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Amiloidose hereditária
ORPHA:444116CID-10 · E85.2CID-11 · 5D00.2DOENÇA RARA

Amiloidose hereditária é um grupo de doenças genéticas (passadas de pais para filhos) que fazem parte dos diferentes tipos de amiloidose. Ela é caracterizada pelo acúmulo de uma proteína anormal chamada amiloide em vários órgãos do corpo, em lugares onde não deveria estar. Esse acúmulo atrapalha a estrutura e o funcionamento normal desses órgãos. Na amiloidose hereditária, os depósitos de amiloide atingem principalmente os tecidos do coração, dos rins e do sistema nervoso. Embora os sintomas da amiloidose hereditária possam surgir na infância, a maioria das pessoas só apresenta sintomas na vida adulta. Existem vários tipos de amiloidose hereditária, ligados a diferentes alterações genéticas (mutações) e proteínas anormais. O tipo mais comum de amiloidose hereditária é a amiloidose por transtirretina (ATTR), uma condição em que os depósitos de amiloide são formados, na maioria das vezes, pela proteína transtirretina, que é produzida no fígado. Outros exemplos de amiloidose hereditária incluem, entre outros: amiloidose por apolipoproteína AI (A ApoAI), amiloidose por gelsolina (A Gel), amiloidose por lisozima (A Lys), amiloidose por cistatina C (A Cys), amiloidose por cadeia alfa de fibrinogênio (A Fib) e amiloidose por apolipoproteína AII (A ApoAII). A maioria dos tipos de amiloidose hereditária é transmitida de forma autossômica dominante, o que significa que basta herdar uma cópia do gene alterado de um dos pais para desenvolver a doença. O tratamento busca lidar com os sintomas causados pelos danos aos órgãos e, quando possível, reduzir a produção de amiloide por meio de métodos como transplantes de fígado.

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Introdução

O que você precisa saber de cara

📋

Amiloidose hereditária é um grupo de doenças genéticas (passadas de pais para filhos) que fazem parte dos diferentes tipos de amiloidose. Ela é caracterizada pelo acúmulo de uma proteína anormal chamada amiloide em vários órgãos do corpo, em lugares onde não deveria estar. Esse acúmulo atrapalha a estrutura e o funcionamento normal desses órgãos. Na amiloidose hereditária, os depósitos de amiloide atingem principalmente os tecidos do coração, dos rins e do sistema nervoso. Embora os sintomas da amiloidose hereditária possam surgir na infância, a maioria das pessoas só apresenta sintomas na vida adulta. Existem vários tipos de amiloidose hereditária, ligados a diferentes alterações genéticas (mutações) e proteínas anormais. O tipo mais comum de amiloidose hereditária é a amiloidose por transtirretina (ATTR), uma condição em que os depósitos de amiloide são formados, na maioria das vezes, pela proteína transtirretina, que é produzida no fígado. Outros exemplos de amiloidose hereditária incluem, entre outros: amiloidose por apolipoproteína AI (A ApoAI), amiloidose por gelsolina (A Gel), amiloidose por lisozima (A Lys), amiloidose por cistatina C (A Cys), amiloidose por cadeia alfa de fibrinogênio (A Fib) e amiloidose por apolipoproteína AII (A ApoAII). A maioria dos tipos de amiloidose hereditária é transmitida de forma autossômica dominante, o que significa que basta herdar uma cópia do gene alterado de um dos pais para desenvolver a doença. O tratamento busca lidar com os sintomas causados pelos danos aos órgãos e, quando possível, reduzir a produção de amiloide por meio de métodos como transplantes de fígado.

Pesquisas ativas
12 ensaios
229 total registrados no ClinicalTrials.gov
Publicações científicas
371 artigos
Último publicado: 2026 Feb
Medicamentos
13 registrados
PATISIRAN SODIUM, VUTRISIRAN SODIUM, INOTERSEN SODIUM

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13 medicamentos registrados
Ver detalhes, fases e interações →
PATISIRAN SODIUMVUTRISIRAN SODIUMINOTERSEN SODIUMVUTRISIRANPATISIRANINOTERSENEPLONTERSENTAFAMIDISACORAMIDISREVUSIRAN
🏥
SUS: Cobertura mínimaScore: 20%
2 medicamentos CEAFCID-10: E85.2
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Sinais e sintomas

O que aparece no corpo e com que frequência cada sintoma acontece

Partes do corpo afetadas

🧠
Neurológico
44 sintomas
🫃
Digestivo
26 sintomas
🫘
Rins
20 sintomas
❤️
Coração
18 sintomas
👁️
Olhos
17 sintomas
🧬
Pele e cabelo
11 sintomas

+ 78 sintomas em outras categorias

Características mais comuns

Psicose
Déficit na memória de curto prazo fonológica
Hipotensão ortostática devido a disfunção autonômica
Amiloidose
Infecção do trato respiratório
Tremor intencional
247sintomas
Sem dados (247)

Os sintomas variam de pessoa para pessoa. Abaixo estão as 247 características clínicas mais associadas, ordenadas por frequência.

PsicosePsychosis
Déficit na memória de curto prazo fonológicaDeficit in phonologic short-term memory
Hipotensão ortostática devido a disfunção autonômicaOrthostatic hypotension due to autonomic dysfunction
AmiloidoseAmyloidosis
Infecção do trato respiratórioRespiratory tract infection

Linha do tempo da pesquisa

Publicações por ano — veja quando o interesse científico cresceu
Anos de pesquisa1desde 2026
Total histórico371PubMed
Últimos 10 anos173publicações
Pico202022 papers
Linha do tempo
2026Hoje · 2026🧪 1979Primeiro ensaio clínico📈 2020Ano de pico
Publicações por ano (últimos 10 anos)

Encontrou um erro ou informação desatualizada? Sugira uma correção →

Genética e causas

O que está alterado no DNA e como passa nas famílias

Genes associados

13 genes identificados com associação a esta condição.

GPNMBTransmembrane glycoprotein NMBDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Could be a melanogenic enzyme

LOCALIZAÇÃO

Cell membraneMelanosome membraneEarly endosome membrane

VIAS BIOLÓGICAS (1)
PTK6 promotes HIF1A stabilization
EXPRESSÃO TECIDUAL(Ubíquo)
Cervix Ectocervix
316.2 TPM
Skin Not Sun Exposed Suprapubic
299.5 TPM
Cervix Endocervix
270.1 TPM
Skin Sun Exposed Lower leg
250.8 TPM
Aorta
177.0 TPM
OUTRAS DOENÇAS (2)
amyloidosis, primary localized cutaneous, 3amyloidosis cutis dyschromia
HGNC:4462UniProt:Q14956
TTRTransthyretinDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Thyroid hormone-binding protein. Probably transports thyroxine from the bloodstream to the brain

LOCALIZAÇÃO

SecretedCytoplasm

VIAS BIOLÓGICAS (6)
The canonical retinoid cycle in rods (twilight vision)Retinoid metabolism and transportDefective visual phototransduction due to STRA6 loss of functionNeutrophil degranulationAmyloid fiber formation
MECANISMO DE DOENÇA

Amyloidosis, hereditary systemic 1

A form of hereditary systemic amyloidosis, a disorder characterized by amyloid deposition in multiple tissues resulting in a wide clinical spectrum. AMYLD1 is an autosomal dominant form due to transthyretin amyloid deposition. Protein fibrils can form in different tissues leading to amyloid polyneuropathies, amyloidotic cardiomyopathy, carpal tunnel syndrome, systemic senile amyloidosis. The disease includes leptomeningeal amyloidosis that is characterized by primary involvement of the central nervous system. Neuropathologic examination shows amyloid in the walls of leptomeningeal vessels, in pia arachnoid, and subpial deposits. Some patients also develop vitreous amyloid deposition that leads to visual impairment (oculoleptomeningeal amyloidosis). Clinical features include seizures, stroke-like episodes, dementia, psychomotor deterioration, variable amyloid deposition in the vitreous humor.

