Pruritus is an essential feature of atopic dermatitis (AD) and the diagnosis of active AD cannot be made without the history of itching Because of the high impact on life quality, most of the patients measure the severity of eczema by the intensity of pruritus rather than appearance of skin lesions However, although pruritus is a cardinal symptom of AD, its mechanism and association with the cutaneous nervous system is not completely understood Recently, a considerable progress has been achieved in clarifying the complex pathophysiology of pruritus in AD As a cutaneous sensory perception, itch requires excitation of neuropeptide-containing free nerve endings of unmyelinated nociceptor fibers It is well known that histamine and acetylcholine provoke itch by direct binding to 'itch receptors' and several mediators such as neuropeptides, proteases or cytokines indirectly via histamine release Interestingly, some variations of these complex mechanisms could be demonstrated in patients with AD This review highlights the recent knowledge of different mechanisms which may be involved in regulating pruritus in patients with AD potentially leading to new therapeutic applications for the treatment of itch in AD

https://onlinelibrary.wiley.com/doi/pdf/10.1034/j.1600-0625.2002.110102.x

Pathophysiology of pruritus in atopic dermatitis: an overview.

https://www.jidonline.org/article/S0022-202X(15)30278-5/pdf

Measuring Atopic Dermatitis Severity in Randomized Controlled Clinical Trials: What Exactly Are We Measuring?

Sir, We present an unusual and striking case of elastosis perforans serpiginosa and cutis laxa in a 36-year-old man previously on long-term, high-dose penicillamine for Wilson's disease. The patient may also have elastolytic involvement of the upper respiratory tract, a rarely reported feature. He originally presented with jaundice at the age of 4 years and by age 8 years progressive dysarthria and clumsiness of the hands had appeared. Wilson's disease was diagnosed and he was treated with the chelating agent dimercaprol. In 1982 the treatment was changed to penicillamine given long-term in a dose of 2±3 g daily. In 1995 he presented with itchy, papular lesions on the left arm, due to penicillamine-induced perforating elastosis. Penicillamine was discontinued in January 1996, and trientine dihydrochloride (triethylene tetramine dihydrochloride), an alternative copper chelator, was commenced. The papular lesions resolved initially but then returned 6 months later on the neck, shoulders and upper arms. Trientine was therefore discontinued and he was maintained on zinc sulphate (up to 600 mg daily),which reduces copper absorption in the intestine. Treatment with topical clobetasol propionate flattened the lesions, and small areas treated with triamcinolone 10 mg/mL injections resolved almost completely. There has also been some spontaneous improvement following the withdrawal of chelation therapy, with fewer new lesions appearing. Subsequently, trientine has been recommenced because of neurological deterioration; new lesions have been partially controlled by the topical steroid therapy. On examination of his skin in 1996 there was generalized cutis laxa (Fig. 1a) with perforating elastolytic nodules on the neck and elastosis perforans serpiginosa over the shoulders (Fig. 1b). General examination revealed dysphonia, dysarthria due to pseudobulbar palsy, upward gaze palsy, reduced speed of tongue movements, and erect gait with truncal rigidity. Ophthalmological examination revealed no elastolytic changes such as angioid streaks in the retina, and no Kayser± Fleischer corneal deposits of copper. Investigations revealed a normal full blood count, biochemistry, autoantibodies and immunoglobulins. Caeruloplasmin, urine copper, serum copper and a magnetic resonance imaging brain scan were consistent with Wilson's disease, in the decoppered state. A barium swallow, performed in 1995 because of his difficulty in swallowing, demonstrated pharyngeal and tongue weakness with aspiration and ineffective cough reflex. We feel that this may in part be caused by the elastolytic effects of penicillamine on the upper respiratory tract and oropharynx and also because of pseudobulbar palsy, as penicillamine is known to cause elastolysis of many tissues including the respiratory tract. Histology of a skin biopsy from the upper arm and a nodule on the neck revealed a perforating channel from the dermis through the epidermis with a surrounding inflammatory infiltrate, and horseshoe-shaped multinucleate giant cells phagocytosing abnormal elastic fibres. Elastin van Gieson stain showed abnormal elastic fibres with a `lumpy-bumpy' or `bramblebush' appearance, which are typically seen in elastolysis due to penicillamine (Fig. 1c).

Penicillamine‐induced elastosis perforans serpiginosa and cutis laxa in Wilson’s disease

Pruritus (itch) is a major characteristic and one of the most debilitating symptoms in allergic and atopic diseases and the diagnostic hallmark of atopic dermatitis. Pruritus is regularly defined as an unpleasant sensation provoking the desire to scratch. Although we achieved rather good knowledge about certain inducers of itch such as neuropeptides, amines, mu-opioids, cytokines and proteases, for example, less is known about the pathophysiological specifities among the different diseases, and the therapeutic consequences which may derive thereoff. This review dissects the role of mediators, receptors and itch inhibitors on peripheral nerve endings, dorsal root ganglia, the spinal cord and the CNS leading to the amplification or - vice versa - suppression of pruritus. As the treatment of pruritus in allergic and atopic skin disease is still not satisfactory, knowing these pathways and mechanisms may lead to novel therapeutic approaches against this frequently encountered skin symptom.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1398-9995.2010.01995.x

Pathophysiology and therapy of pruritus in allergic and atopic diseases

The beneficial effects of ultraviolet (UV) radiation on atopic dermatitis has been appreciated for many years. While broadband UVB and psoralen UVA have been the mainstay of phototherapy for some time, the past 5 years have seen the introduction of phototherapeutic modalities, including UVA-1 and 311nm UVB. The best modality and mode of usage is dependent on the type of atopic dermatitis, severity and body site. T lymphocytes play an important role in disease pathogenesis and UV radiation has profound effects on skin and systemic immune responses.

Phototherapy for atopic dermatitis.

UVA1 irradiation is effective in treatment of chronic vesicular dyshidrotic hand eczema.

Platelet-activating factor (PAF acether) is a lipid mediator with a potent proinflammatory activity. Results derived both from in vitro and in vivo studies suggest a possible role of this substance in the pathophysiology of atopic dermatitis. A double-blind, randomized, multi-center, within-patient study was performed to evaluate the efficacy of a topically applied PAF antagonist (RO-24-0238) in 36 patients with atopic dermatitis. Over a period of 28 days, 0.25 ml of the PAF antagonist and the vehicle (placebo) were applied twice daily on opposite sites of symmetrical lesions (measuring 10 to 20 cm2 each). The overall assessment of the therapeutic efficacy did not demonstrate a superior effect of the PAF antagonist in comparison to placebo, and this was the same with the individual study parameters erythema, scaling, induration and exudation. For reducing pruritus, as assessed by the patient using a visual analogue scale, a statistically significant action was documented during the first 2 weeks of the study (p < 0.04; Wilcoxon rank sum test), with a continued, yet not statistically significant efficacy after weeks 3 and 4. The exact role of the pathological events of atopic dermatitis that might be influenced by a PAF antagonist remains to be determined, but the anti-pruritic component of this substance especially deserves further scientific interest.

Topical application of a platelet-activating factor (PAF) antagonist in atopic dermatitis.

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UVA1 irradiation is effective in treatment of chronic vesicular dyshidrotic hand eczema.

Topical application of a platelet-activating factor (PAF) antagonist in atopic dermatitis.