Lichenoid paraneoplastic pemphigus in the absence of detectable antibodies

Cummins, Deborah L.; Mimouni, Daniel; Tzu, Julia; Owens, Nicole M.; Anhalt, Grant J.; Meyerle, Jon H

doi:10.1016/j.jaad.2006.06.007

Cited by 96 publications

(92 citation statements)

References 19 publications

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“…Another study reported the presence of selective epidermal activated CD8+ T-cells in PNP [34] . There are also four PNP patients without any detectable autoantibodies described by Cummins et al [35] . Furthermore, another study showed that MHC-restricted CD8+ cytotoxic T lymphocytes, non-MHC-restricted CD56+, and CD68+ natural killer cells are at the dermo-epidermal junction of PNP lesions [36] .…”

Section: Pathogenesismentioning

confidence: 83%

“…It is well known that if the principal mechanism is humoral-mediated cytotoxicity, a usual pemphigus appearance might be prominent [3,6] . In contrast, if cell-mediated cytotoxicity is the leading mechanism, lichenoid lesions might be easily seen [33,35,36] . Lichenoid lesions are commonly detected in children, especially on the trunk and limbs [9,10] .…”

Section: Clinical Featuresmentioning

confidence: 99%

“…Furthermore, the presence of dyskeratosis with suprabasal acantholysis is a clue to paraneoplastic pemphigus. On the other hand, interface and lichenoid dermatitis are more easily detected in erythematous inflammatory maculopapular lesions [30,35] . Lesions with a mixed clinical feature might show concomitant acantholysis occurring with lichenoid interface dermatitis [30,38,40] .…”

Section: Histological Featuresmentioning

confidence: 99%

See 2 more Smart Citations

Paraneoplastic pemphigus: A trait d’union between dermatology and oncology

Didona¹,

Didona²,

Richetta³

et al. 2015

Adv Mod Oncol Res

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Paraneoplastic pemphigus is a rare autoimmune disease of the skin associated with neoplasm. Nowadays, the pathogenesis of paraneoplastic pemphigus is not fully understood. Due to its rarity, various criteria have been proposed for the diagnosis. For this reason, several diagnostic methods have been considered useful for the diagnosis of paraneoplastic pemphigus including indirect immunofluorescence, direct immune of fluorescence, immunoprecipitation, immunoblotting, and enzyme-linked immunosorbent assay (ELISA). However, the polymorphic clinical features and the various results of laboratory tests and pathological evaluation present a challenge for the clinicians.

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Section: Pathogenesismentioning

confidence: 83%

Section: Clinical Featuresmentioning

confidence: 99%

Section: Histological Featuresmentioning

confidence: 99%

See 1 more Smart Citation

Paraneoplastic pemphigus: A trait d’union between dermatology and oncology

Didona¹,

Didona²,

Richetta³

et al. 2015

Adv Mod Oncol Res

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“…Клиническая картина и течение заболевания согла-суются с диагнозом «синдром Стивенса-Джонсона». Диагноз «синдром Стивенса-Джонсона» не только клинический, он должен включать гистологическое исследование биоптата пораженного участка кожи [32]. В данном клиническом наблюдении биопсия кожи не проводилась.…”

Section: обсуждение и заключениеunclassified

Stevens-Johnson Syndrome after Treatment of Female Patient with Small Lymphocytic B-Cell Lymphoma, Autoimmune Hemolytic Anemia and Antiphospholipid Antibody Syndrome with Rituximab

Melikyan¹,

Суборцева²,

Ковригина³

et al. 2017

Клиническая онкогематология

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Stevens-Johnson syndrome is a severe delayed type systemic allergic reaction which affects the skin and mucous membranes. In adults, Stevens-Johnson syndrome is usually caused by the administration of drugs or a malignant process. The paper presents a case of Stevens-Johnson syndrome after the treatment of a female patient with small lymphocytic B-cell lymphoma, autoimmune hemolytic anemia and antiphospholipid antibody syndrome with rituximab. A rare combination of Stevens-Johnson syndrome and small lymphocytic B-cell lymphoma of small lymphocytes, as well as the development of severe delayed type systemic allergic reaction to introduction of rituximab are of special interest. A detailed medical history and the clinical manifestations of the disease allowed to diagnose Stevens-Johnson syndrome at early stages and prescribe an adequate therapy. As a result of the treatment, the patient’s condition has improved considerably. Symptoms of general toxicity were arrested completely; there was a complete epithelization of erosive defects. Therefore, the presented clinical observation shows that timely diagnosis, complex drug therapy, and comprehensive care can cure the diseases as soon as possible and prevent complications.

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“…Enzymelinked immunoassay detected no Dsg1-, Dsg3-, desmocollin We examined the pathogenicity of the patient's serum by in vitro dissociation assays, as previously described. 5 IgG fractions were isolated using Hi-Trap Protein G columns (GE Healthcare, Tokyo, Japan). DJM-1 cells, which were cultured as a monolayer sheet to reach confluence, were incubated with each purified IgG at concentrations of 0.3 mg/mL for 24 h. The number of cell dissociations in dishes with the patient's serum (1 on 27 May; 2 on 7 June) was larger than that of the negative control, but smaller than that of the positive control.…”

mentioning

confidence: 99%