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Malignant Intertrigo: a Subset of Toxic Erythema of Chemotherapy Requiring Recognition

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Malignant Intertrigo: a Subset of Toxic Erythema of Chemotherapy Requiring Recognition CASE SERIES Malignant intertrigo: A subset of toxic erythema of chemotherapy requiring recognition SabrinaM.Smith,MD,a Philip B. Milam, MD,a Stephanie K. Fabbro, MD,a AlejandroA.Gru,MD,b and Benjamin H. Kaffenberger, MDa Columbus, Ohio and Charlottesville, Virginia Key words: chemotherapy; drug eruption; graft-versus-host disease; intertrigo; pathogenesis; toxic erythema of chemotherapy. INTRODUCTION Abbreviations used: Toxic erythema of chemotherapy (TEC) encom- passes a broad spectrum of cytotoxic effects on the MI: malignant intertrigo 1 PPE: palmoplantar erythrodysesthesia skin. Despite increasing awareness of TEC, such SDRIFE: symmetrical drug-related intertriginous, eruptions may remain unrecognized and subse- flexural exanthema quently result in unnecessary hospitalizations. Of TEC: toxic erythema of chemotherapy the different variants of TEC, intertriginous eruptions have been reported using many terms, such as intertrigo dermatitis, intertriginous eruption of REPORT OF CASES chemotherapy, flexural erythematous eruption, and Six patients with various malignancies undergo- intertrigo-like eruption associated with chemo- ing chemotherapy presented with intertriginous therapy.1 Intertrigo is a broad term that refers to rashes (Table I and Fig 1). Involved areas included any inflammatory rash of closely opposed skin, cervical, inframammary and inguinal folds, and typically presenting with varying degrees of ery- axillae, abdomen, antecubital fossae, perineum, thema and maceration, and this particular type of buttocks, and thighs. Physical examination found TEC has not been identified with consistent nomen- sharply demarcated, erythematous-to-dusky patches clature. We present 6 cases of this distinct subset of and plaques with focal scaling, crusting, and ero- TEC, all occurring within a 7-month period at a single sions. These lesions were painful and exquisitely institution; these cases were initially unrecognized, tender. Histopathology results showed subtle inter- resulted in hospitalization, and required inpatient face dermatitis with variable epidermal dysmatura- dermatologic consultation to achieve a diagnosis. tion and necrosis, along with perivascular and Although TEC is a clinically useful term intended to periadnexal chronic inflammatory infiltrate. Three improve discernment of its noninfectious and of these cases showed eccrine squamous nonallergic etiology,1 the loss of morphologic spec- syringometaplasia. ificity may prevent its variants from being properly Several patients were initially misdiagnosed in the recognized, especially in the intertriginous regions. outpatient or emergency setting with infections, We therefore propose malignant intertrigo (MI) as a contact dermatitis, and, in one case, atypical useful and encompassing term describing toxic Stevens-Johnson syndrome, leading to treatments erythema of chemotherapy affecting the intertrigi- with antimicrobials and corticosteroids, both topical nous skin. and intravenous. At the time of diagnosis of TEC, From the Department of Internal Medicine, Division of Derma- Correspondence to: Benjamin H. Kaffenberger, MD, 915 Olentangy tology, The Ohio State University Wexner Medical Centera and River Road, Suite 4000, Columbus, OH 43212. E-mail: benjamin. the Department of Pathology, University of Virginia.b [email protected]. Funding sources: None. JAAD Case Reports 2016;2:476-81. Conflicts of interest: Dr Gru discloses that he has a potential 2352-5126 conflict of interest and has received honoraria for consulting Ó 2016 by the American Academy of Dermatology, Inc. Published from Seattle Genetics. The rest of the authors have no conflicts by Elsevier, Inc. This is an open access article under the CC BY- to declare. NC-ND license (http://creativecommons.org/licenses/by-nc-nd/ This work was presented at the American Society for Dermatopa- 4.0/). thology National Conference, San Francisco, California, October http://dx.doi.org/10.1016/j.jdcr.2016.08.016 8-11, 2015. 