Ito A. Mimori Department of Collagen Disease, National Center for Global Health and Medicine, Tokyo, Japan H. Kuroki Department of Orthopedic Surgery, National Center for Global Health and Medicine, Tokyo, Japan
Introduction Tuberculous pericarditis caused by Mycobacterium tuberculosis is found in approximately 1–2% of all cases of pulmonary tuberculosis [1]. However, no reliable diagnostic test is available for accurately evaluating pericardial inflammation [2]. Many previous reports have described the efficacy of imaging modalities for diagnosing pericardial effusion, and a few reports have focused on the usefulness of 18F-fluorodeoxyglycose (18F-FDG) positron emission tomography combined with computed tomography (PET-CT) for the diagnosis and monitoring of tuberculosis. Here, we present two cases of tuberculous pericarditis, focusing on the assessment of pericardial inflammation using 18 F-FDG-PET-CT.
Cases report Case 1 A 26-year-old woman presented with a history of fever and back pain. Laboratory findings revealed a white blood cell count of 12.53 9 103 mL, a gamma GTP level of 77 UI, a C-reactive protein (CRP) level of 14.23 mg/dl, and a soluble IL-2 receptor level of 1,060 U/ml. Others were normal. A chest X-ray and chest and abdominal CT examination were performed. The CT results showed sclerotic and osteolytic lesions in the sacrum and right femoral head, pleural effusion, and pericardial thickening of 1.5 cm. Upper GI fiberscope examination was normal. In view of the patient’s persistent fever and elevated inflammatory markers, an 18F-FDG-PET-CT examination was performed to identify the cause of the inflammation or malignancy.
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Fig. 1 a Initial PET-CT MIP images showing 18F-FDG uptake in the pericardium (max SUV: 13.9), 5th cervical vertebra (13.1), and 2nd and 7th thoracic vertebrae (13.0). 18 F-FDG uptake is also visible in bilateral inguinal lymph nodes, left iliac crest (12.8), and sacrum (18.6). b Coronal PETCT and fusion images showing pericardial FDG uptake. c Posttreatment MIP images showing 18 F-FDG uptake in the pericardial recess (max SUV: 7.1) and sacrum (4.4) only. Some uptake in the lower cervical spine (site of fixation) is visible. d Post-treatment coronal PET, CT and fusion images showing 18F-FDG uptake in the pericardial recess
The 18F-FDG-PET-CT examination protocol was as follows. After at least 6 h of fasting, the patient received an intravenous injection of 370 MBq of 18F-FDG. Threedimensional whole-body PET-CT imaging was then performed using a PET-CT scanner (Siemens Biograph 16). The intensity of the 18F-FDG uptake was quantified by measuring the standardized uptake value (SUV). The PET-CT examination (Fig. 1a) revealed a high 18FFDG uptake in the 5th cervical vertebra and the 2nd thoracic vertebra, in the S1–S2 vertebrae (max SUV: 18.6), and in the right femoral head and acetabulum and the left iliac bone. Evidence of 18F-FDG uptake in the mediastinal lymph nodes and pericardium (max SUV: 13.9) was also observed (Fig. 1b). Bone biopsies of the 2nd thoracic vertebra and the S1–S2 vertebrae were performed. The biopsies showed epithelioid cell granuloma with caseous necrosis, findings that are consistent with a diagnosis of tuberculosis. A QuantiFERON test for Mycobacterium tuberculosis was positive. Antituberculosis treatment was started, and the patient’s CRP level gradually improved. Cervical fixation was also performed. During a follow-up 18 F-FDG-PET-CT examination performed 6 months later, 18 F-FDG uptake was once again observed in the pericardial
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recess (max SUV decreased from 13.9 to 7.1) and sacrum (from 18.6 to 4.4) (Fig 1c, d). All the other previous sites of uptake showed a minimal accumulation of 18F-FDG. The size and extent of the lesions had significantly decreased. Significant improvements in the patient’s signs and symptoms, such as the CRP level and fever, were also observed. Case 2 A 29-year-old woman presented with a fever of unknown origin and lateral chest pain. A physical examination and auscultation yielded normal findings. Echocardiography showed no pericardial effusion, and no hemodynamic compromise was observed on an echocardiogram. A CT examination was performed, and enlarged cervical and mediastinal lymph nodes as well as pericardial thickening and a soft tissue mass in the pericardium were revealed. The laboratory findings were within the normal limits except for the sedimentation rate, which was 74 mm in the first hour. Tumor markers such as soluble IL-2 receptor, Pro-GRP were all normal. Upper GI fiberscope examination was normal. To investigate the septic focus or
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Fig. 2 a Initial PET-CT MIP images showing pericardial thickening and 18F-FDG uptake in the parietal and visceral pericardium (max SUV: 16.5) and cervical (4.9) and mediastinal (19.2) lymph nodes. 18 F-FDG uptake is also visible in the 7th thoracic vertebra (6.3). b PET, CT, and fusion images showing pericardial 18 F-FDG uptake. c Posttreatment CT image showing slight pericardial thickening
possible malignancy, an 18F-FDG-PET-CT examination was performed. The PET-CT examination (Fig. 2a, b) showed a high 18 F-FDG uptake in the 7th thoracic vertebra, in the cervical and mediastinal lymph nodes (maximum SUV: 19.2), and in the pericardium (16.5). The cervical lymph nodes were resected, and a biopsy showed caseation granulomas, suggestive of tuberculosis. Ziehl–Nielsen staining was positive for Mycobacterium tuberculosis. The patient received antitubercular treatment and responded well. A follow-up CT examination showed no pericardial thickening and regression of the lymph nodes (Fig. 2c). Neither of the patients in the present report were infected with human immunodeficiency virus (HIV).
