Ann Thorac Surg 2003;76:219-224
© 2003 The Society of Thoracic Surgeons
Original article: general thoracic
Castleman disease of the pleura: experience with eight surgically proven cases
Sheung-Fat Ko, MDa*,
Shu-Hang Ng, MDd,
Ming-Jang Hsieh, MDb,
Jui-Wei Lin, MDc,
Chung-Cheng Huang, MDa,
Tze-Yu Lee, MDa,
Wei-Jen Chen, MDc
a Departments of Radiology, Keelung Hsien and Taoyuen Hsien, Taiwan
b Department of Cardiovascular and Thoracic Surgery, Keelung Hsien and Taoyuen Hsien, Taiwan
c Department of Pathology, Chang Gung University, Chang Gung Memorial Hospital at Kaohsiung, Kaohsiung Hsien, Taiwan
d Department of Radiology, Chang Gung University, Chang Gung Memorial Hospitals at Keelung and Linkou, Keelung Hsien and Taoyuen Hsien, Taiwan
Accepted for publication January 22, 2003.
* Address reprint requests to Dr Ko, Department of Radiology, Chang Gung University, Chang Gung Memorial Hospital at Kaohsiung, 123, Ta-Pei Road, Niao-Sung Hsiang, Kaohsiung Hsien, 833, Taiwan.
e-mail: sfatko{at}adm.cgmh.org.tw
 |
Abstract
|
|---|
BACKGROUND: Castleman disease of the pleura is unusual, and we present our experience with eight surgically proven cases.
METHODS: Between 1980 and 2002, 8 patients (7 women and 1 man; age range, 20 to 53 years; mean, 26.5 years) with surgically proven, pleural Castleman disease (six hyaline vascular type, one plasma cell type, and one mixed type) were encountered. Their clinical, imaging, and surgical findings were reviewed.
RESULTS: Five patients were asymptomatic, 1 had dyspnea, 1 had cough, and 1 experienced chest discomfort. Chest radiography showed a well-circumscribed interlobar, cardiophrenic, or paraaortic mass in 6 patients, a massive effusion in 1, and a focal diaphragmatic bulge in 1. Six tumors showed varying degrees of contrast enhancement (10 to 95 HU; mean, 46 HU) on computed tomography. Three cases appeared as well-defined, heterogeneously hyperintense pleural masses on magnetic resonance imaging. The masses varied in size from 3 to 10 cm (mean, 5.2 cm). Five masses greater than 5 cm had prominent pleural arterial blood supply and severe adhesions requiring thoracotomy and resection of nearby structures for radical tumor excision. Blood loss from patients varied between 100 and 850 mL (mean, 620 mL). No tumor recurrence was noted during follow-up (range, 1 to 16 years; mean, 6.5 years).
CONCLUSIONS: Pleural Castleman disease predominately affects young women and manifests as a well-circumscribed mass with a varying degree of contrast enhancement on computed tomography and heterogeneity on magnetic resonance imaging. Tumors greater than 5 cm have profuse pleural blood supplies and severe adhesion necessitating open thoracotomy and resection of neighboring structures. Radical resection can produce a satisfactory outcome.
|
Introduction
|
|---|
Most pleural neoplasms are metastatic lesions (95%), and only 5% of pleural neoplasms originate primarily from the pleura, the most common of which are mesothelioma, solitary fibrous tumor, and lipoma [1, 2]. Recently, we encountered two unusual cases of pleural tumors. One presented as a moderately enhanced large mass in the intrapulmonary fissure on computed tomography (CT) and was misdiagnosed as lymphoma based on the specimen from CT-guided biopsy. The other presented with dyspnea and massive pleural effusion. These two cases were eventually proven to be Castleman disease of the pleura, after surgery and detailed histopathologic examinations. As most cases of intrathoracic Castleman disease affect the mediastinum or hila, and there have only been a limited number of previously documented cases of pleural Castleman disease [4–11], we were prompted to search our records for other cases of pleural Castleman disease. The objective of this study was to present the clinical, imaging, and surgical findings of eight cases of Castleman disease of the pleura. To our knowledge, this is the largest case series of this unusual pleural tumor in the literature.
