Role of delayed cellular hypersensitivity and adhesion molecules in amoxicillin-induced morbilliform rashes
A. M. Barbaud, M. C. Bene, J. L. Schmutz, A. Ehlinger, M. Weber and G. C. Faure
Dermatology Department, Fournier Hospital, Nancy, France.
BACKGROUND: Morbilliform rashes induced by amoxicillin are though to be
caused by a delayed cell-mediated immune reaction. The importance of
amoxicillin skin tests is not well defined. A better understanding of the
mechanisms of amoxicillin-induced morbilliform rashes can be obtained by
performing cutaneous immunohistological studies on specimens from
amoxicillin-induced morbilliform rashes and positive amoxicillin skin test
results. OBSERVATIONS: Skin biopsy specimens were obtained from 5 patients
who had developed an amoxicillin-induced morbilliform rash. All patients
underwent amoxicillin prick, patch, and intradermal tests. Similar
immunohistological investigations were performed on amoxicillin-induced
morbilliform rashes and positive skin test biopsy specimens, with a special
focus on the expression of adhesion molecules. Three of the 5 patients
developed delayed positive results to intradermal and patch tests and 2
patients developed delayed positive results to prick tests.
Amoxicillin-induced morbilliform rashes were well reproduced by skin tests,
with similar immunohistological results in amoxicillin-induced morbilliform
rashes and skin test biopsy specimens. Keratinocytes were activated and
expressed CD54 (intercellular adhesion molecule 1); perivascular
lymphocytes were mostly CD2+, CD3+, and CD4+ and exhibited CD11a through
CD18 (leukocyte function-associated antigen 1) and often HLA-DR and/or
CD62L (leukocyte endothelial cell adhesion molecule 1); and endothelial
cells were activated with a strong expression of CD54 (intercellular
adhesion molecule 1), CD62E (endothelial leukocyte adhesion molecule 1),
and CD31 (platelet endothelial cell adhesion molecule 1) in lesser amounts.
CONCLUSIONS: Findings of this clinical and immunohistochemical study
support the theory of a T-cell-mediated immune reaction in patients with
amoxicillin-induced morbilliform rashes, with a strong involvement of
adhesion molecules both on endothelial and infiltrating cells. Our findings
emphasize the importance of delayed readings of amoxicillin prick,
intradermal, and patch tests.
