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A case of multifocal fibrosclerosis with intracardiac solid masses
Human Pathology (2006) 37, 493 – 497
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A case of multifocal fibrosclerosis with intracardiac solid masses Mikiko Takikita-Suzuki MDa,*, Eiji Takeuchi MDb, Yasuaki Nakashima MDc, Takako Yamamoto MDd, Koichi Mukaib, Kazumasa Ogasawara MDa a
Department of Pathology, Shiga University of Medical Science, Otsu 520-2192, Japan Department of Pathology, Shiga Medical Center for Adults, Moriyama 524-8524, Japan c Department of Anatomical Pathology, Faculty of Medicine, Kyoto University Hospital, Kyoto 606-8507, Japan d Department of Medicine, Shiga University of Medical Science, Otsu 520-2192, Japan b
Received 27 July 2005; accepted 18 November 2005
Keywords: Multifocal fibrosclerosis; Intracardiac mass
Summary We report an extremely rare case of multifocal fibrosclerosis (MFS) with intracardiac solid masses. A 70-year-old woman with Hashimoto’s disease had pericardial thickening and intracardiac masses. Histology of pericardiectomy showed only fibrosis. The clinical diagnosis was constrictive pericarditis. She died of postoperative infectious mediastinitis and cerebral infarction. Postmortem examination revealed intracardiac solid masses contiguous to thickened pericardium. Multifocal areas of fibrosis were also seen in the pericardium, mediastinum, abdominal cavity, and the retroperitoneum. The intracardiac masses and the areas of fibrosis were composed of collagenous fibers with various intensities of inflammatory infiltrates and sclerotic changes. Neoplastic changes were not observed. These histological features were similar to that of MFS. The intracardiac masses are interpreted as one of the manifestations of MFS. This is the first case of MFS accompanied with intracardiac solid masses. D 2006 Elsevier Inc. All rights reserved.
1. Introduction Multifocal fibrosclerosis (MFS) is a generic term that has been used to denote a group of fibrosing conditions occurring at different anatomic sites [1]. The condition was defined by Comings [1] and originally included 5 disorders: invasive fibrous thyroiditis of Riedel, idiopathic mediastinal fibrosis, idiopathic retroperitoneal fibrosis, sclerosing cholangitis, and pseudotumor of the orbit. These disorders exhibit similar
* Corresponding author. E-mail address: [email protected] (M. Takikita-Suzuki). 0046-8177/$ – see front matter D 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.humpath.2005.11.017
histology resembling fibrotic tissue changes infiltrated with blood vessels, lymphocytes, and plasma cells. Therefore, it was suggested that they were all interrelated and probably were different manifestations of the same disorder of fibroblastic proliferation. Besides the original definition by Comings [1], MFS may associate with fibrosing lesions in other organs, such as intracranial pachymeningitis [2], sellar pseudotumor [3], paranasal sinusitis [4], pulmonary fibrosis [5], pancreatitis [6], parotitis [7], and fibrosis in the lacrimal gland [8]. However, no case of MFS complicated with intracardiac masses has been published. We report here a case of systemic fibrosclerosis accompanied with intracardiac solid masses with a histology similar to that of MFS.
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M. Takikita-Suzuki et al.
2. Case report A 70-year-old Japanese woman complained of general fatigue and pretibial edema. She had neither family history of thyroid disease nor autoimmune disease. Chest x-ray demonstrated cardiomegaly and bilateral pleural effusions. Laboratory results, including elevated antithyroglobulin antibody titers (1:102 400) and antimicrosomal antibody titers (1:6400), led to the diagnosis of Hashimoto’s thyroiditis. Other autoantibodies including P-/C-ANCA (antineutrophil cytoplasmic antibodies) were negative. Although thyroidal function returned to normal level by medication, cardiomegaly and pleural effusion still remained. Transesophageal echocardiography identified a mass in the atrial septum and a supravalvular mass protruding from the tricuspid valve (Fig. 1A). Paradoxical motion of the septum was also noted. Electrocardiography
Fig. 2 Gross appearance of the autopsied specimen. A, A plaque-like mass lay along the attached border of the tricuspid valve. B, Cut surface of the mass in (A). The right coronary artery (RCA) was situated in the middle of the mass. C, Cut surface of the atrial septum. Note the mass in the atrial septum.
