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Results for “PRURIGO NODULARIS”

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At least 19 recordsLinked to original sources
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↗
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↗
PubMed1990

Hodgkin's disease manifesting as prurigo nodularis.

Prurigo nodularis is an uncommon pediatric cutaneous disorder that is associated with intense pruritus. We report a teenager with prurigo nodularis as the presenting sign of stage IIA Hodgkin's disease, primarily in the mediastinum. The pruritus and associated cutaneous lesions resolved with combination chemotherapy directed at the malignancy. In patients with prurigo nodularis and pruritus of unclear etiology, the possibility of underlying Hodgkin's disease must be considered.

Adolescent↗
PubMed1993

Prurigo nodularis.

Prurigo nodularis is a chronic skin disorder that is frequently misdiagnosed. It is characterized by multiple pea-sized nodules that develop on the skin, particularly on the anterior leg and thigh. These lesions are intensely pruritic and frequently become excoriated and infected. The cause of prurigo nodularis is unknown, and treatment is directed at reducing inflammation and controlling symptoms. The condition is typically of long duration and is refractory to treatment.

Female↗
PubMed2026

Somatic mutations reveal hyperactive Notch signaling in prurigo nodularis.

Prurigo nodularis (PN) is a chronic inflammatory skin disease characterized by pruritic skin nodules of unknown etiology. Little is known about genetic changes in PN pathogenesis, particularly somatic events, which are often implicated in inflammatory conditions. We thus performed whole-exome sequencing on 54 lesional and nonlesional skin biopsies from 17 patients with PN and 10 patients with atopic dermatitis (AD) for comparison. Somatic mutational analysis revealed that PN lesional skin harbors recurrent somatic mutations in fibrotic, neurotropic, and cancer-associated genes that are absent in adjacent PN nonlesional skin. Nonsynonymous mutations were most frequently present in NOTCH1 and the Notch signaling pathway, a key regulator of cellular proliferation and tissue fibrosis. In contrast, NOTCH1 mutations were absent in AD. Somatic copy-number analysis, combined with expression data, identified recurrently deleted and downregulated genes in PN lesional skin, which are associated with axonal guidance and extension. Follow-up immunofluorescence validation demonstrated increased NOTCH1 expression in PN lesional skin fibroblasts and increased Notch signaling in PN lesional dermis. Finally, a multicenter analysis revealed increased risk of NOTCH1-associated diseases in patients with PN. In characterizing the somatic landscape of PN, this study highlights the potential role of Notch pathway dysregulation in PN pathogenesis and fibrosis.

Humans↗
PubMedDate not supplied

Prurigo nodularis (Hyde's prurigo) disclosing celiac disease.

A case of prurigo nodularis (Hyde's prurigo) preceding by 15 years the diagnosis of celiac disease is presented. In particular, the association between the clinical course of prurigo nodularis and the compliance with gluten-free diet is reported and discussed.

Aged↗
PubMed1997

Sequential combined therapy with thalidomide and narrow-band (TL01) UVB in the treatment of prurigo nodularis.

BACKGROUND: Prurigo nodularis (PN) is a chronic disease of which treatment choices are limited. Among them, thalidomide and phototherapy have been used with satisfactory results. Unfortunately, the possibility of side effects limits their use. OBJECTIVE: To evaluate the efficacy of a sequential combined treatment with thalidomide and ultraviolet B (UVB) therapy in order to minimize side effects and, thus, making possible a long-term treatment. METHODS: A prospective open trial combining thalidomide as initial therapy followed by narrow-band UVB (TL01) irradiation until complete or almost complete remission of the disease was achieved. RESULTS: An excellent response was obtained after an average of 12 weeks of thalidomide therapy and 32 UVB courses. CONCLUSIONS: Sequential combined therapy with thalidomide and narrow-band UVB therapy could improve the management of prurigo nodularis with minimal side effects, although it should probably be reserved to men and women over 50 years of age.

Administration, Oral↗
PubMed2005

Prurigo nodularis: a review.

