Lentiginous Eruption Due to Topical Immunotherapy

Tosti, Antonella; Piraccini, Bianca Maria; Misciali, Cosimo; Vincenzi, Colombina

doi:10.1001/archderm.139.4.544

Cited by 16 publications

(6 citation statements)

References 4 publications

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“…10 The use of topical immunomodulatory drugs for the treatment of alopecia universalis (ie, dibutyl squaric acid) has been also associated with the development of simple lentigines in the area under treatment, where an increased number of melanocytes in the dermo-epidermal junction, infiltrated slight surface perivascular lymphocytes, melanophages, and lamellar fibroplasia can be seen. 11 A similar situation was described in cases of atopic dermatitis treated with calcineurin inhibitors. 12,13 Our patient presented the spots in both affected and unaffected areas of vitiligo, where histological studies showed melanocytic hyperplasia and basal layer hyperpigmentation.…”

Section: Discussionmentioning

confidence: 59%

“Eruptive Lentiginosis” in a Patient With Vitiligo and Inflammatory Bowel Disease Treated With Azathioprine

Ramos-Rodríguez

Murillo-Lázaro

Mendoza-Chaparro

2016

The American Journal of Dermatopathology

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Multiple lentiginosis are seen in many multisystemic diseases and during the course of many treatment schemes in the area of application of topical substances, PUVA, or more disseminated reactions in the case of systemic drugs. We report a case of a 67-year-old man with multiple comorbidities including vitiligo, and a recent diagnosis of inflammatory bowel disease, who developed millimeter-size, circular, brown macules in photoexposed areas both affected and not affected by vitiligo while was taken azathioprine, which disappeared after drug withdrawal. Biopsy showed groups of apoptotic keratinocytes, basal hyperpigmentation, and slight dermal inflammation. The authors describe "eruptive lentiginosis" as an adverse event of azathioprine not previously described in the literature.

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Section: Discussionmentioning

confidence: 59%

“Eruptive Lentiginosis” in a Patient With Vitiligo and Inflammatory Bowel Disease Treated With Azathioprine

Ramos-Rodríguez

Murillo-Lázaro

Mendoza-Chaparro

2016

The American Journal of Dermatopathology

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“…However, from the perspective of melanogenesis, phenylazonaphthol (PAN), a well‐known contactant in PCD, reportedly induces a melanogenic‐stimulating factor such as growth‐related oncogene‐α (GRO‐α) using a PCD model of brownish guinea pig skins, 14 suggesting that melanogenesis by the contactants, in part, causes the pathomechanism of PCD. Indeed, lentiginous eruption was reported to be induced during CI with squaric acid dibutylester (SADBE), 15 suggesting that contact sensitizers such as DPCP and SADBE for CI may stimulate melanocyte activity. Alternatively, because melanocytes are possible targets as autoantigens in AA pathogensis, 16–18 it is of interest to elucidate relationship between auto‐antigenicity of melanocytes and inhibitory effect of PCD on CI outcome.…”

Section: Discussionmentioning

confidence: 99%

Pigmented contact dermatitis due to therapeutic sensitizer as complication of contact immunotherapy in alopecia areata

Inui¹,

Nakajima²,

Toda³

et al. 2010

The Journal of Dermatology

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Pigmentary complication by contact immunotherapy (CI) for alopecia areata (AA) has been reported but its pathophysiology remains unknown. To characterize pigmentary complication by CI and its pathophysiology, we examined the incidence of hyperpigmentation in 186 consecutive patients treated with CI using diphenylcyclopropenone. From clinical data of AA totalis (AAT) or universalis (AAU) patients (n = 78), we studied the correlations between this complication and age, sex, atopic background, duration and treatment responsiveness, duration of CI, final concentration of diphenylcyclopropenone and administration of anti-histamines by χ(2)-test or Mann-Whitney U-test. Additionally, the histopathology of pigmentation was studied. As a result, 11 (5.91%) of the 186 patients had hyperpigmentation in this series. All of them had AAT or AAU, suggesting that the pigmentation is apt to occur in severe AA. When the AAT or AAU patients with (n = 11) and without hyperpigmentation (n = 67) were compared, those with pigmentation showed poorer responsiveness to CI (P < 0.05) but no significant tendency for other factors. Histopathologically, skin specimens showed lichenoid or vacuolar interface dermatitis with necrotic keratinocytes and dermal melanophages, consistent with pigmented contact dermatitis (PCD). Together, pigmentary complication by CI corresponds to PCD from therapeutic sensitizer, representing clinical indicator of poor responsiveness.

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“…A wide range of drugs has been implicated, including azathioprine, 3 infliximab, 3 prednisolone, 4 immunosuppressives, 5 cancer chemotherapy drugs, 6 alefacept, 3 etanercept, 3 6‐mercaptopurine, 7 and methotrexate 7,8 . Lentiginoses induced by psoralen UVA therapy, 9 tacrolimus 10 and squaric acid dibutyl ester 11 have been described in the literature. The spectrum of drugs causing eruptive naevi or eruptive lentiginosis indicates that the condition is associated with immunosuppression or immunomodulation.…”

Section: Reportmentioning

confidence: 99%