Generalized lichen amyloidosis associated with chronic lichen planus

Hongcharu, Wichai; Baldassano, Marisa; González, Ernesto Rafael

doi:10.1016/s0190-9622(00)70289-1

Cited by 8 publications

(11 citation statements)

References 7 publications

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“…Several inflammatory dermatoses and systemic disorders have been reported in association with PLCA, both familial and sporadic. Most associations are probably coincidental and based on anecdotal reports, such as PLCA occurring with ankylosing spondylitis and autoimmune thyroiditis, 20 chronic lichen planus, 21 coeliac disease, 22 chronic urticaria, 23 or angiolymphoid hyperplasia with eosinophilia 24 . Other associations may have a more direct relevance to the aetiology of PLCA such as repeated skin friction, 25,26 notalgia paraesthetica 27 or textile contact dermatitis 28 .…”

Section: Conditions Associated With Primary Localized Cutaneous Amylomentioning

confidence: 99%

New insight into mechanisms of pruritus from molecular studies on familial primary localized cutaneous amyloidosis

Tanaka

Arita

Lai-Cheong

et al. 2009

British Journal of Dermatology

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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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Section: Conditions Associated With Primary Localized Cutaneous Amylomentioning

confidence: 99%

New insight into mechanisms of pruritus from molecular studies on familial primary localized cutaneous amyloidosis

Tanaka

Arita

Lai-Cheong

et al. 2009

British Journal of Dermatology

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“…It is rare in the West, but is a relatively common skin disorder in Southern Asia, China, Thailand, and some South American countries 9–11 . The association of LA with human immunodeficiency virus infection, multiple endocrine neoplasia type 2A (Sipple syndrome), atopic dermatitis, lichen planus, mycosis fungoides, thyroiditis, and ankylosing spondilitis has been reported 3–5,7,12 . No other cutaneous or systemic diseases were observed in our patient.…”

Section: Discussionmentioning

confidence: 50%

“…Our patient responded well to topical steroid therapy and antihistamines. Generalized LA is rarely seen in the literature 5,6 …”

Section: Discussionmentioning

confidence: 97%

“…Lichen amyloidosis is a common clinical problem characterized by a persistent, pruritic eruption of multiple discrete hyperkeratotic and hyperpigmented papules, which often coalesce to form plaques, frequently distributed over the shins and extensor aspect of the arms 4 . Widespread involvement is rarely reported 5,6 . Lichen amyloidosis may occur in individuals of all ages 7 .…”

Section: Discussionmentioning

confidence: 99%

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Case of generalized lichen amyloidosis

et al. 2003

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A 23‐year‐old white female patient presented with a 3‐year history of a pruritic rash on the trunk, extensor surfaces of the extremities, back, abdomen, and the glutea. There was no family history of any similar dermatological disease. Dermatological examination revealed generalized rough, mildly keratotic, symmetrical dome‐shaped papules, involving dorsal and extensor surfaces of both the lower and upper extremities, abdomen, back and the glutea (Fig. 1). Physical examination was normal. 1 Dome‐shaped, lichenified papules, 4–5 mm in diameter, on the right lower extremity

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“…Amyloid deposition has only been rarely reported in association with one of the most common forms of interface dermatitis, namely lichen planus. 11 Similarly, amyloid deposition has been documented as an exceptional finding in the context of dermatomyositis or keratosis lichenoides chronica. 12,13 Based upon such reports and also the case reported here, it seems clear that inflammation focused on the epidermal-dermal junction plays a key role in the etiopathogenesis of keratinocytederived amyloidosis.…”

mentioning

confidence: 98%