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Expert consensus recommendations to improve diagnosis of ATTR amyloidosis with polyneuropathy
Amyloid transthyretin (ATTR) amyloidosis with polyneuropathy (PN) is a progressive, debilitating, systemic disease wherein transthyretin protein misfolds to form amyloid, which is deposited in the endoneurium. ATTR amyloidosis with PN is the most serious hereditary polyneuropathy of adult onset. It...
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Published in: | Journal of neurology 2021-06, Vol.268 (6), p.2109-2122 |
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container_title | Journal of neurology |
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description | Amyloid transthyretin (ATTR) amyloidosis with polyneuropathy (PN) is a progressive, debilitating, systemic disease wherein transthyretin protein misfolds to form amyloid, which is deposited in the endoneurium. ATTR amyloidosis with PN is the most serious hereditary polyneuropathy of adult onset. It arises from a hereditary mutation in the
TTR
gene and may involve the heart as well as other organs. It is critical to identify and diagnose the disease earlier because treatments are available to help slow the progression of neuropathy. Early diagnosis is complicated, however, because presentation may vary and family history is not always known. Symptoms may be mistakenly attributed to other diseases such as chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), idiopathic axonal polyneuropathy, lumbar spinal stenosis, and, more rarely, diabetic neuropathy and AL amyloidosis. In endemic countries (e.g., Portugal, Japan, Sweden, Brazil), ATTR amyloidosis with PN should be suspected in any patient who has length-dependent small-fiber PN with autonomic dysfunction and a family history of ATTR amyloidosis, unexplained weight loss, heart rhythm disorders, vitreous opacities, or renal abnormalities. In nonendemic countries, the disease may present as idiopathic rapidly progressive sensory motor axonal neuropathy or atypical CIDP with any of the above symptoms or with bilateral carpal tunnel syndrome, gait disorders, or cardiac hypertrophy. Diagnosis should include DNA testing, biopsy, and amyloid typing. Patients should be followed up every 6–12 months, depending on the severity of the disease and response to therapy. This review outlines detailed recommendations to improve the diagnosis of ATTR amyloidosis with PN. |
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TTR
gene and may involve the heart as well as other organs. It is critical to identify and diagnose the disease earlier because treatments are available to help slow the progression of neuropathy. Early diagnosis is complicated, however, because presentation may vary and family history is not always known. Symptoms may be mistakenly attributed to other diseases such as chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), idiopathic axonal polyneuropathy, lumbar spinal stenosis, and, more rarely, diabetic neuropathy and AL amyloidosis. In endemic countries (e.g., Portugal, Japan, Sweden, Brazil), ATTR amyloidosis with PN should be suspected in any patient who has length-dependent small-fiber PN with autonomic dysfunction and a family history of ATTR amyloidosis, unexplained weight loss, heart rhythm disorders, vitreous opacities, or renal abnormalities. In nonendemic countries, the disease may present as idiopathic rapidly progressive sensory motor axonal neuropathy or atypical CIDP with any of the above symptoms or with bilateral carpal tunnel syndrome, gait disorders, or cardiac hypertrophy. Diagnosis should include DNA testing, biopsy, and amyloid typing. Patients should be followed up every 6–12 months, depending on the severity of the disease and response to therapy. This review outlines detailed recommendations to improve the diagnosis of ATTR amyloidosis with PN.</description><identifier>ISSN: 0340-5354</identifier><identifier>ISSN: 1432-1459</identifier><identifier>EISSN: 1432-1459</identifier><identifier>DOI: 10.1007/s00415-019-09688-0</identifier><identifier>PMID: 31907599</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Amyloidosis ; ATTR amyloidosis ; ATTRv ; Autonomic nervous system ; Biopsy ; Carpal tunnel syndrome ; Demyelination ; Diabetes mellitus ; Diabetic neuropathy ; Diagnosis ; Disease ; Family medical history ; Gait ; hATTR ; Hypertrophy ; Inflammation ; Medicine ; Medicine & Public Health ; Neurology ; Neuroradiology ; Neurosciences ; Peripheral neuropathy ; Polyneuropathy ; Protein folding ; Review ; Spinal stenosis ; Transthyretin ; Transthyretin amyloidosis</subject><ispartof>Journal of neurology, 2021-06, Vol.268 (6), p.2109-2122</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c512t-6fe330a626dfdb99fda6f0b51ec8264b6ae971481fa3cf7e634339791935233a3</citedby><cites>FETCH-LOGICAL-c512t-6fe330a626dfdb99fda6f0b51ec8264b6ae971481fa3cf7e634339791935233a3</cites><orcidid>0000-0002-8722-4108</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31907599$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-176103$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Adams, David</creatorcontrib><creatorcontrib>Ando, Yukio</creatorcontrib><creatorcontrib>Beirão, João Melo</creatorcontrib><creatorcontrib>Coelho, Teresa</creatorcontrib><creatorcontrib>Gertz, Morie A.