Discussion Tuberculous pericarditis caused by Mycobacterium tuberculosis is found in approximately 1% of all autopsied cases
with tuberculosis and in 1–2% of all cases of pulmonary tuberculosis [1]. Tuberculous pericarditis is the most common cause of pericarditis in developing countries [1– 3]. Furthermore, the spread of HIV has led to a resurgence of tuberculosis, and the incidence of tuberculous pericarditis is increasing in populations infected with HIV [4]. Tuberculous pericarditis has a variable clinical presentation and should be considered when evaluating cases of pericarditis without a rapidly self-limiting course. The condition usually develops insidiously, presenting with symptoms such as fever, night sweats, fatigue, weight loss and chest pain. Both of our patients had suffered from longstanding fevers and one had also experienced chest pain. Pericardial involvement usually develops via the retrograde lymphatic spread of M. tuberculosis from peritracheal, peribronchial, or mediastinal lymph nodes or by hematogenous spread from the primary site of tuberculous infection. In rare cases, the pericardium becomes involved as a result of the breakdown and contiguous spread of a tuberculous lesion in the lung or hematogenous spread from a distant secondary extrapulmonary skeletal or urogenital infection [1]. The lymphatic drainage of the
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pericardium is primarily to the anterior and posterior and the tracheobronchial lymph nodes, and this drainage route is reflected by the pattern of lymphadenopathy seen in cases with tuberculous pericarditis. In other conditions associated with mediastinal lymph node involvement, such as lymphoma, malignancy and sarcoidosis, hilar lymph node involvement is prominent [2, 3]. In patients with lymphoma, pericardial involvement is rare and tuberculosis should be suspected even in patients who are not infected with HIV. Neither of the patients in the present report were infected with HIV. Four pathologic stages of tuberculous pericarditis are recognized (1) fibrinous exudation with initial polymorphonuclear leukocytosis, relatively abundant mycobacteria, and early granuloma formation with loose organization of macrophages and T cells, (2) serosanguineous effusion with predominantly lymphocytic exudate containing monocytes and foam cells, (3) the absorption of effusion with organization of granulomatous caseation and pericardial thickening caused by fibrin, collagenosis and ultimately fibrosis, and (4) constrictive scarring as the fibrosing visceral and parietal pericardium contracts on the cardiac chamber and possibly becomes calcified, encasing the heart in a fibroelastic skin that impedes diastolic filling and causes the classic syndrome of constrictive pericarditis [1–3]. Although biopsies of the pericardium were not performed in the present patients, the pathological stage was estimated as being between 1 and 2 in both cases, because both cases showed dramatic improvement in pericardial thickening and activity of inflammation after the introduction of therapy. Recent data suggest that the histological pattern is affected by the immune status of the patient, with fewer granulomas being observed in HIVinfected patients with severely depleted CD4 lymphocyte counts [1, 2]. The role of imaging in the diagnosis of pulmonary tuberculosis is well established [4, 5]. Since other diagnostic tools are time-consuming and sometimes produce negative results despite the presence of active disease, antitubercular treatment is typically started before the final laboratory results become available. 18F-FDG-PET is playing an increasingly important role in the diagnosis, staging and monitoring of malignant tumors [6, 7]. Not only tumors, but also infections show an increased uptake of 18F-FDG. 18F-FDG uptake depends on the increase in glucose metabolism in activated inflammatory cells such as leukocytes, granulocytes and macrophages [8]. Some reports and clinical studies have dealt with the usefulness of 18F-FDG-PET-CT for the diagnosis and monitoring of pulmonary tuberculosis [9, 10]. PET scans using 18F-FDG are useful for differentiating tuberculous pulmonary nodules from malignancies but can also provide information about disease activity, enabling the immediate start of
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antitubercular treatment before a definite diagnosis based on bacteriology, which is time-consuming and sometimes produces false-negative results, becomes available in patients with active pulmonary tuberculosis [10–12]. In the present cases, FDG-PET-CT provided valuable information regarding the degree of inflammatory activity in the pericardium without requiring an invasive diagnostic procedure to confirm pericardial involvement and disease activity. A previous case report [10] showed FDG uptake in the pericardium in a patient with tuberculous pericarditis, but whole-body imaging, which aids physicians to understand how this disease spreads from the lungs to the pericardium and other areas of the body, was not performed. Also, the usefulness of FDG-PET for monitoring of the response of tuberculous pericarditis to treatment was clearly demonstrated in the present cases. Our report emphasizes the unique ability of 18F-FDG-PET to visualize active inflammation associated with tuberculous pericarditis. No other imaging modality is capable of demonstrating pericardial disease activity, which may be critical for reducing the mortality rate associated with this disease. In conclusion, 18F-FDG-PET could be an important noninvasive method for diagnosing active disease and enabling the management of extrapulmonary mycobacterial infections, including pericarditis. Furthermore, our study provides additional evidence that 18F-FDG-PET is useful for evaluating the therapeutic response of patients with tuberculosis. Acknowledgments The authors would like to thank Mr. Kazuhiko Nakajima, Mr. Takuya Mitsumoto, and Mr. Nao Fujiki for their excellent support. This work was supported by a Grant for International Health Research (21A126) from the Japanese Ministry of Health, Labour and Welfare.
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