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Hipotireoidismo congênito permanente
ORPHA:226292CID-11 · 5A00.0YPCDT · SUSDOENÇA RARA

O hipotireoidismo congênito permanente é um tipo de hipotireoidismo congênito, ou seja, uma falta de hormônio da tireoide que já existe desde o nascimento.

Mantido por Agente Raras·Colaborar como especialista →

Introdução

O que você precisa saber de cara

📋

O hipotireoidismo congênito permanente é um tipo de hipotireoidismo congênito, ou seja, uma falta de hormônio da tireoide que já existe desde o nascimento.

Pesquisas ativas
1 ensaio
1 total registrados no ClinicalTrials.gov
Publicações científicas
122 artigos
Último publicado: 2026 Mar 17

Escala de raridade

CLASSIFICAÇÃO ORPHANET · BRASIL 2024
Unknown
Ultra-rara
<1/50k
Muito rara
1/20k
Rara
1/10k
Pouco freq.
1/5k
Incomum
1/2k
Prevalência
0.0
Worldwide
Início
Infancy
+ neonatal
🏥
SUS: Cobertura parcialScore: 60%
PCDT disponívelTriagem neonatal (Fase 1)Centros em: PA, PR, SC, RS, ES +10
Você se identifica com essa condição?
O Raras está aqui pra te apoiar — com ou sem diagnóstico

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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

📏
Crescimento
27 sintomas
🦴
Ossos e articulações
9 sintomas
🧠
Neurológico
7 sintomas
😀
Face
6 sintomas
💪
Músculos
4 sintomas
👁️
Olhos
2 sintomas

+ 47 sintomas em outras categorias

Características mais comuns

Aumento da concentração circulante de prolactina
Hipoplasia do nervo óptico
Pescoço curto
Retrusão médio-facial
Hipófise posterior ectópica
Nível diminuído de ACTH circulante
110sintomas
Sem dados (110)

Os sintomas variam de pessoa para pessoa. Abaixo estão as 110 características clínicas mais associadas, ordenadas por frequência.

Aumento da concentração circulante de prolactinaIncreased circulating prolactin concentration
Hipoplasia do nervo ópticoOptic nerve hypoplasia
Pescoço curtoShort neck
Retrusão médio-facialMidface retrusion
Hipófise posterior ectópicaEctopic posterior pituitary

Linha do tempo da pesquisa

Publicações por ano — veja quando o interesse científico cresceu
Anos de pesquisa1desde 2026
Total histórico122PubMed
Últimos 10 anos79publicações
Pico202515 papers
Linha do tempo
2026Hoje · 2026🧪 2006Primeiro ensaio clínico📈 2025Ano de pico
Publicações por ano (últimos 10 anos)

Triagem neonatal (Teste do Pezinho)

👶
Teste: TSH neonatal em sangue seco
Fase 1 do PNTNTriagem nacionalimplemented_nationally
Incidência no Brasil: 1:3.500

A triagem neonatal permite diagnóstico precoce e início imediato do tratamento.

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

11 genes identificados com associação a esta condição. Padrão de herança: Autosomal recessive, Not applicable.

TSHBThyrotropin subunit betaDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Indispensable for the control of thyroid structure and metabolism

LOCALIZAÇÃO

Secreted

VIAS BIOLÓGICAS (4)
G alpha (s) signalling eventsHormone ligand-binding receptorsThyroxine biosynthesisGlycoprotein hormones
MECANISMO DE DOENÇA

Hypothyroidism, congenital, non-goitrous, 4

A form of central hypothyroidism, a disorder characterized by insufficient stimulation by thyroid stimulating hormone of an otherwise normal thyroid gland. CHNG4 is an autosomal recessive form characterized by isolated thyrotropin deficiency that, if untreated, results in severe growth retardation and intellectual disability.

