Journal of women's health (2002) · 2011
A case of progesterone-induced anaphylaxis, cyclic urticaria/angioedema, and autoimmune dermatitis.
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Bernstein I Leonard, Bernstein David I, Lummus Zana L, Bernstein Jonathan A
Аннотация
OBJECTIVE: Women have exhibited anaphylaxis, urticaria/angioedema, and autoimmune progesterone dermatitis (APD) coinciding with the progesterone premenstrual rise. We report a detailed immunological evaluation of such a woman responsive to a gonadotropin hormone-releasing agonist (GHRA).
METHODS: Skin testing, enzyme-linked immunosorbent assays (ELISAs), leukocyte histamine release (LHR), and inhibition assays were performed to demonstrate progesterone immunoresponsiveness.
RESULTS: Serum specific-progesterone immunoglobulin G (IgG) and IgE were detected initially and disappeared 6 months after GHRA treatment. Dose-response LHR using patient basophils was observed for different hormones but after 3 months persisted only for 5β-pregnanediol. Preincubation with mouse antiprogesterone monoclonal antibody (PmAb) or mifepristone, a progesterone inhibitor, over a range of doses inhibited specific progesterone-induced LHR. Experiments with varying progesterone concentrations and a fixed dose of anti-IgE resulted in 100% LHR at a concentration as low as 0.016 nmol/mL, which, without anti-IgE, failed to release histamine.
CONCLUSIONS: This is the first report of combined recurrent anaphylaxis, cyclic urticaria/angioedema, and APD induced by immunoresponsiveness to progesterone.
METHODS: Skin testing, enzyme-linked immunosorbent assays (ELISAs), leukocyte histamine release (LHR), and inhibition assays were performed to demonstrate progesterone immunoresponsiveness.
RESULTS: Serum specific-progesterone immunoglobulin G (IgG) and IgE were detected initially and disappeared 6 months after GHRA treatment. Dose-response LHR using patient basophils was observed for different hormones but after 3 months persisted only for 5β-pregnanediol. Preincubation with mouse antiprogesterone monoclonal antibody (PmAb) or mifepristone, a progesterone inhibitor, over a range of doses inhibited specific progesterone-induced LHR. Experiments with varying progesterone concentrations and a fixed dose of anti-IgE resulted in 100% LHR at a concentration as low as 0.016 nmol/mL, which, without anti-IgE, failed to release histamine.
CONCLUSIONS: This is the first report of combined recurrent anaphylaxis, cyclic urticaria/angioedema, and APD induced by immunoresponsiveness to progesterone.
Предметные рубрики MeSH
AnaphylaxisAngioedemaAnimalsAntibodies, Monoclonal, Murine-DerivedAutoimmune DiseasesContraceptives, Oral, CombinedContraceptives, Oral, SyntheticDermatitisDrug EruptionsEnzyme-Linked Immunosorbent AssayEstrogensEthinyl EstradiolFemaleFertility Agents, FemaleGonadotropin-Releasing HormoneHormone AntagonistsHumansImmunoglobulin EImmunoglobulin GMiceMiddle AgedMifepristoneNafarelinNorethindroneProgesteroneUrticaria