Actinic prurigo (Hutchinson's summer prurigo).
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Adult↗
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Treatment of prurigo nodularis, chronic prurigo and neurodermatitis circumscripta with topical capsaicin.
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Administration, Cutaneous↗
[Pruritus sine materia and prurigo. II. Prurigo].
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Adolescent↗
[Nodular prurigo (Hyde's prurigo nodularis)].
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Adult↗
[Pruritus and prurigo].
Prurigo occurs in the acute form of the disease (strophulus), in the subacute frorm (prurigo simplex subacuta), and the chronic form (prurigo nodularis Hyde). Transition stages between the subacute and the chronic form of the disease are common. Strophulus is characterized by few papulovesicles, which are disseminated on the trunk. Likewise, the lesions of prurigo simplex subacuta may be disseminated, or they may be acneiform, or are localised on the extremities only. Typically, prurigo nodularis Hyde occurs on the lower extremities. Strophulus is caused by the bites of insects or by gastrointestinal disorders. The causes of prurigo simplex subacuta include metabolic and endocrine disorders as well as skin diseases. The occurrence of the latter is demonstrated by the combination of atopic dermatitis and prurigo (prurigo diathetique Besnier). The metabolic and endocrine disorders include diabetes mellitus, hyperlipidemia, diseases of the liver, the stomach and the bowels, finally increased androgene levels in women. The same pathological conditions are found in prurigo nodularis Hyde. The extreme chronicity of the prurigo is most probably caused by the inefficiency of the therapy of internal diseases.
Adolescent↗
Increased sensory neuropeptides in nodular prurigo: a quantitative immunohistochemical analysis.
Seven patients with nodular prurigo, five patients with lichenified eczema and seven control volunteers were studied immunohistochemically using antisera to the pan-neuronal marker protein gene product 9.5 (PGP), and the neuropeptides calcitonin gene-related peptide (CGRP), substance P (SP), tyrosine hydroxylase (TH), vasoactive intestinal polypeptide (VIP) and the C-flanking region of neuropeptide Y (C-PON). PGP-, CGRP- and SP-immunoreactivities were also evaluated using image analysis quantification, and the data compared by statistical analysis. No significant changes were noted in the lichenified skin of patients with chronic eczema, compared with the control groups. In contrast, a significant increase in PGP immunoreactive nerve fibers was seen in lesional skin of all nodular prurigo cases studied, when compared with non-lesional skin from the same patient or from control subjects (P < 0.001). In one case massive neural hyperplasia was also identified. Staining for CGRP and SP showed a large increase of immunoreactive nerves in lesional skin of nodular prurigo patients, which closely paralleled that of PGP. Staining with VIP, C-PON and TH was similar in both lesional and non-lesional skin. These results indicate that neural changes in nodular prurigo are associated with an increase of sensory neuropeptides, which could be related to the intense pruritus which accompanies nodular prurigo. The absence of significant changes in lichenified skin suggests that the increase in CGRP- and SP-immunoreactive nerve fibres is a characteristic feature of nodular prurigo and may be important in its pathogenesis.
Adult↗
Demonstration by S-100 protein staining of increased numbers of nerves in the papillary dermis of patients with prurigo nodularis.
BACKGROUND: We hypothesized that hyperplasia of papillary dermal nerves was a constant feature of prurigo nodularis. OBJECTIVE: We tested this hypothesis by examining sections from 25 cases of prurigo nodularis, 25 cases of skin lesions characterized by epidermal hyperplasia without clinical pruritus, and 22 cases of clinically pruritic dermatoses with variable degrees of epidermal response for the presence of papillary dermal nerves. METHODS: We used a standard immunohistochemical assay with an antibody to S-100 protein as a means of identification of nerves. RESULTS: In 24 of 25 cases of prurigo nodularis, papillary dermal nerves were identified by immunostaining. Cutaneous nerves were present in 1 of 22 cases of epidermal hyperplasia with pruritus and were absent in the papillary dermis in nonpruritic cases. CONCLUSION: We conclude that hypertrophy of cutaneous papillary dermal nerves is a relatively constant feature of prurigo nodularis. The presence of papillary dermal nerves suggests a neurocutaneous component in the pathogenesis of prurigo nodularis.
Humans↗
Actinic prurigo.