EXPRESSÃO TECIDUAL(Tecido-específico)
Fígado
2734.3 TPM
Pâncreas
202.8 TPM
Hipocampo
43.8 TPM
Brain Spinal cord cervical c-1
26.7 TPM
Substância negra
16.7 TPM
OUTRAS DOENÇAS (6)
hyperthyroxinemia, dystransthyretinemiccarpal tunnel syndrome 1amyloidosis, hereditary systemic 1euthyroid dysprealbuminemic hyperthyroxinemia
HGNC:12405UniProt:P02766
LYZLysozyme CDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Lysozymes have primarily a bacteriolytic function; those in tissues and body fluids are associated with the monocyte-macrophage system and enhance the activity of immunoagents

LOCALIZAÇÃO

Secreted

VIAS BIOLÓGICAS (1)
Neutrophil degranulation
MECANISMO DE DOENÇA

Amyloidosis, hereditary systemic 5

A form of hereditary systemic amyloidosis, a disorder characterized by amyloid deposition in multiple tissues resulting in a wide clinical spectrum. AMYLD5 primarily affects the viscera, and the predominant clinical features are renal dysfunction of varying severity, and intra-abdominal bleeding. Inheritance is autosomal dominant.

EXPRESSÃO TECIDUAL(Ubíquo)
Glândula salivar
9548.0 TPM
Sangue
1687.4 TPM
Intestino delgado
304.3 TPM
Pulmão
296.5 TPM
Baço
177.4 TPM
OUTRAS DOENÇAS (2)
amyloidosis, hereditary systemic 5ALys amyloidosis
HGNC:6740UniProt:P61626
APOA2Apolipoprotein A-IICandidate gene tested inModerado
FUNÇÃO

May stabilize HDL (high density lipoprotein) structure by its association with lipids, and affect the HDL metabolism

LOCALIZAÇÃO

Secreted

VIAS BIOLÓGICAS (2)
Post-translational protein phosphorylationRegulation of Insulin-like Growth Factor (IGF) transport and uptake by Insulin-like Growth Factor Binding Proteins (IGFBPs)
OUTRAS DOENÇAS (2)
apolipoprotein A-II amyloidosishypercholesterolemia, familial, 1
HGNC:601UniProt:P02652
ITM2BIntegral membrane protein 2BDisease-causing germline mutation(s) inModerado
FUNÇÃO

Plays a regulatory role in the processing of the amyloid-beta A4 precursor protein (APP) and acts as an inhibitor of the amyloid-beta peptide aggregation and fibrils deposition. Plays a role in the induction of neurite outgrowth. Functions as a protease inhibitor by blocking access of secretases to APP cleavage sites Mature BRI2 (mBRI2) functions as a modulator of the amyloid-beta A4 precursor protein (APP) processing leading to a strong reduction in the secretion of secretase-processed amyloid-

LOCALIZAÇÃO

Golgi apparatus membraneCell membraneEndosome membraneSecreted

VIAS BIOLÓGICAS (1)
Amyloid fiber formation
MECANISMO DE DOENÇA

Cerebral amyloid angiopathy, ITM2B-related 1

A disorder characterized by amyloid deposition in the walls of cerebral blood vessels and neurodegeneration in the central nervous system. Cerebral amyloid angiopathy, non-neuritic and perivascular plaques and neurofibrillary tangles are the predominant pathological lesions. Clinical features include progressive mental deterioration, spasticity and muscular rigidity.

VIAS REACTOME (1)
EXPRESSÃO TECIDUAL(Ubíquo)
Ovário
241.1 TPM
Sangue
208.7 TPM
Cérebro - Hemisfério cerebelar
204.2 TPM
Cervix Ectocervix
200.0 TPM
Cervix Endocervix
193.0 TPM
INTERAÇÕES PROTEICAS (2)
OUTRAS DOENÇAS (3)
ABri amyloidosisADan amyloidosisretinal dystrophy with inner retinal dysfunction and ganglion cell anomalies
HGNC:6174UniProt:Q9Y287
OSMROncostatin-M-specific receptor subunit betaDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Associates with IL31RA to form the IL31 receptor. Binds IL31 to activate STAT3 and possibly STAT1 and STAT5. Capable of transducing OSM-specific signaling events

LOCALIZAÇÃO

Membrane

VIAS BIOLÓGICAS (1)
IL-6-type cytokine receptor ligand interactions
MECANISMO DE DOENÇA

Amyloidosis, primary localized cutaneous, 1

A primary amyloidosis characterized by localized cutaneous amyloid deposition. This condition usually presents with itching (especially on the lower legs) and visible changes of skin hyperpigmentation and thickening that may be exacerbated by chronic scratching and rubbing. Primary localized cutaneous amyloidosis is often divided into macular and lichen subtypes although many affected individuals often show both variants coexisting. Lichen amyloidosis characteristically presents as a pruritic eruption of grouped hyperkeratotic papules with a predilection for the shins, calves, ankles and dorsa of feet and thighs. Papules may coalesce to form hyperkeratotic plaques that can resemble lichen planus, lichen simplex or nodular prurigo. Macular amyloidosis is characterized by small pigmented macules that may merge to produce macular hyperpigmentation, sometimes with a reticulate or rippled pattern. In macular and lichen amyloidosis, amyloid is deposited in the papillary dermis in association with grouped colloid bodies, thought to represent degenerate basal keratinocytes. The amyloid deposits probably reflect a combination of degenerate keratin filaments, serum amyloid P component, and deposition of immunoglobulins.

EXPRESSÃO TECIDUAL(Ubíquo)
Fibroblastos
117.0 TPM
Adipose Visceral Omentum
72.4 TPM
Pulmão
67.0 TPM
Artéria tibial
57.4 TPM
Aorta
55.9 TPM
OUTRAS DOENÇAS (2)
amyloidosis, primary localized cutaneous, 1familial primary localized cutaneous amyloidosis
HGNC:8507UniProt:Q99650
APOA1Apolipoprotein A-IDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Participates in the reverse transport of cholesterol from tissues to the liver for excretion by promoting cholesterol efflux from tissues and by acting as a cofactor for the lecithin cholesterol acyltransferase (LCAT). As part of the SPAP complex, activates spermatozoa motility

LOCALIZAÇÃO

Secreted

VIAS BIOLÓGICAS (2)
Post-translational protein phosphorylationRegulation of Insulin-like Growth Factor (IGF) transport and uptake by Insulin-like Growth Factor Binding Proteins (IGFBPs)
MECANISMO DE DOENÇA

Hypoalphalipoproteinemia, primary, 2

An autosomal recessive disorder of lipoprotein metabolism, biochemically characterized by severe apoA-I deficiency and severely reduced serum high-density lipoprotein cholesterol (HDL-C). Affected individuals have undetectable serum levels of apoA-I, and develop xanthomas and corneal opacities. The disease is generally associated with atherosclerosis and markedly increased cardiovascular risk.

OUTRAS DOENÇAS (4)
hypoalphalipoproteinemia, primary, 2, intermediateamyloidosis, hereditary systemic 3hypoalphalipoproteinemia, primary, 2AApoAI amyloidosis
HGNC:600UniProt:P02647
FGAFibrinogen alpha chainDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Cleaved by the protease thrombin to yield monomers which, together with fibrinogen beta (FGB) and fibrinogen gamma (FGG), polymerize to form an insoluble fibrin matrix. Fibrin has a major function in hemostasis as one of the primary components of blood clots. In addition, functions during the early stages of wound repair to stabilize the lesion and guide cell migration during re-epithelialization. Was originally thought to be essential for platelet aggregation, based on in vitro studies using an

LOCALIZAÇÃO

Secreted

VIAS BIOLÓGICAS (10)
Paradoxical activation of RAF signaling by kinase inactive BRAFSignaling by moderate kinase activity BRAF mutantsSignaling by high-kinase activity BRAF mutantsSignaling downstream of RAS mutantsMAP2K and MAPK activation
MECANISMO DE DOENÇA

Congenital afibrinogenemia

Rare autosomal recessive disorder is characterized by bleeding that varies from mild to severe and by complete absence or extremely low levels of plasma and platelet fibrinogen.