EXPRESSÃO TECIDUAL(Tecido-específico)
Pituitária
634.8 TPM
Testículo
1.0 TPM
Útero
0.9 TPM
Artéria tibial
0.9 TPM
Cólon sigmoide
0.7 TPM
OUTRAS DOENÇAS (1)
isolated thyroid-stimulating hormone deficiency
HGNC:12372UniProt:P01222
HESX1Homeobox expressed in ES cells 1Candidate gene tested inTolerante
FUNÇÃO

Required for the normal development of the forebrain, eyes and other anterior structures such as the olfactory placodes and pituitary gland. Possible transcriptional repressor. Binds to the palindromic PIII sequence, 5'-AGCTTGAGTCTAATTGAATTAACTGTAC-3'. HESX1 and PROP1 bind as heterodimers on this palindromic site, and, in vitro, HESX1 can antagonize PROP1 activation

LOCALIZAÇÃO

Nucleus

MECANISMO DE DOENÇA

Septooptic dysplasia

A clinically heterogeneous disorder defined by any combination of optic nerve hypoplasia, pituitary gland hypoplasia with panhypopopituitarism, and midline abnormalities of the brain, including absence of the corpus callosum and septum pellucidum.

EXPRESSÃO TECIDUAL(Ubíquo)
Testículo
9.7 TPM
Linfócitos
4.2 TPM
Pituitária
2.4 TPM
Nervo tibial
2.3 TPM
Tireoide
2.3 TPM
OUTRAS DOENÇAS (5)
septooptic dysplasiaKallmann syndromehypothyroidism due to deficient transcription factors involved in pituitary development or functionpituitary stalk interruption syndrome
HGNC:4877UniProt:Q9UBX0
POU1F1Pituitary-specific positive transcription factor 1Candidate gene tested inTolerante
FUNÇÃO

Transcription factor involved in the specification of the lactotrope, somatotrope, and thyrotrope phenotypes in the developing anterior pituitary. Specifically binds to the consensus sequence 5'-TAAAT-3'. Activates growth hormone and prolactin genes (PubMed:22010633, PubMed:26612202)

LOCALIZAÇÃO

Nucleus

MECANISMO DE DOENÇA

Pituitary hormone deficiency, combined, 1

Combined pituitary hormone deficiency is defined as the impaired production of growth hormone and one or more of the other five anterior pituitary hormones. CPHD1 is characterized by pleiotropic deficiencies of growth hormone, prolactin and thyroid-stimulating hormone, while the production of adrenocorticotropic hormone, luteinizing hormone, and follicle-stimulating hormone are preserved. In infancy severe growth deficiency from birth as well as distinctive facial features with prominent forehead, marked midfacial hypoplasia with depressed nasal bridge, deep-set eyes, and a short nose with anteverted nostrils and hypoplastic pituitary gland by MRI examination can be seen. Some cases present with severe intellectual disability along with short stature.

EXPRESSÃO TECIDUAL(Tecido-específico)
Pituitária
111.3 TPM
Cérebro - Hemisfério cerebelar
0.3 TPM
Cerebelo
0.2 TPM
Cervix Ectocervix
0.1 TPM
Fallopian Tube
0.1 TPM
OUTRAS DOENÇAS (4)
pituitary hormone deficiency, combined, 1hypothyroidism due to deficient transcription factors involved in pituitary development or functionisolated growth hormone deficiency type IIcombined pituitary hormone deficiencies, genetic form
HGNC:9210UniProt:P28069
LHX3LIM/homeobox protein Lhx3Candidate gene tested inTolerante
FUNÇÃO

Transcription factor. Recognizes and binds to the consensus sequence motif 5'-AATTAATTA-3' in the regulatory elements of target genes, such as glycoprotein hormones alpha chain CGA and visual system homeobox CHX10, positively modulating transcription; transcription can be co-activated by LDB2. Synergistically enhances transcription from the prolactin promoter in cooperation with POU1F1/Pit-1 (By similarity). Required for the establishment of the specialized cells of the pituitary gland and the n

LOCALIZAÇÃO

Nucleus

VIAS BIOLÓGICAS (1)
Regulation of expression of SLITs and ROBOs
MECANISMO DE DOENÇA

Pituitary hormone deficiency, combined, 3

Combined pituitary hormone deficiency is defined as the impaired production of growth hormone and one or more of the other five anterior pituitary hormones. CPHD3 is characterized by a complete deficit in all but one (adrenocorticotropin) anterior pituitary hormone and a rigid cervical spine leading to limited head rotation.

