Clinicopathologic Correlation:

Clinical Feature

Histopathologic Correlate

Dusky lesion

Extensive necrosis of keratinocytes

Bullous lesion

Confluent vacuolar alteration of basal keratinocytes resulting in subepidermal cleft

Differential Diagnosis:

Fixed Drug Eruption Erythema Multiforme

Sparse to moderate inflammatory Sparse superficial lymphohistiocytic cell infiltrate with eosinophils infiltrate; eosinophils usually absent


■ Pityriasis lichenoides and varioliformis acuta is believed to be a benign clonal lymphoproliferative disorder, the etiology of which has not yet been elucidated

■ Activated T lymphocytes in the dermis are thought to effect epidermal necrosis through directly cytotoxic immune mechanisms


1. Hood AF, Mark EJ. Histopathologic diagnosis of pityriasis lichenoides et varioliformis acuta and its clinical correlation. Arch Dermatol 1982; 118:478.

2. Dereure O, Levi E, Kadin ME. T-cell clonality in pityriasis lichenoides et varioliformis acuta. A heteroduplex analysis of 20 cases. Arch Dermatol 2000; 136:1483-1486.

FIXED DRUG ERUPTION Clinical Presentation:

■ Typically presents as a circumscribed, round or oval, erythematous-to-dusky patch, which develops within hours of consuming the offending drug

■ Recurs at the same site with each subsequent exposure to the offending agent

■ Characteristic sites of predilection include the face, lips, buttocks, and genitals

■ Upon discontinuation of the offending drug, eruption resolves with hyperpigmentation

■ Lesions are usually single but may be multiple or generalized, and a bullous variant exists

■ Most commonly implicated drugs: trimethoprim-sulfamethoxazole, phenolphthalein, tetracycline, acetyl salicylic acid, and barbiturates


■ Vacuolar alteration of basal keratinocytes (Fig. 7A)

■ Necrotic keratinocytes along the dermoepidermal junction and at higher levels of the epidermis; sometimes epidermal necrosis becomes confluent (Figs. 7A and B)

■ Mixed, superficial and deep perivascular inflammatory cell infiltrate composed of lymphocytes, eosinophils and neutrophils (Fig. 7C)

■ Melanophages are frequently present in the upper dermis


■ The offending drug acts as a hapten which binds to a protein in basal keratinocytes or in melanocytes within the basal layer of the epidermis

■ The hapten-host protein complex appears to activate T lymphocytes, thereby inciting a cytotoxic immune reaction that may be antibody-mediated

■ The site-specificity and sharp circumscription of the clinical lesions may be due to localized expression on keratinocytes of a cell-adhesion antigen (CD54, ICAM-1) involved in the adherence between keratinocytes and lymphocytes


1. KorkijW, Soltani K. Fixed drug eruption. A brief review. Arch Dermatol 1984; 120:520-524.

2. Smoller BR, Luster AD, Krane JF, et al. Fixed drug eruptions: evidence for a cytokine-mediated process. J Cutan Pathol 1991; 18:13-19.

3. Teraki Y, Moriya N, Shiohara T. Drug-induced expression of intercellular adhesion molecule-1 on lesional keratinocytes in fixed drug eruption. Am J Pathol 1995; 145:550.

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