DOI: 10.1148/radiol.2402050886
(Radiology 2006;240:559-564.)
© RSNA, 2006
Pulmonary CT Findings in 320 Carriers of Human T-Lymphotropic Virus Type 11
Fumito Okada, MD,
Yumiko Ando, MD,
Sachie Yoshitake, MD,
Shinji Yotsumoto, MD,
Shunro Matsumoto, MD,
Masaki Wakisaka, MD,
Toru Maeda, MD and
Hiromu Mori, MD
1 From the Department of Diagnostic and Interventional Radiology, Oita University Faculty of Medicine, Idaigaoka 1-1, Hasama-machi, Oita 879-5593, Japan. Received May 27, 2005; revision requested July 21; revision received September 15; accepted October 14; final version accepted November 2.
Address correspondence to F.O. (e-mail: fumitook{at}med.oita-u.ac.jp).
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ABSTRACT
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Purpose: To retrospectively evaluate pulmonary computed tomographic (CT) findings in human T-lymphotropic virus type 1 (HTLV-1) carriers, who were characterized by means of polyclonal integration of proviral DNA.
Materials and Methods: Institutional review board approval was obtained, and informed consent was waived. Chest CT scans obtained between January 1996 and October 2004 in 320 (154 men, 166 women; age range, 31–86 years; mean, 64 years) patients with HTLV-1 were retrospectively evaluated by three chest radiologists. Parenchymal abnormalities (ground-glass opacity, consolidation, centrilobular nodules, thickening of bronchovascular bundles, interlobular septal thickening, and bronchiectasis) were evaluated, along with enlarged lymph nodes and pleural effusion. In 58 patients who underwent surgical biopsy or transbronchial biopsy, comparison of CT images with the actual specimens was performed by a pathologist and three chest radiologists.
Results: On CT scans, abnormal findings were seen in 98 (30.1%) patients and consisted of centrilobular nodules (n = 95), thickening of bronchovascular bundles (n = 55), ground-glass opacity (n = 51), bronchiectasis (n = 50), interlobular septal thickening (n = 28), and consolidation (n = 5). These abnormalities were predominantly seen in the peripheral lung parenchyma (n = 70). Pathologically, these findings corresponded to lymphocytic infiltration along respiratory bronchioles and bronchovascular bundles. Pleural effusion and enlarged lymph nodes were found in two and five patients, respectively.
Conclusion: CT findings in patients with HTLV-1 consisted mainly of centrilobular nodules, ground-glass opacity, and thickening of the bronchovascular bundles in the peripheral lung. These CT findings are considered suggestive of thoracic involvement in patients with HTLV-1.
© RSNA, 2006
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INTRODUCTION
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Human T-lymphotropic virus type 1 (HTLV-1) is an etiologic retrovirus of adult T-cell leukemia or lymphoma (1). This viral infection is endemic in Caribbean countries, South America, Africa, and southwestern Japan and has sporadically been identified in the United States and some European countries (2,3). Interestingly, this virus is also associated with several nonmalignant disorders such as HTLV-1–associated myelopathy or tropical spastic paraparesis (HAM/TSP) (4), HTLV-1–associated uveitis (5), and HTLV-1–associated arthropathy (6). These disorders often occur simultaneously in an individual, which indicates that systemic involvement occurs in HTLV-1 infection.
Patients with HAM/TSP and HTLV-1–associated uveitis who are in the carrier state, as shown with polyclonal integration of proviral DNA, demonstrate frequent pulmonary complications characterized by T-lymphocytic alveolitis (7). However, unlike patients with adult T-cell leukemia or lymphoma, neither leukemic cells nor pathogens associated with opportunistic infections are found in the lungs of carriers of HTLV-1. Surprisingly, a similar pulmonary involvement has been observed in asymptomatic carriers of HTLV-1 (8). These reports suggest the possibility that the lung is the preferential site for HTLV-1 infection and that this peculiar tropism is responsible for the high incidence of pulmonary involvement.
