Forma comum de amiloidose sistêmica caracterizada pela deposição de transtirretina, do tipo selvagem, predominantemente no coração e nos tecidos moles (principalmente na região do túnel do carpo, canal lombar e tendões).
Introdução
O que você precisa saber de cara
Visão geral
A Amiloidose ATTR tipo selvagem (do inglês wild type ATTR amyloidosis, categorizada sob o código CID-10 E85.8 e identificador MONDO:0018018) é uma condição clínica com prevalência estimada entre 1 e 5 casos a cada 10.000 pessoas. Trata-se de uma patologia cujo início das manifestações costuma ocorrer em indivíduos adultos ou idosos.[1][2]
Sinais e sintomas
O quadro clínico envolve com frequência amiloidose cardíaca por transtirretina, cardiomiopatia hipertrófica, insuficiência cardíaca congestiva, bradicardia, eletrocardiograma anormal, estenose da valva aórtica, infarto do miocárdio, edema pedal, edema pulmonar e derrame pleural.[1][2]
Manifestações neurológicas e do sistema nervoso periférico ou autônomo abrangem neuropatia sensorial, neuropatia mediana constritiva, estenose do canal espinhal, reflexos do tornozelo diminuídos ou ausentes, fisiologia anormal do sistema nervoso autônomo, hipotensão ortostática devido a disfunção autonômica e disfunção autonômica da bexiga.[1][2]
Outros sinais e sintomas descritos incluem dismotilidade gastrointestinal, diarreia crônica, incontinência intestinal, insuficiência renal, síndrome nefrótica, hepatomegalia, concentração elevada de fosfatase alcalina circulante e perda de peso.[1][2]
Causas genéticas
Diagnóstico
Tratamento e manejo
No Sistema Único de Saúde (SUS), o medicamento Tafamidis cápsula 61 mg é dispensado para o tratamento de Amiloidoses Associadas à Transtirretina, conforme estabelecido pelo protocolo clínico correspondente na Portaria Conjunta SAES-SECTICS/MS nº 12, com data de 24 de julho de 2025. Consta ainda a existência de 1 ensaio clínico ativo para a condição.[4]
Conteúdo informativo gerado e mantido automaticamente a partir de fontes oficiais (Orphanet, HPO, OMIM, SUS). Não substitui avaliação médica.
A **amiloidose ATTR tipo selvagem** é uma doença que surge na idade adulta ou avançada quando uma proteína normal chamada transtirretina começa a se acumular em órgãos vitais, principalmente no coração. Os sintomas mais frequentes costumam ser o inchaço nas pernas, falta de ar, batimentos irregulares no coração e formigamento ou dormência nas mãos. Diferente de outras formas da doença, ela não tem herança genética transmitida de pais para filhos e não decorre de mutações no gene. No Brasil, o Sistema Único de Saúde (SUS) disponibiliza o medicamento **Tafamidis cápsula 61 mg** por meio do protocolo clínico vigente.
Forma comum de amiloidose sistêmica caracterizada pela deposição de transtirretina, do tipo selvagem, predominantemente no coração e nos tecidos moles (principalmente na região do túnel do carpo, canal lombar e tendões).
Tem tratamento?
Escala de raridade
<1/50kMuito rara
1/20kRara
1/10kPouco freq.
1/5kIncomum
1/2k
Encontrou um erro ou informação desatualizada? Sugira uma correção →
Entender a doença
Do básico ao detalhe, leia no seu ritmo
Preparando trilha educativa...
Sinais e sintomas
O que aparece no corpo e com que frequência cada sintoma acontece
Partes do corpo afetadas
+ 8 sintomas em outras categorias
Características mais comuns
Os sintomas variam de pessoa para pessoa. Abaixo estão as 32 características clínicas mais associadas, ordenadas por frequência.
Linha do tempo da pesquisa
Encontrou um erro ou informação desatualizada? Sugira uma correção →
Genética e causas
O que está alterado no DNA e como passa nas famílias
Nenhum gene associado encontrado
Os dados genéticos desta condição ainda estão sendo catalogados.
Diagnóstico
Os sinais que médicos procuram e os exames que confirmam
Tratamento e manejo
Remédios, cuidados de apoio e o que precisa acompanhar
Onde tratar no SUS
Hospitais de referência no Brasil e o protocolo oficial do SUS (PCDT)
🇧🇷 Atendimento SUS — Amiloidose ATTR tipo selvagem
Selecione um estado ou use sua localização para ver resultados.
Dados de DATASUS/CNES, SBGM, ABNeuro e Ministério da Saúde. Sempre confirme a disponibilidade diretamente com o estabelecimento.
Pesquisa ativa
Ensaios clínicos abertos e novidades científicas recentes
Ensaios em destaque
Com ensaio aberto em 1 país. O ponto verde marca onde há vaga agora.