EXPRESSÃO TECIDUAL(Tecido-específico)
Fígado
5497.7 TPM
Estômago
12.4 TPM
Testículo
5.1 TPM
Rim - Medula
2.7 TPM
Rim - Córtex
1.7 TPM
OUTRAS DOENÇAS (6)
familial dysfibrinogenemiafamilial visceral amyloidosiscongenital afibrinogenemiaAFib amyloidosis
HGNC:3661UniProt:P02671
APPAmyloid-beta precursor proteinDisease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Functions as a cell surface receptor and performs physiological functions on the surface of neurons relevant to neurite growth, neuronal adhesion and axonogenesis. Interaction between APP molecules on neighboring cells promotes synaptogenesis (PubMed:25122912). Involved in cell mobility and transcription regulation through protein-protein interactions. Can promote transcription activation through binding to APBB1-KAT5 and inhibits Notch signaling through interaction with Numb. Couples to apoptos

LOCALIZAÇÃO

Cell membraneMembranePerikaryonCell projection, growth coneMembrane, clathrin-coated pitEarly endosomeCytoplasmic vesicleEndoplasmic reticulumGolgi apparatusSecretedCell surfaceNucleusCytoplasm

VIAS BIOLÓGICAS (2)
Post-translational protein phosphorylationRegulation of Insulin-like Growth Factor (IGF) transport and uptake by Insulin-like Growth Factor Binding Proteins (IGFBPs)
MECANISMO DE DOENÇA

Alzheimer disease 1

A form of Alzheimer disease, a neurodegenerative disorder characterized by progressive dementia, loss of cognitive abilities, and deposition of fibrillar amyloid proteins as intraneuronal neurofibrillary tangles, extracellular amyloid plaques and vascular amyloid deposits. The major constituents of these plaques are neurotoxic amyloid-beta protein 40 and amyloid-beta protein 42, that are produced by the proteolysis of the transmembrane APP protein. The cytotoxic C-terminal fragments (CTFs) and the caspase-cleaved products, such as C31, are also implicated in neuronal death. It can be associated with cerebral amyloid angiopathy. Alzheimer disease can be associated with cerebral amyloid angiopathy.

OUTRAS DOENÇAS (9)
cerebral amyloid angiopathy, APP-relatedAlzheimer disease type 1ABeta amyloidosis, Italian typeearly-onset autosomal dominant Alzheimer disease
HGNC:620UniProt:P05067
IL31RAInterleukin-31 receptor subunit alphaDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Associates with OSMR to form the interleukin-31 receptor which activates STAT3 and to a lower extent STAT1 and STAT5 (PubMed:11877449, PubMed:14504285, PubMed:15194700, PubMed:15627637). May function in skin immunity (PubMed:15184896). Mediates IL31-induced itch, probably in a manner dependent on cation channels TRPA1 and TRPV1 (By similarity). Positively regulates numbers and cycling status of immature subsets of myeloid progenitor cells in bone marrow in vivo and enhances myeloid progenitor ce

LOCALIZAÇÃO

Cell membranePresynaptic cell membraneCell projection, axon

VIAS BIOLÓGICAS (1)
IL-6-type cytokine receptor ligand interactions
MECANISMO DE DOENÇA

Amyloidosis, primary localized cutaneous, 2

A primary amyloidosis characterized by localized cutaneous amyloid deposition. This condition usually presents with itching (especially on the lower legs) and visible changes of skin hyperpigmentation and thickening that may be exacerbated by chronic scratching and rubbing. Primary localized cutaneous amyloidosis is often divided into macular and lichen subtypes although many affected individuals often show both variants coexisting. Lichen amyloidosis characteristically presents as a pruritic eruption of grouped hyperkeratotic papules with a predilection for the shins, calves, ankles and dorsa of feet and thighs. Papules may coalesce to form hyperkeratotic plaques that can resemble lichen planus, lichen simplex or nodular prurigo. Macular amyloidosis is characterized by small pigmented macules that may merge to produce macular hyperpigmentation, sometimes with a reticulate or rippled pattern. In macular and lichen amyloidosis, amyloid is deposited in the papillary dermis in association with grouped colloid bodies, thought to represent degenerate basal keratinocytes. The amyloid deposits probably reflect a combination of degenerate keratin filaments, serum amyloid P component, and deposition of immunoglobulins.

EXPRESSÃO TECIDUAL(Baixa expressão)
Aorta
1.9 TPM
Testículo
1.8 TPM
Fibroblastos
0.8 TPM
Skin Sun Exposed Lower leg
0.5 TPM
Skin Not Sun Exposed Suprapubic
0.5 TPM
INTERAÇÕES PROTEICAS (5)
OUTRAS DOENÇAS (2)
amyloidosis, primary localized cutaneous, 2familial primary localized cutaneous amyloidosis
HGNC:18969UniProt:Q8NI17
B2MBeta-2-microglobulinDisease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Component of the class I major histocompatibility complex (MHC). Involved in the presentation of peptide antigens to the immune system. Exogenously applied M.tuberculosis EsxA or EsxA-EsxB (or EsxA expressed in host) binds B2M and decreases its export to the cell surface (total protein levels do not change), probably leading to defects in class I antigen presentation (PubMed:25356553)

LOCALIZAÇÃO

SecretedCell surface

VIAS BIOLÓGICAS (2)
Antigen Presentation: Folding, assembly and peptide loading of class I MHCNef mediated downregulation of MHC class I complex cell surface expression
MECANISMO DE DOENÇA

Immunodeficiency 43

A disorder characterized by marked reduction in serum concentrations of immunoglobulins and albumin, and hypoproteinemia due to hypercatabolism. Patients may suffer from recurrent respiratory tract infections and severe skin disease.

OUTRAS DOENÇAS (4)
hypoproteinemia, hypercatabolicamyloidosis, hereditary systemic 6variant ABeta2M amyloidosisMHC class I deficiency
HGNC:914UniProt:P61769
GSNGelsolinDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Calcium-regulated, actin-modulating protein that binds to the plus (or barbed) ends of actin monomers or filaments, preventing monomer exchange (end-blocking or capping). It can promote the assembly of monomers into filaments (nucleation) as well as sever filaments already formed (PubMed:19666512). Plays a role in ciliogenesis (PubMed:20393563)

LOCALIZAÇÃO

Cytoplasm, cytoskeletonSecreted

MECANISMO DE DOENÇA

Amyloidosis, hereditary systemic 4, Finnish type

A form of hereditary systemic amyloidosis, a disorder characterized by amyloid deposition in multiple tissues resulting in a wide clinical spectrum. AMYLD4 is due to gelsolin amyloid deposition and is typically characterized by cranial neuropathy and lattice corneal dystrophy. Most patients have modest involvement of internal organs, but severe systemic disease can develop in some individuals causing peripheral polyneuropathy, amyloid cardiomyopathy, and nephrotic syndrome leading to renal failure. AMYLD4 is usually inherited in an autosomal dominant pattern. However, homozygotes with a more severe phenotype have also been reported.

EXPRESSÃO TECIDUAL(Ubíquo)
Tecido adiposo
2343.5 TPM
Nervo tibial
1919.4 TPM
Artéria tibial
1624.6 TPM
Aorta
1619.7 TPM
Artéria coronária
1564.3 TPM
OUTRAS DOENÇAS (1)
Finnish type amyloidosis
HGNC:4620UniProt:P06396
CST3Cystatin-CDisease-causing germline mutation(s) inTolerante
FUNÇÃO

As an inhibitor of cysteine proteinases, this protein is thought to serve an important physiological role as a local regulator of this enzyme activity

LOCALIZAÇÃO

Secreted

VIAS BIOLÓGICAS (2)
Post-translational protein phosphorylationRegulation of Insulin-like Growth Factor (IGF) transport and uptake by Insulin-like Growth Factor Binding Proteins (IGFBPs)
MECANISMO DE DOENÇA

Cerebral amyloid angiopathy, CST3-related

An autosomal dominant disorder characterized by cystatin C amyloid accumulation in the walls of arteries, arterioles, and sometimes capillaries and veins of the brain, and in various organs including lymphoid tissue, spleen, salivary glands, and seminal vesicles. Amyloid deposition in the cerebral vessels results in intracranial hemorrhage and premature stroke. Cystatin C levels in the cerebrospinal fluid are abnormally low.