Prurigo nodularis is a chronic condition characterized by a papulonodular pruriginous eruption of unknown aetiology. This condition is a difficult disease to treat and causes frustration to both the patient and the treating doctor. A variety of systemic conditions have been reported to be associated with prurigo nodularis. The mechanism by which these disorders may trigger prurigo nodularis is unknown. Nerve growth factor has been implicated in the pathogenesis of prurigo nodularis. Calcitonin gene-related peptide and substance P immunoreactive nerves are markedly increased in prurigo nodularis when compared with normal skin. These neuropeptides may mediate the cutaneous neurogenic inflammation and pruritus in prurigo nodularis. Topical or intralesional glucocorticoids are the treatment of choice. Other topical treatments such as topical vitamin D3, and topical capsaicin have also been reported to be effective. Oral treatments such as cyclosporin and thalidomide have been shown to improve both appearance of the skin and pruritus. We review the clinical features, associations, pathology, pathogenesis and treatment of prurigo nodularis.

Administration, Topical↗
PubMed1993

Mast cells, neutrophils, and eosinophils in prurigo nodularis.

BACKGROUND AND DESIGN: Prurigo nodularis is a disease of unknown cause. To characterize the involvement of mast cells, neutrophils, and eosinophils in lesional tissue, we analyzed seven skin biopsy specimens by an indirect immunofluorescence technique for localization of mast cell tryptase, neutrophil elastase, and eosinophil granule major basic protein, eosinophil cationic protein, and eosinophil-derived neurotoxin. RESULTS: Mast cells were detected in all of the specimens, with prominent numbers of mast cells in three specimens; there was minimal or no extracellular deposition of tryptase in any of the tissues. Neutrophil infiltration was observed in all specimens, but few cells were observed in four; extracellular elastase was minimal or absent in all but one specimen in which prominent dermal elastase deposition was found. Scanty eosinophil infiltration was present in all specimens; however, extracellular deposition of the eosinophil granule proteins including major basic protein, eosinophil-derived neurotoxin, and eosinophil cationic protein was present in all but one specimen and striking deposition of at least one eosinophil granule protein was present in six of the seven specimens. CONCLUSIONS: These studies suggest that mast cell numbers are increased in prurigo nodularis and that eosinophil degranulation as evidenced by striking extracellular deposition of granule proteins is prominent in lesions. In contrast, extracellular deposition of mast cell and neutrophil proteins is absent. The distinctive proteins of the eosinophil granule have potent effects on tissues; the toxicity of these proteins and their deposition in lesional tissue suggest a pathogenic role for the eosinophil in prurigo nodularis.

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↗
PubMed2000

Squamous cell carcinoma complicating prurigo nodularis.

Squamous cell carcinoma complicating ulcerative prurigo nodularis is described in 2 patients who were having prurigo nodularis on dorsum of the feet for duration of many years. Biopsy specimens from the ulcerating nodules showed features of squamous cell carcinoma. This finding has not been previously reported. Squamous cell carcinoma should be considered in the evaluation of long standing ulcerative lesion of prurigo nodularis especially when not responding to conventional therapy.

Biopsy↗
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↗
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↗
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↗
PubMed1989

Patch testing in prurigo nodularis.

32 patients with prurigo nodularis evaluated at the Mayo Clinic from 1975 to 1987 have been patch tested for sensitivity to appropriate allergen series; 25 of these had relevant positive reactions and subsequent follow-up to 5 to 14 years was available for 11. 6 patients had persistent disease and 5 had resolution or marked improvement. 3 of these latter patients noted a strong positive correlation between improvement and avoidance of contact allergens. Screening for contact sensitivity may be helpful in the management of this refractory dermatosis, particularly if there is a coexistent dermatitis.

Adrenal Cortex Hormones↗
PubMed1988

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↗
PubMed2000

The combined occurrence of macular amyloidosis and prurigo nodularis.

The association of prurigo nodularis (PN) and macular amyloidosis (MA) has not been reported before. Although pruritus related frictional trauma is a well-known cause of PN, its role in the development of MA has always been questioned. We herein report two cases with chronic liver disease and iron deficiency who concomitantly developed MA and PN lesions. Pruritus was the preceding factor and both lesions were confined to scratched areas. The association of two otherwise uncommon dermatoses in pruritic patients and their characteristic distribution might indicate an important role for pruritus-induced scratching in the pathogenesis of MA, too.

Amyloid↗