Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033774 (pruritus)
 14,546 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pigmented purpuric dermatosis (PPD) is a chronic disorder of unknown etiology. It is quite common, and no therapy is significantly effective. Calcium dobesilate (Cd) has been tried successfully in many vascular disorders. The aim of this study was to evaluate the usefulness and efficacy of Cd in PPD. Nine male patients (7 with Schamberg's and 1 each with lichenoid dermatosis of Gougerot and Blum and lichen aureus) were given Cd 500 mg twice daily for two initial weeks and then 500 mg once daily for a total period of three months. All the patients were followed up for one year after cessation of therapy. The improvement was moderate in 11.11% and mild in 66.67% of cases; 22.22% did not show any improvement. New lesions stopped appearing in two weeks in all patients, and itching also improved in symptomatic cases without any significant side effects. Based upon the results of this pilot study we recommend Cd as the first line therapy for PPD.
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PMID:Calcium dobesilate (Cd) in pigmented purpuric dermatosis (PPD): a pilot evaluation. 1516 Aug 62

We hereby report a case of lichen amyloidosus in a 69-year-old man unresponsive to various treatments. The patient was treated by occlusion with hydrocolloid dressings. Considerable subjective and objective improvement was observed with respect to the pruritus and cosmetic appearance. We suggest this convenient and efficacious treatment as first line therapy.
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PMID:Lichen amyloidosus treated by hydrocolloid dressings. 1548 97

A 36-year-old man presented with a linear erythematous eruption along his right forearm and dystrophy of his right thumbnail. These changes had developed 2 weeks after his right thumb had been pricked by a pineapple leaf and evolved over a 6-week period. Histopathology revealed features consistent with lichen striatus. He complained of mild intermittent pruritus, which responded to moderate-potency topical corticosteroids. At 12 months the skin eruption had improved, but the nail changes persisted.
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PMID:Lichen striatus in an adult following trauma. 1567 Jan 74

Lichen amyloidosis (LA) is a chronic, pruritic skin disorder characterized by brownish-grey papules on extensor surfaces of legs and rarely on the trunk. Thioflavin T-positive amyloid deposits are found in the papillary dermis of affected skin, which is the only organ involved. A variety of therapeutic regimens for lichen amyloidosis have been described; however, in many cases with only limited effect. We report on two patients with lichen amyloidosis with typical clinical symptoms not responding to local treatment. A combined regimen with bath psoralen ultraviolet A (PUVA) and oral acitretin was initiated, resulting in nearly complete resolution of the papules and impressive relief from the severe pruritus. The beneficial response has persisted for 8 months. The suggested combined therapy with bath PUVA photochemotherapy and oral acitretin represents an efficacious and practical treatment modality for lichen amyloidosis with long-lasting effects.
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PMID:Successful treatment of lichen amyloidosis with combined bath PUVA photochemotherapy and oral acitretin. 1700 89

Twenty-seven patients with chronic lichen simplex involving various parts of the body were treated. Hydrocotyle was prescribed to 21 patients in different potencies (6c, 30c, 200c, 1 M, 10 M), Thuja to three patients (1 M, 10 M), Graphites (6c), Kali bich (30c) and Sulphur (200c) to one patient each during 1 year study period. Only two patients showed complete improvement with Thuja and one with Graphites. In other cases, the response was limited to partial relief of [corrected] itching.
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PMID:Homoeopathy for the treatment of lichen simplex chronicus: a case series. 1701 96

Dystrophic epidermolysis bullosa is a rare and clinically heterogeneous mechanobullous disorder. One unusual clinical variant is epidermolysis bullosa pruriginosa (EBP), in which the combination of pruritus and skin fragility can lead to hypertrophic, lichenified nodules and plaques. This form of inherited epidermolysis bullosa may not develop clinically until adult life, leading to diagnostic confusion with acquired disorders, such as nodular prurigo, lichen simplex, lichen planus, hypertrophic scarring, or dermatitis artefacta. As in all other forms of dystrophic epidermolysis bullosa, the molecular pathology involves mutations in the gene encoding the anchoring fibril protein, type VII collagen (COL7A1), but there is no clear genotype-phenotype correlation in EBP. In this report, we describe a Chinese-Singaporean family with EBP in whom an autosomal dominant glycine substitution mutation, p.G2251E, was identified in exon 86 of the COL7A1 gene. This heterozygous mutation was identified in the genomic DNA of all 4 affected adults tested, as well as 2 clinically unaffected offspring (aged 9-29 years). Based on DNA sequencing, we predict that these individuals may develop EBP later in life, although additional factors leading to disease expression may determine phenotypic expression. Nevertheless, we plan to closely monitor these potentially presymptomatic individuals for symptoms of pruritus and early signs of the genetic disorder.
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PMID:Clinical and molecular dilemmas in the diagnosis of familial epidermolysis bullosa pruriginosa. 1743 45