Respiratory symptoms and chest radiographic abnormalities are rarely found in these patients. Findings in a report (9) from Japan showed chest radiographic abnormalities manifested as diffuse micronodular shadows in five of 30 patients with HAM/TSP. To our knowledge, no radiologic studies of pulmonary CT in HTLV-1 carriers have been performed. Thus, the purpose of our study was to retrospectively evaluate the pulmonary CT findings in HTLV-1 carriers, who were characterized by means of polyclonal integration of proviral DNA.
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MATERIALS AND METHODS
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Patients
The authors retrospectively reviewed CT scans of the lung in 320 patients (154 men, 166 women; age range, 31–86 years; mean, 64 years) with HTLV-1 who had undergone chest CT between January 1996 and October 2004 at three institutions. The institutional review boards of the three institutions approved this retrospective study and waived informed consent.
HTLV-1 carriers were characterized by means of positive HTLV-1 antibody staining and polyclonal integration of proviral DNA in the peripheral blood or tissues that were sampled at biopsy. On the other hand, adult T-cell leukemia or lymphoma was diagnosed by means of monoclonal integration of proviral DNA and the presence of abnormal lymphocytes with convoluted nuclei (adult T-cell leukemia or lymphoma cells) in the peripheral blood or histologic findings compatible with diagnosis of adult T-cell leukemia or lymphoma in tissue that was sampled at biopsy.
In 221 of 320 patients, a diagnosis of HTLV-1 was made 3–85 days (mean, 55 days) prior to CT examinations. Ninety-nine patients underwent CT 8–31 days (mean, 22 days) before the diagnosis was evident. Patients with concurrent infectious disease, collagen disease, diffuse panbronchiolitis, or sarcoidosis diagnosed by means of serologic tests and clinical and pathologic findings were not included in this study, because these diseases can manifest CT findings such as ground-glass opacity, consolidation, nodules, or thickening of bronchovascular bundles.
Among the patients with abnormal findings on chest CT scans, 60 patients were treated with low doses of 14-membered ring macrolide antibiotics for 2–30 months (mean, 14.3 months) after the diagnosis. Among the patients who received treatment, follow-up CT scans were obtained in 46 patients. These patients did not receive any other medication during the entire study, except for short-term antibiotics if their condition became acutely exacerbated. On the other hand, among the patients who did not receive treatment (n = 260), follow-up CT scans were obtained in 33 patients. All follow-up CT scans were also evaluated. A total of 421 CT scans were obtained in these patients, and intravenously administered contrast material was used for 178 of the CT scans.
CT Examinations
CT examinations were performed with either a HiSpeed Advantage (GE Medical Systems, Milwaukee, Wis), a HiSpeed LX/i Advantage (GE Medical Systems), or an X-press (Toshiba, Tokyo, Japan) unit. Thin-section CT was performed with 1-mm collimation at 10-mm intervals. Images were obtained at lung (width, 1500 HU; level, –700 HU) and mediastinal (width, 400 HU; level, 20–40 HU) window settings. Two hundred twenty-seven patients underwent thin-section CT with 1-mm collimation, and 93 patients underwent CT with 7–10-mm collimation. In 88 patients, follow-up CT scans were obtained 3–32 months after the initial scan. These CT scans extended from the lung apices to the costophrenic angle. With the HiSpeed Advantage unit, the scanning time of each section was 2 seconds at 120 kVp and 150 mA; with the Hi Speed Lx/i Advantage unit, the scanning time of each section was 2 seconds at 140 kVp and 160 mA; and with the X-press unit, the scanning time was 2 seconds at 140 kVp and 150 mA. All CT scans were obtained during suspended end inspiration with the patient in the supine position.