|
Patients and methods
|
|---|
Between January 1980 and September 2002, a total of eight cases of surgically proven Castleman disease of the pleura were collected in our hospital’s three medical facilities (one being in southern Taiwan and the other two in the north). The patients’ medical records were reviewed for clinical manifestations, past known diseases, and available laboratory data pertaining to their condition. All patients had undergone preoperative chest radiographs, but there was no previous study before the preoperative study for comparison. There were six CT and three magnetic resonance (MR) imaging studies (1 patient underwent both CT and MR studies), with the results being available for analysis. The imaging findings were reviewed and special attention was given to the following findings: tumor size, margin, location, relation of fissure, presence of any internal calcifications, presence of effusion, CT density and enhancement value, the presence of any adjacent bone changes, inherent MR signal intensities, and morphologic characteristics of the tumors. The CT enhancement attenuation value was defined as the attenuation value after enhancement minus the preenhanced attenuation value of the same region of interest (approximately 60% of central area) of the tumor. The enhancement was arbitrarily defined as being poor when the net enhancement value was less than or equal to 30 HU, moderate when the net enhancement was more than 30 HU but less than 60 HU, and strong when the net enhancement was more than 60 HU.
The surgical findings, including an investigation of tumor origin and blood supplies to the tumors, surgical methods adopted, any blood loss during surgery, and the presence of any adhesion or invasion of adjacent structures, were recorded. The pathologic examinations were reviewed by two pathologists. The lesions were classified as follows: (1) hyaline vascular type when the lesions were characterized by follicles with hyalinized vessels surrounded by circumferentially arranged layers of small lymphocytes, while the interfollicular tissues were composed of lymphocytic infiltrations with prominent vascular stroma; (2) plasma cell type when the lesions were characterized by a paucity of follicular hyalinized vessels within the tumor mass, while the interfollicular tissues were composed of continuous sheets of dense plasma cells in conjunction with a less vascular stroma; and (3) mixed type when the lesions were characterized by features of both subtypes.
|
Results
|
|---|
The clinical and imaging findings of the patients are summarized in Table 1,
and operative findings and follow-up are summarized in Table 2.
Clinical features
There were 7 women and 1 man in our study, ranging in age from 20 to 53 years (mean, 26.5 years). Of these 8 patients, 1 had dyspnea, 1 had cough, and 1 experienced chest discomfort, and the other 5 patients were, seemingly, asymptomatic and their lesions were, incidentally, found on chest radiographs. The past history of all our patients was unremarkable, apart from patient 2, who revealed a previous history of tuberculosis. None of them had any comorbid disease such as human immunodeficiency virus infection, immunosuppression, or collagen disease. On physical examination, only patient 2 had decreased breathing sound over the left hemithorax, in whom thoracentesis yielded 3 L of straw-colored effusion with a protein concentration of 63 g/L that was suggestive of an exudative process. Laboratory findings were unremarkable in the other patients. None of our patients had anemia, hypoalbuminemia, or hypergammaglobulinemia. C-reactive protein and erythrocyte sedimentation rate were available in 5 and 4 patients, respectively, and no abnormality was noted.
Imaging features
Chest radiography showed a well-circumscribed interlobar mass in 4 patients and one instance each of a cardiophrenic mass, a paraaortic mass, a massive effusion, and a focal diaphragmatic bulge, but no calcification could be identified. Six available CT scans showed varying degrees of contrast enhancement of the tumors (10 to 95 HU; mean, 46 HU), with strong enhancement in 1 patient, moderate enhancement in 3 patients, and poor enhancement in 2 patients, whereas punctate intratumoral calcifications were noted in two tumors. In patient 1 (Fig 1A),
a CT-guided biopsy was performed, from which the specimen was misinterpreted as lymphoma. In patient 2, a tumor was associated with massive effusion and focal rib erosion (Fig 2).
Magnetic resonance imaging demonstrated well-defined hyperintense pleural masses (Fig 3)
(two hyaline vascular type and one mixed type) in patients 6, 7, and 8.
View larger version (152K):
[in this window]
[in a new window]
|
Fig 1. Patient 1. (A) Enhanced chest computed tomography shows a homogeneous mass with moderate enhancement in the left major fissure. (B) At surgery, an intrafissural mass (arrows) between the left upper and lower lobes (triangles) with prominent superficial arterial supplies from the pleural vessels and severe adhesion to adjacent lung tissues was noted. (C and D) Histopathologic sections (hematoxylin & eosin stain) at two magnifications, (C) original magnification x40 and (D) original magnification x100, show typical features of hyaline-vascular Castleman disease with hyalinized vessels within germinal follicles that are surrounded by onion-like lymphocytes.
