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Mixed-Type Multicentric Castleman's Disease Developing During a 17-Year Follow-Up of Sarcoidosis

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Mixed-Type Multicentric Castleman's Disease Developing During a 17-Year Follow-Up of Sarcoidosis □ CASE REPORT □ Mixed-type Multicentric Castleman’s Disease Developing during a 17-year Follow-up of Sarcoidosis Nobuyasu Awano 1, Minoru Inomata 1, Keisuke Kondoh 1, Kohta Satake 1, Hiroyuki Kamiya 1, Atsuko Moriya 1, Tsunehiro Ando 1, Toshio Kumasaka 2, Tamiko Takemura 2, Kengo Takeuchi 3 and Soichiro Ikushima 1 Abstract Multicentric Castleman’s Disease (MCD) is a systemic disease characterized by generalized lymphadeno- pathy and the proliferation of plasma cells. The development of MCD in a patient with preexisting sarcoido- sis has not been previously reported. We herein describe a case of MCD developing in a 78-year-old woman with a 17-year history of sarcoidosis. The patient’s serum interleukin-6 (IL-6) levels were only slightly ele- vated; however, the IL-6 levels in the fluid of both pleural effusion and ascites were markedly elevated. The administration of steroid-pulse therapy and prednisolone was ineffective in treating the MCD, although treat- ment with tocilizumab proved highly effective. Key words: sarcoidosis, Multicentric Castleman’s Disease (MCD), tocilizumab, IL-6 (Intern Med 51: 3061-3066, 2012) (DOI: 10.2169/internalmedicine.51.8120) eases as well as treatment selection. Introduction Case Report Castleman’s Disease (CD) is a rare lymphoproliferative disease associated with human immunodeficiency virus A 60-year-old woman developed bilateral lower leg (HIV), human herpesvirus 8 (HHV-8), Kaposi’s sarcoma- erythema and a mass in the right breast in 1993. Skin and associated herpesvirus (KSHV), secondary amyloidosis and breast biopsies conducted elsewhere revealed non-caseating a number of malignancies, including malignant lymphoma, epithelioid cell granulomas (Fig. 1). The laboratory data polyneuropathy, organomegaly, endocrinopathy, M-protein showed elevations in the levels of serum angiotensin- and skin change syndrome (POEMS syndrome) (1, 2). Clini- converting enzyme (ACE) (23.6 IU/L) and lysozyme (10.8 cally, CD is divided into two variants: unicentric (UCD) and μg/mL), while a tuberculin test was negative. The patient multicentric (MCD) (3). Pathologically, it is divided into was diagnosed with sarcoidosis according to the criteria es- three variants: hyaline-vascular, plasma-cell and mixed (4). tablished in 1991 (6), and her case was followed by obser- Sarcoidosis is a multisystem granulomatous disorder of vation without the administration of any treatment, again unknown etiology. Although patients with sarcoidosis often satisfying criteria updated in 1999 (7). In 2003, she devel- develop lymphoproliferative or malignant diseases, the de- oped third-degree atrioventricular block as a result of car- velopment of MCD in a patient with preexisting sarcoidosis diac sarcoidosis. A pacemaker was implanted, and again no has not been previously reported, and only one report has follow-up treatment was administered. In December 2010, at described the coexistence of sarcoidosis with UCD (5). the age of 77, the patient came to our hospital with a slight We herein present the first case of sarcoidosis preceding fever and epigastric pain. Two weeks later, she developed MCD and discuss the possible relationship between the dis- dyspnea and systemic edema and was admitted to our hospi- １Department of Respiratory Medicine, Japanese Red Cross Medical Center, Japan, ２Department of Pathology, Japanese Red Cross Medical Cen- ter, Japan and ３Department of Pathology, the Cancer Institute Hospital of JFCR, Japan Received for publication May 9, 2012; Accepted for publication August 1, 2012 Correspondence to Dr. Nobuyasu Awano, [email protected] 3061 Intern Med 51: 3061-3066, 2012 DOI: 10.2169/internalmedicine.51.8120 A B Figure 1. A) A skin biopsy performed in 1993 revealed non-caseating epithelioid cell granulomas around a small blood vessel and hair follicle in the dermis (Hematoxylin and Eosin staining, ×20). B) A right breast biopsy performed in 1993 revealed non-caseating epthelioid cell granulomas with gi- ant cells. A lobule of a mammary gland in the right corner shows lymphocyte infiltration and granu- lomas (Hematoxylin and Eosin staining, ×15). Table 1. Laboratory Data and the Examination Results of the Pleural Effusion and Ascites WBC 8,600/ȝL Na: 136 mEq/L [pleural effusion] RBC 380×104ȝ/ K: 4.8 mEq/L Alb: 1.2g/dL Hb 10.3g/dL Cl: 106 mEq/L TG: 6mg/dL Plt 16.0×104ȝL Ca: 7.2 mg/dL protein: 2,400mg/dL PT%: 70% Fe: 7ȝg/dL glucose: 148mg/dL PT-INR: 1.17 Glucose: 10ȝg/dL LDH: 56 IU/L APTT: 46.2 sec ACE: 5.6 