Hypersensitivity Disorders

Abstract

The classic hypersensitivity disease is a drug eruption; such eruptions can assume many forms and are included in all dermatologic differential diagnoses including bullous diseases. Other diseases included on many differential listings include syphilis, lupus erythematosus, sarcoidosis, and Hansen disease (leprosy); but with the exception of lupus and special situations in syphilis (congenital syphilis and HIV infection), bullous lesions are not included. The triggering factor for the classic hypersensitivity situations is an antigen in the dermis that creates inflammation visible both clinically and histologically. Clinically, the inflammation is red or pink, and histologically there is a lymphohistiocytic perivascular infiltrate along with eosinophils. On occasion, the neutrophil mediates the inflammation, but typically it is the eosinophil.

Erythema multiforme is thought by many to represent a hypersensitivity disease at the end of a spectrum that includes Stevens–Johnson syndrome and toxic epidermal necrolysis at the other. The “target lesion” that is the keyword for this disease is small in contrast to the large target of Lyme disease. The lesion generally is 1–2 cm, and the large target is 10 or more times that size. The two diseases can be differentiated by pathology as well, with Lyme disease showing a “coat-sleeving” arrangement of lymphocytes around upper and mid dermal blood vessels and erythema multiforme showing necrotic keratinocytes, marked upper dermal edema, and extravasated red blood cells in the upper dermis along with a stromal and perivascular lymphohistiocytic infiltrate. The most common cause of erythema multiforme is a reaction to herpes simplex virus; if recurrences are numerous and clinically disturbing, they can be suppressed with daily acyclovir or valacyclovir. If the erythema multiforme reaction has not been suppressed with antiviral agents, prednisone in a short tapered dose begun at the very first symptom prevents widespread eruption.