CT Image Interpretation
Three chest radiologists (F.O., Y.A., and S.M., with 17, 9, and 20 years, respectively, of experience in chest CT image interpretation), who were aware of the underlying diagnosis, retrospectively interpreted the CT scans by using hard-copy images and reached their conclusion in consensus. All initial scans were evaluated. There was an average of two sessions per week reserved for reviewing CT scans, and there were a total of about 50 sessions. CT images were assessed with regard to each of the following radiologic patterns: ground-glass opacity, consolidation, centrilobular nodules, thickening of bronchovascular bundles, interlobular septal thickening, honeycombing, crazy-paving appearance, bronchiectasis, enlarged hilar and/or mediastinal lymph node(s) (>1 cm in diameter of the short axis), pleural effusion (unilateral or bilateral), and pericardial effusion. The combination of these CT findings was also assessed. Areas of ground-glass opacity were defined as hazy increases in attenuation without obscuration of vascular markings. Areas of consolidation were defined as areas of increased attenuation that caused obscuration of the normal lung markings with or without air bronchograms. If a small nodule was identified around peripheral pulmonary arterial branches or 3–5 mm away from the pleura, interlobular septa, or pulmonary veins, it was defined as a centrilobular nodule. Centrilobular nodules were categorized according to the diameter of the short axis as smaller than 5 mm, 5–10 mm, or larger than 10 mm.
The distribution of parenchymal disease was also noted. If the main lesion was located predominantly in the inner third of the lung, the disease was classified as having a central distribution. If the lesion was predominantly in the outer third of the lung, the disease was classified as having peripheral distribution. If the lesions showed no predominant distribution, the disease was classified as having random distribution. In addition, zonal predominance was classified as upper, lower, or random. The upper lung zone predominance was considered to be present when most abnormalities were seen at the upper level to the tracheal carina; likewise, the lower lung zone predominance was considered to be present when most abnormalities were seen below the upper zone. When abnormalities showed no definite zonal predominance, the lung disease was classified as having a random distribution.
Moreover, four radiologists (F.O., Y.A., S. Yoshitake, and S.M.) reviewed abnormal findings on chest radiographs, and five radiologists (F.O., Y.A., S. Yoshitake, S. Yotsumoto, and T.M.) reviewed respiratory symptoms regarding the clinical features in patients with abnormal findings on chest CT scans.
Comparison with Pathologic Findings
Comparison of CT and pathologic findings was performed with actual specimens by a pathologist and three chest radiologists (F.O., Y.A., S. Yotsumoto) in 58 patients by using surgical biopsy in one, transbronchial lung biopsy in 44, and both transbronchial lung biopsy and surgical specimens in 13 patients. Surgical lung biopsy and transbronchial lung biopsy, findings of which corresponded to abnormal regions on chest CT scans, were performed within 14 and 22 days, respectively, after CT.
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RESULTS
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CT Pattern
The chest CT scans revealed abnormalities in 98 (30.1%) of 320 patients with HTLV-1 (Table). Among the 98 patients, centrilobular nodules (n = 95, 97%) (Figs 1–5) were seen most frequently, followed by thickening of bronchovascular bundles (n = 55, 56%) (Figs 2, 4). Centrilobular nodules smaller than 5 mm in diameter were identified in all patients, and centrilobular nodules 5–10 mm in diameter were identified in 17 patients. No nodules larger than 10 mm in diameter were observed. The nodules were diffuse in both lungs and were frequently associated with centrilobular branching linear structures. Ground-glass opacity (n = 51, 52%) (Figs 1, 2, 4), bronchiectasis (n = 50, 51%) (Fig 3), and interlobular septal thickening (n = 28, 29%) (Fig 4) were also observed frequently. Areas of consolidation were also observed in five (5%) patients. CT findings of honeycombing or crazy-paving appearance were not found. The combination of centrilobular nodules and thickening of bronchovascular bundles (n = 52, 53%) was seen most frequently, followed by centrilobular nodules and ground-glass opacity (n = 49, 50%). Some ground-glass opacity was detected in areas near centrilobular nodules or thickened bronchovascular bundles.
