Atopic dermatitis with CD30-positive anaplastic large cell lymphoma

Yasukochi, Yoshiki; Takenaka, Katsuto; Yurino, Ayano; Kurihara, Yusuke; Miake, Shunji; Uchi, Hiroshi; Takeuchi, Satoshi; Kohda, Futoshi; Moroi, Yoichi; Okano, Shinji; Yamamoto, Hidetaka; Furue, Masutaka

doi:10.1684/ejd.2013.2253

Cited by 4 publications

(1 citation statement)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The relationship between AD and primary cutaneous CD30 + lymphoproliferative disorders appears to be even more complex. So far, 9 cases, including one case series of 4 patients, of LyP (n = 3) or pc-ALCL (n = 6) in adult patients with persistent AD have been reported in the English literature (7)(8)(9)(10)(11)(12). Four of the 9 patients have been treated with CsA during or prior to the development of lymphoproliferative disease.…”

Section: Discussionmentioning

confidence: 99%

Primary Cutaneous CD30+ Lymphoproliferative Disorders in a Patient with Severe Atopic Dermatitis: Is There a Causative Link?

Żychowska

Woźniak²,

Maj³

2018

Acta Derm Venerol

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Primary Cutaneous CD30+ Lymphoproliferative Disorders in a Patient with Severe Atopic Dermatitis: Is There a Causative Link?

Żychowska

Woźniak²,

Maj³

2018

Acta Derm Venerol

View full text Add to dashboard Cite

show abstract

The Inflammatory Effects of Breast Implant Particulate Shedding: Comparison With Orthopedic Implants

Hallab

Samelko

Hammond³

2019

Aesthetic Surgery Journal

View full text Add to dashboard Cite

Currently, there is a dearth of information regarding the degree of particle shedding from breast implants (BIs) and what are the general biological consequences of BI debris. Thus, it is unclear to what degree BI debris compromises the long-term biological performance of BIs. For orthopedic implants, it is well established that the severity of biological reactivity to implant debris governs long-term clinical performance. Orthopedic implant particulate debris is generally in the range of 0.01 to 100 μm in diameter. Implant debris-induced bioreactivity/inflammation is mostly a peri-implant phenomenon caused by local innate immune cells (eg, macrophages) that produce proinflammatory cytokines such as tumor necrosis factor-α, interleukin-1β, interleukin-6, and prostaglandin 2 (PGE2). In orthopedics, there have been few systemic concerns associated with polymeric implant debris (like silicone) other than documented dissemination to remote organs (eg, liver, spleen, etc.) with no known associated pathogenicity. This is not true of metal implant debris where normal (well-functioning) implants can induce systemic reactions such as delayed type hypersensitivity. Diagnostic analysis of orthopedic tissues has focused on innate (macrophage mediated) and adaptive (lymphocyte-mediated hypersensitivity) immune responses. Orthopedic implant debris-associated lymphocyte cancers have not been reported in over 40 years of orthopedic literature. Adaptive immune responses such as hypersensitivity reactions to orthopedic implant debris have been dominated by certain implant types that produce specific kinds of debris (eg, metal-on-metal total joint prostheses). Orthopedic hypersensitivity responses and atypical BI bioreactivity such as BI-associated anaplastic large cell lymphoma share crossover markers for diagnosis. Differentiating normal innate immune reactivity to particles from anaplastic large cell lymphoma reactions from delayed type hypersensitivity reactions to BI-associated implant debris remains unclear but vital to patients and surgeons.

show abstract