EXPRESSÃO TECIDUAL(Tecido-específico)
Pituitária
89.7 TPM
Testículo
0.4 TPM
Skin Not Sun Exposed Suprapubic
0.1 TPM
Cerebelo
0.1 TPM
Cérebro - Hemisfério cerebelar
0.0 TPM
OUTRAS DOENÇAS (2)
non-acquired combined pituitary hormone deficiency with spine abnormalitieshypothyroidism due to deficient transcription factors involved in pituitary development or function
HGNC:6595UniProt:Q9UBR4
PROP1Homeobox protein prophet of Pit-1Candidate gene tested inTolerante
FUNÇÃO

Possibly involved in the ontogenesis of pituitary gonadotropes, as well as somatotropes, lactotropes and caudomedial thyrotropes

LOCALIZAÇÃO

Nucleus

MECANISMO DE DOENÇA

Pituitary hormone deficiency, combined, 2

Combined pituitary hormone deficiency is defined as the impaired production of growth hormone and one or more of the other five anterior pituitary hormones. CPHD2 is characterized by pleiotropic deficiencies of growth hormone, thyroid-stimulating hormone, follicle-stimulating hormone, luteinizing hormone, prolactin and adrenocorticotropic hormone.

EXPRESSÃO TECIDUAL(Baixa expressão)
Pituitária
2.0 TPM
Cerebelo
0.3 TPM
Cérebro - Hemisfério cerebelar
0.3 TPM
Testículo
0.1 TPM
Próstata
0.0 TPM
OUTRAS DOENÇAS (4)
pituitary hormone deficiency, combined, 2combined pituitary hormone deficiencies, genetic formhypothyroidism due to deficient transcription factors involved in pituitary development or functionpanhypopituitarism
HGNC:9455UniProt:O75360
TRHPro-thyrotropin-releasing hormoneCandidate gene tested inTolerante
FUNÇÃO

As a component of the hypothalamic-pituitary-thyroid axis, it controls the secretion of thyroid-stimulating hormone (TSH) and is involved in thyroid hormone synthesis regulation. It also operates as modulator of hair growth. It promotes hair-shaft elongation, prolongs the hair cycle growth phase (anagen) and antagonizes its termination (catagen) by TGFB2. It stimulates proliferation and inhibits apoptosis of hair matrix keratinocytes

LOCALIZAÇÃO

Secreted

VIAS BIOLÓGICAS (2)
G alpha (q) signalling eventsPeptide ligand-binding receptors
EXPRESSÃO TECIDUAL(Tecido-específico)
Hipotálamo
19.7 TPM
Cervix Endocervix
4.3 TPM
Ovário
3.7 TPM
Testículo
2.7 TPM
Brain Caudate basal ganglia
1.9 TPM
OUTRAS DOENÇAS (1)
isolated thyrotropin-releasing hormone deficiency
HGNC:12298UniProt:P20396
LHX4LIM/homeobox protein Lhx4Candidate gene tested inModerado
FUNÇÃO

May play a critical role in the development of respiratory control mechanisms and in the normal growth and maturation of the lung. Binds preferentially to methylated DNA (PubMed:28473536)

LOCALIZAÇÃO

Nucleus

VIAS BIOLÓGICAS (1)
Regulation of expression of SLITs and ROBOs
MECANISMO DE DOENÇA

Pituitary hormone deficiency, combined, 4

Combined pituitary hormone deficiency is defined as the impaired production of growth hormone and one or more of the other five anterior pituitary hormones. CPHD4 is characterized by complete or partial deficiencies of growth hormone, thyroid-stimulating hormone, luteinizing hormone, follicle stimulating hormone and adrenocorticotropic hormone. Clinical features include short stature, cerebellar defects, and small sella turcica.

