A possible new morphological variant of mantle cell lymphoma with plasma-cell type Castleman disease-like features

2017 ◽  
Vol 213 (11) ◽  
pp. 1378-1383 ◽  
Author(s):  
Takuro Igawa ◽  
Rika Omote ◽  
Hiaki Sato ◽  
Kohei Taniguchi ◽  
Katsuya Miyatani ◽  
...  
Diagnostics ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1150
Author(s):  
Magda Zanelli ◽  
Luca Stingeni ◽  
Maurizio Zizzo ◽  
Giovanni Martino ◽  
Francesca Sanguedolce ◽  
...  

A 73-year-old man presented with multiple lymphadenopathy. He had a 20-year history of palmoplantar psoriasis evolved to a diffuse erythrodermic picture in the last two years. Topic and systemic medications including prednisolone, acitretin, anti-IL17 (ixekizumab), TNF inhibitor (adalimumab), anti-IL23 (guselkumab), methotrexate, cyclosporine, and phosphodiesterase 4 inhibitor (apremilast) were ineffective. Repeated skin biopsies excluded mycosis fungoides, confirming psoriasis; molecular analysis of T-cell receptor genes ruled out clonality. The axillary lymph node histology documented a dermatopathic lymphadenitis, often associated with chronic cutaneous inflammatory diseases. At an accurate morphological evaluation, features of HHV8-positive multicentric Castleman disease were observed. Moreover, in a few follicles, in situ mantle cell neoplasia was identified. The translocation t(11;14)(q13;q32), characteristic of mantle cell lymphoma, and the monoclonal IGH gene rearrangement were present. HHV8 DNA was identified on plasma sample. Multicentric Castleman disease in psoriatic patients is a rare event and it might be favored by the immunomodulatory treatment in longstanding psoriasis. Multicentric Castleman disease patients are predisposed to developing simultaneous or subsequent lymphoma. In situ mantle cell neoplasia often behaves indolently, although it may progress to overt mantle cell lymphoma. Rituximab achieved a good control of psoriasis. Unfortunately, the patient developed Staphylococcus aureus sepsis for which he is currently on antibiotic therapy.


2018 ◽  
Vol 17 (5) ◽  
pp. 0-10
Author(s):  
Claudio De Vito ◽  
Thomas Papathomas G. ◽  
Federica Pedica ◽  
Pauline Kane ◽  
Ali Amir ◽  
...  

Systemic symptoms such as fever and fatigue are non-specific manifestations spanning from inflammation to neoplasia. Here we report the case of a 34 year-old man who presented with systemic symptoms for four months. CT-scan and MRI revealed a 3.4 cm arterialized hepatic lesion and a 7 cm paraduodenal mass. Surgical resection of both lesions and histological examination revealed an inflammatory hepatocellular adenoma and a unicentric plasma cell type of Castleman disease. Moreover, a diffuse AA amyloid deposition in the liver was observed. Resection of both lesions was associated with an improvement of the symptoms. To our knowledge, this is the first report of a synchronous presentation of a unicentric plasma cell type of Castleman disease, inflammatory hepatocellular adenoma and AA amyloidosis.


2017 ◽  
Vol 74 (4) ◽  
pp. 367-370
Author(s):  
Bosko Milev ◽  
Borka Milev ◽  
Zoran Kostic ◽  
Darko Mirkovic ◽  
Nenad Perisic ◽  
...  

Introduction. Castleman disease is a rare disease of the unknown etiology, occuring in two clinical forms: unicentric or multicentric. It is characterized by the hyperplasia of lymph glands. In literature the four pathohistological forms were described: hyaline vascular type, plasma cell type, mixed type and a recently recognized plasmablastic type. The most frequent changes are localized in the mediastinum, while the abdominal localization is with significatly rare occurrence, and that was the motive for presentation of this case. Case report. In a 41-year old male magnetic resonance (MR) enterography showed a change in the ileocecal area without the presence of subjective symptoms of digestive tract and without loss of body mass. Due to the suspicion of stromal tumor, surgical intervention was indicated. Pathohistological findings showed Castleman lymphadenopathia reactiva mesenterii (plasma cell type) which was in the unicentric form. There were present only anaemia and the increased value of sedimentation from the laboratory analyses. Conclusion. Abdominal localization of unicentric plasma cell form occurs rarely and the surgical method of treatment presents the golden standard as it was shown in the presented case.


2011 ◽  
Vol 35 (2) ◽  
pp. 177-189 ◽  
Author(s):  
Carlo Visco ◽  
Sylvia Hoeller ◽  
Jeffrey T. Malik ◽  
Zijun Y. Xu-Monette ◽  
Michele L. Wiggins ◽  
...  

2014 ◽  
Vol 47 (2) ◽  
pp. 110-113 ◽  
Author(s):  
Carlos Humberto Gordillo Vélez ◽  
Israel Bernal Becerra ◽  
Carmen Bárcena García ◽  
Federico Álvarez Rodríguez ◽  
José Antonio Jiménez Heffernan

2014 ◽  
Vol 21 (2) ◽  
pp. 157-162
Author(s):  
Tae Hoon Heo ◽  
Hyun Wook Lim ◽  
Ji Hyun Sim ◽  
Jung Hwa Lee ◽  
Eun Hee Lee ◽  
...  

Blood ◽  
2012 ◽  
Vol 119 (22) ◽  
pp. 5173-5181 ◽  
Author(s):  
Jan Suthaus ◽  
Christiane Stuhlmann-Laeisz ◽  
Van S. Tompkins ◽  
Timothy R. Rosean ◽  
Wolfram Klapper ◽  
...  

Human herpes virus 8 (HHV-8) or Kaposi sarcoma-associated herpes virus is the etiologic agent of Kaposi sarcoma, primary effusion lymphoma, and plasma cell-type multicentric Castleman disease (MCD). HHV-8 encodes a viral homolog of human IL-6, called viral IL-6 (vIL-6), which does not require the cellular IL-6 receptor for binding to the ubiquitously expressed gp130 receptor subunit and subsequent JAK-STAT signaling. Thus, in contrast to IL-6, vIL-6 can stimulate virtually all cells in the body. To elucidate the mechanism by which vIL-6 drives human diseases, we generated transgenic mice that constitutively express vIL-6 under control of the MHC class I promoter. The mice were found to exhibit vIL-6 serum levels comparable with those observed in HHV-8–infected patients, to contain elevated amounts of phosphorylated STAT3 in spleen and lymph nodes, where vIL-6 was produced, and to spontaneously develop key features of human plasma cell-type MCD, including splenomegaly, multifocal lymphadenopathy, hypergammaglobulin-emia, and plasmacytosis. Transfer of the vIL-6 transgene onto an IL-6–deficient genetic background abrogated MCD-like phenotypes, indicating that endogenous mouse IL-6 is a crucial cofactor in the natural history of the disease. Our results in mice suggest that human IL-6 plays an important role in the pathogenesis of HHV-8–associated MCD.


2013 ◽  
Vol 35 (7) ◽  
pp. e306-e308 ◽  
Author(s):  
Tuba H. Karapinar ◽  
Özlem Tüfekçi ◽  
Salih Gözmen ◽  
Şebnem Yilmaz ◽  
Gülersu İrken ◽  
...  

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