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Histopathologic Overlap between Fibrosing Mediastinitis and IgG4-Related Disease

DOI: 10.1155/2012/207056

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Abstract:

Fibrosing mediastinitis (FM) and IgG4-related disease (IgG4-RD) are two fibroinflammatory disorders with potentially overlapping clinical and radiological features. In this paper, we looked for histopathologic features of IgG4-RD and enumerated infiltrating IgG4-positive plasma cells within mediastinal tissue biopsies from FM patients. We identified 15 consecutive FM surgical mediastinal tissue biopsies between 1985 and 2006. All patients satisfied the clinical and radiological diagnostic criteria for FM. All patients had either serological or radiological evidence of prior histoplasmosis or granulomatous disease, respectively. Formalin-fixed paraffin-embedded tissue sections of all patients were stained for H&E, IgG, and IgG4. Three samples met the predefined diagnostic criteria for IgG4-RD. In addition, characteristic histopathologic changes of IgG4-RD in the absence of diagnostic numbers of tissue infiltrating IgG4-positive plasma cells were seen in a number of additional cases (storiform cell-rich fibrosis in 11 cases, lymphoplasmacytic infiltrate in 7 cases, and obliterative phlebitis/arteritis in 2 cases). We conclude that up to one-third of histoplasmosis or granulomatous-disease-associated FM cases demonstrate histopathological features of IgG4-RD spectrum. Whether these changes occur as the host immune response against Histoplasma or represent a manifestation of IgG4-RD remains to be determined. Studies to prospectively identify these cases and evaluate their therapeutic responses to glucocorticoids and/or other immunosuppressive agents such as rituximab are warranted. 1. Background IgG4-related disease (IgG4-RD) is recognized to include a growing number of fibroinflammatory disorders [1–5]. Histopathologic evaluation typically demonstrates distinctive cellular fibrosis organized in an irregular whorled pattern (often referred to as “storiform fibrosis”), obliterative phlebitis/arteritis, and prominent lymphoplasmacytic tissue infiltration [6]. Tissue immunostaining and serum IgG-subclass assessment characteristically reveal large numbers of IgG4 producing plasma cells and elevated serum IgG4 levels, respectively [6]. IgG4-RD was first described in the context of autoimmune pancreatitis presenting with obstructive jaundice due to a space-occupying lesion within the pancreas [7, 8]. Since these initial reports, IgG4-RD has been demonstrated to involve various other organs including the biliary tree (sclerosing cholangitis), salivary (sclerosing sialadenitis), and lacrimal glands (sclerosing dacroadenitis) in isolation or in combination