Fig. 1 Imaging studies. A, Transesophageal echocardiography revealed a thickened pericardium with masses (arrows) in the atrial septum and the supravalvular region of the tricuspid valve. B, CT showed soft tissue density (an arrow) in the right atrioventricular sulcal region with pericardial thickening and massive pleural and pericardial effusion.
indicated low voltage. Cardiac catheterization displayed a dip and plateau in the right ventricle pressure curve and elevated pressure of both superior and inferior venae cavae. Coronary angiography was normal. Several myocardial biopsies suggested normal tissue. The results of these examinations led to the diagnosis of constrictive pericarditis. On computed tomography (CT) and magnetic resonance imaging analyses, the right atrioventricular sulcal region had the density of soft tissue or with an intensity suggesting pericardial thickening and massive pleural and pericardial effusions (Fig. 1B). Abdominal CT presented soft tissue density in the retroperitoneum and in the mesentery, suggesting that retroperitoneal fibrosis might be present.
A case of multifocal fibrosclerosis with intracardiac solid masses
495
Fig. 3 Microscopic appearance of intracardiac masses. A, Low-power view of the mass in Fig. 2B. B, Prominent sclerosis with few inflammatory cells. C, Circumferential fibrosis around small vessels. D, Mononuclear infiltrates. High-power view of (A) (hematoxylin and eosin, original magnification 5 [A], 100 [B], 100 [C], and 400 [D]). E, KP-1 staining showed many histiocytes (original magnification 200). F, CD38 staining revealed a small number of plasma cells (original magnification 200).
496 To rule out cardiac neoplasms, pericardiectomy was performed. Histological examination detected only nonspecific chronic fibrosing process. After the operation, the patient experienced infectious mediastinitis and subsequently died of cerebral infarction and diffuse alveolar damage.
3. Pathological findings On postmortem examination, intracardiac solid masses accompanied with thickened pericardium were apparent (Fig. 2A). Areas of fibrosis in the mediastinum, the abdominal cavity, and the retroperitoneum were also observed. The thickened pericardium encased the heart that weighed 480 g. A plaque-like mass lay along the attached border of the tricuspid valve and continued as an area of fibrosis around the right coronary artery (Fig. 2A, B). A solid mass, measuring 45 25 20 mm, was situated in the atrial septum (Fig. 2C). Fibrosis further spread around the other valves, the aorta, the superior and the inferior venae cavae, pleurae, and bilateral hilus of the lungs (Fig. 2D), suggesting the presence of fibrosing mediastinitis. In the abdominal cavity, fibrosis was also observed around the pancreas, gallbladder, and hilus of the liver. The mesentery was densely thickened. In the retroperitoneum, fibrosis spread around the ureters, the adrenal glands, and bilateral hilus of the kidneys. Microscopically, all the above fibrotic lesions and cardiac masses were composed of dense bundles and whorls of collagenous fibers with various intensity of inflammatory infiltrates of histiocytes, lymphocytes, and plasma cells (Fig. 3A-D). Blood vessels were rimmed by collarettes of collagen (Fig. 3C). Fibrosis spread in an infiltrating manner and caused atrophic changes in adjacent structures (Fig. 3A). Some areas were completely replaced with paucicellular fibrosclerosis and others showed fibrosis with moderate infiltration of mononuclear cells. Considerable degree of focal histiocytic infiltration was observed. Neither granuloma nor vasculitis was observed. Histology of the thyroid was compatible with Hashimoto’s thyroiditis, but not with Riedel’s thyroiditis. Immunohistochemical studies revealed a small number of aggregates of CD3- and CD20-positive lymphocytes. CD30-positive cells were not present. KP-1 staining uncovered a large number of histiocytes (Fig. 3E). Small number of CD38-positive cells (plasma cells) was also seen (Fig. 3F). Labeled streptavidin biotin method (Ventana HX system) and all the antibodies against above antigens from Novocastra (Newcastle, UK) were used.