|
|
View larger version (125K):
[in this window]
[in a new window]
|
Fig 2. Patient 2. Enhanced chest computed tomography shows massive left pleural effusion and a slightly lobulated parietal pleural mass with strong enhancement and focal erosion of the adjacent rib (arrow).
|
|
View larger version (111K):
[in this window]
[in a new window]
|
Fig 3. Patient 6. Magnetic resonance imaging of the thorax depicts a heterogeneously hyperintense pleural mass (arrow) attaching to the descending aorta and pericardium.
|
|
Surgical findings and treatment outcome
During surgery, multiple prominent pleural arteries (Fig 1B) over the lesions were noted, and patient 5 had additional blood supply originating from the pulmonary artery. Four tumors originated from the visceral pleura and were intrafissurally located, of which, three were located in the right major fissure, and one was situated in the left major fissure. The other four tumors originated from the parietal pleura, one located in the right cardiophrenic region exhibiting tight adhesion to the right hemidiaphragm and right pericardium, one occurred in the pericardioaortic region, and one affected the right basal pleura with tight adhesion to the right hemidiaphragm. The remaining tumor (patient 2) originated from the left posterior parietal pleura with involvement of the adjacent rib. Three tumors were smaller than 5 cm in diameter, in which video-assisted thoracoscopic surgery (VATS) was successful in tumor resection in two (patients 3 and 6), whereas the remaining one was resected by thoracotomy with minimal resection of nearby lung tissues. Those five tumors larger than 5 cm in diameter revealed severe adhesion to the adjacent lungs, pericardium, or pleura, and even the rib. In two of these five tumors (patients 2 and 7), VATS was initially applied but was ineffective due to the presence of profuse pleural arterial blood supplies over the tumor surfaces and severe adhesion to adjacent tissues, and a conversion to open thoracotomy was subsequently performed. For the other 3 patients, thoracotomy was performed in the first instance. In addition, among these five cases, the wedge resection of nearby lungs, a partial pericardiectomy, decortication of the pleura, or partial resection of the involved rib was undertaken in order to perform a radical removal of the lesion. Blood loss from patients varied between 100 and 850 mL. No postsurgical complication was noted and no further treatment was used for any patient. At the time of writing, all patients were alive and seemingly well, with no recurrent lesion being detected during follow-up, with duration ranging from 1 to 16 years (mean, 6.5 years).
Pathologic finding and correlation with imaging studies
All eight tumors presented as solitary, well-encapsulated masses possessing rubbery consistency, but six of them had moderate to marked adhesion to the adjacent structures. The masses varied from 3 to 10 cm (mean, 5.2 cm). Six masses showed typical histopathological features of hyaline vascular type Castleman disease (Fig 1C, 1D). Of the remaining two masses, one was plasma cell type and one was a mixed type. Cut sections of the resected specimens revealed grayish yellow, pinkish tan, to yellowish brown content. Four tumors with strong or moderate enhancement on CT were characterized by proliferative vascular stroma between germinal follicles, whereas distorted germinal follicles with prominent necrosis and fibrosis in the intervening tissues were noted in the other two poorly enhanced tumors. Inhomogeneous arrangement of germinal follicles with intervening focal degeneration changes or fibrotic septa accounted for heterogeneous hyperintense appearances on MR imaging. Immunohistochemical profiles were available in four cases, with the tumor cells staining positively for CD45 (or T200), CD45RO (or UCHL-1), and CD20 (or L26), but negatively for high- and low-molecular weight cytokeratins. These tumors were also negatively stained for congo red.
|
Comment
|
|---|
Castleman and associates first described the characteristic clinical and pathologic findings of Castleman disease and established two characteristic histologic types, of which, 91% of cases belonged to the hyaline vascular type characterized by hyaline-vascular follicles and interfollicular capillary proliferations. The remaining 9% of cases belonged to the plasma cells type, as distinguished by poorly vascularized follicles with intervening sheets of dense plasma cells. Occasionally, a mixed form may also be seen [2, 3]. Alternatively, based on biological behavior, Castleman disease is currently divided into two forms, including a localized or unicentric form, which is usually asymptomatic and amenable to surgical treatment, and a disseminated or multicentric form, which exhibits complicated systemic manifestations [4, 5]. Castleman disease occurs at any age, with a peak in the fourth decade of life and without particular gender preference [3–6, 12], although the disseminated form frequently affects older individuals [6, 12].
