DERMATOPATHOLOGY CASES: Self-Assessment Cases: Editor - Dr Sampurna Roy MD

Digital Images of interesting cases that will include the full spectrum of Dermatopathology, presented in the form of quiz.

The answer of the cases include related links and recent abstracts of articles.








Monday, August 16, 2010

Answer of Dermatopathology Case 58


Fixed Drug Eruption

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Abstract:

Clinical resemblance of widespread bullous fixed drug eruption to Stevens-Johnson syndrome or toxic epidermal necrolysis: report of two cases.J Formos Med Assoc. 2002 Aug;101(8):572-6.

Widespread bullous fixed drug eruption (FDE) is the most severe form of FDE and may be mistaken clinically for Stevens-Johnson syndrome or toxic epidermal necrolysis (SJS/TEN). We report two cases of generalized bullous drug eruption with extensive epidermal necrosis and detachment mimicking SJS/TEN overlap and TEN, respectively. The first patient, a 78-year-old man, developed SJS/TEN-like eruption with widespread dusky red patches and denuded areas shortly after taking multiple nonsteroidal antiinflammatory drugs (NSAIDs). Histopathology showed vacuolar interface dermatitis with numerous necrotic keratinocytes and a superficial and deep perivascular infiltrate containing lymphocytes, eosinophils, neutrophils and melanophages. These findings are consistent with FDE. The second patient, a 61-year-old woman, had three episodes of near-total body epidermal detachment shortly after taking NSAIDs. TEN was diagnosed clinically in all three episodes without pathologic confirmation. FDE was suspected due to lack of involvement of two mucosal sites and uneventful recovery. These cases highlight the importance of considering severe bullous FDE in the differential diagnosis of SJS and TEN, and the necessity of skin biopsy in such cases.

Fixed drug eruption: pathogenesis and diagnostic tests. Curr Opin Allergy Clin Immunol.2009 Aug;9(4):316-21.

PURPOSE OF REVIEW: Fixed drug eruption is a simplified disease model for elucidating the mechanism(s) of how skin inflammation is induced by skin-resident T cells. In this review, we focus on how the presence of intraepidermal CD8+T cells resident in the fixed drug eruption lesions can provide exciting new clues to our understanding of pathomechanisms of inflammatory skin diseases.
RECENT FINDINGS: Intraepidermal CD8+T cells with an effector-memory phenotype resident in fixed drug eruption lesions have a major contributing role in the development of localized tissue damage. Activation of these CD8+T cells is sufficient for triggering the lesion, however, but not sufficient to cause extensive tissue damage observed in the fully evolved lesions; additional recruitment of CD4+ and CD8+T cells to a specific tissue site would also contribute to the late stage of lesion development. The influx of regulatory T cells into the epidermis observed in fully evolved lesions would serve to limit harmful immune reactions. Consistent with this, positive patch test reactions are only observed at the site of previous lesions harboring significant numbers of intraepidermal CD8+T cells.
SUMMARY: Intraepidermal CD8+T cells may represent double-edged swords of the skin immune system with protective and destructive capacity.

Histological phases of Bactrim-induced fixed drug eruption. The report of one case.Am J Dermatopathol. 1987 Dec;9(6):528-32.

A case is described of a patient with Bactrim-induced fixed drug eruption (FDE). Histological studies were performed at 1 day and 5 days after the drug exposure. While the 5-day-old lesion showed changes classically recognized as FDE, the 1-day-old lesion showed changes typical of a hypersensitivity response: diffuse spongiosis, dermal edema and hemorrhage, neutrophilic polymorphonuclear leukocyte abscess formations, and large numbers of eosinophils. This report underscores the dynamic cellular changes that occur in the evolving FDE lesion.

Pigmentary incontinence in fixed drug eruptions. Histologic and electron microscopic findings.J Am Acad Dermatol.1983 Apr;8(4):525-32.

Pigmentary incontinence is a phenomenon observed in some inflammatory skin disorders. Clinically it may be seen as a slate-colored pigmentation. Histologically it is seen as an accumulation of melanin in the upper dermis. The possible mechanism for development of pigmentary incontinence is discussed based on a review of the literature and electron microscopic studies of fixed drug eruption.