Nonimmediate reactions to betalactams.

PURPOSE OF REVIEW

Nonimmediate reactions to beta-lactams include several clinical entities, from maculopapular rash to severe reactions such as Steven-Johnson syndrome. Toxic epidermal necrolysis and organ-specific reactions may also occur.

RECENT FINDINGS

Progress has been made in understanding the role of the immunological system in nonimmediate reactions to beta-lactams. Different T-cell subsets recognize beta-lactams after haptenation of serum or cell proteins in the context of major histocompatibility complex. Studies using T-cell lines and clones have shown that a heterogeneous response is generated, with the expression of different cytokine profiles. Betalactams also act on dendritic cells, inducing changes that enable them to interact with naïve lymphocytes, becoming memory T cells. Tissue-activated CD4 and CD8 cells express perforin and other cytotoxic mediators that elicit the lesions. Studies on the clinical course of these entities indicate that cells migrate, establishing a recirculation with homing to the skin and back to the circulation. These cells thus participate not only in skin lesions but probably also in the repair process.

SUMMARY

Understanding the immunological mechanisms involved in nonimmediate reactions to beta-lactams has improved over the last few years, with better definition of the different T-cell subpopulations involved. Experimental studies and monitoring of the response support the implication of different cell subsets.