Actinic prurigo is a chronic photodermatitis found predominantly in North American Indians. Other terms have been used to describe similar cases in Central and South America and in Europe. Relatively little has been written about this condition in the English literature, and confusion exists over whether this is a form of polymorphic light eruption. Actinic prurigo can be considered a unique variant of polymorphic light eruption; however, we believe that certain differences help to distinguish actinic prurigo as a separate disease entity. Herein we report three cases of this disease and review the related literature. Characteristic clinical features include prurigolike papules and cheilitis. Pruritus is the predominant symptom, and a familial tendency and an early age at onset are usually noted. Results of karyotyping and analysis of sister chromatid exchanges were normal in two of our patients so tested. Skin testing for photosensitivity has yielded inconsistent results, and use of light testing for diagnosing actinic prurigo does not seem to be a predictable procedure. Actinic prurigo is a chronic disease that often is refractory to therapy.
Adult↗
Merkel cells and prurigo nodularis.
BACKGROUND: Increased numbers of dermal nerves have been demonstrated in prurigo nodularis and have been theoretically linked to the intense pruritus. We hypothesized that the neuronal proliferation in prurigo nodularis might be associated with an increased density of Merkel cells because they are also a component of the neurocutaneous system. METHODS: We examined skin biopsy specimens from 20 cases of prurigo nodularis for Merkel cells with the use of a standard immunohistochemical assay (avidin-biotin-peroxidase complex system) with an antibody to cytokeratin 8 (CAM 5.2). Six cases of lichen simplex chronicus were examined as controls. RESULTS: Merkel cells were present in the interfollicular area of the basal cell layer in 15 (75%) of 20 prurigo nodularis cases and in one (17%) of six cases of lichen simplex chronicus. CONCLUSION: Merkel cells are increased in number in prurigo nodularis and may be a component of the neurocutaneous abnormality associated with this disorder.
Humans↗
[Prurigo in tropical area. Importance of its association with HIV infection].
The term prurigo applies to a classic chronic skin disease of children (P. strophulus) which is becoming found very seldom in developed countries, but remains extraordinarily prevalent in tropical areas. This striking geographical distribution relies on its ectoparasitic origin. Some peculiar aspects of prurigo, observed in French Guyana (South America), are reported. The original point is a new aspect of adult acquired prurigo, associated with HIV infection, which appears to be one of the features characteristic of tropical AIDS. This HIV associated prurigo (HAP) is the revelating event, in as high as 20% of HIV infected people, significatively those with less than 200 CD4 cells. HAP appears as a marker of HIV infection with poor sensitivity, but much higher specificity (92%), with no correlation with acquisition's risk factors. Just like infantile prurigo, HAP can be considered an arthropod bite reaction which seems to be enhanced in HIV infected people living in tropical environment.
CD4 Lymphocyte Count↗
Actinic prurigo: clinical features and prognosis.
BACKGROUND: Actinic prurigo, an idiopathic familial photodermatosis, has been described in Amerindians in Manitoba, Canada, as well as in the United States, Mexico, and South America. OBJECTIVE: Our purpose was to describe the clinical features and prognosis of actinic prurigo in Amerindians in Saskatchewan, Canada. METHODS: Clinical examinations, questionnaires, phototesting, and laboratory tests were used. RESULTS: We present a series of 93 Amerindian patients. The face is the most commonly involved area. A hereditary tendency, cheilitis, and pruritus are prominent features. One third of patients report some lesions, often minor, during the winter. The majority of patients phototested were sensitive to ultraviolet A light. CONCLUSION: We find the age of onset of actinic prurigo to be the most important feature in determining the type of eruption and the prognosis for the patient. In general the younger ages of onset (up to 20 years of age) are associated with cheilitis and more acute eruptions and are more likely to improve over 5 years. Those who develop actinic prurigo as adults (21 years of age and older) tend to have a milder and more persistent dermatosis.
Adolescent↗
Bullous pemphigoid and prurigo nodularis.
Bullous pemphigoid is a chronic blistering disorder characterized by specific clinical, histologic, and immunofluorescent findings. Several variants have been described, including pemphigoid nodularis, which may mimic or evolve from or into prurigo nodularis. The casual relationship between prurigo nodularis and bullous pemphigoid is unknown. We describe a patient with prurigo nodularis and no immunologic evidence of pemphigoid who subsequently developed bullae. Direct immunofluorescence then confirmed the diagnosis of bullous pemphigoid. Apparently this patient had prurigo nodularis and then developed bullous pemphigoid.
Aged↗
Follicular occurrence of prurigo nodularis.
