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PubMed1992

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↗
PubMed1981

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↗
PubMed1994

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↗
PubMed1998

Langerhans cells in prurigo nodularis investigated by HLA-DR and S-100 immunofluorescence double staining.

The Langerhans cell is one of the antigen-presenting cells in the immune system. To study the presence of cutaneous Langerhans cells in prurigo nodularis, age- and sex-matched prurigo nodularis patients and healthy volunteer skin biopsies were investigated by an HLA-DR and S-100 immunohistochemical double staining method. The results showed that the HLA-DR- and S-100-immunoreactive (IR) Langerhans cells were altered in prurigo nodularis epidermis and dermis. The number of epidermal Langerhans cells in the prurigo nodularis patients was decreased in five and increased in two cases. In the dermis, the HLA-DR- and S-100-IR cells were apparently more numerous than in the controls. In the involved skin there were also more S-100-IR coarse nerve fibres in the dermis as compared to controls. The results indicate that dermal Langerhans cells (HLA-DR and S-100 double-labeled) as well as other dermal HLA-DR- and S-100-IR dendritic cells, but most likely not epidermal Langerhans cells, may be critically involved in the development or persistence of prurigo nodularis.

Aged↗
PubMed2002

Lymphocyte subtypes and adhesion molecules in actinic prurigo: observations with cyclosporin A.

BACKGROUND: Actinic prurigo is a photodermatitis in which UV light is implicated by an unknown mechanism. METHODS: Skin biopsies of 19 patients with actinic prurigo and 11 controls were analyzed by immunohistochemistry. RESULTS: In actinic prurigo patients, there was a significant increase in the number of CD3, CD4, CD8, CD45RA, CD45RO, and CD45RB lymphocytes and Langerhans cells, as well as in the level of human leukocyte antigen-DR (HLA-DR) expression and cell adhesion molecules lymphocyte functional antigen-1 (LFA-1), intercellular adhesion molecule-1 (ICAM-1), and endothelial leukocyte adhesion molecule-1 (ELAM-1). Actinic prurigo patients were treated with cyclosporin A (CsA), and a final skin biopsy was taken after 6 months of treatment. All the cell populations and markers studied, except for the CD4 lymphocytes, Langerhans cells, and HLA-DR expression, returned to normal levels. CONCLUSIONS: CsA was found to be effective in relieving the clinical symptoms of actinic prurigo.

Adolescent↗
PubMed2003

Prurigo pigmentosa: a distinctive inflammatory disease of the skin.

More than 200 patients with prurigo pigmentosa, a disease described first by Nagashima in 1971, have been reported on in Japan, but only 28 non-Japanese patients have come to notice as of today. In order to establish reliable, repeatable criteria for diagnosis of the disease, we studied 25 patients with prurigo pigmentosa and reviewed the literature pertaining to it as recorded in another 182 patients.Clinically, prurigo pigmentosa presents itself as pruritic urticarial papules, papulovesicles, and vesicles arranged in reticular pattern and distributed symmetrically on the back, neck, and chest. Lesions involute in a matter of days, leaving behind netlike pigmentation. Exacerbations and recurrences are the rule. Histopathologically, prurigo pigmentosa begins with a superficial perivascular infiltrate of neutrophils. Shortly thereafter, neutrophils are scattered in dermal papillae and then sweep rapidly through an epidermis in which spongiosis, ballooning, and necrotic keratocytes are accompaniments. En route, abscesses may form in the surface epithelium. Very soon, eosinophils and lymphocytes come to predominate over neutrophils in a dermal infiltrate that assumes a patchy lichenoid pattern. Intraepidermal vesiculation follows on spongiosis and ballooning and, sometimes, subepidermal vesiculation on vacuolar alteration at the dermo-epidermal junction. As the epidermis becomes hyperplastic, parakeratotic, and slightly hyperpigmented, melanophages begin to appear in the dermis. Studies by immunofluorescence are negative invariably. Dapsone or minocyclin are effective treatments; both of those agents inhibit migration and/or function of neutrophils. The cause and pathogenesis have yet to be determined. Prurigo pigmentosa is unique among inflammatory diseases of the skin and the singularity of it is manifest both clinically and histopathologically.