EXPRESSÃO TECIDUAL(Ubíquo)
Brain Putamen basal ganglia
653.3 TPM
Brain Caudate basal ganglia
619.9 TPM
Cérebro - Amígdala
598.5 TPM
Córtex cerebral
585.7 TPM
Brain Frontal Cortex BA9
531.0 TPM
OUTRAS DOENÇAS (2)
ACys amyloidosisage related macular degeneration 11
HGNC:2475UniProt:P01034

Medicamentos e terapias

PATISIRAN SODIUMPhase 4

Mecanismo: Transthyretin mRNA RNAi inhibitor

VUTRISIRAN SODIUMPhase 4

Mecanismo: Transthyretin mRNA rnai inhibitor

INOTERSEN SODIUMPhase 4

Mecanismo: Transthyretin mRNA antisense inhibitor

VUTRISIRANPhase 4

Mecanismo: Transthyretin mRNA rnai inhibitor

PATISIRANPhase 3

Mecanismo: Transthyretin mRNA RNAi inhibitor

INOTERSENPhase 3

Mecanismo: Transthyretin mRNA antisense inhibitor

EPLONTERSENPhase 3

Mecanismo: Transthyretin mRNA antisense inhibitor

TAFAMIDISPhase 3

Mecanismo: Transthyretin stabiliser

ACORAMIDISPhase 3

Mecanismo: Transthyretin stabiliser

REVUSIRANPhase 3

Mecanismo: Transthyretin mRNA RNAi inhibitor

Ver mais no OpenTargets

Variantes genéticas (ClinVar)

292 variantes patogênicas registradas no ClinVar.

🧬 GPNMB: GRCh37/hg19 7p22.3-14.3(chr7:158725-29918785)x3 ()
🧬 GPNMB: GRCh37/hg19 7p21.1-15.3(chr7:18093509-25363633)x1 ()
🧬 GPNMB: GRCh37/hg19 7p21.2-15.2(chr7:16417575-27541028)x3 ()
🧬 GPNMB: NM_002510.3(GPNMB):c.1019-316G>A ()
🧬 GPNMB: NM_002510.3(GPNMB):c.701-1G>T ()
Ver todas no ClinVar

Classificação de variantes (ClinVar)

Distribuição de 2 variantes classificadas pelo ClinVar.

2
Patogênica (100.0%)
VARIANTES MAIS SIGNIFICATIVAS
TTR: NM_000371.4(TTR):c.277A>G (p.Ile93Val) [Pathogenic/Likely pathogenic]
TTR: NM_000371.4(TTR):c.379A>G (p.Ile127Val) [Pathogenic/Likely pathogenic]

Vias biológicas (Reactome)

68 vias biológicas associadas aos genes desta condição.

PTK6 promotes HIF1A stabilization The canonical retinoid cycle in rods (twilight vision) Non-integrin membrane-ECM interactions Neutrophil degranulation Retinoid metabolism and transport Amyloid fiber formation Defective visual phototransduction due to STRA6 loss of function Antimicrobial peptides PPARA activates gene expression Regulation of Insulin-like Growth Factor (IGF) transport and uptake by Insulin-like Growth Factor Binding Proteins (IGFBPs) Post-translational protein phosphorylation Chylomicron assembly Chylomicron remodeling IL-6-type cytokine receptor ligand interactions Platelet degranulation ABC transporters in lipid homeostasis Scavenging of heme from plasma Scavenging by Class B Receptors Scavenging by Class A Receptors Defective ABCA1 causes TGD HDL assembly HDL clearance HDL remodeling Heme signaling Maturation of DENV proteins Dengue Virus-Host Interactions Dengue virus activates/modulates innate and adaptive immune responses ER-Phagosome pathway Common Pathway of Fibrin Clot Formation MyD88:MAL(TIRAP) cascade initiated on plasma membrane Integrin cell surface interactions Integrin signaling GRB2:SOS provides linkage to MAPK signaling for Integrins p130Cas linkage to MAPK signaling for integrins MyD88 deficiency (TLR2/4) IRAK4 deficiency (TLR2/4) MAP2K and MAPK activation Regulation of TLR by endogenous ligand Signaling by moderate kinase activity BRAF mutants Signaling by high-kinase activity BRAF mutants Signaling by BRAF and RAF1 fusions Paradoxical activation of RAF signaling by kinase inactive BRAF Signaling downstream of RAS mutants Signaling by RAF1 mutants ECM proteoglycans G alpha (q) signalling events G alpha (i) signalling events Lysosome Vesicle Biogenesis Formyl peptide receptors bind formyl peptides and many other ligands TAK1-dependent IKK and NF-kappa-B activation The NLRP3 inflammasome Advanced glycosylation endproduct receptor signaling Deregulated CDK5 triggers multiple neurodegenerative pathways in Alzheimer's disease models TRAF6 mediated NF-kB activation Insertion of tail-anchored proteins into the endoplasmic reticulum membrane Purinergic signaling in leishmaniasis infection Mitochondrial protein degradation Endosomal/Vacuolar pathway Nef mediated downregulation of MHC class I complex cell surface expression Immunoregulatory interactions between a Lymphoid and a non-Lymphoid cell DAP12 interactions DAP12 signaling Interferon gamma signaling Modulation by Mtb of host immune system SARS-CoV-2 activates/modulates innate and adaptive immune responses Antigen Presentation: Folding, assembly and peptide loading of class I MHC Caspase-mediated cleavage of cytoskeletal proteins Sensory processing of sound by outer hair cells of the cochlea

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Publicações mais relevantes

Timeline de publicações
172 papers (10 anos)
#1

Therapeutic Efficacy and Safety Profile of Eplontersen in Hereditary Transthyretin-Mediated Amyloidosis: A Systematic Review.

Health science reports2026 Mar

Hereditary transthyretin-mediated amyloidosis (hATTR) is a disorder that affects several body systems and can result in life-threatening conditions like cardiomyopathy and polyneuropathy. For treatment of hATTR in the new medical realm, there is a breakthrough discovery of a medicine called Eplontersen, which targets the underlying genetic mutation causing the condition. This review aims to summarize Eplontersen's mechanism of action, efficacy, safety profile, and ongoing clinical trials. A systematic review of the literature was conducted following PRISMA guidelines. Databases searched included PubMed, Cochrane, and Science Direct using terms related to Eplontersen and hereditary amyloidosis. Studies were selected based on defined inclusion and exclusion criteria. Eplontersen was approved by the FDA after the NEURO-TTRansform phase 3 trial showed substantial safety and efficacy. The drug demonstrated a significant reduction in serum TTR levels and improvements in neurological function and quality of life in patients with hATTR. The review also explored contraindications, dosing, safety monitoring, and patient support programs. Although data gaps remain, Eplontersen represents a promising advancement in the treatment of hATTR-induced polyneuropathy. Future research is needed on long-term safety, early diagnosis, personalized treatments, and combination therapies. This drug emphasizes the importance of continued research for optimal patient care and outcomes.

#2

Central Nervous System Manifestations Associated with Hereditary Transthyretin Amyloidosis: a Narrative Review.

Arquivos de neuro-psiquiatria2026 Feb

Hereditary transthyretin amyloidosis (ATTRv) is a rare, autosomal dominant, inherited disease caused by variants in the gene encoding the transthyretin (TTR) protein. These variants lead to TTR tetramer destabilization, resulting in the formation and progressive deposition of insoluble amyloid fibrils in various tissues, including those of the central nervous system (CNS). Although previously neglected, the recognition of CNS involvement in ATTRv has become progressively relevant due to prolonged patient survival and the ineffectiveness of the current therapies in addressing CNS synthesis of TTR. The first descriptions of the pathological involvement of the CNS in ATTRv date from the 1960s; however, this topic has not been fully explored. In the present article, the main CNS clinical manifestations of ATTRv, such as transient focal neurological episodes, bleeding complications, leptomeningeal amyloidosis, and cognitive impairment, are reviewed, and the phenotypic variability of this condition is highlighted. A literature review of the PubMed/Medline database was conducted using the following keywords: hereditary amyloidosis, transthyretin amyloidosis, familial amyloidosis, central nervous system, neurological manifestations, leptomeningeal amyloidosis, cognition, and cognitive impairment. Studies published in the last 15 years, including review articles, prospective observational studies, experimental studies and clinical trials, were evaluated. Improving our understanding of CNS involvement in ATTRv will enable the early identification of neurological symptoms in this condition, which will enhance the understanding of the pathophysiological mechanisms and boost the advancement of research, expanding potential treatments and improving the quality of life of these individuals.