🟢 Recrutando agora
1 pesquisa recrutando participantes. Converse com seu médico sobre a possibilidade de participar.
Outros ensaios clínicos
5 ensaios clínicos encontrados, 1 ativos.
Publicações mais relevantes
Pittsburgh compound B positron emission tomography detects cardiomyopathy in hereditary transthyretin amyloidosis patients with negative bone scintigraphy: a pilot study.
To evaluate the effectiveness of positron emission tomography (PET) with [11C]-Pittsburgh Compound-B ([11C]PiB) for detecting transthyretin amyloid (ATTR) cardiomyopathy in patients with transthyretin gene (TTR) variants associated with reduced bone scintigraphy sensitivity, and its ability to detect brain involvement in hereditary transthyretin amyloidosis. This prospective case series included four hereditary ATTR amyloidosis patients with TTR variants associated with reduced bone scintigraphy sensitivity, and two patients with positive bone scintigraphy (one hereditary ATTR and one wild-type ATTR amyloidosis patient). All patients underwent diagnostic work-up at the Groningen Amyloidosis Centre of Expertise between April 2024 and March 2025, including [11C]PiB PET/CT. Cardiac and brain [11C]PiB uptake were assessed visually. Target-to-background ratios (TBRs) and cortical SUV ratios were calculated. TBR ≥1.09 was considered positive for ATTR cardiomyopathy and SUV ratios ≥0.7 was considered positive for brain involvement. Cardiac [11C]PiB uptake was observed in three of four hereditary ATTR amyloidosis patients despite negative bone scintigraphy. In one of four patients, there was visually equivocal radiotracer uptake, but elevated TBRs did indicate ATTR cardiomyopathy. Conversely, both hereditary ATTR and wild-type ATTR amyloidosis patients with a positive bone scintigraphy had negative or inconclusive [11C]PiB PET results. Brain uptake was observed in two asymptomatic patients, while no uptake was seen in two patients with suspected brain involvement. [11C]PiB PET could be an effective tool for detecting ATTR cardiomyopathy in patients with TTR variants associated with reduced bone scintigraphy sensitivity. However, its utility for detecting brain involvement in symptomatic hereditary ATTR patients remains uncertain.
Progression of QRS duration - a potential surrogate marker of survival in ATTRwt amyloidosis patients.
In wild-type transthyretin amyloidosis (ATTRwt), the deposition of transthyretin in the myocardium leads to progressive heart failure. However, little is known about the short-term natural progression of this disease and potential predictors of outcome. Therefore, this study longitudinally analyzed the clinical findings (ECG, echocardiography, and laboratory tests) of 65 patients suffering from ATTRwt at baseline and at follow-up visits after 12 months. In total, 44 patients (67.7%) presented with abnormal ECGs, prolonged PR and QRS durations and low-voltage patterns. Pacemaker placement was performed in eleven patients (16.9%). At the one-year follow-up visit, we detected significant increases in the QRS duration (from 119.7 ± 4.0 to 125.9 ± 4.3 ms; p < 0.05), intraventricular septum thickness (from 18.9 ± 0.5 mm to 19.9 ± 0.5 mm; p < 0.05) and ejection fraction (EF) (from 45.4 ± 2.1% to 38.9 ± 2.6%; p < 0.05) compared with those at the baseline visit. During follow-up, 16 patients (24.6%) died. Predictors of worse outcomes were progression in QRS duration, low EF, reduced renal function, impaired right ventricular function and the need for pacemaker implantation. In ATTRwt, precise evaluation via routine cardiac diagnosis helps to identify patients with an elevated risk of mortality. Patients with prolonged QRS duration, progressive myocardial hypertrophy, right ventricular failure, reduced renal function and the need for cardiac pacemakers are at increased risk for one-year mortality. The online version contains supplementary material available at 10.1186/s13023-025-04078-4.
Neurological Examinations of Patients Initially Diagnosed With Wild-Type Transthyretin Amyloidosis (wtATTR).
Relevance of wild-type ATTR amyloidosis (wtATTR) is increasing, due to improved therapeutic and diagnostic options. Despite the significant prevalence of neurological manifestations, there remains low awareness towards the disease, resulting in delayed diagnoses and treatment commencements. Systematic clinical and neurophysiological characterisations of large neurological collectives are lacking, as well as examination of correlations between neurological and cardiological involvement. 75 patients with confirmed initial diagnosis of wtATTR amyloidosis underwent standardised clinical and extended neurophysiological examination (quantitative sensory testing, nerve conduction studies, sympathetic skin response, autonomic testing). Furthermore, cardiac involvement was quantified using laboratory and clinical scores, as well as cardiac tracer uptake in scintigraphy. 84% of the patients suffered from carpal tunnel syndrome (CTS), 62% with bilateral involvement. Neuropathy was present in 71%; one third showed spinal stenosis. CTS operation was performed a median of 10 years before diagnosis. Clinically, the absence of Achilles reflexes and impaired pallesthesia were particularly impressive. No correlation was found between the severity of neurological symptoms and cardiological or scintigraphic parameters. We were able to perform a precise clinical and neurophysiological characterisation in a large cohort of patients. We detected a predominant peripheral neuropathy pattern in a large majority of patients. However, the extent of neurological damage did not correlate with cardiac involvement. The findings may contribute to enhanced awareness among neurologists, potentially leading to earlier diagnosis and initiation of treatment.
