LAS VEGAS Most experts in psychodermatology long ago abandoned the psychoanalytic theory of atopic eczema, characterized in 1940 by Dr. Franz Alexander as an outgrowth of a child's emotional angst at being unable to express anger and hostility arising from maternal rejection.
Still, increasing evidence points to a psychoneuroimmunologic "setup" for atopic dermatitis (AD), if not an eczema personality profile, asserts Dr. Torello M. Lotti, professor and chair of dermatology at the University of Florence, Italy.
Dr. Lotti and other researchers have hypothesized that an interconnection between genetic and environmental factors may predispose a patient to allergic inflammation, which may then cascade in a vulnerable individual into a long-lasting diminished capacity for appropriate protective reactivity within the hypothalamus-pituitary-adrenal (HPA) axis.
Certain responses to experimental conditions point to notable differences in the psycho-neuroendocrine-immune function of people with atopic dermatitis and other inflammatory allergic diseases, Dr. Lotti said during a seminar on dermatology sponsored by Skin Disease Education Foundation.
He cited numerous studies:
▸ Diurnal plasma cortisol (stress marker) variations in AD patients were found to rise and fall with atopy-relevant inflammatory parameters, with associated waxing and waning of allergic symptom severity (J. Clin. Invest. 1992;90:596603).
▸ AD-like symptoms were actually precipitated in healthy volunteers after treatment with the glucocorticoid receptor antagonist RU 486 (J. Clin. Endocrinol. Metab 1990;71:147480).
▸ When exposed to experimental stressor conditions (asking volunteers to speak and do mental arithmetic tasks in front of an audience), eosinophil counts and IgE levels rose significantly in atopic eczema sufferers, but not in healthy volunteers (J. Neuroimmunol. 2002;129:1617).
▸ Finally, epidemiologic evidence appears to bolster the argument that stresseither exerted by outside events or exquisitely experienced by a vulnerable personalitycontributes to the cycle of events perpetuating atopic dermatitis, he said.
A severe shock or emotional event has been found to precede the onset or aggravation of AD in patients in early dermatologic studies, which also tracks with his clinical experience, he noted. An increasing prevalence of AD in children in the Western World may be symptomatic of the more highly-stressed, pressured environments in which they live.
In Dr. Lotti's view, a "biochemical setup" for atopic dermatitis activates not only stress (influencing the sympathetic nervous system and immune response), but also behavior and personality.
An appropriate approach, he said, is to utilize treatments that impact psychological symptoms of distress as well as physiologic symptoms such as pruritus.
He favors doxepin (10 mg at bedtime) or amitriptyline (starting at a dose of 50 mg/day) over antihistamines for "the itch of atopic dermatitis," which he said "is not a regular itch."
Direct acknowledgement of the psychological contributors to atopic dermatitis facilitates "liaison consultations," in which Dr. Lotti sees patients sometimes in the same room at the same time as do psychologists or psychiatrists.
Dr. Lotti disclosed receiving grant or research support or speakers bureau contributions from Merck-Serono, Wyeth, Abbott, and Schering-Plough.
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