EXPRESSÃO TECIDUAL(Ubíquo)
Testículo
5.2 TPM
Cerebelo
5.0 TPM
Cérebro - Hemisfério cerebelar
3.9 TPM
Pituitária
3.4 TPM
Tireoide
3.2 TPM
OUTRAS DOENÇAS (4)
short stature-pituitary and cerebellar defects-small sella turcica syndromehypothyroidism due to deficient transcription factors involved in pituitary development or functionpituitary stalk interruption syndromecombined pituitary hormone deficiencies, genetic form
HGNC:21734UniProt:Q969G2
TRHRThyrotropin-releasing hormone receptorDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Receptor for thyrotropin-releasing hormone (TRH). Upon ligand binding, this G-protein-coupled receptor triggers activation of the phosphatidylinositol (IP3)-calcium-protein kinase C (PKC) pathway

LOCALIZAÇÃO

Cell membrane

VIAS BIOLÓGICAS (2)
G alpha (q) signalling eventsPeptide ligand-binding receptors
MECANISMO DE DOENÇA

Hypothyroidism, congenital, non-goitrous, 7

A form of central hypothyroidism, a disorder characterized by sub-optimal thyroid hormone secretion, due to insufficient stimulation by thyrotropin of an otherwise normal thyroid gland. It may be caused by congenital or acquired disorders of the pituitary gland or hypothalamus. CHNG7 is a congenital, autosomal recessive form characterized by normal-to-low T4 and normal-to-high thyrotropin levels, and reduced or absent pituitary responsiveness to thyrotropin-releasing hormone. Patients may exhibit short stature, growth retardation, and delayed bone age, as well as lethargy or fatigue.

EXPRESSÃO TECIDUAL(Baixa expressão)
Pituitária
0.9 TPM
Tireoide
0.1 TPM
Nervo tibial
0.1 TPM
Tecido adiposo
0.1 TPM
Músculo esquelético
0.0 TPM
OUTRAS DOENÇAS (1)
hypothyroidism, congenital, nongoitrous, 7
HGNC:12299UniProt:P34981
IGSF1Immunoglobulin superfamily member 1Disease-causing germline mutation(s) inRestrito
FUNÇÃO

Seems to be a coreceptor in inhibin signaling, but seems not to be a high-affinity inhibin receptor. Antagonizes activin A signaling in the presence or absence of inhibin B (By similarity). Necessary to mediate a specific antagonistic effect of inhibin B on activin-stimulated transcription

LOCALIZAÇÃO

MembraneSecreted

MECANISMO DE DOENÇA

Hypothyroidism, central, and testicular enlargement

A disorder characterized by insufficient thyroid gland stimulation by thyroid stimulating hormone (TSH), resulting from hypothalamic and/or pituitary dysfunction. CHTE patients have delayed testosterone increase at puberty with normal testosterone levels in adulthood, normal testicular volume in childhood and enlarged testicles in adulthood.

EXPRESSÃO TECIDUAL(Tecido-específico)
Pituitária
185.6 TPM
Hipotálamo
14.0 TPM
Nervo tibial
11.1 TPM
Testículo
9.8 TPM
Brain Nucleus accumbens basal ganglia
6.1 TPM
INTERAÇÕES PROTEICAS (1)
OUTRAS DOENÇAS (1)
X-linked central congenital hypothyroidism with late-onset testicular enlargement
HGNC:5948UniProt:Q8N6C5
SECISBP2Selenocysteine insertion sequence-binding protein 2Disease-causing germline mutation(s) inTolerante
FUNÇÃO

mRNA-binding protein that binds to the SECIS (selenocysteine insertion sequence) element present in the 3'-UTR of mRNAs encoding selenoproteins and facilitates the incorporation of the rare amino acid selenocysteine (PubMed:35709277). Insertion of selenocysteine at UGA codons is mediated by SECISBP2 and EEFSEC: SECISBP2 (1) specifically binds the SECIS sequence once the 80S ribosome encounters an in-frame UGA codon and (2) contacts the RPS27A/eS31 of the 40S ribosome before ribosome stalling (Pu

LOCALIZAÇÃO

NucleusMitochondrion

VIAS BIOLÓGICAS (1)
Selenocysteine synthesis
MECANISMO DE DOENÇA

Thyroid hormone metabolism, abnormal, 1

A disorder associated with a reduction in type II iodothyronine deiodinase activity.