Adult↗
PubMed1996

Treatment of actinic prurigo in Chimila Indians.

BACKGROUND: Actinic prurigo has a high prevalence in women of child-bearing age. Its treatment has been, among others, with thalidomide. To avoid the deleterious effects of this drug on the embryo, therapeutic alternatives have been sought. Among these, tetracycline and vitamin E have been investigated as to their influence on the symptoms of actinic prurigo. Both these drugs affect superoxide radicals that are thought to be involved in the pathogenesis of actinic prurigo. MATERIALS AND METHODS: Patients (Chimila Indians with a high prevalence of actinic prurigo) received either (a) tetracycline, 500 mg three times daily, for 6 months, or (b) vitamin E, 100 IU daily, for 6 months. The patients were seen once monthly. There were eight patients in each group. RESULTS: Both drugs used were effective. Pruritus was remarkably improved by either treatment. None of the side effects were severe enough to lead to interruption of treatment, but the observation period posttreatment was relatively short, 4 months for tetracycline and 2 months for vitamin E. The improvement occurred in spite of the continuation of extensive exposure to the sun. CONCLUSIONS: Tetracycline and vitamin E are efficacious in relieving the pruritus of actinic prurigo. Preliminary trials of a combination treatment with these two drugs is a new avenue which has shown in preliminary trials to yield synergistic effects which might allow the dosage of tetracycline to be reduced.

Anti-Bacterial Agents↗
PubMed1997

Histopathological and bacteriological findings in prurigo nodularis.

Prurigo nodularis is a chronic disease with unknown aetiology. Biopsy specimens of 43 patients with prurigo nodularis were taken for histopathological and mycobacteriological analyses. By conventional histopathology, 25 (58%) samples, and by immunostaining for S100 protein, 31 (72%) samples had changes relevant to prurigo nodularis. Twelve (28%) of the samples were positive for acid fast bacilli in tissue staining by Ziehl-Neelsen technique, including 4 of the 6 samples also positive for mycobacteria in cultivation. The results verified the usefulness of S100 staining in detection of neural hyperplasia in dermal nerves, a feature regarded as diagnostic for prurigo nodularis. They also indicated that atypical mycobacteria may be a contributing factor in prurigo nodularis.

Adult↗
PubMed2004

[Hepatitis C virus RNA in the skin eruption from patients with prurigo and chronic hepatitis C].

UNLABELLED: Hepatitis C virus RNA in the skin eruption from patients with prurigo and chronic hepatitis C. Since the discovery of hepatitis C virus (HCV) in 1989, many cutaneous disorders have been observed in patients suffering from chronic HCV infection. The relationship between HCV infection and cryoglobulinemia and porphyria cutanea tarda is clearly established, however, the link between HCV and other skin diseases is still controversial. AIM: Two patients with intense pruritus and secondary prurigo in chronic C hepatitis have been presented. METHODS: The chronic hepatitis C of the patients were proved by elevated ALT and AST level, anti HCV (ELISA), HCV-PCR serological examination and liver biopsy. The skin lesions were accompanied by severe itching. According to clinical symptoms the patients suffered from prurigo simplex. RESULTS: HCV RNA in the skin specimen from the biopsy of the skin lesion was detected by RT PCR method, but the non affected skin specimen from the patients was HCV RNA negative. CONCLUSIONS: This report is a case of prurigo simplex with chronic C hepatitis proving a direct relation between the HCV infection and prurigo.

Female↗
PubMed1993

[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↗
PubMed2004

Thalidomide treatment for prurigo nodularis in human immunodeficiency virus-infected subjects: efficacy and risk of neuropathy.