M. Takikita-Suzuki et al. pericarditis [9,10]. For this reason, the patient was not properly diagnosed clinically. Autopsy clarified that she had MFS and the intracardiac masses were one of the manifestations of MFS. The intracardiac masses and the other areas of fibrosis shared the histological features of MFS. Multifocal fibrosclerosis is a chronic inflammatory disease and its histological hallmark is fibrosis with various intensities of inflammation. In the area where the disease had advanced, the areas of collagenous fibrosis were hyalinized and sclerotic with few cellular components. Anatomic structures were compressed and were surrounded by fibrotic lesions, but not obliterated as in the case of infection or malignancy. The areas of fibrosis were observed in multiple regions such as the pericardium, the mediastinum, the abdominal cavity, and the retroperitoneum. Therefore, her disease was diagnosed as MFS accompanied with peculiar intracardiac masses. Differential diagnosis of this case includes neoplastic and nonneoplastic lesions with severe fibrosis. Malignant lymphoma was ruled out because lymphocytes had neither nuclear atypia nor monoclonality. The possibility of Hodgkin’s disease with substantial fibrous reaction was also investigated, but there were no CD30-positive cells. Concentric fibrosis and lymphocytic infiltration were reminiscent of Castleman’s disease, but its peculiar lymphoid follicles were not detected. A variety of causes have been assigned to MFS. For example, hereditary cause [1], vasculitis [11], occlusive phlebitis [12], and inflammatory periaortitis [13] have been described. Idiopathic retroperitoneal fibrosis with ANCApositive vacuities has also been reported [14], suggesting the association with autoimmune disease. These hypotheses, however, did not support the mechanism of MFS in detail. The pathogenesis of this case remains unknown. The patient had neither family history of systemic fibrosis nor vasculitis. An autoimmune process may be involved as the patient had Hashimoto’s thyroiditis with elevated antithyroglobulin antibody titers and antimicrosomal antibody titers. Histiocytic infiltration may also play a role in the fibrosing process because histiocytes themselves are the likely source of the cytokines [15]. In conclusion, we present an unusual case of MFS accompanied with intracardiac solid masses. Multifocal fibrosclerosis is a chronic inflammatory disease and its histological features are fibrosis with various intensities of inflammation. Its etiology is still unknown, but the present case suggests that autoimmune process may play some role in the development of this disease. We conclude that MFS may form a tumor-like mass.
4. Discussion The present case is quite rare because intracardiac masses demonstrating histological features similar to MFS have not been reported. Although 12 cases of cardiac involvement in systemic fibrosis have been published, they described only
References [1] Comings DE. Familial multifocal fibrosclerosis. Ann Intern Med 1967;66:884 - 92.
A case of multifocal fibrosclerosis with intracardiac solid masses [2] Kishimoto M, Okimura Y, Kimura K, et al. Multifocal fibrosclerosis as a possible cause of panhypopituitarism with central diabetes insipidus. Endocr J 2000;47:335 - 42. [3] Olmos PR, Falko JM, Rea GL, et al. Fibrosing pseudotumor of the sella and parasellar area producing hypopituitarism and multiple cranial nerve palsies. Neurosurgery 1993;32:1015 - 21. [4] Noble SC, Chandler WF, Lloyd RV. Intracranial extension of orbital pseudotumor: a case report. Neurosurgery 1986;18:798 - 801. [5] Temperley JA. Multifocal fibrosclerosis. Br J Clin Pract 1974;28: 217 - 9. [6] Kamisawa T, Funata N, Hayashi Y, et al. Close relationship between autoimmune pancreatitis and multifocal fibrosclerosis. Gut 2003;52: 683 - 7. [7] Hines RC, Scheuermann HA, Royster HP, et al. Invasive fibrous (Riedel’s) thyroiditis with bilateral fibrous parotitis. JAMA 1970;213: 869 - 71. [8] Sclare G, Luxton RW. Fibrosis of the thyroid and lacrimal glands. Br J Ophthalmol 1967;51:173 - 7.
497
[9] Klisnick A, Fourcade J, Ruivard M, et al. Combined idiopathic retroperitoneal and mediastinal fibrosis with pericardial involvement. Clin Nephrol 1999;52:51 - 5. [10] Hanley PC, Shub C, Lie JT. Constrictive pericarditis associated with combined idiopathic retroperitoneal and mediastinal fibrosis. Mayo Clin Proc 1984;59:300 - 4. [11] Hoffman WW, Trippel OH. Retroperitoneal fibrosis: etiologic considerations. J Urol 1961;86:222. [12] Meyer S, Hausman R. Occlusive phlebitis in multifocal fibrosclerosis. Am J Clin Pathol 1976;65:274 - 83. [13] Ramshaw AL, Roskell DE, Parums DV. Cytokine gene expression in aortic adventitial inflammation associated with advanced atherosclerosis (chronic periaortitis). J Clin Pathol 1994;47:721 - 7. [14] Kaipiainen-Seppanen O, Jantunen E, Kuusisto J, et al. Retroperitoneal fibrosis with antineutrophil cytoplasmic antibodies. J Rheumatol 1996;23:779 - 81. [15] Dehner LP, Coffin CM. Idiopathic fibrosclerotic disorders and other inflammatory pseudotumors. Semin Diagn Pathol 1998;15:161 - 73.
