Coeliac disease with primary cutaneous amyloidosis

Presbury, D. G. C.; Griffiths, W.A.D.

doi:10.1111/j.1365-2133.1975.tb03042.x

Cited by 6 publications

(4 citation statements)

References 9 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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“…17 Furthermore, there is only 1 report of celiac disease and primary cutaneous amyloidosis. 18 To our knowledge, this is the first case of coexistence of celiac disease, primary Sjögren syndrome, and secondary cutaneous amyloidosis. Although secondary AA amyloidosis is a wellknown complication in specific autoimmune diseases (such as rheumatoid arthritis, juvenile chronic arthritis, ankylosing spondylitis, psoriatic arthritis, Crohn disease) it is extremely unusual in others (such as systemic lupus erythematosus, Sjögren syndrome).…”

Section: Discussionmentioning

confidence: 90%

Secondary Cutaneous Nodular AA Amyloidosis in a Patient With Primary Sjögren Syndrome and Celiac Disease

Katsikas¹,

Maragou²,

Rontogianni³

et al. 2008

JCR: Journal of Clinical Rheumatology

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We describe a 62-year-old female with primary Sjögren syndrome and myopathy, severe osteoporosis, and vertebral fractures that were attributed to celiac disease. A year after the diagnosis, she developed a skin nodule on the extensor surface of her right elbow, which was due to an amyloid deposit of AA type. Amyloidosis, although relatively common in some chronic inflammatory diseases, has been uncommon in Sjögren syndrome or celiac disease. Visceral amyloid was not found in this patient.

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“…The underlying etiologies of secondary amyloidosis include chronic inflammatory arthritis, periodic fever syndromes, inflammatory bowel disease, neoplasms, and infections. 16 - 18 Autoimmune disorders were ruled out by negative serology; he was evaluated for liver disease and underwent CT chest and abdomen imaging to rule out possible infective foci or malignancies. The serological evidence of celiac disease, i.e., serum anti-TTG positivity in our case, favored the likelihood of celiac disease in the presence of villous atrophy and inflammatory changes in duodenal biopsy.…”

Section: Discussionmentioning

confidence: 99%

“…Isolated cases of cutaneous amyloidosis, both primary and secondary, have been reported to be associated with celiac disease. 18 , 19 However, there is only one other case reported in the literature about the association between celiac and systemic secondary amyloidosis. 20 To our knowledge, our case is only the second reported of its kind, and it underscores the importance of considering celiac disease as a possible etiology of secondary renal amyloidosis.…”

Section: Discussionmentioning

confidence: 99%

Celiac Disease and Secondary Amyloidosis: A Possible Causal Association?

Chhoda

Jain

Daga

et al. 2018

ACG Case Reports Journal

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We report a rare case of secondary renal amyloidosis in a patient with probable celiac disease presenting as nephrotic syndrome. A 30-year-old man with chronic diarrhea presented with progressive anasarca for 2 years. On further evaluation, he had hypoalbuminemia, significant nephrotic-range proteinuria, and elevated levels of anti-tissue transglutaminase. Renal biopsy suggested deposition of amorphous Congo red–positive material in the glomerular mesangium, positive for amyloid A amyloidosis. Endoscopic duodenal biopsy suggested blunting of the villous architecture and chronic inflammation of the lamina propria. The patient subsequently developed massive pulmonary embolism and died due to refractory cardiogenic shock.

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Coeliac disease with primary cutaneous amyloidosis

Abstract: SUMMARY A case is described where the patient suffered from coeliac disease, and a widespread eczema which was succeeded by lichen amyloidosus.

Cited by 6 publications

References 9 publications

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

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

Secondary Cutaneous Nodular AA Amyloidosis in a Patient With Primary Sjögren Syndrome and Celiac Disease

Celiac Disease and Secondary Amyloidosis: A Possible Causal Association?

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