Glucocorticoid resistance in atopic dermatitis associated with decreased expression of glucocorticoid receptor-alpha in peripheral blood mononuclear cells.
A 51-year-old man had been followed up for approximately 10 years at our clinic for persistent itchy eczematous lesions on his limbs and trunk. At the first visit, physical examination revealed itchy lichenificated and eczematous eruptions and many pruriginous papules over his entire body. Laboratory data showed remarkably high levels of immunoglobulin E (20,000 IU/mL). He was diagnosed as having severe atopic dermatitis (AD). Topical treatment with a potent corticosteroid (class I-II) did not significantly decrease the eruptions and occasional administration of a systemic corticosteroid elicited only a subtle response. The pruriginous lesions did not respond at all to topical or systemic corticosteroids. We used semiquantitative reverse transcription polymerase chain reaction to examine the expression of glucocorticoid receptor (GR)alpha and GRbeta mRNA in peripheral blood mononuclear cells (PBMC) of this patient and compared those with six other patients with AD and three normal controls. As a result, the expression of GRalpha was remarkably decreased compared to normal controls and the other AD patients. Therefore, his poor response to corticosteroid was at least partially caused by this GRalpha decrease in the PBMC.
Inui
Shigeki
S
Department of Regenerative Dermatology, Osaka University School of Medicine, Suita-shi, Osaka, Japan. inui@r-derma.med.osaka-u.ac.jp
Sumikawa
Yasuyuki
Y
Asada
Hideo
H
Itami
Satoshi
S
D003876:Dermatitis, Atopic / Q000175:diagnosis / Q000378:metabolism*; D004351:Drug Resistance; D005500:Follow-Up Studies; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D011965:Receptors, Glucocorticoid / Q000235:genetics / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016896:Treatment Outcome
D011965:Receptors, Glucocorticoid; C411470:glucocorticoid receptor alpha