www.elsevier.com/locate/humpath
A case of multifocal fibrosclerosis with intracardiac solid masses Mikiko Takikita-Suzuki MDa,*, Eiji Takeuchi MDb, Yasuaki Nakashima MDc, Takako Yamamoto MDd, Koichi Mukaib, Kazumasa Ogasawara MDa a
Department of Pathology, Shiga University of Medical Science, Otsu 520-2192, Japan Department of Pathology, Shiga Medical Center for Adults, Moriyama 524-8524, Japan c Department of Anatomical Pathology, Faculty of Medicine, Kyoto University Hospital, Kyoto 606-8507, Japan d Department of Medicine, Shiga University of Medical Science, Otsu 520-2192, Japan b
Received 27 July 2005; accepted 18 November 2005
Keywords: Multifocal fibrosclerosis; Intracardiac mass
Summary We report an extremely rare case of multifocal fibrosclerosis (MFS) with intracardiac solid masses. A 70-year-old woman with Hashimoto’s disease had pericardial thickening and intracardiac masses. Histology of pericardiectomy showed only fibrosis. The clinical diagnosis was constrictive pericarditis. She died of postoperative infectious mediastinitis and cerebral infarction. Postmortem examination revealed intracardiac solid masses contiguous to thickened pericardium. Multifocal areas of fibrosis were also seen in the pericardium, mediastinum, abdominal cavity, and the retroperitoneum. The intracardiac masses and the areas of fibrosis were composed of collagenous fibers with various intensities of inflammatory infiltrates and sclerotic changes. Neoplastic changes were not observed. These histological features were similar to that of MFS. The intracardiac masses are interpreted as one of the manifestations of MFS. This is the first case of MFS accompanied with intracardiac solid masses. D 2006 Elsevier Inc. All rights reserved.
1. Introduction Multifocal fibrosclerosis (MFS) is a generic term that has been used to denote a group of fibrosing conditions occurring at different anatomic sites [1]. The condition was defined by Comings [1] and originally included 5 disorders: invasive fibrous thyroiditis of Riedel, idiopathic mediastinal fibrosis, idiopathic retroperitoneal fibrosis, sclerosing cholangitis, and pseudotumor of the orbit. These disorders exhibit similar
* Corresponding author. E-mail address: [email protected] (M. Takikita-Suzuki). 0046-8177/$ – see front matter D 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.humpath.2005.11.017
histology resembling fibrotic tissue changes infiltrated with blood vessels, lymphocytes, and plasma cells. Therefore, it was suggested that they were all interrelated and probably were different manifestations of the same disorder of fibroblastic proliferation. Besides the original definition by Comings [1], MFS may associate with fibrosing lesions in other organs, such as intracranial pachymeningitis [2], sellar pseudotumor [3], paranasal sinusitis [4], pulmonary fibrosis [5], pancreatitis [6], parotitis [7], and fibrosis in the lacrimal gland [8]. However, no case of MFS complicated with intracardiac masses has been published. We report here a case of systemic fibrosclerosis accompanied with intracardiac solid masses with a histology similar to that of MFS.
494
M. Takikita-Suzuki et al.
2. Case report A 70-year-old Japanese woman complained of general fatigue and pretibial edema. She had neither family history of thyroid disease nor autoimmune disease. Chest x-ray demonstrated cardiomegaly and bilateral pleural effusions. Laboratory results, including elevated antithyroglobulin antibody titers (1:102 400) and antimicrosomal antibody titers (1:6400), led to the diagnosis of Hashimoto’s thyroiditis. Other autoantibodies including P-/C-ANCA (antineutrophil cytoplasmic antibodies) were negative. Although thyroidal function returned to normal level by medication, cardiomegaly and pleural effusion still remained. Transesophageal echocardiography identified a mass in the atrial septum and a supravalvular mass protruding from the tricuspid valve (Fig. 1A). Paradoxical motion of the septum was also noted. Electrocardiography
Fig. 2 Gross appearance of the autopsied specimen. A, A plaque-like mass lay along the attached border of the tricuspid valve. B, Cut surface of the mass in (A). The right coronary artery (RCA) was situated in the middle of the mass. C, Cut surface of the atrial septum. Note the mass in the atrial septum.