#3

Hereditary Transthyretin Amyloidosis in Austria: Clinical, Genetic, and Demographic Insights from a Nationwide Cohort.

Journal of clinical medicine2026 Mar 04

Background/Objectives: Hereditary transthyretin amyloidosis (ATTRv) is a heterogeneous multisystem disease caused by pathogenic transthyretin gene (TTR) variants. Increased awareness and availability of disease-modifying therapies have resulted in increased diagnoses, even in previously nonendemic regions. The aim of this study was to update the nationwide Austrian ATTRv registry by characterizing the clinical, genetic, and regional distribution of TTR variants. Methods: This multicenter, observational analysis examined ATTRv cases diagnosed in Austria between 2014 and 2025. Individuals were included according to the presence of pathogenic or likely pathogenic variants or variants of uncertain significance (VUSs) in TTR. Results: In total, 100 individuals were identified, including symptomatic and asymptomatic carriers. Compared with our previously presented data, the number of genetically confirmed ATTRv cases has more than doubled. Twenty-three TTR variants were identified. The most frequent pathologic variants were p.His108Arg (26%), p.Ile127Phe (11%), and p.Thr69Ile (9%), while p.Val113Leu (9%) represented the most frequent VUS. Significant regional clustering of p.His108Arg was documented in Vienna and Lower Austria. Other findings included a rising number of p.Val142Ile carriers and phenotypically relevant VUSs in 20 patients. Conclusions: Our findings revealed an increasing detection rate of ATTRv in a nonendemic European region. These data underscore the importance of multidisciplinary evaluation, cascade testing, and long-term monitoring to improve early diagnosis and timely management in hereditary amyloidosis.

#4

A Cautionary Tale: An Instructive Case of Recognising Non-Amyloid Light Chain Renal Amyloidosis.

Nephrology (Carlton, Vic.)2026 Feb

Amyloidosis is a group of diseases characterised by tissue deposition of misfolded proteins, leading to organ dysfunction without appropriate therapy. Fibrinogen A α-chain amyloidosis is a rare hereditary amyloidosis that can be difficult to distinguish from other causes of renal amyloidosis. We report on a 66-year-old female who presented with deteriorating kidney function. Serum kappa/lambda free light chain ratio was normal with no detectable paraprotein. Kidney biopsy showed marked glomerular expansion and architectural destruction due to amyloid deposition with no vascular amyloid deposits and moderate kappa staining on immunohistochemistry. Despite bone marrow aspirate and trephine showing no evidence of plasma cell dyscrasia, light chain amyloidosis was diagnosed, and she was treated with chemotherapy, eventually progressing to kidney failure. Subsequent genetic testing revealed the amyloidogenic variant of fibrinogen A α due to mutation Glu526Val, confirming a diagnosis of fibrinogen A α-chain amyloidosis and not light chain amyloidosis. She received a deceased donor kidney transplant and was treated with doxycycline for its anti-fibrillogenesis effect with no amyloid recurrence on post-transplant surveillance biopsies, satisfactory kidney function and no proteinuria 6 years post-transplant. Renal amyloidosis cannot be attributed to the light chain subtype without evidence of plasma cell dyscrasia. Understanding of patterns of amyloid deposition in all renal amyloidosis subtypes is necessary, and genetic testing and mass spectrometry should be considered when immunohistochemistry is inconclusive. Correct subtyping of renal amyloidosis is crucial to avoid unnecessary toxicity from chemotherapy and determine the risk of recurrence for kidney transplantation. A multidisciplinary team approach with amyloidosis expertise is recommended.

#5

Natural variants of apolipoprotein A1 L99P and R173P exhibited a high degree of amyloid fibril formation: Implications for high-density lipoprotein functions and disease pathogenesis.

International journal of biological macromolecules2026 Feb

Apolipoprotein A1 (ApoA1), the primary protein component of high-density lipoprotein (HDL), plays a crucial role in cholesterol transport and cardiovascular protection. However, specific mutations in ApoA1 are associated with hereditary amyloidosis, a condition marked by protein misfolding and deposition of amyloid fibrils in various tissues. This study aimed to experimentally characterize the structural and functional consequences of four disease-associated ApoA1 mutations (G26R, L84P, L99P, and R173P), previously predicted to be amyloidogenic via computational analysis. Recombinant ApoA1 variants were expressed in Bacillus subtilis, purified, and characterized using a combination of biophysical, structural, and cellular assays. The L99P and R173P mutants exhibited significant structural destabilization, increased exposure of hydrophobic surfaces, enhanced β-sheet formation, and a strong tendency to aggregate. These properties were associated with the formation of elongated fibrils and a marked increase in cytotoxicity in HEK293 cells. In contrast, the L84P variant formed spherical aggregates with relatively preserved secondary structure and showed minimal cytotoxic effects, suggesting a distinct, possibly less pathogenic aggregation pathway. G26R displayed intermediate behavior, with notable amyloidogenic potential and cellular toxicity. This study provides experimental validation for the amyloidogenic nature of select ApoA1 mutations and highlights the structural heterogeneity underlying their aggregation behavior.

Publicações recentes

Ver todas no PubMed

📚 EuropePMC123 artigos no totalmostrando 170

2026

Central Nervous System Manifestations Associated with Hereditary Transthyretin Amyloidosis: a Narrative Review.

Arquivos de neuro-psiquiatria
2026

Hereditary Transthyretin Amyloidosis in Austria: Clinical, Genetic, and Demographic Insights from a Nationwide Cohort.

Journal of clinical medicine
2026

Therapeutic Efficacy and Safety Profile of Eplontersen in Hereditary Transthyretin-Mediated Amyloidosis: A Systematic Review.

Health science reports
2026

A Cautionary Tale: An Instructive Case of Recognising Non-Amyloid Light Chain Renal Amyloidosis.

Nephrology (Carlton, Vic.)
2026

Natural variants of apolipoprotein A1 L99P and R173P exhibited a high degree of amyloid fibril formation: Implications for high-density lipoprotein functions and disease pathogenesis.

International journal of biological macromolecules
2026

Genetic and Clinical Spectrum of Hereditary Transthyretin Amyloidosis in Brazil.

Journal of the peripheral nervous system : JPNS
2025

Predictors of poor prognosis in a large cohort of patients with hereditary cardiac transthyretin amyloidosis.

Revista espanola de cardiologia (English ed.)
2025

Efficacy and safety of patisiran for the treatment of acquired amyloid polyneuropathy in domino liver transplant recipients.

Therapeutic advances in neurological disorders
2025

Revolutionizing pediatric gene and cell therapy: The hope for lipid-based nanoparticles in blood disorders.

Current research in translational medicine
2025

Sixty years of experience with hereditary transthyretin amyloidosis: Insights from the Swedish transthyretin amyloidosis registry.

Journal of internal medicine
2025

Transthyretin variant cerebral amyloid angiopathy fulfilling the modified Boston criteria: Retrospective data from the Bicêtre hospital cohort.

Revue neurologique
2025

The Structure of the Apolipoprotein A-I Monomer Provides Insights Into Its Oligomerisation and Lipid-binding Mechanisms.

Journal of molecular biology
2025

A mutation in transthyretin gene in a Mexican patient leading to hereditary amyloidosis: a case report.

Journal of medical case reports
2025

Introducing a revised version of the Kumamoto scale as an easy-to-use clinical tool for monitoring multisystemic changes in hereditary transthyretin amyloidosis.