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Figure 1a: Images in a 26-year-old woman. (a) Transverse CT scan obtained 1 cm below the level of tracheal carina shows centrilobular nodules (arrows) in peripheral distribution. Ground-glass opacity is also present (arrowheads). (b) Photomicrograph of surgical biopsy specimen from right upper lobe shows infiltration of lymphocytes into respiratory bronchioles and alveolar walls (arrows). (Hematoxylin-eosin stain; original magnification, x100.)
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Figure 1b: Images in a 26-year-old woman. (a) Transverse CT scan obtained 1 cm below the level of tracheal carina shows centrilobular nodules (arrows) in peripheral distribution. Ground-glass opacity is also present (arrowheads). (b) Photomicrograph of surgical biopsy specimen from right upper lobe shows infiltration of lymphocytes into respiratory bronchioles and alveolar walls (arrows). (Hematoxylin-eosin stain; original magnification, x100.)
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Figure 2: Transverse CT scan in a 76-year-old woman obtained at the level of carina shows thickening of bronchovascular bundles (arrows) and presence of centrilobular nodules (tree-in-bud pattern) (arrowhead). Surgical biopsy specimen (not shown) from left upper lobe demonstrated lymphocytes infiltrating along bronchovascular bundles with mild fibrosis.
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Figure 3: Transverse CT scan in a 72-year-old woman obtained at the level of right hemidiaphragm shows centrilobular nodules (black arrows), bronchiectasis (arrowheads), and bronchial wall thickening (white arrows). Surgical biopsy specimen (not shown) from right lower lobe demonstrated mild bronchiectasis and lymphocytes without any nuclear atypia infiltrating the walls of respiratory bronchioles and extending into the adjacent peribronchiolar interstitium.
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Figure 5: Transverse CT scan in a 27-year-old woman obtained at the level of right hemidiaphragm shows centrilobular nodules (tree-in-bud pattern) (arrows) and mild thickening of bronchial wall (arrowheads). Surgical biopsy specimen (not shown) from right lower lobe demonstrated infiltration of lymphocytes along the bronchial wall.
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Distribution of Disease
Among the 98 patients with parenchymal disease, abnormal findings were predominantly seen in the peripheral lung (n = 70, 71%). There were 28 patients with disease showing random distribution (29%) and no patients with a predominantly central distribution. The predominant zonal distribution was at the lower zone in 12 (12%) patients and at the middle zone in 15 (15%) patients; random distribution was observed in 71 (72%) patients.
Treatment versus No Treatment
Among the patients with macrolide treatment and follow-up CT scans (n = 46), centrilobular nodules (n = 46) had improved in seven patients, remained unchanged in 35, and worsened in four. Thickening of bronchovascular bundles (n = 25) had improved in five patients, remained unchanged in 18, and worsened in two. Ground-glass opacity (n = 37) had improved in nine patients and remained unchanged in 28. Among patients without treatment and follow-up CT scans (n = 33), 20 patients had abnormal findings on the initial CT scans. The centrilobular nodules (n = 19) remained unchanged in 12 and worsened in seven patients. Thickening of bronchovascular bundles (n = 13) remained unchanged in eight patients and worsened in five. Among the remaining 13 patients with no abnormal findings on the initial CT scans, centrilobular nodules newly appeared in two patients on follow-up CT scans.
Effusion and Lymph Nodes
There were small pleural effusions in two (2%) patients. Bilateral effusion was observed in one patient; unilateral effusion, in the other. Pleural effusion disappeared in both patients after treatment. Mediastinal and hilar lymph node enlargement (11–17 mm) were found in five (5%) patients. Enlarged lymph nodes were generally found at the pretracheal, paratracheal, tracheobronchial, or subcarinal regions. At follow-up CT in four patients who received treatment, lymph node enlargement improved in one patient and remained unchanged in three. No enlarged lymph nodes were found in axillary regions. None of the patients had pericardial effusions.
Chest Radiographs and Clinical Features
We also reviewed chest radiographs and clinical features in the 98 patients with abnormal findings on chest CT scans. Fourteen patients had abnormal radiographic findings that manifested as diffuse micronodular and reticular opacities. Among respiratory symptoms, 47 patients had cough and productive sputum.