VIAS REACTOME (1)
EXPRESSÃO TECIDUAL(Ubíquo)
Testículo
41.8 TPM
Ovário
40.0 TPM
Útero
32.8 TPM
Cervix Endocervix
31.7 TPM
Nervo tibial
30.9 TPM
OUTRAS DOENÇAS (1)
thyroid hormone metabolism, abnormal 1
HGNC:30972UniProt:Q96T21
THRAThyroid hormone receptor alphaDisease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Nuclear hormone receptor that can act as a repressor or activator of transcription. High affinity receptor for thyroid hormones, including triiodothyronine and thyroxine Does not bind thyroid hormone and functions as a weak dominant negative inhibitor of thyroid hormone action

LOCALIZAÇÃO

NucleusCytoplasm

VIAS BIOLÓGICAS (1)
Nuclear Receptor transcription pathway
MECANISMO DE DOENÇA

Hypothyroidism, congenital, non-goitrous, 6

A disease characterized by growth retardation, developmental retardation, skeletal dysplasia, borderline low thyroxine levels and high triiodothyronine levels. There is differential sensitivity to thyroid hormone action, with retention of hormone responsiveness in the hypothalamic pituitary axis and liver but skeletal, gastrointestinal, and myocardial resistance.

EXPRESSÃO TECIDUAL(Ubíquo)
Brain Nucleus accumbens basal ganglia
172.8 TPM
Cérebro - Hemisfério cerebelar
144.5 TPM
Cerebelo
126.3 TPM
Brain Caudate basal ganglia
110.4 TPM
Brain Anterior cingulate cortex BA24
109.7 TPM
OUTRAS DOENÇAS (2)
congenital nongoitrous hypothyroidism 6resistance to thyroid hormone due to a mutation in thyroid hormone receptor alpha
HGNC:11796UniProt:P10827

Variantes genéticas (ClinVar)

154 variantes patogênicas registradas no ClinVar.

🧬 TSHB: NM_000549.5(TSHB):c.226_227del (p.Asp76fs) ()
🧬 TSHB: NM_000549.5(TSHB):c.315T>A (p.Cys105Ter) ()
🧬 TSHB: NM_000549.5(TSHB):c.-1_5del (p.Met1_Thr2del) ()
🧬 TSHB: NM_000549.5(TSHB):c.141T>G (p.Cys47Trp) ()
🧬 TSHB: NC_000001.10:g.(?_115575984)_(115576848_?)del ()
Ver todas no ClinVar

Diagnóstico

Os sinais que médicos procuram e os exames que confirmam

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Tratamento e manejo

Remédios, cuidados de apoio e o que precisa acompanhar

Pipeline de tratamentos
Pipeline regulatório — de medicamentos já aprovados a drogas em pesquisa exploratória.
·Pré-clínico1
Medicamentos catalogadosEnsaios clínicos· 0 medicamentos · 1 ensaio
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Onde tratar no SUS

Hospitais de referência no Brasil e o protocolo oficial do SUS (PCDT)

🇧🇷 Atendimento SUS — Hipotireoidismo congênito permanente

Centros de Referência SUS

24 centros habilitados pelo SUS para Hipotireoidismo congênito permanente

Centros para Hipotireoidismo congênito permanente

Detalhes dos centros

Hospital Universitário Prof. Edgard Santos (HUPES)