High Sensitivity Troponin for Contemporary Risk Stratification in Wild-Type ATTR Amyloidosis.
Beyond hypertrophy: unmasking sarcomeric hypertrophic cardiomyopathy in a patient with wild-type ATTR amyloidosis.
Publicações recentes
Pittsburgh compound B positron emission tomography detects cardiomyopathy in hereditary transthyretin amyloidosis patients with negative bone scintigraphy: a pilot study.
Sodium-glucose cotransporter 2 inhibitors for wild-type transthyretin amyloidosis: Insights from a global database.
The FLC Ratio Reframed: Averting Unnecessary Heart Biopsies in Wild-Type ATTR Amyloidosis.
Progression of QRS duration - a potential surrogate marker of survival in ATTRwt amyloidosis patients.
Neurological Examinations of Patients Initially Diagnosed With Wild-Type Transthyretin Amyloidosis (wtATTR).
📚 EuropePMC11 artigos no totalmostrando 35
Pittsburgh compound B positron emission tomography detects cardiomyopathy in hereditary transthyretin amyloidosis patients with negative bone scintigraphy: a pilot study.
Frontiers in nuclear medicineSodium-glucose cotransporter 2 inhibitors for wild-type transthyretin amyloidosis: Insights from a global database.
American heart journal plus : cardiology research and practiceThe FLC Ratio Reframed: Averting Unnecessary Heart Biopsies in Wild-Type ATTR Amyloidosis.
JACC. CardioOncologyProgression of QRS duration - a potential surrogate marker of survival in ATTRwt amyloidosis patients.
Orphanet journal of rare diseasesNeurological Examinations of Patients Initially Diagnosed With Wild-Type Transthyretin Amyloidosis (wtATTR).
European journal of neurologyHigh Sensitivity Troponin for Contemporary Risk Stratification in Wild-Type ATTR Amyloidosis.
Circulation. Heart failureThe Relationship between Carpal Tunnel Syndrome and Wild-Type ATTR Amyloidosis.
The journal of hand surgery Asian-Pacific volumeA Challenging Case of Wild-Type Transthyretin Amyloidosis (ATTR) Amyloidosis Treated With Cardiac Resynchronization Therapy.
CureusUnusual hypertrophic cardiomyopathy: case report of an early onset wild-type ATTR amyloidosis accompanied by a chromosomal duplication involving the MYH6 and MYH7 gene.
Frontiers in cardiovascular medicineBeyond hypertrophy: unmasking sarcomeric hypertrophic cardiomyopathy in a patient with wild-type ATTR amyloidosis.
European heart journal. Cardiovascular ImagingTransthyretin Cardiac Amyloidosis in an Elderly Male With Heart Failure Intolerant to Guideline-Directed Medical Therapy.
CureusWild-Type Transthyretin Amyloidosis: A Prevalent and Underdiagnosed Cause of Heart Failure With Preserved Ejection Fraction.
CureusClinical clues for suspecting wild-type transthyretin cardiac amyloidosis in patients with monoclonal gammopathy of undetermined significance: a case report.
The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of CardiologyAdvancing Transthyretin Amyloidosis Drug Development in an Evolving Treatment Landscape: Amyloidosis Forum Meeting Proceedings.
Advances in therapyThermal evaporation as sample preparation for silver-assisted laser desorption/ionization mass spectrometry imaging of cholesterol in amyloid tissues.
The AnalystLessons from the first-in-human in vivo CRISPR/Cas9 editing of the TTR gene by NTLA-2001 trial in patients with transthyretin amyloidosis with cardiomyopathy.
Global cardiology science & practice[Neurological manifestations of ATTR amyloidosis].
Innere Medizin (Heidelberg, Germany)Early and aggressive presentation of wild-type transthyretin amyloid cardiomyopathy: A case report.
World journal of cardiologyWild-type Transthyretin Amyloidosis with Diffuse Alveolar-septal Amyloidosis Diagnosed by a Transbronchial Lung Biopsy.
Internal medicine (Tokyo, Japan)Amyloid myopathy: expanding the clinical spectrum of transthyretin amyloidosis-case report and literature review.