476 V JAAD C Table I. Epidemiologic and clinicopathologic findings in the 6 cases OLUME Onset of rash 2, N (season and ASE Age/ chemotherapy R Case sex Malignancy Prior therapy Most recent therapy* cycle) Clinical findings Histologic findings Course and response UMBER EPORTS 1 60 F AML: 47,XX, None Decitabine priming Autumn, Tender erythematous Atrophic epidermis Complete re- 18, t(9;11) with ‘‘713’’ cycle 1 patches in the with prominent epithelialization 6 cytarabine and bilateral interface changes achieved after daunorubicin inframammary folds, displaying a hydropic application of topical left axilla, left pattern of the basal steroids, silver- anterior chest, and keratinocytes, early impregnated mesh cervical skin folds squamous gauze, and metaplasia of the aluminum acetate dermal eccrine ducts, soaks and superficial and perivascular lymphocytic inflammatory infiltrate, consistent with interface dermatitis with early associated changes of squamous syringometaplasia 2 43 F Metastatic rectal Surgical debulking FOLFIRI and Summer, cycle Tender, sharply Prominent compact Initially treated for adenocarcinoma bevacizumab 3 (interrupted demarcated hyperkeratosis of the suspected cutaneous and renal cell because of hyperpigmented and epidermis with candidiasis, cellulitis, carcinoma nausea and erythematous scaly patchy parakeratosis and ACD without vomiting) patches in the and focal ulceration improvement. inframammary with a mild chronic Treatment included regions and inguinal inflammatory nystatin cream, folds bilaterally, with infiltrate admixed fluconazole (both focal serous crusting with occasional topical powder and in the right neutrophils and oral), empiric IV inframammary patch some antibiotics, and impetiginization; topical Smith et al mild, predominantly corticosteroids. perivascular and Astringent soaks and periadnexal chronic higher-potency inflammatory topical steroids Continued 477 Table I. Cont’d 478 Onset of rash Smith et al (season and Age/ chemotherapy Case sex Malignancy Prior therapy Most recent therapy* cycle) Clinical findings Histologic findings Course and response infiltrate in the resulted in initial dermis improvement. 3 68 F Metastatic breast Lumpectomy with Doxorubicin Summer, Extensive Interface dermatitis Treated with topical carcinoma: axillary node cycle 2 hyperpigmentation with keratinocyte corticosteroids with 1 1 ER ,PR , dissection, adjuvant and exquisitely necrosis and lidocaine and an oral - Her 2/neu- external beam tender, associated squamous prednisone taper radiation, erythematous rash syringometaplasia, with subsequent doxorubicin and with thin scale on marked surface improvement. cyclophosphamide, the buttocks, hyperorthokeratosis, Patient discontinued paclitaxel, posterior thighs, and and superficial and cytotoxic anastrozole, inframmamory perivascular chemotherapy docetaxel, regions lymphocytic and because of severity fulvestrant, letrozole, histiocytic of the skin reaction capecitabine inflammation and was restarted on hormonal agents 4 26 M Recurrent HL ABVD GND Winter, Erythematous and No biopsy performed Initially treated for cycle 2 dusky papules and suspected cellulitis plaques intermixed with TMP-SMX with with erosions on the subsequent bilateral antecubital worsening of rash. fossae, umbilicus, Supportive and groin with treatment with crusting of the magic mouthwash scrotum. Dusky and aluminum erythema of the acetate soaks palmar and dorsal resulted in surfaces of the improvement. bilateral hands without evidence of oral mucositis 5 52 F Metastatic ovarian Neoadjuvant Experimental trial of Summer, Painful, dusky plaques Interface dermatitis Initially treated for JAAD C adenocarcinoma carboplatin and doxorubicin and cycle 4 on the upper with alternating suspected atypical N paclitaxel, surgical study drug VTX-2337 abdomen; large, hyper- and SJS with pulse-dosed OVEMBER debulking, and erythematous hypokeratosis, IV steroids, topical ASE adjuvant carboplatin erosions and clusters of steroids, topical R EPORTS and paclitaxel desquamation on neutrophils and mupirocin, and 2016 V JAAD C the bilateral parakeratosis in the aggressive pain OLUME posterior thighs, and stratum corneum, control with gradual 2, N scattered follicular lymphoid cells at the improvement over ASE erythematous dermal-epidermal weeks R UMBER papules on the junction with focal EPORTS bilateral interface reaction, anterosuperior and a superficial and 6 thighs deep dermal, predominantly perivascular and periadnexal chronic inflammatory infiltrate admixed with rare eosinophils 6 60 F Metastatic Nephrectomy, Axitinib Winter, Well-demarcated Parakeratosis, mild Initially treated with renal cell pazopanib, cycle 1 erythema of the perivascular antimicrobial silver carcinoma cabozantinib intertriginous zones dermatitis with red complex moisture of the panniculus, blood cell wicking fabric. axillae and perineum extravasation; Axitinib was with several erosions eccrine squamous stopped. Wounds draining serous fluid syringometaplasia improved over identified in several several days, but sections patient switched to comfort care because of disease progression. AML, Acute myelogenous leukemia; FOLFIRI, leucovorin, 5-fluorouracil, and irinotecan; ACD, allergic contact dermatitis; IV, intravenous; ER, estrogen receptor; PR, progesterone receptor; HL, Hodgkin’s lymphoma; ABVD, doxorubicin, bleomycin, vinblastine, and dacarbazine; GND, gemcitabine, Navelbine, and doxorubicin; TMP-SMX, trimethoprim-sulfamethoxazole; SJS, Stevens-Johnson syndrome. *Before or during development of rash. Smith et al
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