In the present series of eight cases, all were classified as the localized form of Castleman disease, among which, six cases belonged to the hyaline vascular type, one belonged to the plasma cell type, and the remaining one belonged to the mixed type. Interestingly, this unusual pleural tumor predominantly affected young women (7:1 female-to-male ratio). Only 1 patient suffered from marked dyspnea due to massive effusion requiring thoracentesis for symptom relief. None of our patients had any constitutional symptoms, systemic abnormalities, or comorbid diseases.
The etiology and pathogenesis of Castleman disease are still uncertain. Various theories, including hyperplasia of hamartomatous lymphoid tissue [13], a chronic low-grade inflammatory process [3, 4], autoimmunity or an inappropriate immune response [10, 14, 15], and an immunodeficiency state [16–18], have been postulated. A relationship between human herpesvirus-8, Kaposi’s sarcoma herpesvirus, or human immunodeficiency virus, and multicentric Castleman disease has been shown [16–18]. Human herpesvirus-8, which encodes a homologue of human interleukin-6 (IL-6) and overexpression of a viral IL-6 homologue as a causative agent for the lymph node hyperplasia and the commonly observed systemic manifestations of multicentric Castleman disease, has also been reported [18–20]. However, none of our patients showed any related comorbid disease such as human immunodeficiency virus infection, immunosuppression, or autoimmunity that may have contributed to the development of this tumor. On the other hand, Castleman disease arises from the lymph nodes and there are no lymph nodes in the pleural space, whereas the subpleural space contains well-developed clusters of lymphoid cells and occasionally lymph nodes are found located subpleurally. It is thus possible to theorize that intrapleural Castleman disease may arise from the subpleural lymph nodes and grow toward the pleural space rather than into the lung parenchyma. Furthermore, in the present series, the surgical findings revealed a variable degree of adhesion of the affected pleura and nearby structures associated with multiple prominent overlying pleural arteries as well as the histopathological demonstration of intranodular degeneration and fibrosis. These findings may be suggestive of chronic inflammatory processes of the pleura.
On chest radiographs, in the present study, half of our cases manifested as well-defined interlobar masses, and the definitive differentiation from other pleural masses such as mesothelioma, fibrous tumor, solitary metastatic tumor, loculated effusion, fibrin body, or hematoma may be difficult [1–4]. Furthermore, three partially well-defined masses mimicked a pericardial cyst [21], a saccular aortic aneurysm, or focal bulging of the diaphragm. As in the present study, intratumoral calcifications in Castleman disease are rarely seen on chest radiographs, but when present, it is typically dense and coarse [4, 5]. Rarely, as in our patient 2, Castleman disease may associate with a massive effusion [5, 9, 11].
Morphologically, localized thoracic Castleman disease may appear on CT or MR imaging as a solitary mass that can be easily excised surgically (50% of the cases), a dominant mass that invades contiguous structures (40% of the cases), or unresectable matted lymphadenopathy (10% of the cases) [5, 6]. Disseminated Castleman disease is characterized by bilateral hilar or mediastinal lymphadenopathy and centrilobular nodular opacities in the thorax, and by retroperitoneal lymphadenopathy, hepatosplenomegaly, and ascites in the abdomen [4–6, 22]. Castleman disease typically shows intense contrast enhancement, whereas characteristic discrete or "arborizing" calcifications are found in only 5% to 10% of the cases [5–8, 23]. In the present study, all cases of pleural Castleman disease appeared as solitary, well-defined masses featuring smooth or slightly lobulated margins with variable degrees of contrast enhancement on CT and hyperintense on MR imaging. However, only two tumors could be effectively excised by VATS. The remaining six tumors exhibited moderate to severe adhesion to the contiguous anatomical structures, rendering radical resection by VATS difficult. Unfortunately, in our series, there were no specific CT or MR features that were useful in predicting the presence or severity of possible adhesion.