We present two cases of lichen amyloidosus treated with retinoids. A 57-year-old Vietnamese woman has had extensive generalized recalcitrant lichen amyloidosus for 23 years. Treatment with oral etretinate (25 mg/day) for 3 years, and later oral acitretin (10 mg/day) for the past 10 years, has controlled the pruritus and flattened the hyperkeratotic papules. Whenever the acitretin was ceased her symptoms flared within weeks. On each occasion reintroduction of acitretin was effective within 1-2 months. The second case is that of a 51-year-old Australian Aboriginal woman who had a 2-year history of lichen amyloidosus affecting her lower legs. A 2-month course of oral acitretin (25 mg b.d.) produced a marked improvement in both the pruritus and hyperkeratotic papules. She was then lost to follow up for 2 years, during which time her symptoms recurred.
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PMID:Acitretin for lichen amyloidosus. 1841 14

A 34-year-old woman presented with large, scaly patches of alopecia with a peripheral rim of violaceous, folliculocentric papules and appreciable pruritus of one-year duration. Histopathologic examination showed changes consistent with lichen planopilaris and psoriasis, which was suggested by neutrophilic spongiosis. Consequently, cyclosporine and betamethasone valerate topical 0.12 percent foam twice daily were initiated. A short time after, there was clinical reduction of perifollicular erythema and attenuation of pruritus. However, there was no decrease of scale. Although LLP is classified in the lymphocytic group of cicatricial alopecias, this case demonstrates a clinical and histopathologic overlap with a psoriasiform dermatosis which may represent a collision of two diseases.
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PMID:Lichen planopilaris and psoriasis. 1906 3

Macular and lichen amyloidosis are common variants of primary localized cutaneous amyloidosis (PLCA) in which clinical features of pruritus and skin scratching are associated with histological findings of deposits of amyloid staining on keratinous debris in the papillary dermis. Most cases are sporadic, but an autosomal dominant family history may be present in up to 10% of cases, consistent with a genetic predisposition in some individuals. Familial PLCA has been mapped to a locus on 5p13.1-q11.2 and in 2008 pathogenic heterozygous missense mutations were identified in the OSMR gene, which encodes oncostatin M receptor beta (OSMRbeta), an interleukin (IL)-6 family cytokine receptor. OSMRbeta is expressed in various cell types, including keratinocytes, cutaneous nerves and nociceptive neurones in dorsal root ganglia; its ligands are oncostatin M and IL-31. All pathogenic mutations are clustered in the fibronectin-III repeat domains of the extracellular part of OSMRbeta, sites that are critical for receptor dimerization (with either gp130 or IL-31RA), and lead to defective signalling through Janus kinase-signal transducers and activators of transcription, extracellular signal-regulated protein kinase 1/2 and phosphoinositide 3 kinase/Akt pathways. Elucidating the molecular pathology of familial PLCA provides new insight into mechanisms of pruritus in human skin, findings that may have relevance to developing novel treatments for skin itching. This review provides a clinicopathological and molecular update on familial PLCA.
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PMID:New insight into mechanisms of pruritus from molecular studies on familial primary localized cutaneous amyloidosis. 1966 69

UVB 311 nm phototherapy (NUVB) is used successfully in the treatment of psoriasis or atopic dermatitis and is often chosen as "first-line" therapy. In a prospective study we investigated the efficacy of the targeted UVB 308 phototherapy by excimer laser in the treatment of 57 patients with localized, mild therapy-resistant atopic dermatitis. We achieved a complete remission (CR) in nearly 85% and a partial remission (PR) in 15% after 10 treatments during 6-8 weeks in all patients. A mean reduction in patient-reported pruritus was one hallmark after 3-4 treatments. 48 other patients with lichen simplex chronicus Vidal, nodular prurigo, granuloma anulare, alopezia areata (AA) and lichen ruber planus were also treated by targeted NUVB. We found higher rates of CR and PR only in patients with AA and in patients with oral Lichen ruber mucosae. These results and the systematically reviewing of the current medical literature shows that targeted NUVB by excimer laser cannot be successfully transferred for all inflammatory skin diseases. In particular, Excimer UVB treatment expands the therapeutic options in patients with localized and therapy-resistant atopic dermatitis enormously.
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PMID:[Targeted UVB-308 nm (NUVB) therapy with excimer laser in the treatment of atopic dermatitis and other inflammatory dermatoses]. 1971 Oct 24


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