CT and Pathologic Comparison
In all 58 patients who underwent surgical biopsy or transbronchial lung biopsy, the extent of centrilobular nodules pathologically corresponded to that of lymphocytic infiltration along respiratory bronchioles (Figs 1–3). In addition, thickening of the bronchovascular bundles corresponded to infiltration of lymphocytes along bronchovascular bundles (Figs 2, 3, and 5).
The extent of ground-glass opacity also corresponded to the extent of lymphocytic infiltration into the interstitium (Fig 1). In 13 patients, both surgical biopsy and transbronchial lung biopsy were performed, and histologic findings of the surgical biopsies were identical to those of the transbronchial lung biopsy specimens.
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DISCUSSION
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HTLV-1 infection is endemic in tropical areas and in southwestern Japan and has been identified in the United States and in the United Kingdom (10). In Japan, antibodies against HTLV-1 have been found in more than 1 million people, and approximately 500 patients develop adult T-cell leukemia or lymphoma annually. HTLV-1 is most often transmitted vertically by means of breast feeding and occasionally by means of blood transfusion. There is a long latency period of 10–30 years between the initial infection with HTLV-1 and the development of adult T-cell leukemia or lymphoma (11). The cumulative lifetime risk for an infected individual to develop adult T-cell leukemia or lymphoma is estimated to be 0.5%-5% (12–14). Specific risk factors for developing adult T-cell leukemia or lymphoma remain unclear.
Pulmonary involvement in patients with HAM/TSP and HTLV-1–associated uveitis is mostly subclinical. Respiratory symptoms and chest radiographic abnormalities are rarely found in these patients, although 60%–80% have T-lymphocytic alveolitis as demonstrated by bronchoalveolar lavage. A report (9) from Japan demonstrated chest radiographic abnormalities that manifested as diffuse micronodular shadows in five of 30 patients with HAM/TSP. Similarly, all 11 patients with HTLV-1–associated uveitis had normal chest radiographs, and six of these cases were associated with bronchoalveolar T lymphocytosis (7). In pulmonary function testing, seven of 30 patients with HAM/TSP showed decreased diffusing capacity to carbon monoxide (9). Such abnormalities in pulmonary function testing were demonstrated not only in patients with abnormal chest radiographs but also in patients with normal chest radiographs. In our study, 14 patients had abnormal radiographic findings, which are similar to those of previous reports. Among respiratory symptoms, 47 patients had cough and productive sputum.
To our knowledge, no radiologic studies of pulmonary CT findings in HTLV-1 carriers have been performed. Of the 320 carriers with HTLV-1 antibodies we reviewed, 98 (30.1%) had CT abnormalities. The most common CT findings were centrilobular nodules, followed by thickening of bronchovascular bundles and ground-glass opacity. Centrilobular nodules corresponded to the extent of lymphocytic infiltration into the wall of respiratory bronchioles extending into the adjacent peribronchiaolar interstitium. Thickening of bronchovascular bundles corresponded to the presence of lymphocytes along the bronchovascular bundles with mild fibrosis. In addition, the extent of ground-glass opacity corresponded to the extent of lymphocytic infiltration into the interstitium.
Previously, we reported the pulmonary CT findings and CT-pathologic correlation in 60 patients with adult T-cell leukemia or lymphoma (15). The CT findings of these patients consisted of ground-glass opacity, centrilobular nodules, thickening of bronchovascular bundles, and consolidation in peripheral lung parenchyma. Pleural effusion and lymph node enlargement were also observed frequently.
In comparison with CT findings in adult T-cell leukemia or lymphoma patients, CT findings in HTLV-1 carriers were substantially different from those in HTLV-1 patients. Consolidation, a nodule larger than 1 cm in diameter, pleural effusion, or pleural thickening corresponding to atypical lymphocytic infiltration were less common. Since the HTLV-1–associated bronchopulmonary disorder is chronic bronchiolitis, lymph node enlargement, pleural thickening, or pleural effusion are rare in HTLV-1 carriers.