Preoperatively, among our cases, the differential diagnoses included mesothelioma, solitary fibrous tumor, lymphoma, pulmonary hyalinzing granuloma, lymphoma of mucosa-associated lymphoid tissue (MALToma), lymphocyte-rich thymoma, and nodular amyliodosis. Frozen section is often misleading, and Kim and associates have reported that positive correct diagnosis based on frozen section was available in only half of their cases [8]. In addition, as seen in 1 of our patients, percutaneous biopsy may yield an incorrect diagnosis of lymphoma, and inadvertent biopsy of this tumor may also lead to profuse bleeding because Castleman disease is quite vascular [8, 19]. Definitive diagnosis of Castleman disease usually relies on detailed histopathologic examinations after excision of the mass. Histopathologically, typical arrangement of germinal follicles with hyalinized vessels and mixed populations of interfollicular lymphocytes in Castleman disease allows definitive differentiation from mesothelioma and solitary fibrous tumor. Lymphoma is usually composed of monotonous T-cells or B-cells. Pulmonary hyalinizing granuloma is characterized by lamellar hyaline collagen arrayed in a storiform fashion with scattered mononuclear cells [24]. Immunohistochemically, Castleman disease is positive for CD45, CD45RO, and CD20, but negative for epithelial markers such as cytokeratins. Therefore, it can easily be differentiated from MALToma, which is negative for CD45RO, and lymphocyte-rich thymoma, which is positive for cytokeratins. In addition, Castleman disease is negative for special stain congo red, and thus, appears different from nodular amyloidosis, which typically shows positive stain for congo red with apple-green birefringence when examined by polarizing microscopy [24].
Despite Castleman disease being an essentially benign condition, surgical resection would appear to be mandatory in order to avoid the potential transformation of the lesion to malignant lymphoma, vascular neoplasia, or sarcoma [25–27]. Video-assisted thoracoscopic surgery (VATS) has been reported to be safe and less invasive than open thoracotomy in the diagnosis and treatment of a great variety of thoracic lesions, including mediastinal masses, lung cancer, and pleural lesions with shorter hospitalization, with a more rapid recovery than is the case for open chest surgery [28–30]. When there is risk of massive bleeding, or when the tumor size is large, impaired lesion exposure, or rib attachment of the tumor, the conversion of VATS to thoracotomy is usually necessitated, and the conversion rate is approximately 4% to 6% [27–29]. In our series, only two of three cases of tumor size less than 5 cm could be successfully resected by VATS. The remaining one and all the other five cases greater than 5 cm necessitated thoracotomy for radical excision, due to moderate to severe adhesion in the vicinity and the presence of prominent pleural arteries on the tumor surfaces. For a tumor that cannot be totally excised, subtotal excision with no short-term recurrence has been reported [9]. Nevertheless, radical surgical resection of localized pleural Castleman disease, irrespective of the cell type, offered an extremely satisfactory outcome with no tumor recurrence being noted for our patients even after long-term follow-up.
In conclusion, in our series of eight cases, Castleman disease of the pleura predominately affects young women, often without symptoms. This unusual tumor shows a variable degree of enhancement on CT and is typically inhomogeneously hyperintense on T2-weighted or enhanced T1-weighted MR images. High incidence of severe adhesion to the contiguous anatomical structures occurs in lesions greater than 5 cm in diameter. Thoracotomy and radical excision of the lesion can produce a satisfactory outcome for this uncommon disease.
|
References
|
|---|
- Theros E.G., Feigin D.S. Pleural tumors and pulmonary tumors: differential diagnosis. Semin Roentgenol 1977;12:239-247.[Medline]
- Sahn S.A. The pleura. Am Rev Resp Dis 1988;138:184-234.[Medline]
- Castleman B., Inverson L., Menendex V. Localized mediastinal lymph node hyperplasia resembling thymoma. Cancer 1956;9:822-830.[Medline]
- Keller A.R., Hochholzer L., Castleman B. Hyaline-vascular and plasma-cell types of giant lymph node hyperplasia of the mediastinum and other locations. Cancer 1972;29:670-683.[Medline]
- McAdams H.P., Rosado-de-Christenson M., Fishback N.F., Templeton P.A. Castleman disease of the thorax: radiologic features with clinical and histopathologic correlation. Radiology 1998;209:221-228.[Abstract/Free Full Text]
- Bowne W.B., Lewis J.J., Filippa D.A., et al. The management of unicentric and multicentric Castleman’s disease: a report of 16 cases and a review of the literature. Cancer 1999;85:706-717.[Medline]
- Moon W.K., Im J.G., Choi C.G., Kim H.C., Yeon K.M., Han M.C. Mediastinal Castleman disease: CT findings. J Comput Assist Tomogr 1994;18:43-46.[Medline]
- Kim J.H., Jun T.G., Sung S.W., et al. Giant lymph node hyperplasia (Castleman’s disease) in the chest. Ann Thorac Surg 1995;589:1162-1165.