OBJECTIVE: To evaluate safety and efficacy of thalidomide in the treatment of prurigo nodularis in a group of human immunodeficiency virus (HIV)-infected patients whose condition was recalcitrant to standard treatment. DESIGN: Prospective study. SETTING: Outpatient dermatology and neurology clinic, both referral settings. PATIENTS: Eight HIV-infected patients with refractory prurigo nodularis; a total of 10 met inclusion criteria, but 2 could not be followed up. INTERVENTIONS: Treatment with thalidomide, 100 mg/d. Subjects were randomized after 1 month to receive 100 or 200 mg/d. If side effects were noted, the drug was reduced to a tolerable dose or discontinued. Subjects were monitored at baseline and monthly for degree of pruritus and total area of body involvement of prurigo nodularis. Sequential neurologic assessments were performed. MAIN OUTCOME MEASURES: Efficacy and toxic effects. RESULTS: The dosage of thalidomide ranged from 33 to 200 mg/d. Eight subjects had a greater than 50% response in reduction of itch over 3.4 months (average). Seven subjects had a greater than 50% reduction of skin involvement over 5 months (average). Three subjects developed thalidomide peripheral neuropathy (TPN). There was no correlation between duration of treatment, daily or cumulative dose, and TPN. A change in the Neuropathy Impairment Score of 10 points was a good marker of TPN, as was a greater than 50% decrease in the sural sensory nerve action potential amplitude. CONCLUSIONS: Thalidomide reduced the signs and symptoms of prurigo nodularis in HIV-infected subjects. One third of subjects developed TPN, underscoring the importance of careful neurologic assessment.

Administration, Oral↗
PubMed1999

Light and electron microscopic immunohistochemical observations of p75 nerve growth factor receptor-immunoreactive dermal nerves in prurigo nodularis.

Prurigo nodularis is an inflammatory skin disease characterized by neurohyperplasia. Neurotrophins and their receptors play a critical role in nerve growth, differentiation, maturation and maintenance, including cutaneous nerve fiber growth and innervation. They may also be responsible for events related to the growth and differentiation control of keratinocytes. To explore the exact distribution of the p75 low-affinity nerve growth factor receptor (p75 NGFr) in the cutaneous nerve components, p75 NGFr immunofluorescence as well as ultrastructural immunohistochemical studies were performed on prurigo nodularis lesional skin and normal human skin samples. The immunofluorescence results revealed that nerve fibers and bundles were increased in number and size in lesional upper dermis with stronger p75 NGFr immunoreactivity than in the corresponding normal tissue. At the ultrastructural level, a lot of nerve fibers clustered together in the prurigo nodularis dermal tissue. The axons were enlarged and branched, but the axons themselves seldom showed any NGFr immunoreactivity. The Schwann cell bodies were extended and irregularly shaped, and tended to separate into many branches enveloping the axons. The Schwann cell membrane showed strong p75 NGFr immunoreactivity. The perineurium cells also revealed strong p75 NGFr immunoreactivity. The Schwann cells inside the perineurium were less p75 NGFr-immunoreactive than those outside the perineurium. The membrane of certain basal keratinocytes showed NGFr immunoreactivity as well. The present results indicate that overexpression of p75 NGFr in Schwann cells and perineurium cells could contribute to the neurohyperplasia in prurigo nodularis.

Aged↗
PubMed1992

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↗
PubMed1986

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↗
PubMed2001

Prurigo pigmentosa from contact allergy to chrome in detergent.

Prurigo pigmentosa is a recurrent inflammatory dermatosis characterized by pruritic erythematous papules and reticulate hyperpigmentation that occurs most frequently in spring and summer. The etiology of prurigo pigmentosa remains unknown. Numerous authors have suggested that various contact allergens may be pathogenic or triggering factors, but nearly all attempts to identify an allergen have been unsuccessful. We report a case of prurigo pigmentosa induced by contact allergy to chrome in detergent, supporting the conclusion that contact allergens such as chrome may play a rôle in inducing prurigo pigmentosa.