Thirty-eight biopsies of prurigo lesions (22 large, mature nodules and 16 smaller, intermediately developed nodules) were obtained from 17 patients with idiopathic prurigo nodularis Hyde who had not been bitten by insects, nor had other underlying diseases. Each biopsy was serially sectioned to reveal its histological structure. In 88% (14/16) of the smaller nodules and in 55% (12/22) of the large ones, a hair follicle was observed in the center of the prurigo lesion. The follicular epidermis and the adjacent surface epidermis showed various degrees of acanthosis and spongiosis. The dermal infiltrates extended from the superficial dermis into the middle dermis in a triangular fashion around the involved hair follicle. It is suggested that idiopathic prurigo nodularis most frequently occurs in connection with a hair follicle.
Adult↗
Actinic prurigo, tropical (South-East Asian) variant.
Actinic prurigo is a chronic familial photodermatitis found predominantly among the Amerindians. It has been reported from North and South America, Britain and Japan. We report a case of actinic prurigo seen in Singapore. A 20-year-old Malay female presented with a persistent pruriginous eruption in the sun-exposed parts and on her abdomen. She also had lower lip cheilitis and thinning of the outer eyebrows, features often seen in actinic prurigo. The minimal erythema dose to ultraviolet A (UVA) and UVB were persistently lowered. We propose that this condition be called actinic prurigo, tropical (South-East Asian) variant.
Adult↗
[Prurigo diseases].
The term "prurigo" is universally used in dermatology. But, up to now, no definition of this term has been generally accepted. The "classic" description of the "urticarial papules" as the primary skin eruptions of prurigo is not correct, for these papules do not show any momentary edema but a persistent cellular infiltration. In the past, some authors already pointed out that the histologic structure of such papules looks very much like that of the characteristic papulovesicles in eczema--especially those in atopic dermatitis. The various forms of the prurigo nodes secondarily develop in case of the coincidence of three main factors: (1) the particular cutaneous response to repeated irritation (especially in autosomally dominant ichthyosis simplex), (2) reduced threshold for or constitutional disposition to pruritus (especially in atopy), and (3) internal (e.g. intestinal disorders) or external (e.g. insect bites) triggers. Probably none of the prurigo diseases represents a nosologic entity.
Dermatitis, Atopic↗
Actinic prurigo--a specific photodermatosis?
Actinic prurigo can be defined as an idiopathic photodermatosis which usually starts in childhood, particularly affects the female, with some evidence for an atopic and familial photosensitivity background. It affects both exposed and covered skin but mainly the former and although it may be present all the year round is usually maximal on the exposed skin during months of sunshine. The changes are those of a chronic prurigo along with more acute episodes following sunshine exposure in which there is a background of edematous erythema. It usually lasts throughout childhood and adolescence, but tends to wane and even to clear in late adolescence or early adult life. The etiology is unknown, as are the mechanisms involved. Action spectrum studies have produced no evidence for the involvement of specific wavelengths other than the presence of UV sensitivity in some subjects and a suggestion that the longer wavelength UVA may be more important than the sunburn waveband around 305 nm. Based on a study of 60 personal cases with actinic prurigo the authors agree with the longheld view of Calnan & Meara (1) that actinic prurigo is a separate and distinct photodermatosis.
Adolescent↗
[Multiple keratoacanthomas (Witten-Zak type) in prurigo simplex subacuta].
We report on the case of a 51-year-old female patient who had been suffering from multiple itching nodules for 3 years. Some of these lesions were classified clinically and histologically as keratoacanthomas (KA), whereas the multiple smaller nodules were found on histological examination to be either early stage KA or lesions of prurigo simplex subacuta. In two KA, HPV subtype 2 was identified by in situ hybridization. Treatment with etretinate resulted in remission of the fully developed KA and reduced the occurrence of new ones. The outbreak of multiple KA in our patient resembled a rare subtype described by Witten and Zak. Postclinical follow-up for 28 months to date has revealed that the KA arise from the subacute prurigo lesions. This mode of prurigo-dependent KA development has not previously been reported.
Biopsy↗
HLA typing in actinic prurigo.
Thirty-two actinic prurigo patients of Cree ancestry underwent human lymphocyte antigen (HLA) typing and were compared with 32 control subjects of Cree ancestry. We found a significantly increased frequency of HLA-A24 and Cw4 antigens and a significant decrease in the frequency of the A3 antigen in actinic prurigo patients. These HLA associations may be helpful in determining whether actinic prurigo is a distinct disease or a variant of polymorphous light eruption.
Adolescent↗