- Reynold S.P., Gibbs A.R., Weeks R., Adams H., Davies B.H. Massive pleural effusion: an unusual presentation of Castleman’s disease. Eur Respir J 1992;5:1150-1153.[Abstract]
- Mohamedani A.A., Bennett M.K. Angiofollicular lymphoid hyperplasia in a pulmonary fissure. Thorax 1985;40:686-687.[Free Full Text]
- Awotedu A.A., Otulana B.A. Giant lymph node hyperplasia of the lung (Castleman’s disease) associated with recurrent pleural effusion. Thorax 1990;45:775-776.[Abstract/Free Full Text]
- McCarthy M.J., Vukelja S.J., Banks P.M., Weiss R.B. Angiofollicular lymph node hyperplasia (Castleman’s disease). Cancer Treat Rev 1995;21:291-310.[Medline]
- Latters R., Pachter R. Benign lymphoid masses of probable hamartomatous nature: analysis of 12 cases. Cancer 1962;15:197-213.
- Frizzera G. Castleman’ disease: more questions than answer. Hum Pathol 1985;156:202-205.
- Suwannaroj S., Eljins S.L., McMurrray R.W. Systemic lupus erythematosus and Castleman’s disease. J Rheumatol 1999;26:1400-1403.[Medline]
- Lachant N.A., Sun Nora C.J., Leong L.A., Oseas R.S., Prince H.E. Multicentric angiofollicular lymph node hyperplasia (Castleman’s disease followed by Kaposi’s sarcoma in two homosexual males with acquired immunodeficiency syndrome (AIDS). Am J Clin Pathol 1985;83:27-33.[Medline]
- Oksenhendler E., Duarte M., Soulier J., et al. Multicentric Castleman’s disease in HIV infection: a clinical and pathological study of 20 patients. AIDS 1996;10:61-67.[Medline]
- Luppi M, Barozzi P, Maioriana A, et al. Human herpesvirus-8 DNA sequences in human immunodeficiency virus-negative angioimmunoblastic lymphadenopathy, and benign lymphadenopathy, and benign lymphadenopathy with giant germinal center hyperplasia, and increased vascularity. Blood 1996;87:3903–9
- Yoshizaki K., Matsuda T., Nishimoto K.N., et al. Pathogenic significance of interleukin-6 (IL-6/BSF-2) in Castleman’s disease. Blood 1989;74:1360-1367.[Abstract/Free Full Text]
- Hsu S.M., Waldron J.A., Xie S.S., Barlogie B. Expression of interleukin-6 in Castleman’s disease. Hum Pathol 1993;24:833-839.[Medline]
- Gibbons J.A., Rosencrantz H., Posey D.J., Watts M. Angiofollicular lymphoid hyperplasia (Castleman’s tumor) resembling a pericardial cyst: differentiation by computerized tomography. Ann Thorac Surg 1981;32:193-196.[Medline]
- Johkoh T., Müller N.L., Ichikado K., et al. Intrathoracic multicentric Castleman disese: CT findings in 12 patients. Radiology 1998;209:477-481.[Abstract/Free Full Text]
- Ecklund K., Hartnell G.G. Mediastinal Castleman disease. MR and MRA features. J Thorac Imaging 1994;9:156-159.[Medline]
- Colby T.V., Koss M.N., Travis W.D. Tumors of the lower respiratory tract: atlas of tumor pathology, series 3, fascicles 13. Washington DC: Armed Forces Institute of Pathology, 1995:495-513.
- Gerald W., Ariza A., Doglionic C., Rosai J. Sarcomas with features of vascular differentiation arising in Castleman’s disease [abstract]. Lab Invest 1988;58:34.
- Gerald W., Kostianovsky M., Rosai J. Development of vascular neoplasia in Castleman’s disease: report of seven cases. Am J Surg Path 1990;14:603-614.[Medline]
- Vasef M., Katsin W.E., Mendelsohn G., Reydman M. Report of a case of localized Castleman’s disease with progression to malignant lymphoma. Am J Path 1992;98:633-636.
- Demmy T.L., Krasna M.J., Detterbeck F.C., et al. Multicenter VATS experience with mediastinal tumors. Ann Thorac Surg 1998;66:187-192.[Abstract/Free Full Text]
- Zierold D., Halow K.D. Thoracoscopic resection as the preferred approach to posterior mediastinal neurogenic tumors. Surg Laparos Endos Percutaneous Technique 2000;10:222-225.
- Ronson R.S., Miller J.I., Jr. Video-assisted thoracoscopy for pleural disease. Chest Surg Clin North Am 1998;8:919-932.[Medline]
Top
Abstract
Introduction