Journal of nuclear cardiology : official publication of the American Society of Nuclear CardiologyA case of localized colorectal wild-type ATTR amyloidosis complicated by early stage colorectal cancer and a CMV-associated ulcer during the long-term follow-up.
Clinical journal of gastroenterologyTransthyretin: Its function and amyloid formation.
Neurochemistry internationalSuccessful management of refractory constipation using Kampo medicine Mashiningan in a patient with wild-type ATTR cardiac amyloidosis.
Journal of cardiology casesAssociation between spinal stenosis and wild-type ATTR amyloidosis.
Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of AmyloidosisTafamidis: a selective transthyretin stabilizer to treat wild-type ATTR amyloidosis and hereditary ATTR amyloidosis with cardiomyopathy.
Drugs of today (Barcelona, Spain : 1998)Amyloidosis in Heart Failure.
Current heart failure reportsWild-type ATTR amyloidosis may be associated with unexpected death among the elderly.
Legal medicine (Tokyo, Japan)Transthyretin Amyloid Cardiomyopathy: JACC State-of-the-Art Review.
Journal of the American College of CardiologyWhen and how do patients with cardiac amyloidosis die?
Clinical research in cardiology : official journal of the German Cardiac SocietyFirst nationwide survey on systemic wild-type ATTR amyloidosis in Japan.
Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of AmyloidosisSafety and efficacy of a TTR specific antisense oligonucleotide in patients with transthyretin amyloid cardiomyopathy.
Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of AmyloidosisCardiac amyloidosis: An update on pathophysiology, diagnosis, and treatment.
Trends in cardiovascular medicine(99m)Tc-DPD uptake reflects amyloid fibril composition in hereditary transthyretin amyloidosis.
Upsala journal of medical sciencesWild-type ATTR amyloidosis of the ureter in a 56-year-old woman with rheumatoid arthritis and Sjögren's syndrome.
International journal of clinical and experimental pathologyTransthyretin (ATTR) amyloidosis: clinical spectrum, molecular pathogenesis and disease-modifying treatments.
Journal of neurology, neurosurgery, and psychiatryAssociações
Organizações que acompanham esta doença — pra ter apoio e orientação
Ainda não temos associações cadastradas para Amiloidose ATTR tipo selvagem.
É de uma associação que acompanha esta doença? Fale com a gente →
Doença com base genética
Um médico geneticista pode ajudar no diagnóstico de Amiloidose ATTR tipo selvagem e no aconselhamento genético da família.
Doenças relacionadas
Doenças com sintomas parecidos — ajudam quem ainda está buscando diagnóstico
Perguntas frequentes
O que as famílias mais perguntam sobre esta doença — cada resposta com a fonte de onde saiu
Existe um documento oficial para "Amiloidoses Associadas à Transtirretina". Ele pode não cobrir esta forma específica da doença — confira no texto do protocolo antes de contar com ele.
É uma doença rara que atinge principalmente adultos e idosos, caracterizada pelo depósito anormal da proteína transtirretina normal em órgãos como o coração. Nos registros internacionais, é identificada pelo código Orpha 330001 e CID-10 E85.8.
Referências
Fontes citadas no texto, publicações do grafo e bases de dados usadas neste verbete
5 fontes citadas no texto · 7 publicações do grafo RarasNet (PubMed) · 5 bases de dados. Títulos, periódicos e PMIDs vêm direto da fonte, sem intermediação de IA.
Dados compilados pelo RarasNet a partir de fontes abertas (Orphanet, OMIM, MONDO, PubMed/EuropePMC, ClinicalTrials.gov, DATASUS, PCDT/MS). Este conteúdo é informativo e não substitui avaliação médica.
Citar este verbete
Raras. (2026). Amiloidose ATTR tipo selvagem. Em Raras — Enciclopédia de Doenças Raras do Brasil. https://raras.org/doenca/amiloidose-attr-tipo-selvagem
Formato APA. Conteúdo sob CC BY 4.0 — reuso livre com atribuição.
Conteúdo mantido por Agente Raras · Médicos e pesquisadores podem colaborar
Amiloidose ATTR tipo selvagem
📋 Origem dos dados
Esta página agrega dados de fontes públicas e oficiais. Dados sobre cobertura no SUS (PCDT, CEAF) são verificados ativamente por agente proativo (ver badge no infobox). Demais dados têm atribuição de fonte + data da última sincronização — clique para abrir o original.
- Doença rara (ontologia)
- fonte: Orphanet
- Identificador unificado
- fonte: MONDO
- Codificação WHO/SUS
- fonte: WHO ICD-10 / DATASUS
- CID-11 (futuro)
- fonte: WHO ICD-11
- NIH/GARD
- fonte: GARD (NIH)
- Dado público estruturado
- fonte: Wikidata
- Medicamentos aprovados FDA
- fonte: FDA OpenFDA
- Ensaios clínicos
- fonte: ClinicalTrials.gov