Fig. 1 Imaging studies. A, Transesophageal echocardiography revealed a thickened pericardium with masses (arrows) in the atrial septum and the supravalvular region of the tricuspid valve. B, CT showed soft tissue density (an arrow) in the right atrioventricular sulcal region with pericardial thickening and massive pleural and pericardial effusion.
indicated low voltage. Cardiac catheterization displayed a dip and plateau in the right ventricle pressure curve and elevated pressure of both superior and inferior venae cavae. Coronary angiography was normal. Several myocardial biopsies suggested normal tissue. The results of these examinations led to the diagnosis of constrictive pericarditis. On computed tomography (CT) and magnetic resonance imaging analyses, the right atrioventricular sulcal region had the density of soft tissue or with an intensity suggesting pericardial thickening and massive pleural and pericardial effusions (Fig. 1B). Abdominal CT presented soft tissue density in the retroperitoneum and in the mesentery, suggesting that retroperitoneal fibrosis might be present.
A case of multifocal fibrosclerosis with intracardiac solid masses
495
Fig. 3 Microscopic appearance of intracardiac masses. A, Low-power view of the mass in Fig. 2B. B, Prominent sclerosis with few inflammatory cells. C, Circumferential fibrosis around small vessels. D, Mononuclear infiltrates. High-power view of (A) (hematoxylin and eosin, original magnification 5 [A], 100 [B], 100 [C], and 400 [D]). E, KP-1 staining showed many histiocytes (original magnification 200). F, CD38 staining revealed a small number of plasma cells (original magnification 200).
496 To rule out cardiac neoplasms, pericardiectomy was performed. Histological examination detected only nonspecific chronic fibrosing process. After the operation, the patient experienced infectious mediastinitis and subsequently died of cerebral infarction and diffuse alveolar damage.
3. Pathological findings On postmortem examination, intracardiac solid masses accompanied with thickened pericardium were apparent (Fig. 2A). Areas of fibrosis in the mediastinum, the abdominal cavity, and the retroperitoneum were also observed. The thickened pericardium encased the heart that weighed 480 g. A plaque-like mass lay along the attached border of the tricuspid valve and continued as an area of fibrosis around the right coronary artery (Fig. 2A, B). A solid mass, measuring 45 25 20 mm, was situated in the atrial septum (Fig. 2C). Fibrosis further spread around the other valves, the aorta, the superior and the inferior venae cavae, pleurae, and bilateral hilus of the lungs (Fig. 2D), suggesting the presence of fibrosing mediastinitis. In the abdominal cavity, fibrosis was also observed around the pancreas, gallbladder, and hilus of the liver. The mesentery was densely thickened. In the retroperitoneum, fibrosis spread around the ureters, the adrenal glands, and bilateral hilus of the kidneys. Microscopically, all the above fibrotic lesions and cardiac masses were composed of dense bundles and whorls of collagenous fibers with various intensity of inflammatory infiltrates of histiocytes, lymphocytes, and plasma cells (Fig. 3A-D). Blood vessels were rimmed by collarettes of collagen (Fig. 3C). Fibrosis spread in an infiltrating manner and caused atrophic changes in adjacent structures (Fig. 3A). Some areas were completely replaced with paucicellular fibrosclerosis and others showed fibrosis with moderate infiltration of mononuclear cells. Considerable degree of focal histiocytic infiltration was observed. Neither granuloma nor vasculitis was observed. Histology of the thyroid was compatible with Hashimoto’s thyroiditis, but not with Riedel’s thyroiditis. Immunohistochemical studies revealed a small number of aggregates of CD3- and CD20-positive lymphocytes. CD30-positive cells were not present. KP-1 staining uncovered a large number of histiocytes (Fig. 3E). Small number of CD38-positive cells (plasma cells) was also seen (Fig. 3F). Labeled streptavidin biotin method (Ventana HX system) and all the antibodies against above antigens from Novocastra (Newcastle, UK) were used.