Orphanet journal of rare diseases
2025

Realizing the therapeutic potential of rapid knockdown of transthyretin via RNA interference in transthyretin amyloidosis.

Molecular therapy. Nucleic acids
2025

Scalloped pupil in a patient with hereditary amyloidosis transthyretin.

Medicina clinica
2025

Progress and Criteria in Public Health Applications of Gene Therapy and Gene Editing: Beyond the White Paper.

Public health genomics
2025

ATTRV30M amyloidosis post-liver transplant: cognition and long-term survival.

Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
2025

Multigene panel analysis has limited additional value compared to transthyretin gene analysis in Dutch patients with suspected cardiac amyloidosis.

Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
2025

Exploring Cardiac Sympathetic Denervation in Transthyretin-Mediated Hereditary Amyloidosis (ATTRv): Insights from 123I-mIBG Scintigraphy.

Diagnostics (Basel, Switzerland)
2025

Cardiac amyloidosis: A diagnosis made from an ophthalmological finding and suspicion.

Revista espanola de patologia : publicacion oficial de la Sociedad Espanola de Anatomia Patologica y de la Sociedad Espanola de Citologia
2025

Insights into the structural and biophysical mechanisms of benzamidine-driven inhibition of human lysozyme aggregation.

International journal of biological macromolecules
2025

Hereditary transthyretin amyloidosis (ATTRv).

Current problems in cardiology
2025

Hereditary Transthyretin Amyloidosis in Israel: Genetic Landscape and Clinical Characteristics.

European journal of neurology
2025

Amyloidosis and Heart Transplantation in a New Era.

Clinical transplantation
2025

Prevalence of Pathogenic Transthyretin Gene Variants in the Rocky Mountain Region.

Muscle & nerve
2025

Clinicopathologic, Proteomic and Outcome Characteristics of Renal Apolipoprotein C-II Amyloidosis: A Case Series.

American journal of kidney diseases : the official journal of the National Kidney Foundation
2024

Cryo-EM structure of a lysozyme-derived amyloid fibril from hereditary amyloidosis.

Nature communications
2024

Experience of Hereditary Amyloidosis with Rare Variant in Ecuador: Case Reports.

Medical sciences (Basel, Switzerland)
2025

The Role of Neuromuscular Ultrasound in the Diagnosis of Peripheral Neuropathy.

Seminars in neurology
2024

Assessing the effectiveness and safety of Patisiran and Vutrisiran in ATTRv amyloidosis with polyneuropathy: a systematic review.

Frontiers in neurology
2024

Hereditary transthyretin amyloidosis with hydrocephalus at 27 years old: A case report.

Journal of cardiology cases
2024

RNA Interference Therapeutics for Hereditary Amyloidosis: A Narrative Review of Clinical Trial Outcomes and Future Directions.

Cureus
2024

Hereditary Amyloidosis: Insights Into a Fibrinogen A Variant Protein.

Proteins
2024

Neurofilament light chain as a biomarker for acute hepatic porphyrias.

Frontiers in neurology
2024

Unravelling complexity: A case of progressive cardiac involvement in hereditary amyloidosis after liver transplant.

Kardiologia polska
2024

Late-onset familial amyloidosis polyneuropathy associated with c.186G>C in transthyretin.

Revista de la Facultad de Ciencias Medicas (Cordoba, Argentina)
2024

Circulating transthyretin and retinol binding protein 4 levels among middle-age V122I TTR carriers in the general population.

Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
2024

Apolipoprotein C-III amyloidosis in white lions (Panthera leo).

Veterinary pathology
2024

Trypsin-induced aggregation of transthyretin Valine 30 variants associated with hereditary amyloidosis.

The FEBS journal
2024

An ultra performance liquid chromatography method for transthyretin variants screening and heart failure assisting diagnosis.

Clinica chimica acta; international journal of clinical chemistry
2024

Generation of two induced pluripotent stem cell lines from hereditary amyloidosis patients with polyneuropathy carrying heterozygous transthyretin (TTR) mutation.

Stem cell research
2023

Real-world utilization of guideline-directed genetic testing in inherited cardiovascular diseases.

Frontiers in cardiovascular medicine
2024

RNA Interference and Neuromuscular Diseases: A Focus on Hereditary Transthyretin Amyloidosis.

Current gene therapy
2023

Cardiac Amyloid Quantification Using 124I-Evuzamitide (124I-P5+14) Versus 18F-Florbetapir: A Pilot PET/CT Study.

JACC. Cardiovascular imaging
2023

Comparison of cardiac involvement, extracardiac manifestations and outcomes between homozygote and heterozygote transthyretin p.Val142Ile (V122I) variant in patients with hereditary transthyretin amyloidosis: a cohort study.

Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
2023

Indirect treatment comparison (ITC) of the efficacy of vutrisiran and tafamidis for hereditary transthyretin-mediated amyloidosis with polyneuropathy.

Expert opinion on pharmacotherapy
2023

[Therapeutic Strategies for Hereditary Transthyretin Amyloidosis].

Brain and nerve = Shinkei kenkyu no shinpo
2023

Hereditary gelsolin amyloidosis: a rare cause of cranial, peripheral and autonomic neuropathies linked to D187N and Y447H substitutions.

Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
2023

Renal Amyloidosis (AL Kappa Type) With an Uncommon Presentation: A Case Report.

Cureus
2023

Small interfering RNA (siRNA)-based therapeutics.

Drug and therapeutics bulletin
2023

Corneal confocal microscopy identifies corneal nerve loss and increased Langerhans cells in presymptomatic carriers and patients with hereditary transthyretin amyloidosis.

Journal of neurology
2023

Amyloidosis of the Heart: A Comprehensive Review.

Cureus
2023

The value of electrochemical skin conductance measurement by Sudoscan® for assessing autonomic dysfunction in peripheral neuropathies beyond diabetes.

Neurophysiologie clinique = Clinical neurophysiology
2023

Neuropathic pain experience in symptomatic and presymptomatic subjects carrying a transthyretin gene mutation.

Frontiers in neurology
2023

A Comprehensive Multidisciplinary Diagnostic Algorithm for the Early and Efficient Detection of Amyloidosis.

Clinical lymphoma, myeloma & leukemia
2024

Severe Polyneuropathy in Hereditary Transthyretin Amyloidosis Caused by H90D Variant.

The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques
2022

A Metabolic Signature of Hereditary Transthyretin Amyloidosis: A Pilot Study.

International journal of molecular sciences
2022

Trajectories of Kidney Function in Patients with ATTRv Treated with Gene Silencers.

Genes
2022

Noncardiac Manifestations of Hereditary Amyloidosis.

The American journal of cardiology
2022

Hereditary Transthyretin-Related Amyloidosis: Genetic Heterogeneity and Early Personalized Gene Therapy.

Biomedicines
2022

Regression of left ventricular hypertrophy after tafamidis therapy in a patient with transthyretin amyloidosis variant.

The journal of medical investigation : JMI
2022

Renal amyloidosis: a new time for a complete diagnosis.

Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
2022

Gait Characterization and Analysis of Hereditary Amyloidosis Associated with Transthyretin Patients: A Case Series.

Journal of clinical medicine
2022

A patient with hereditary transthyretin amyloidosis involving multiple cranial nerves due to a rare p.(Phe84Ser) variant.

Translational neuroscience
2022

The effect of mutation on an aggregation-prone protein: An in vivo, in vitro, and in silico analysis.

Proceedings of the National Academy of Sciences of the United States of America
2022

Lysozyme amyloidosis-a report on a large German cohort and the characterisation of a novel amyloidogenic lysozyme gene variant.

Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
2022

Antisense therapies in neurological diseases.

Brain : a journal of neurology
2022

Patisiran treatment in patients with hereditary transthyretin-mediated amyloidosis with polyneuropathy after liver transplantation.

American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons
2022

Angiographic dark choroid in systemic non-hereditary amyloidosis.

American journal of ophthalmology case reports
2022

Three patients of transthyretin amyloidosis in a Japanese family with amyloidogenic transthyretin Thr49Ser (p.Thr69Ser) variant.