Abdomen↗
PubMed2002

Prurigo pigmentosa.

BACKGROUND: Prurigo pigmentosa is a rare inflammatory dermatosis of unknown etiology characterized by recurrent, pruritic erythematous papules and gross reticulate hyperpigmentation. It is seen most commonly among young adult Japanese females. Only 20 cases have been described outside Japan. METHODS: We report two female, Turkish patients aged 20 and 26 years who had a pruritic rash with the characteristic clinical appearance and supportive histopathology of prurigo pigmentosa. RESULTS: They were successfully treated with minocycline and doxycycline. CONCLUSIONS: Prurigo pigmentosa is a relatively new clinical entity, and we believe that a more widespread knowledge of this disease will lessen its misdiagnosis. We find it noteworthy to point out that there may be a predisposition to prurigo pigmentosa amongst the Turkish and Sicilian populations.

Adult↗
PubMed2001

Treatment of prurigo nodularis with topical capsaicin.

BACKGROUND: Prurigo nodularis is an eruption of lichenified or excoriated nodules caused by intractable pruritus that is difficult to treat. Therefore the antipruritic efficacy of capsaicin seemed to be of particular interest because this alkaloid, extractable from red pepper, interferes with the perception of pruritus and pain by depletion of neuropeptides in small sensory cutaneous nerves. OBJECTIVE: The aim of this concentration- and regimen-ranging study was to evaluate the efficacy, safety, and practicability of capsaicin in the topical treatment of prurigo nodularis in a large series of patients. METHODS: A total of 33 patients with prurigo nodularis of various origins were selected to receive capsaicin (0.025% to 0.3%) 4 to 6 times daily for 2 weeks up to 10 months. The consecutive follow-up period was up to 6 months. In 7 patients, skin biopsy specimens were taken before, during, and after therapy and investigated histologically, immunohistochemically, and ultrastructurally. RESULTS: All 33 patients could be evaluated for efficacy. After cessation of the symptoms of neurogenic inflammation, such as burning sensations or erythema, all of them experienced a complete elimination of pruritus within 12 days. In addition, capsaicin largely contributed to the gradual healing of the skin lesions. After discontinuation of the therapy, pruritus returned in 16 of 33 patients within 2 months. At the ultrastructural level, no degenerative changes of cutaneous nerves could be found during or after capsaicin therapy. Depletion of substance P was demonstrated by confocal laser scanning microscopy thus confirming the specific effect of capsaicin in vivo. CONCLUSION: Topical treatment of prurigo nodularis with capsaicin proved to be an effective and safe regimen resulting in clearing of the skin lesions.

Administration, Topical↗
PubMed2001

Effectors of inflammation in actinic prurigo.

BACKGROUND: Actinic prurigo is a specific familial photodermatosis of uncertain pathogenesis. OBJECTIVE: Our purpose was to investigate the immunohistologic presentation of actinic prurigo to explore the involved pathomechanisms. METHODS: The present immunohistochemical study was performed on biopsy specimens from 20 Mexican patients presenting with a severe and perennial form of the disease. RESULTS: The dense inflammatory infiltrate was composed predominantly of helper T type 1 lymphocytes admixed with scattered B-cell lymphoid follicles and numerous dermal dendrocytes. Keratinocytes contained abundant tumor necrosis factor-alpha and calprotectin. CONCLUSION: In subjects genetically predisposed to actinic prurigo, ultraviolet light may trigger excessive tumor necrosis factor-alpha production by keratinocytes whose sustained release in turn exerts its proinflammatory activity and deleterious epidermal effects. Such a cascade of events is in line with the therapeutic benefit already reported when thalidomide is used to treat actinic prurigo.

Adolescent↗