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Virtually any longstanding, recalcitrant inflammatory dermatosis may evolve into a cutaneous T-cell lymphoma. Although several entities within the parapsoriasis group can undergo malignant degeneration, most cases of cutaneous T-cell lymphoma are not preceded by parapsoriasis; a preceding inflammatory dermatosis that is not a parapsoriasis may be much more common. Among the parapsoriasis, lymphomatoid papulosis and large-plaque parapsoriasis and its variant, retiform parapsoriasis, have a variable tendency to undergo malignant degeneration. For any dermatosis deemed to have a significant premalignant potential, a plan of aggressive management with relatively non-aggressive modalities (for example, topical steroids, UVB light, and psoralen plus UVA light) should be considered.

We report a case of a pityriasis rosea-like eruption in a 12-year-old boy several days following BCG vaccination. It is suggested that the BCG vaccination be included in the etiology of pityriasis rosea-like eruptions.

The common feature of all the conditions discussed in this article is that they are inflammatory vascular dermatoses that may occur as reactive processes in association with other diseases. The histopathologic characteristics of the lesions range from mild, perivascular dermal infiltration with inflammatory cells and vasodilation to various degrees of vessel damage (endothelial swelling to fibrinoid necrosis). The vessel damage is reflected in varying degrees of secondary changes including extravasation of edema fluid, extravasation of erythrocytes, epidermal necrosis, separation of the dermal-epidermal junction zone, and widespread tissue necrosis. The etiology of most of these conditions is still unknown, although strong evidence indicates that type III (circulating immune-complex-mediated) pathogenesis may be responsible for necrotizing venulitis (leukocytoclastic vasculitis) and that a type I (IgE-mediated) pathogenesis may be involved in some types of urticaria. For many of the reactions described, the patients have serum sickness-like systemic signs and symptoms in addition to cutaneous lesions, and a circulating immune-complex-mediated pathogenesis has been considered. Future investigations must address the types of antigens and antibodies present in the circulating immune complexes, the detection of specific antigen in cutaneous blood vessels, the reproduction of lesions in experimental animals, and the mechanisms responsible for the spectrum of clinicopathologic lesions produced, with special attention to the possibility that vessel damage results from circulating immune complex-induced lymphocytic rather than only leukocytoclastic vasculitis.

2 patients with long-standing and wide-spread pityriasis lichenoides chronica were treated with orally administered 8-methyoxypsoralen and UVA irradiation (PUVA therapy). After 15--21 PUVA treatments the patients were completely cleared. 3 and 4 weeks after the initial PUVA treatment, phase recurrences occurred in both patients. In 1 patient the lesions appeared clinically and histologically as pityriasis lichenoides et varioliformis acuta.