Anaphylaxis induced by intramuscular betamethasone disodium phosphate: reflections on a clinical case.

Glucocorticoids could be responsible for allergic symptoms correlated to an Ig-E mediated hypersensitivity mechanism. We describe the case of an anaphylactic reaction in a professional nurse, occurring after an intramuscular administration of Betamethasone. After performing skin prick tests, intramuscular tests and patch tests we concluded that the patient had Ig-E mediated sensitization. She was prescribed oral Prednisone and Deflazacort and shows good tolerance of these drugs. This demonstrates that in these patients it is possible to administrate glucocorticoids without the changes in the sites indicated by Wilkinson. Nevertheless, our patient showed a negative allergy test for Dexamethasone disodium phosphate, and in those patients sensitized to fluorinated glucocorticoids, tolerance to other glucocorticoids is not so easily predictable as in patients with hypersensitivity to first generation steroids or in corticosteroid contact dermatitis, according to the four patterns of cross-reactivity proposed by Coopman and Dooms-Goossens.

Distinct delayed T-cell response to beta-methasone and penicillin-G in the same patient.

BACKGROUND: Multiple drug allergy syndrome is a clinical condition characterized by reactions against more than one different class of, both pharmacologically and structurally, unrelated drugs. Scanty data are available to date about a multiple drug delayed hypersensitivity syndrome. Our aim was to report the case of a delayed reaction to both beta-methasone (beta-MT) and penicillin-G (pen-G) occurring in the same patient, and analyse beta-MT- and pen-G-specific T-cell Lines (TCLs) with regard to their specificity, phenotype and cytokine profile. METHODS: We generated two drug-specific TCLs from biopsies at the site of positive intradermal reactions, and analysed their immunophenotype, T-cell receptor Vbeta (TCR-Vbeta) domains expression and cytokine profile. RESULTS: We demonstrated the specificity of the T cells isolated from positive intradermal test reactions to pen-G and beta-MT through the strict dose-dependent proliferation in response to drug-pulsed autologous antigen presenting cells. Fluorescence activated cell sorter (FACS) analysis revealed a predominance of CD4+ cells in the inflammatory cell infiltrate of intradermal test with beta-MT, while a predominance of CD8+ T cells in the site of delayed reaction to pen-G was found. The drug specific CD4+ and CD8+ T cells were heterogeneous, with regard to TCR-Vbeta usage. CD8+ pen-G-TCL displayed a preferential T helper 2 (Th2) profile, while a substantially heterogeneous pattern of cytokine production characterized specific beta-MT TCL. CONCLUSION: The study describes the coexistence in the same patient of a delayed hypersensitivity to both penicillin G and beta-MT, driven, respectively, by pen-G-specificTh2-skewed CD8+ and beta-MT specificTh0 CD4+ T cells. This case further support the existence of a multiple drug allergy syndrome also for delayed hypersensitivity.

Changes in leukocyte, granulocyte and lymphocyte counts following antenatal betamethasone administration to pregnant women.

OBJECTIVE: Preterm labor and premature rupture of membranes are associated with a mild leukocytosis. However, we have observed a higher maternal leukocyte count after antenatal betamethasone therapy. We planned this study to evaluate the effects of antenatal betamethasone treatment on maternal leukocyte, granulocyte and lymphocyte count. METHODS: Forty-six pregnant women with the diagnosis of preterm labor between 28 and 33 weeks of gestation age received 12 mg betamethasone at a 12-h interval. The control group consisted of 50 pregnant women between 28 and 33 weeks of gestational age with no medical or obstetrics problems. After a baseline venous sampling, serial leukocyte, granulocyte and lymphocyte counts were obtained every 6 h until it returned to baseline value. RESULTS: There were no statistically significant differences in the control group with respect to the total leukocyte, lymphocyte, and neutrophil count. Total leukocyte and granulocyte counts were increased by 29.8% and 17.8% within 24 and 12 h after betamethasone injection, respectively (P < 0.01). A significant reduction in lymphocyte count was observed within 12 h (45.4%) after betamethasone injection (P < 0.01). All changes in leukocyte, granulocyte and lymphocyte counts returned to baseline values within 3 days. CONCLUSION: Antenatal betamethasone therapy leads to an increase in maternal leukocyte count and a decrease in lymphocyte count. This effect is transient and any leukocytosis persisting for more than 3 days is not due to betamethasone administration.

Radioimmunoassay for plasma betamethasone 17-benzoate.

A sensitive radioimmunoassay for plasma betamethasone 17-benzoate has been developed. The antiserum used was obtained by immunizing rabbits with betamethasone 17-benzoate-21-hemisuccinate-bovine-serum-albumin conjugate. All of the endogenous steroids tested cross reacted less than 0.10%. A standard curve was established with a useful range from 0.05-5 ng. Reliability criteria were satisfactory. Measurement of plasma concentrations of betamethasone 17-benzoate was performed in patients and in rabbits following occlusive dressing of betamethasone 17-benzoate cream and gel base.