</creatorcontrib><creatorcontrib>Gillmore, Julian D.</creatorcontrib><creatorcontrib>Hawkins, Philip N.</creatorcontrib><creatorcontrib>Lousada, Isabelle</creatorcontrib><creatorcontrib>Suhr, Ole B.</creatorcontrib><creatorcontrib>Merlini, Giampaolo</creatorcontrib><title>Expert consensus recommendations to improve diagnosis of ATTR amyloidosis with polyneuropathy</title><title>Journal of neurology</title><addtitle>J Neurol</addtitle><addtitle>J Neurol</addtitle><description>Amyloid transthyretin (ATTR) amyloidosis with polyneuropathy (PN) is a progressive, debilitating, systemic disease wherein transthyretin protein misfolds to form amyloid, which is deposited in the endoneurium. ATTR amyloidosis with PN is the most serious hereditary polyneuropathy of adult onset. It arises from a hereditary mutation in the
TTR
gene and may involve the heart as well as other organs. It is critical to identify and diagnose the disease earlier because treatments are available to help slow the progression of neuropathy. Early diagnosis is complicated, however, because presentation may vary and family history is not always known. Symptoms may be mistakenly attributed to other diseases such as chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), idiopathic axonal polyneuropathy, lumbar spinal stenosis, and, more rarely, diabetic neuropathy and AL amyloidosis. In endemic countries (e.g., Portugal, Japan, Sweden, Brazil), ATTR amyloidosis with PN should be suspected in any patient who has length-dependent small-fiber PN with autonomic dysfunction and a family history of ATTR amyloidosis, unexplained weight loss, heart rhythm disorders, vitreous opacities, or renal abnormalities. In nonendemic countries, the disease may present as idiopathic rapidly progressive sensory motor axonal neuropathy or atypical CIDP with any of the above symptoms or with bilateral carpal tunnel syndrome, gait disorders, or cardiac hypertrophy. Diagnosis should include DNA testing, biopsy, and amyloid typing. Patients should be followed up every 6–12 months, depending on the severity of the disease and response to therapy. This review outlines detailed recommendations to improve the diagnosis of ATTR amyloidosis with PN.</description><subject>Amyloidosis</subject><subject>ATTR amyloidosis</subject><subject>ATTRv</subject><subject>Autonomic nervous system</subject><subject>Biopsy</subject><subject>Carpal tunnel syndrome</subject><subject>Demyelination</subject><subject>Diabetes mellitus</subject><subject>Diabetic neuropathy</subject><subject>Diagnosis</subject><subject>Disease</subject><subject>Family medical history</subject><subject>Gait</subject><subject>hATTR</subject><subject>Hypertrophy</subject><subject>Inflammation</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Neurology</subject><subject>Neuroradiology</subject><subject>Neurosciences</subject><subject>Peripheral neuropathy</subject><subject>Polyneuropathy</subject><subject>Protein folding</subject><subject>Review</subject><subject>Spinal stenosis</subject><subject>Transthyretin</subject><subject>Transthyretin amyloidosis</subject><issn>0340-5354</issn><issn>1432-1459</issn><issn>1432-1459</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNp9kU9v1DAQxS0EokvhC3BAkbhwCcz4X-IL0qotUKkSUrVwQ5Y3cXZdJXawk5b99pju0lIOPVma-b3nmXmEvEZ4jwDVhwTAUZSAqgQl67qEJ2SBnNESuVBPyQIYh1IwwY_Ii5SuAKDOjefkiKGCSii1ID_Ofo02TkUTfLI-zamItgnDYH1rJpeLxRQKN4wxXNuidWbjQ3KpCF2xXK0uCzPs-uDa29qNm7bFGPqdt3MMo5m2u5fkWWf6ZF8d3mPy7dPZ6uRLefH18_nJ8qJsBNKplJ1lDIyksu3atVJda2QHa4G2qanka2msqpDX2BnWdJWVjDOmKoWKCcqYYcek3PumGzvOaz1GN5i408E4feq-L3WIGz0Ps8ZKIrDMf9zzGR5s21g_RdM_kD3seLfVm3Cta6yUQpoN3h0MYvg52zTpwaXG9r3xNsxJ56k4xQqwzujb_9CrMEefz6GpYBUqQaXKFN1TTQwpRdvdDYOg_6St92nrnLa-TVtDFr35d407yd94M8AOd8ktv7Hx_u9HbH8DaUa3wg</recordid><startdate>20210601</startdate><enddate>20210601</enddate><creator>Adams, David</creator><creator>Ando, Yukio</creator><creator>Beirão, João Melo</creator><creator>Coelho, Teresa</creator><creator>Gertz, Morie A.</creator><creator>Gillmore, Julian D.</creator><creator>Hawkins, Philip N.</creator><creator>Lousada, Isabelle</creator><creator>Suhr, Ole B.