M. Takikita-Suzuki et al. pericarditis [9,10]. For this reason, the patient was not properly diagnosed clinically. Autopsy clarified that she had MFS and the intracardiac masses were one of the manifestations of MFS. The intracardiac masses and the other areas of fibrosis shared the histological features of MFS. Multifocal fibrosclerosis is a chronic inflammatory disease and its histological hallmark is fibrosis with various intensities of inflammation. In the area where the disease had advanced, the areas of collagenous fibrosis were hyalinized and sclerotic with few cellular components. Anatomic structures were compressed and were surrounded by fibrotic lesions, but not obliterated as in the case of infection or malignancy. The areas of fibrosis were observed in multiple regions such as the pericardium, the mediastinum, the abdominal cavity, and the retroperitoneum. Therefore, her disease was diagnosed as MFS accompanied with peculiar intracardiac masses. Differential diagnosis of this case includes neoplastic and nonneoplastic lesions with severe fibrosis. Malignant lymphoma was ruled out because lymphocytes had neither nuclear atypia nor monoclonality. The possibility of Hodgkin’s disease with substantial fibrous reaction was also investigated, but there were no CD30-positive cells. Concentric fibrosis and lymphocytic infiltration were reminiscent of Castleman’s disease, but its peculiar lymphoid follicles were not detected. A variety of causes have been assigned to MFS. For example, hereditary cause [1], vasculitis [11], occlusive phlebitis [12], and inflammatory periaortitis [13] have been described. Idiopathic retroperitoneal fibrosis with ANCApositive vacuities has also been reported [14], suggesting the association with autoimmune disease. These hypotheses, however, did not support the mechanism of MFS in detail. The pathogenesis of this case remains unknown. The patient had neither family history of systemic fibrosis nor vasculitis. An autoimmune process may be involved as the patient had Hashimoto’s thyroiditis with elevated antithyroglobulin antibody titers and antimicrosomal antibody titers. Histiocytic infiltration may also play a role in the fibrosing process because histiocytes themselves are the likely source of the cytokines [15]. In conclusion, we present an unusual case of MFS accompanied with intracardiac solid masses. Multifocal fibrosclerosis is a chronic inflammatory disease and its histological features are fibrosis with various intensities of inflammation. Its etiology is still unknown, but the present case suggests that autoimmune process may play some role in the development of this disease. We conclude that MFS may form a tumor-like mass.
4. Discussion The present case is quite rare because intracardiac masses demonstrating histological features similar to MFS have not been reported. Although 12 cases of cardiac involvement in systemic fibrosis have been published, they described only
References [1] Comings DE. Familial multifocal fibrosclerosis. Ann Intern Med 1967;66:884 - 92.
A case of multifocal fibrosclerosis with intracardiac solid masses [2] Kishimoto M, Okimura Y, Kimura K, et al. Multifocal fibrosclerosis as a possible cause of panhypopituitarism with central diabetes insipidus. Endocr J 2000;47:335 - 42. [3] Olmos PR, Falko JM, Rea GL, et al. Fibrosing pseudotumor of the sella and parasellar area producing hypopituitarism and multiple cranial nerve palsies. Neurosurgery 1993;32:1015 - 21. [4] Noble SC, Chandler WF, Lloyd RV. Intracranial extension of orbital pseudotumor: a case report. Neurosurgery 1986;18:798 - 801. [5] Temperley JA. Multifocal fibrosclerosis. Br J Clin Pract 1974;28: 217 - 9. [6] Kamisawa T, Funata N, Hayashi Y, et al. Close relationship between autoimmune pancreatitis and multifocal fibrosclerosis. Gut 2003;52: 683 - 7. [7] Hines RC, Scheuermann HA, Royster HP, et al. Invasive fibrous (Riedel’s) thyroiditis with bilateral fibrous parotitis. JAMA 1970;213: 869 - 71. [8] Sclare G, Luxton RW. Fibrosis of the thyroid and lacrimal glands. Br J Ophthalmol 1967;51:173 - 7.
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[9] Klisnick A, Fourcade J, Ruivard M, et al. Combined idiopathic retroperitoneal and mediastinal fibrosis with pericardial involvement. Clin Nephrol 1999;52:51 - 5. [10] Hanley PC, Shub C, Lie JT. Constrictive pericarditis associated with combined idiopathic retroperitoneal and mediastinal fibrosis. Mayo Clin Proc 1984;59:300 - 4. [11] Hoffman WW, Trippel OH. Retroperitoneal fibrosis: etiologic considerations. J Urol 1961;86:222. [12] Meyer S, Hausman R. Occlusive phlebitis in multifocal fibrosclerosis. Am J Clin Pathol 1976;65:274 - 83. [13] Ramshaw AL, Roskell DE, Parums DV. Cytokine gene expression in aortic adventitial inflammation associated with advanced atherosclerosis (chronic periaortitis). J Clin Pathol 1994;47:721 - 7. [14] Kaipiainen-Seppanen O, Jantunen E, Kuusisto J, et al. Retroperitoneal fibrosis with antineutrophil cytoplasmic antibodies. J Rheumatol 1996;23:779 - 81. [15] Dehner LP, Coffin CM. Idiopathic fibrosclerotic disorders and other inflammatory pseudotumors. Semin Diagn Pathol 1998;15:161 - 73.