Kimura (16) described a close relationship between diffuse panbronchiolitis or idiopathic interstitial pneumonia and HTLV-1. In his article, the author speculated that the accumulation of precancerous lymphoid cells in bronchoalveolar areas would lead to diffuse panbronchiolitis or idiopathic interstitial pneumonia due to host response.
Recently, Kadota et al (17) reported that the clinicopathologic features of diffuse panbronchiolitis and HTLV-1–associated bronchitis were similar. However, HTLV-1–associated bronchitis might be associated with conditions that are distinct from those of diffuse panbronchiolitis due to the different responses to macrolide treatment and the difference in the number of activated T cells bearing interleukin-2 receptor in the lungs.
In our study, follow-up CT scans after treatment showed that centrilobular nodules (n = 46) had improved in only seven cases, remained unchanged in 35, and worsened in four. In addition, lung biopsy specimens were obtained from 22 patients in the group with centrilobular nodules, and all revealed pathologic changes unlike those of diffuse panbronchiolitis. Our results regarding the effects of macrolide treatment were similar to those of previous reports (17). Thus, HTLV-1–associated bronchiolitis can be distinguished from diffuse panbronchiolitis by means of pathologic and clinical findings.
On the other hand, CT findings of pulmonary fibrosis (ie, honeycombing) were not found in our study. This result is probably due to the fact that patients with a collagen disease or a collagen-related disease were excluded from the study. Furthermore, none of the patients showed any sign of substantial fibrotic disease in the upper lobe, which is frequently seen in patients with chronic hypersensitivity pneumonitis, sarcoidosis, or pneumoconiosis.
It should be noted that there were several limitations to our study. First, this was a retrospective study, and CT image interpretation was performed by consensus. Second, CT findings were not compared with pathologic findings in all patients, because some patients were asymptomatic. In addition, CT scans and histologic specimens were not obtained on the same day, although surgical biopsies and transbronchial lung biopsies were performed within 14 and 22 days, respectively, after CT. Third, it is difficult to distinguish between diffuse panbronchiolitis, follicular bronchiolitis, collagen-related bronchiolitis, or respiratory bronchiolitis associated interstitial lung disease or diffuse aspiration bronchiolitis only on the basis of CT findings. Finally, some of the CT examinations were performed several years ago, and, more important, not all CT studies included 1-mm thin-section images. If all patients had undergone thin-section CT, the abnormal findings may have resulted in a different frequency than that observed in our study.
In summary, pulmonary CT findings in carriers of HTLV-1 consisted mainly of centrilobular nodules, thickening of bronchovascular bundles, and ground-glass opacity in the peripheral lung. These findings corresponded pathologically to lymphocytic infiltration into the respiratory bronchial wall, into the bronchovascular bundles, and into the interstitium. These CT findings are considered suggestive of pulmonary involvement in patients with positive HTLV-1.
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ADVANCES IN KNOWLEDGE
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- Pulmonary CT scans revealed abnormalities in 98 (30.1%) of 320 carriers of human T-lymphotropic virus type 1.
- The most common CT finding was the centrilobular nodule, which corresponded pathologically to the extent of lymphocytic infiltration into the wall of respiratory bronchioles.
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FOOTNOTES
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Abbreviations: HAM/TSP = HTLV-1–associated myelopathy or tropical spastic paraparesis • HTLV-1 = human T-lymphotropic virus type 1
Authors stated no financial relationship to disclose.
Author contributions: Guarantor of integrity of entire study, F.O.; study concepts/study design or data acquisition or data analysis/interpretation, all authors; manuscript drafting or manuscript revision for important intellectual content, all authors; approval of final version of submitted manuscript, all authors; literature research, S.M., M.W., T.M.; clinical studies, F.O., Y.A., S. Yoshitake, S. Yotsumoto, T.M.; and manuscript editing, F.O., Y.A., S.M., M.W., H.M.
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ABSTRACT
INTRODUCTION