European journal of medical genetics
2022

Vitreous involvement as initial presentation of hereditary transthyretin amyloidosis related to the rare TTR Ile107Met (p.Ile127Met) pathogenic variant.

Ophthalmic genetics
2021

A Pilot Study of Rare Renal Amyloidosis Based on FFPE Proteomics.

Molecules (Basel, Switzerland)
2021

A Brief Journey through Protein Misfolding in Transthyretin Amyloidosis (ATTR Amyloidosis).

International journal of molecular sciences
2022

Changes in nerve conduction studies predate clinical symptoms onset in early onset Val30Met hereditary ATTR amyloidosis.

European journal of neurology
2021

Toward Population-Based Genetic Screening for Hereditary Amyloidosis.

JACC. CardioOncology
2021

TRANSTHYRETIN AMYLOIDOSIS THERAPIES: GUIDING THE FUTURE.

Revista de investigacion clinica; organo del Hospital de Enfermedades de la Nutricion
2021

Cardiomyopathy and Refractory Tachycardia in a Patient With Hereditary Amyloidosis.

Circulation. Heart failure
2021

Ocular Involvement in Hereditary Amyloidosis.

Genes
2021

A Case of Hearing Impairment with Renal Dysfunction.

Indian journal of nephrology
2021

Patisiran in hATTR Amyloidosis: Six-Month Latency Period before Efficacy.

Brain sciences
2022

Clinical comparison of V122I genotypic variant of transthyretin amyloid cardiomyopathy with wild-type and other hereditary variants: a systematic review.

Heart failure reviews
2021

Estimating the annual economic burden for the management of patients with transthyretin amyloid polyneuropathy in Spain.

Expert review of pharmacoeconomics & outcomes research
2021

Deposits on Retinal Surface Seen on OCT in Ocular Amyloidosis.

Ophthalmology. Retina
2021

Apolipoprotein genetic variants and hereditary amyloidosis.

Current opinion in lipidology
2020

Clinical 3-D Gait Assessment of Patients With Polyneuropathy Associated With Hereditary Transthyretin Amyloidosis.

Frontiers in neurology
2020

Analyses Mutations in GSN, CST3, TTR, and ITM2B Genes in Chinese Patients With Alzheimer's Disease.

Frontiers in aging neuroscience
2021

Targeting transthyretin - Mechanism-based treatment approaches and future perspectives in hereditary amyloidosis.

Journal of neurochemistry
2020

A case of cardiac amyloidosis in an elderly Japanese patient with amyloidogenic transthyretin Val122Ile variant.

Journal of cardiology cases
2021

Low Prevalence of Clinically Apparent Cardiac Amyloidosis Among Carriers of Transthyretin V122I Variant in a Large Electronic Medical Record.

The American journal of medicine
2020

Amyloid Typing by Mass Spectrometry in Clinical Practice: a Comprehensive Review of 16,175 Samples.

Mayo Clinic proceedings
2020

The effects of mutation and modification on the structure and stability of human lysozyme: A molecular link between carbamylation and atherosclerosis.

Journal of molecular graphics & modelling
2020

A Review of Patisiran (ONPATTRO®) for the Treatment of Polyneuropathy in People with Hereditary Transthyretin Amyloidosis.

Neurology and therapy
2020

Expression of Amyloidogenic Transthyretin Drives Hepatic Proteostasis Remodeling in an Induced Pluripotent Stem Cell Model of Systemic Amyloid Disease.

Stem cell reports
2020

Overview of treatments used in transthyretin-related hereditary amyloidosis: a systematic review.

European journal of hospital pharmacy : science and practice
2020

The sensitivity of DPD scintigraphy to detect transthyretin cardiac amyloidosis in V30M mutation depends on the phenotypic expression of the disease.

Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
2020

Renal amyloidosis: an update on diagnosis and pathogenesis.

Protoplasma
2020

Presence of val30Met and val122ile mutations in a patient with hereditary amyloidosis.

Journal of human genetics
2020

Cytodiagnosis and protein typing of amyloid from a vitreous washing: initial diagnostic workup of hereditary amyloidosis.

Journal of the American Society of Cytopathology
2020

In vitro investigation of the effect of mesalazine on amyloid fibril formation of hen egg-white lysozyme and defibrillation lysozyme fibrils.

European journal of pharmacology
2020

Regression of cardiac amyloid load documented by cardiovascular magnetic resonance in a patient with hereditary amyloidosis.

Clinical research in cardiology : official journal of the German Cardiac Society
2020

Clinical characteristics in patients with hereditary amyloidosis with Glu54Gln transthyretin identified in the Romanian population.

Orphanet journal of rare diseases
2020

Skin Biopsy in Evaluation of Autonomic Disorders.

Continuum (Minneapolis, Minn.)
2020

Finnish gelsolin amyloidosis causes significant disease burden but does not affect survival: FIN-GAR phase II study.

Orphanet journal of rare diseases
2020

Clinical manifestations in hereditary amyloidosis with the variant Glu54Gln transthyretin: a comment.

Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
2020

Fibrillar conformation of an apolipoprotein A-I variant involved in amyloidosis and atherosclerosis.

Biochimica et biophysica acta. General subjects
2019

Typing of hereditary renal amyloidosis presenting with isolated glomerular amyloid deposition.

BMC nephrology
2019

LEFT ATRIAL FUNCTION AND VOLUME BY MAGNETIC RESONANCE IN PATIENTS WITH HEREDITARY AMYLOIDOSIS.

Revista de investigacion clinica; organo del Hospital de Enfermedades de la Nutricion
2020

Diagnosis of genetic amyloidosis through the analysis of transthyretin gene mutation using high-resolution melting.

International journal of cardiology
2019

Neuropathy Associated with Systemic Amyloidosis.

Seminars in neurology
2019

An evaluation of patisiran: a viable treatment option for transthyretin-related hereditary amyloidosis.

Expert opinion on pharmacotherapy
2020

Transthyretin Cardiac Amyloidosis and Aortic Stenosis: Connection and Therapeutic Implications.

Current cardiology reviews
2019

Impact of Genetic Testing in Transthyretin (ATTR) Cardiac Amyloidosis.

Current heart failure reports
2019

Novel RNA-targeted therapies for hereditary ATTR amyloidosis and their impact on the autonomic nervous system.

Clinical autonomic research : official journal of the Clinical Autonomic Research Society
2019

Hereditary renal amyloidosis with a variant lysozyme p.Trp82Arg in a Chinese family: case report and literature review.

BMC nephrology
2019

Early diagnostic tools in hereditary amyloidosis related to transthyretin (hATTR) V30M autonomic neuropathy.

Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
2019

Clinical manifestations in hereditary amyloidosis with the variant Glu54Gln transthyretin.

Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
2019

Primary squamous cell carcinoma of the peristomal skin of gastrostomy in a transplant patient: a first case report.

Journal of gastrointestinal oncology
2019

Amyloid in parenchymal organs in gelsolin (AGel) amyloidosis.

Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
2019

Clinical Presentation, Diagnosis and Treatment of TTR Amyloidosis.

Journal of neuromuscular diseases
2018

Electrochemical skin conductance in hereditary amyloidosis related to transthyretin V30M - a promising tool to assess treatment efficacy?

Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
2019

Estimating the prevalence of allelic variants in the transthyretin gene by analysing large-scale sequencing data.

European journal of human genetics : EJHG
2019

A new genetic variant of hereditary apolipoprotein A-I amyloidosis: a case-report followed by discussion of diagnostic challenges and therapeutic options.

BMC medical genetics
2018

[What's new in dermatological treatment?].

Annales de dermatologie et de venereologie
2020

Cardiomyopathy and autonomic neuropathy in hereditary amyloidosis: Defining the cart and the horse.

Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology
2019

Atypical presentation of transthyretin amyloidosis in a non-endemic area.

Revista clinica espanola
2018

Non-parametric estimation of survival in age-dependent genetic disease and application to the transthyretin-related hereditary amyloidosis.