</creator><creator>Merlini, Giampaolo</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>ADHXS</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>D8T</scope><scope>D93</scope><scope>ZZAVC</scope><orcidid>https://orcid.org/0000-0002-8722-4108</orcidid></search><sort><creationdate>20210601</creationdate><title>Expert consensus recommendations to improve diagnosis of ATTR amyloidosis with polyneuropathy</title><author>Adams, David ; Ando, Yukio ; Beirão, João Melo ; Coelho, Teresa ; Gertz, Morie A. ; Gillmore, Julian D. ; Hawkins, Philip N. ; Lousada, Isabelle ; Suhr, Ole B. ; Merlini, Giampaolo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c512t-6fe330a626dfdb99fda6f0b51ec8264b6ae971481fa3cf7e634339791935233a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Amyloidosis</topic><topic>ATTR amyloidosis</topic><topic>ATTRv</topic><topic>Autonomic nervous system</topic><topic>Biopsy</topic><topic>Carpal tunnel syndrome</topic><topic>Demyelination</topic><topic>Diabetes mellitus</topic><topic>Diabetic neuropathy</topic><topic>Diagnosis</topic><topic>Disease</topic><topic>Family medical history</topic><topic>Gait</topic><topic>hATTR</topic><topic>Hypertrophy</topic><topic>Inflammation</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Neurology</topic><topic>Neuroradiology</topic><topic>Neurosciences</topic><topic>Peripheral neuropathy</topic><topic>Polyneuropathy</topic><topic>Protein folding</topic><topic>Review</topic><topic>Spinal stenosis</topic><topic>Transthyretin</topic><topic>Transthyretin amyloidosis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Adams, David</creatorcontrib><creatorcontrib>Ando, Yukio</creatorcontrib><creatorcontrib>Beirão, João Melo</creatorcontrib><creatorcontrib>Coelho, Teresa</creatorcontrib><creatorcontrib>Gertz, Morie A.</creatorcontrib><creatorcontrib>Gillmore, Julian D.</creatorcontrib><creatorcontrib>Hawkins, Philip N.</creatorcontrib><creatorcontrib>Lousada, Isabelle</creatorcontrib><creatorcontrib>Suhr, Ole B.</creatorcontrib><creatorcontrib>Merlini, Giampaolo</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>SWEPUB Umeå universitet full text</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SWEPUB Umeå universitet</collection><collection>SwePub Articles full text</collection><jtitle>Journal of neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Adams, David</au><au>Ando, Yukio</au><au>Beirão, João Melo</au><au>Coelho, Teresa</au><au>Gertz, Morie A.</au><au>Gillmore, Julian D.</au><au>Hawkins, Philip N.</au><au>Lousada, Isabelle</au><au>Suhr, Ole B.</au><au>Merlini, Giampaolo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expert consensus recommendations to improve diagnosis of ATTR amyloidosis with polyneuropathy</atitle><jtitle>Journal of neurology</jtitle><stitle>J Neurol</stitle><addtitle>J Neurol</addtitle><date>2021-06-01</date><risdate>2021</risdate><volume>268</volume><issue>6</issue><spage>2109</spage><epage>2122</epage><pages>2109-2122</pages><issn>0340-5354</issn><issn>1432-1459</issn><eissn>1432-1459</eissn><abstract>Amyloid transthyretin (ATTR) amyloidosis with polyneuropathy (PN) is a progressive, debilitating, systemic disease wherein transthyretin protein misfolds to form amyloid, which is deposited in the endoneurium. ATTR amyloidosis with PN is the most serious hereditary polyneuropathy of adult onset. It arises from a hereditary mutation in the
TTR
gene and may involve the heart as well as other organs. It is critical to identify and diagnose the disease earlier because treatments are available to help slow the progression of neuropathy. Early diagnosis is complicated, however, because presentation may vary and family history is not always known. Symptoms may be mistakenly attributed to other diseases such as chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), idiopathic axonal polyneuropathy, lumbar spinal stenosis, and, more rarely, diabetic neuropathy and AL amyloidosis. In endemic countries (e.g., Portugal, Japan, Sweden, Brazil), ATTR amyloidosis with PN should be suspected in any patient who has length-dependent small-fiber PN with autonomic dysfunction and a family history of ATTR amyloidosis, unexplained weight loss, heart rhythm disorders, vitreous opacities, or renal abnormalities. In nonendemic countries, the disease may present as idiopathic rapidly progressive sensory motor axonal neuropathy or atypical CIDP with any of the above symptoms or with bilateral carpal tunnel syndrome, gait disorders, or cardiac hypertrophy. Diagnosis should include DNA testing, biopsy, and amyloid typing. Patients should be followed up every 6–12 months, depending on the severity of the disease and response to therapy. This review outlines detailed recommendations to improve the diagnosis of ATTR amyloidosis with PN.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>31907599</pmid><doi>10.1007/s00415-019-09688-0</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-8722-4108</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Amyloidosis ATTR amyloidosis ATTRv Autonomic nervous system Biopsy Carpal tunnel syndrome Demyelination Diabetes mellitus Diabetic neuropathy Diagnosis Disease Family medical history Gait hATTR Hypertrophy Inflammation Medicine Medicine & Public Health Neurology Neuroradiology Neurosciences Peripheral neuropathy Polyneuropathy Protein folding Review Spinal stenosis Transthyretin Transthyretin amyloidosis |
title | Expert consensus recommendations to improve diagnosis of ATTR amyloidosis with polyneuropathy |
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