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Dialogues in Dermatology, a monthly audio program from the American Academy of Dermatology, contains discussions between dermatologists on timely topics. Commentaries from Dialogues Editor-in-Chief Warren R. Heymann, MD, are provided after each discussion as a topic summary and are provided here as a special service to readers of the Journal of the American Academy of Dermatology.
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In previous research we reported attenuated responsiveness of the hypothalamus-pituitary-adrenal (HPA) axis and further, an increased reactivity of the sympathetic adrenomedullary (SAM) system to stress in patients suffering from atopic dermatitis (AD). AD is a chronic inflammatory skin disease mainly triggered by TH(2)-dependent inflammatory processes. The specific goal of the present study was to investigate whether altered HPA axis and SAM system responsiveness to stress can also be found in TH(1)-mediated inflammatory conditions. Patients with psoriasis (PSO; n=23), a TH(1)-mediated inflammatory (autoimmune) skin disease and healthy controls (n=25) were exposed to a standardized laboratory stressor (TSST) which mainly consists of a free speech and a mental arithmetic task in front of an audience. To investigate HPA axis and SAM system responsiveness, cortisol, ACTH, and catecholamines were determined before and after the stress test. In addition, cortisol levels after awakening and cortisol levels during the day (short diurnal profile) were determined. In order to test feedback sensitivity of the HPA axis, a dexamethasone (DEX) suppression test (0.5 mg) was performed. Analysis of cortisol and ACTH levels after the stress test yielded no significant differences between PSO subjects and controls indicating no altered HPA axis function in this patient group. Further, no between-group differences were found in cortisol levels after awakening or during the day (short diurnal profile). Additionally, no difference between PSO and healthy subjects in the feedback sensitivity of the system could be found (DEX test). However, PSO patients showed elevated epinephrine (F(3,102)=4.7; p<0.005) and norepinephrine (F(3,135)=2.7; p<0.05) levels in response to the stress test when compared to the controls. These findings suggest no altered HPA axis responsiveness, but increased reactivity of the SAM system in TH(1)-mediated chronic inflammatory skin disease.
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This review begins with a brief survey of the neurophysiology and neuroanatomy of pruritus, and goes on to describe the etiology of the major allergic and nonallergic pruritic disorders. The etiology of pruritus often suggests the appropriate treatment. For example, urticaria, which is primarily mediated by histamine, is amenable to treatment with H1 antihistamines. Second-generation, nonsedating antihistamines appear to be more effective than sedating antihistamines, perhaps because of better compliance. Other systemic pharmacologic options may be useful in nonhistamine-mediated disorders, for example, immunomodulators for inflammation-induced pruritus or opiate antagonists for atopic dermatitis. Nonpharmacologic measures, such as proper skin care, and physical modalities, such as phototherapy or acupuncture, may also be helpful.
Skin diseases are an essential part of primary care medicine. Most dermatologic care is delivered in an outpatient setting. The initial evaluation is usually performed by the primary care physician. Women account for nearly 60% of all visits for dermatologic complaints.
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International tourism to tropical and sub-tropical areas, both to resource-poor and developed countries, has almost trebled within the past 20 years. We examined the records of patients referred to the Liverpool School of Tropical Medicine over 6 years. 46 (63%) of infestations originated in the UK. Ticks were most common in the UK (19 cases, 41%) whereas myiasis was most common in travellers (18 cases, 67%). These records suggest that whereas many overseas acquired infestations are potentially dangerous if infections are transmitted, ticks constitute the greatest risk, and both domestic and exotic species may act as disease vectors.
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