R. Dr. Augusto Viana, s/n - Canela, Salvador - BA, 40110-060 · CNES 0003808

Serviço de Referência

Rota
Anomalias CongênitasErros Inatos do Metabolismo

Hospital Infantil Albert Sabin

R. Tertuliano Sales, 544 - Vila União, Fortaleza - CE, 60410-794 · CNES 2407876

Serviço de Referência

Rota
Anomalias CongênitasDeficiência Intelectual

Hospital de Apoio de Brasília (HAB)

AENW 3 Lote A Setor Noroeste - Plano Piloto, Brasília - DF, 70684-831 · CNES 0010456

Serviço de Referência

Rota
Anomalias CongênitasErros Inatos do MetabolismoDeficiência Intelectual

Hospital Estadual Infantil e Maternidade Alzir Bernardino Alves (HIABA)

Av. Min. Salgado Filho, 918 - Soteco, Vila Velha - ES, 29106-010 · CNES 6631207

Serviço de Referência

Rota
Anomalias CongênitasErros Inatos do MetabolismoDeficiência Intelectual

Hospital das Clínicas da UFG

Rua 235 QD. 68 Lote Área, Nº 285, s/nº - Setor Leste Universitário, Goiânia - GO, 74605-050 · CNES 2338424

Serviço de Referência

Rota
Anomalias CongênitasErros Inatos do Metabolismo

Hospital Universitário da UFJF

R. Catulo Breviglieri, Bairro - s/n - Santa Catarina, Juiz de Fora - MG, 36036-110 · CNES 2297442

Atenção Especializada

Rota
Anomalias Congênitas

Hospital das Clínicas da UFMG

Av. Prof. Alfredo Balena, 110 - Santa Efigênia, Belo Horizonte - MG, 30130-100 · CNES 2280167

Serviço de Referência

Rota
Anomalias CongênitasErros Inatos do MetabolismoDeficiência Intelectual

Hospital Universitário Julio Müller (HUJM)

R. Luis Philippe Pereira Leite, s/n - Alvorada, Cuiabá - MT, 78048-902 · CNES 2726092

Atenção Especializada

Rota
Anomalias Congênitas

Hospital Universitário João de Barros Barreto

R. dos Mundurucus, 4487 - Guamá, Belém - PA, 66073-000 · CNES 2337878

Serviço de Referência

Rota
Anomalias CongênitasErros Inatos do MetabolismoDeficiência Intelectual

Hospital Universitário Lauro Wanderley (HULW)

R. Tabeliao Estanislau Eloy, 585 - Castelo Branco, João Pessoa - PB, 58050-585 · CNES 0002470

Atenção Especializada

Rota
Anomalias Congênitas

Instituto de Medicina Integral Prof. Fernando Figueira (IMIP)

R. dos Coelhos, 300 - Boa Vista, Recife - PE, 50070-902 · CNES 0000647

Serviço de Referência

Rota
Anomalias CongênitasErros Inatos do MetabolismoDeficiência Intelectual

Hospital Pequeno Príncipe

R. Des. Motta, 1070 - Água Verde, Curitiba - PR, 80250-060 · CNES 3143805

Serviço de Referência

Rota
Anomalias CongênitasDeficiência Intelectual

Hospital Universitário Regional de Maringá (HUM)

Av. Mandacaru, 1590 - Parque das Laranjeiras, Maringá - PR, 87083-240 · CNES 2216108

Atenção Especializada

Rota
Anomalias Congênitas

Hospital de Clínicas da UFPR

R. Gen. Carneiro, 181 - Alto da Glória, Curitiba - PR, 80060-900 · CNES 2364980

Serviço de Referência

Rota
Anomalias CongênitasErros Inatos do MetabolismoDeficiência Intelectual

Hospital Universitário Pedro Ernesto (HUPE-UERJ)

Blvd. 28 de Setembro, 77 - Vila Isabel, Rio de Janeiro - RJ, 20551-030 · CNES 2280221

Serviço de Referência

Rota
Anomalias CongênitasErros Inatos do Metabolismo

Instituto Nacional de Saúde da Mulher, da Criança e do Adolescente Fernandes Figueira (IFF/Fiocruz)