PloS one
2018

A Patient With Hereditary ATTR and a Novel AGel p.Ala578Pro Amyloidosis.

Mayo Clinic proceedings
2018

Phenotypic profile of Ile68Leu transthyretin amyloidosis: an underdiagnosed cause of heart failure.

European journal of heart failure
2018

Effects of Disease-Causing Mutations on the Conformation of Human Apolipoprotein A-I in Model Lipoproteins.

Biochemistry
2018

Amyloidosis due to TTR mutations in Mexico with 4 distincts genotypes in the index cases.

Orphanet journal of rare diseases
2018

Hereditary amyloidosis related to transthyretin V30M: disease progression in treated and untreated patients.

European journal of neurology
2019

Autonomic involvement in hereditary transthyretin amyloidosis (hATTR amyloidosis).

Clinical autonomic research : official journal of the Clinical Autonomic Research Society
2018

Newly designed 11-gene panel reveals first case of hereditary amyloidosis captured by massive parallel sequencing.

Journal of clinical pathology
2018

Primary adrenal insufficiency due to hereditary apolipoprotein AI amyloidosis: endocrine involvement beyond hypogonadism.

Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
2017

Psychopathological Dimensions in Portuguese Subjects with Transthyretin Familial Amyloid Polyneuropathy.

Biomedicine hub
2017

Renal Amyloidosis Associated With 5 Novel Variants in the Fibrinogen A Alpha Chain Protein.

Kidney international reports
2018

Clinical outcomes after preimplantation genetic diagnosis of patients with Corino de Andrade disease (familial amyloid polyneuropathy).

Reproductive biomedicine online
2018

Life paths of patients with transthyretin-related familial amyloid polyneuropathy Val30Met: a descriptive study.

Journal of community genetics
2017

Peptide probes detect misfolded transthyretin oligomers in plasma of hereditary amyloidosis patients.

Science translational medicine
2017

Structural determinants in ApoA-I amyloidogenic variants explain improved cholesterol metabolism despite low HDL levels.

Biochimica et biophysica acta. Molecular basis of disease
2017

Transthyretin Cardiac Amyloidosis.

Current cardiology reports
2016

[Transthyretin-related hereditary amyloidosis].

Revue medicale suisse
2017

Corino de Andrade disease: mechanisms and impact on reproduction.

JBRA assisted reproduction
2017

Familial progressive bilateral facial paralysis in Finnish type hereditary amyloidosis.

Practical neurology
2017

Long-term effects of liver transplantation on small-fiber dysfunction in Japanese transthyretin (ATTR) V30M hereditary amyloidosis with polyneuropathy (FAP).

Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
2017

Transthyretin-related hereditary amyloidosis in an Argentinian family with TTR Tyr114Cys mutation.

Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
2017

Transthyretin amyloidosis: a little history of hereditary amyloidosis.

Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
2017

Amyloid detection in the transverse carpal ligament of patients with hereditary ATTR V30M amyloidosis and carpal tunnel syndrome.

Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
2017

Transthyretin-related hereditary amyloidosis with recurrent vomiting and renal insufficiency as the initial presentation: A case report.

Medicine
2017

Amyloidosis: A cancer-derived paraproteinemia and kidney involvement.

Advances in medical sciences
2017

Hereditary Lysozyme Amyloidosis Variant p.Leu102Ser Associates with Unique Phenotype.

Journal of the American Society of Nephrology : JASN
2017

Exome sequencing establishes a gelsolin mutation as the cause of inherited bulbar-onset neuropathy.

Muscle & nerve
2016

Hereditary Amyloidosis with Recurrent Lung Infiltrates.

The American journal of case reports
2016

Apolipoprotein C-II Deposition Amyloidosis: A Potential Misdiagnosis as Light Chain Amyloidosis.

Case reports in nephrology
2016

Hereditary amyloidosis with cardiomyopathy caused by the novel variant transthyretin A36D.

Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
2016

Amyloidosis of the gastrointestinal tract and the liver: clinical context, diagnosis and management.

European journal of gastroenterology & hepatology
2017

Novel Type of Renal Amyloidosis Derived from Apolipoprotein-CII.

Journal of the American Society of Nephrology : JASN
2016

"Red-flag" symptom clusters in transthyretin familial amyloid polyneuropathy.

Journal of the peripheral nervous system : JPNS
2015

Structural and Functional Analysis of the ApolipoproteinA-I A164S Variant.

PloS one
2016

Protein conformational perturbations in hereditary amyloidosis: Differential impact of single point mutations in ApoAI amyloidogenic variants.

Biochimica et biophysica acta
2015

[Kidney Transplantation and inborn errors of metabolism].

Giornale italiano di nefrologia : organo ufficiale della Societa italiana di nefrologia
2015

Pathological, biochemical, and biophysical characteristics of the transthyretin variant Y114H (p.Y134H) explain its very mild clinical phenotype.

Journal of the peripheral nervous system : JPNS
2015

Hereditary apolipoprotein AI-associated renal amyloidosis: A diagnostic challenge.

Nefrologia : publicacion oficial de la Sociedad Espanola Nefrologia
2015

Vascular alterations in apolipoprotein A-I amyloidosis (Leu75Pro). A case-control study.

Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
2015

Three Turkish families with different transthyretin mutations.

Neuromuscular disorders : NMD
2015

Evaluation of operative risk in de novo familial amyloid polyneuropathy retransplantation.

Transplantation proceedings
2015

Transthyretin V122I amyloidosis with clinical and histological evidence of amyloid neuropathy and myopathy.

Neuromuscular disorders : NMD
2015

Myeloperoxidase-mediated Methionine Oxidation Promotes an Amyloidogenic Outcome for Apolipoprotein A-I.

The Journal of biological chemistry
2015

Transthyretin (ATTR) amyloidosis: clinical spectrum, molecular pathogenesis and disease-modifying treatments.

Journal of neurology, neurosurgery, and psychiatry

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Doenças relacionadas

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Referências e fontes

Bases de dados externas citadas neste artigo

Publicações científicas

Artigos indexados no PubMed ligados a esta doença no grafo RarasNet — título, periódico e PMID direto da fonte, sem intermediação de IA.

  1. Therapeutic Efficacy and Safety Profile of Eplontersen in Hereditary Transthyretin-Mediated Amyloidosis: A Systematic Review.
    Health science reports· 2026· PMID 41788641mais citado
  2. Central Nervous System Manifestations Associated with Hereditary Transthyretin Amyloidosis: a Narrative Review.
    Arquivos de neuro-psiquiatria· 2026· PMID 41871624mais citado
  3. Hereditary Transthyretin Amyloidosis in Austria: Clinical, Genetic, and Demographic Insights from a Nationwide Cohort.
    Journal of clinical medicine· 2026· PMID 41827375mais citado
  4. A Cautionary Tale: An Instructive Case of Recognising Non-Amyloid Light Chain Renal Amyloidosis.
    Nephrology (Carlton, Vic.)· 2026· PMID 41629223mais citado
  5. Natural variants of apolipoprotein A1 L99P and R173P exhibited a high degree of amyloid fibril formation: Implications for high-density lipoprotein functions and disease pathogenesis.
    International journal of biological macromolecules· 2026· PMID 41577276mais citado

Bases de dados e fontes oficiais

Identificadores e referências canônicas usadas para montar este verbete.

  1. ORPHA:444116(Orphanet)
  2. MONDO:0018634(MONDO)
  3. GARD:6611(GARD (NIH))
  4. Variantes catalogadas(ClinVar)
  5. Busca completa no PubMed(PubMed)
  6. Q5737919(Wikidata)

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.

Conteúdo mantido por Agente Raras · Médicos e pesquisadores podem colaborar

Amiloidose hereditária
Compêndio · Raras BR

Amiloidose hereditária

ORPHA:444116 · MONDO:0018634
🇧🇷 Brasil SUS
CEAF
1ATafamidisEplontersena
Geral
CID-10
E85.2 · Amiloidose heredofamiliar não especificada
CID-11
Ensaios
12 ativos
Medicamentos
13 registrados
MedGen
UMLS
C0206246
EuropePMC
Wikidata
Papers 10a
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