IU/L Hyaluronic acid 24,400ng/dL Fbg: 543 mg/dL BNP: 126.0 pg/mL CEA: 0.6ng/mL FDP: 51.3 ȝg/mL SCC: 0.6ng/mL CYFRA: 1.3ng/mL D-dimer 24.9 ȝg/mL CYFRA: 1.3ng/mL ADA: 6.7IU/L TP: 5.4g/dL NSE: 8.3ng/mL Cytology: Class II Alb: 2.5g/dL lysozyme: ȝg/mL [ascites] AST: 26 IU/L CRP: 15.94 mg/dL TG: 20mg/dL ALT: 19 IU/L IgG: 1,066 mg/dL protein: 2,700mg/dL LDH: 148 IU/L (polyclonal pattern) glucose: 15mg/dL ALP: 459IU/L sIL2R: 1,630 U/mL LDH: 65 IU/L Tcho: 95 mg/dL IL-6: 18pg/mL CEA: 0.5ng/mL BUN: 15 mg/dL IgG-4: 31mg/dL CA-19-9: 1U/mL Cre: 0.93 mg/dL VEGF: 69.4 pg/mL Cytology: Class II Reference range: ACE: 8.3-21.4 IU/L, lysozyme: 5-10.2 μg/mL Measurement method: IL-6: chemiluminescent enzyme immunoassay, VEGF: enzyme immunoassay tal. Her weight had increased from 48.0 to 57.1 kg in one the serum IL-6 level was found to have increased slightly to month. A physical examination revealed bilateral cervical 18 pg/mL. The serum level of vascular endothelial growth and axillary lymph node swelling and leg-pitting edema; factor (VEGF) increased to 69.4 pg/mL. HHV-8 deoxyribo- however, no dermatological, neurological or ophthalmologi- nucleic acid (DNA) was not found in the serum. Table 1 cal abnormalities were observed. The laboratory findings shows additional data. A serological test for HIV was nega- showed a white blood cell (WBC) count of 8,600/μL; how- tive, as were both quantiFERONⓇ-TB and tuberculin tests. ever, the C-reactive protein (CRP) level had increased to The arterial blood gas test was unremarkable, and cultures 15.94 mg/dL. The hemoglobin level was 10.3 g/dL, the of blood, sputum and the fluids of ascites and pleural effu- platelet count was 16.0×104/μL and a coagulation disorder sion were sterile. A closer inspection of the ascites and pleu- was evident with an fibrinogen degradation products (FDP) ral effusion revealed unremarkable results, except for a level of 51.3 μg/mL and a D-dimer level of 24.9 μg/mL. marked increase in the IL-6 levels. Chest radiography While the serum levels of calcium, ACE, lysozyme, immu- showed bilateral hilar lymphadenopathy and dull costo- noglobulin G (IgG) and IgG-4 were within normal limits, phrenic angles; however, no abnormal opacities were ob- 3062 Intern Med 51: 3061-3066, 2012 DOI: 10.2169/internalmedicine.51.8120 Figure 2. Computed tomography (CT) showed bilateral pleural effusion and ascites. Lymph nodes in the bilateral cervix, axilla, hilum, mediastinum and abdominal cavity showed swelling. There were no abnormal opacities in the lungs. A B C D E Figure 3. A right axillary lymph node biopsy showed two characteristic features: A) onion skin- like small vessels in the germinal center (Hematoxylin and Eosin staining) and B) CD21-positive dendric cell proliferation in the germinal center (immunohistochemical staining). C) and D) Marked interfolicular plasma cell infiltration (Hematoxylin and Eosin staining). E) CD138-positive cell pro- liferation around the lymphoid follicle (immunohistochemical staining). served in the lung lesion. Computed tomography (CT) fusion (Fig. 2). Both electrocardiogram and transthoracic ul- showed multiple lymphadenopathies, ascites and pleural ef- trasonic cardiograph were normal, and Gallium scintigraphy 3063 Intern Med 51: 3061-3066, 2012 DOI: 10.2169/internalmedicine.51.8120 D-dimer (ug/mL) Plt (×10~4/uL) 1,000 3days 1,000 3days PSL CRP (mg/dL) (mg) CRP Plt D-dimer CTRX CEZ 60 60 50 40 (×10ǹ4/uL) 18 70 400mg 400mg 400mg Tocilizumab 16 60 14 10 1015 10 10 50 Plt transfusion (U) 12 40 10 D-dimer 8 30 Plt 6 20 4 10 2 CRP 0 0 st 1 day 5 10 15 20 25 30 35 4045 50 55 60 65 70 75 80 unit S 18 8 181 71 27 pg/mL IL-6 P 768 802 pg/mL I L- 6 A 2375 1986 pg/mL IL-6 BW 57 57 61 64 64 65 60 58 53 47 46 44 43 kg AC 85 88 90 102 101 97 96 91 83 78 77 77 cm Figure 4. The patient’s clinical course. Plt: platelet, PSL: prednisolone, CTRX: ceftriaxone, CEZ: cefazolin, S IL-6: serum IL-6, P IL-6: pleural effusion IL-6, A IL-6: ascites IL-6, BW: body weight, AC: abdominal circumference showed no abnormal uptake in the lymph nodes or systemic has continued to be administered every two weeks. Her con- organs. Histology of a right axillary lymph node biopsy dition is presently stable with no recurrence of MCD as of showed two abnormal features: 1) onion skin-like small ves- May 2012. sels and CD21-positive follicular dendric cell proliferation in the germinal center, a characteristic of hyaline-vascular type Discussion CD (Fig. 3A and B); and 2) marked interfollicular plasma cell infiltration and CD138-positive cell proliferation around CD is a lymphoproliferative disorder characterized by en- the lymphoid follicle, a characteristic of plasma-cell type larged hyperplastic lymph nodes and striking vascular and CD.
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