ArticleClujul medical (1957)2014
Castleman Disease. A Report of Six Cases.
Article in Clujul medical (1957), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Adult Langerhans cell histiocytosis of skull in a patient with synchronous papillary thyroid carcinoma and Castleman disease.BMJ case reports · 2021Article
- Multicentric Plasma-Cell Type Castleman Disease Masquerading As Hodgkin Lymphoma: A Case Report.Journal of laboratory physicians · 2020Article
- Castleman's disease in the HIV-endemic setting.Cancer management and research · 2018Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsCastleman's disease is a rare disorder situated at the boundary between reactive and neoplastic conditions. The pathogenesis is a subject of debate and the limited number of cases renders the study of the disease difficult. In our paper we present a series of six cases of Castleman disease with emphasis on the clinical presentation, pathology examination and the use of immunohistochemistry in the final diagnosis of the cases. PATIENTS AND
methodThe classification of the disease was based on clinical, imaging and pathological assessment. Specimens were obtained by surgical excision and were routinely processed for the pathology examination.
resultsAll cases were unicentric disease. Two cases were locally extensive. The clinical symptoms were related mostly to compression effects. Five case were of the hyaline-vascular type and one was included in the plasma cell variant. One case showed angiomyoid differentiation.
conclusionsWe strongly believe that by understanding the pathogenesis of the precursor lesions we will gain better understanding of the pathways that lead to neoplasia and that Castleman disesase is a very interesting "natural experiment" illustrating the progression from chronic antigen stimulation to reactive lymphoid hyperplasia and finally to overt lymphoid neoplasia.
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