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CORRESPONDENCE
Year : 2016  |  Volume : 61  |  Issue : 4  |  Page : 446-447
Letter in response to previous publication in IJD®
Drug-induced CD30 + skin lesions: Complex interplay between infectious agents, human leukocyte antigen system and mast cells/T cells


Department of Allergy and Immunology, Apollo Gleneagles Hospital, Kolkata, West Bengal, India

Date of Web Publication7-Jul-2016

Correspondence Address:
Sujoy Khan
Department of Allergy and Immunology, Apollo Gleneagles Hospital, Kolkata, West Bengal
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-5154.185721

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How to cite this article:
Khan S. Letter in response to previous publication in IJD®
Drug-induced CD30 + skin lesions: Complex interplay between infectious agents, human leukocyte antigen system and mast cells/T cells. Indian J Dermatol 2016;61:446-7

How to cite this URL:
Khan S. Letter in response to previous publication in IJD®
Drug-induced CD30 + skin lesions: Complex interplay between infectious agents, human leukocyte antigen system and mast cells/T cells. Indian J Dermatol [serial online] 2016 [cited 2017 Nov 24];61:446-7. Available from: http://www.e-ijd.org/text.asp?2016/61/4/446/185721


Sir,

The report by Stephan et al. on a patient with lamotrigine-induced hypersensitivity syndrome and histologic features of CD30 + lymphoma suggest a complex interplay of a known infectious agent human herpesvirus-6 and hitherto unknown human leukocyte antigen (HLA) haplotype interacting with CD3 + T cells of the immune system. [1] Such case reports throw light into possible mechanisms responsible for such serious cutaneous adverse reactions (SCARs). Lamotrigine, including other anticonvulsants, and allopurinol are well known to cause SCARs but unlike HLA-B*53:01 that increases allopurinol sensitivity, the HLA association(s) for most drugs remain unknown. Several other drugs including the biologics such as anti-tumor necrosis factor-α (TNF-α) have been reported to cause a cutaneous pseudolymphoma like lesion due to intense CD30 positivity [Table 1].
Table 1: Reports of drug-induced cutaneous adverse reactions with CD30+ skin lesions


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Drug-reactive T cells are thought to cause SCARs, and CD30/Ki-1 is a cell-surface molecule of the TNF receptor family that is expressed on a subset of activated T cells and B cells. [2] This cell surface molecule is up-regulated on T cells when exposed to allogeneic antigens, and these CD30 + T cells produce interleukin-5 (IL-5) and interferon-g and exhibit enhanced B-cell helper activity. If the drug behaves as the allogeneic antigen, the ensuing cytokine storm with IL-5 would lead to eosinophil recruitment and drug rash, eosinophilia, systemic symptoms. [3] The other cell of interest is the mast cell that can produce and release numerous powerful mediators (serine proteinases tryptase and chymase, histamine, heparin, leukotriene C4, prostaglandin D2, wide range of cytokines, chemokines) that enable their participation in both adaptive and innate immune responses. Mast cells can express functional CD30 ligand (CD30L/CD153), a member of the TNF superfamily, that could interact with activated T cells. CD30 expression is also seen in activated lymphoid cells and cell infiltrates of atopic dermatitis, scabies, reactions to insect bites, graft versus host disease, infiltrates of viral infections of herpes simplex, orf virus and molluscum contagiosum. [4] Hence, CD30 staining patterns in a cutaneous lymphoid infiltrate should be interpreted with caution to avoid misdiagnosis of malignancy.

Clinicians should take note that even cytopenias or features of hemophagocytic lymphohistiocytosis could be part of SCARs and immediate discontinuation of offending drug(s) should be the first line of management. This is more difficult with newer drugs such as the mean interval between first administration of anti-TNF-α and appearance of CD30 + skin lesions or pseudolymphoma was longer (mean 218.8 days) than that of nonbiologic drugs. [5] Until robust biomarkers or HLA associations are available to prevent SCARs, patient education remains the key to prevent unnecessary morbidity and mortality associated with drug reactions.

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Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Stephan F, Haber R, Kechichian E, Kamar F. Lamotrigine-induced hypersensitivity syndrome with histologic features of CD30 + lymphoma. Indian J Dermatol 2016;61:235.  Back to cited text no. 1
    
2.
Ellis TM, Simms PE, Slivnick DJ, Jäck HM, Fisher RI. CD30 is a signal-transducing molecule that defines a subset of human activated CD45RO+ T cells. J Immunol 1993;151:2380-9.  Back to cited text no. 2
    
3.
Khan S. Anti-IL-5 therapy and DRESS. CMAJ 2010;182:941.  Back to cited text no. 3
    
4.
Kahn A, Horenstein M. Inflammatory dermatopathology: The diagnosis of cutaneous inflammatory infiltrates with atypical CD30-positive cells. Pathol Case Rev 2004;9:60-5.  Back to cited text no. 4
    
5.
Fukamachi S, Sugita K, Sawada Y, Bito T, Nakamura M, Tokura Y. Drug-induced CD30+ T cell pseudolymphoma. Eur J Dermatol 2009;19:292-4.  Back to cited text no. 5
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