References

[1]  W. Cheuk and J. K. C. Chan, “IgG4-related sclerosing disease a critical appraisal of an evolving clinicopathologic entity,” Advances in Anatomic Pathology, vol. 17, no. 5, pp. 303–332, 2010.
[2]  T. Kamisawa and A. Okamoto, “IgG4-related sclerosing disease,” World Journal of Gastroenterology, vol. 14, no. 25, pp. 3948–3955, 2008.
[3]  A. Khosroshahi and J. H. Stone, “A clinical overview of IgG4-related systemic disease,” Current Opinion in Rheumatology, vol. 23, no. 1, pp. 57–66, 2011.
[4]  Y. Zen and Y. Nakanuma, “IgG4-related disease: a cross-sectional study of 114 cases,” American Journal of Surgical Pathology, vol. 34, no. 12, pp. 1812–1819, 2010.
[5]  M. Ebbo, L. Daniel, M. Pavic et al., “IgG4-related systemic disease: features and treatment response in a French cohort: results of a multicenter registry,” Medicine, vol. 91, no. 1, pp. 49–56, 2012.
[6]  M. N. Carruthers, J. H. Stone, and A. Khosroshahi, “The latest on IgG4-RD: a rapidly emerging disease,” Current Opinion in Rheumatology, vol. 24, no. 1, pp. 60–69, 2012.
[7]  T. Kamisawa and A. Okamoto, “Autoimmune pancreatitis: proposal of IgG4-related sclerosing disease,” Journal of Gastroenterology, vol. 41, no. 7, pp. 613–625, 2006.
[8]  K. Yoshida, F. Toki, T. Takeuchi, S. I. Watanabe, K. Shiratori, and N. Hayashi, “Chronic pancreatitis caused by an autoimmune abnormality. Proposal of the concept of autoimmune pancreatitis,” Digestive Diseases and Sciences, vol. 40, no. 7, pp. 1561–1568, 1995.
[9]  A. Khosroshahi, V. Deshpande, and J. H. Stone, “The clinical and pathological features of IgG(4)-related disease,” Current Rheumatology Reports, vol. 13, no. 6, pp. 473–481, 2011.
[10]  K. Nakatani, Y. Nakamoto, and K. Togashi, “Utility of FDG PET/CT in IgG4-related systemic disease,” Clinical Radiology, vol. 67, no. 4, pp. 297–305, 2012.
[11]  A. Khosroshahi and J. H. Stone, “Treatment approaches to IgG4-related systemic disease,” Current Opinion in Rheumatology, vol. 23, no. 1, pp. 67–71, 2011.
[12]  D. B. Flieder, S. Suster, and C. A. Moran, “Idiopathic fibroinflammatory (Fibrosing/Sclerosing) lesions of the mediastinum: a study of 30 cases with emphasis on morphologic heterogeneity,” Modern Pathology, vol. 12, no. 3, pp. 257–264, 1999.
[13]  J. E. Loyd, B. F. Tillman, J. B. Atkinson, and R. M. Des Prez, “Mediastinal fibrosis complicating histoplasmosis,” Medicine, vol. 67, no. 5, pp. 295–310, 1988.
[14]  T. Peikert, T. V. Colby, D. E. Midthun et al., “Fibrosing mediastinitis: clinical presentation, therapeutic outcomes, and adaptive immune response,” Medicine, vol. 90, no. 6, pp. 412–423, 2011.
[15]  S. E. Rossi, H. P. McAdams, M. L. Rosado-de-Christenson, T. J. Franks, and J. R. Galvin, “From the archives of the AFIP: fibrosing mediastinitis,” Radiographics, vol. 21, no. 3, pp. 737–757, 2001.
[16]  R. A. Goodwin, J. A. Nickell, and R. M. Des Prez, “Mediastinal fibrosis complicating healed primary histoplasmosis and tuberculosis,” Medicine, vol. 51, no. 3, pp. 227–246, 1972.
[17]  C. G. Schowengerdt, R. Suyemoto, and F. B. Main, “Granulomatous and fibrous mediastinitis. A review and analysis of 180 cases,” Journal of Thoracic and Cardiovascular Surgery, vol. 57, no. 3, pp. 365–379, 1969.
[18]  S. E. Straus and E. S. Jacobson, “The spectrum of histoplasmosis in a general hospital: a review of 55 cases diagnosed at Barnes Hospital between 1966 and 1977,” American Journal of the Medical Sciences, vol. 279, no. 3, pp. 147–158, 1980.
[19]  A. Devaraj, N. Griffin, A. G. Nicholson, and S. P. G. Padley, “Computed tomography findings in fibrosing mediastinitis,” Clinical Radiology, vol. 62, no. 8, pp. 781–786, 2007.
[20]  A. D. Sherrick, L. R. Brown, G. F. Harms, and J. L. Myers, “The radiographic findings of fibrosing mediastinitis,” Chest, vol. 106, no. 2, pp. 484–489, 1994.
[21]  I. Naitoh, T. Nakazawa, H. Ohara et al., “Clinical significance of extrapancreatic lesions in autoimmune pancreatitis,” Pancreas, vol. 39, no. 1, pp. e1–e5, 2010.
[22]  K. Tsushima, T. Tanabe, H. Yamamoto et al., “Pulmonary involvement of autoimmune pancreatitis,” European Journal of Clinical Investigation, vol. 39, no. 8, pp. 714–722, 2009.
[23]  M. Inoue, N. Nose, H. Nishikawa, M. Takahashi, Y. Zen, and M. Kawaguchi, “Successful treatment of sclerosing mediastinitis with a high serum IgG4 level,” General Thoracic and Cardiovascular Surgery, vol. 55, no. 10, pp. 431–433, 2007.
[24]  A. Sakamoto, R. Nagai, K. Saito et al., “Idiopathic retroperitoneal fibrosis, inflammatory aortic aneurysm, and inflammatory pericarditis-Retrospective analysis of 11 case histories,” Journal of Cardiology, vol. 59, no. 2, pp. 139–146, 2012.
[25]  T. Taniguchi, H. Kobayashi, S. Fukui, K. Ogura, T. Saiga, and M. Okamoto, “A case of multifocal fibrosclerosis involving posterior mediastinal fibrosis, retroperitoneal fibrosis, and a left seminal vesicle with elevated serum IgG4,” Human Pathology, vol. 37, no. 9, pp. 1237–1239, 2006.
[26]  Y. Zen, A. Sawazaki, S. Miyayama, K. Notsumata, N. Tanaka, and Y. Nakanuma, “A case of retroperitoneal and mediastinal fibrosis exhibiting elevated levels of IgG4 in the absence of sclerosing pancreatitis (autoimmune pancreatitis),” Human Pathology, vol. 37, no. 2, pp. 239–243, 2006.
[27]  A. Khosroshahi, D. B. Bloch, V. Deshpande, and J. H. Stone, “Rituximab therapy leads to rapid decline of serum IgG4 levels and prompt clinical improvement in IgG4-related systemic disease,” Arthritis and Rheumatism, vol. 62, no. 6, pp. 1755–1762, 2010.
[28]  J. D. Strehl, A. Hartmann, and A. Agaimy, “Numerous IgG4-positive plasma cells are ubiquitous in diverse localised non-specific chronic inflammatory conditions and need to be distinguished from IgG4-related systemic disorders,” Journal of Clinical Pathology, vol. 64, no. 3, pp. 237–243, 2011.
[29]  A. Vaglio, J. D. Strehl, B. Manger et al., “IgG4 immune response in Churg-Strauss syndrome,” Annals of the Rheumatic Diseases, vol. 71, no. 3, pp. 390–393, 2012.
[30]  M. Yamamoto, H. Takahashi, C. Suzuki et al., “Analysis of serum IgG subclasses in churg-strauss syndrome-The meaning of elevated serum levels of IgG4,” Internal Medicine, vol. 49, no. 14, pp. 1365–1370, 2010.
[31]  R. P. Sah and S. T. Chari, “Serologic issues in IgG4-related systemic disease and autoimmune pancreatitis,” Current Opinion in Rheumatology, vol. 23, no. 1, pp. 108–113, 2011.
[32]  M. J. Levy, M. J. Wiersema, and S. T. Chari, “Chronic pancreatitis: focal pancreatitis or cancer? Is there a role for FNA/biopsy? Autoimmune pancreatitis,” Endoscopy, vol. 38, supplement 1, pp. S30–S35, 2006.

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