Av. Rui Barbosa, 716 - Flamengo, Rio de Janeiro - RJ, 22250-020 · CNES 2269988

Serviço de Referência

Rota
Anomalias CongênitasErros Inatos do MetabolismoDeficiência Intelectual

Hospital São Lucas da PUCRS

Av. Ipiranga, 6690 - Jardim Botânico, Porto Alegre - RS, 90610-000 · CNES 2232928

Serviço de Referência

Rota
Anomalias CongênitasErros Inatos do Metabolismo

Hospital de Clínicas de Porto Alegre (HCPA)

Rua Ramiro Barcelos, 2350 Bloco A - Av. Protásio Alves, 211 - Bloco B e C - Santa Cecília, Porto Alegre - RS, 90035-903 · CNES 2237601

Serviço de Referência

Rota
Anomalias CongênitasErros Inatos do MetabolismoDeficiência Intelectual

Hospital Universitário da UFSC (HU-UFSC)

R. Profa. Maria Flora Pausewang - Trindade, Florianópolis - SC, 88036-800 · CNES 2560356

Serviço de Referência

Rota
Anomalias CongênitasErros Inatos do Metabolismo

Hospital das Clínicas da FMUSP

R. Dr. Ovídio Pires de Campos, 225 - Cerqueira César, São Paulo - SP, 05403-010 · CNES 2077485

Serviço de Referência

Rota
Anomalias CongênitasErros Inatos do MetabolismoDeficiência Intelectual

Hospital de Base de São José do Rio Preto

Av. Brg. Faria Lima, 5544 - Vila Sao Jose, São José do Rio Preto - SP, 15090-000 · CNES 2079798

Atenção Especializada

Rota
Anomalias Congênitas

Hospital de Clínicas da UNICAMP

R. Vital Brasil, 251 - Cidade Universitária, Campinas - SP, 13083-888 · CNES 2748223

Serviço de Referência

Rota
Anomalias CongênitasErros Inatos do MetabolismoDeficiência Intelectual

Hospital de Clínicas de Ribeirão Preto (HCRP-USP)

R. Ten. Catão Roxo, 3900 - Vila Monte Alegre, Ribeirão Preto - SP, 14015-010 · CNES 2082187

Serviço de Referência

Rota
Anomalias CongênitasErros Inatos do MetabolismoDeficiência Intelectual

UNIFESP / Hospital São Paulo

R. Napoleão de Barros, 715 - Vila Clementino, São Paulo - SP, 04024-002 · CNES 2688689

Serviço de Referência

Rota
Anomalias CongênitasErros Inatos do Metabolismo
Sobre os centros SUS: Estes centros são habilitados pelo Ministério da Saúde como Serviços de Referência em Doenças Raras ou Serviços de Atenção Especializada. O atendimento é pelo SUS, com encaminhamento da rede de atenção básica.

Dados de DATASUS/CNES, SBGM, ABNeuro e Ministério da Saúde. Sempre confirme a disponibilidade diretamente com o estabelecimento.

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Publicações mais relevantes

Timeline de publicações
79 papers (10 anos)
#1

Early prediction of transient versus permanent congenital hypothyroidism: a retrospective cohort study.

Annals of pediatric endocrinology &amp; metabolism2026 Feb

Early differentiation between transient congenital hypothyroidism (TCH) and permanent congenital hypothyroidism (PCH) is crucial for optimizing the duration of treatment. This retrospective cohort study aimed to evaluate whether levothyroxine (LT4) dose requirements over time can predict TCH and guide earlier discontinuation of treatment. We retrospectively analyzed 105 infants with congenital hypothyroidism and normal thyroid glands confirmed by imaging at a single tertiary care center (Inha University Hospital) between January 2013 and December 2022. Patients were classified into TCH (n=70) or PCH (n=35) based on thyroid function after LT4 withdrawal at 3 years of age. LT4 dose/kg at 6, 12, and 24 months, along with clinical and biochemical parameters, were compared between the 2 groups. Receiver operating characteristic (ROC) curve analysis was used to assess the predictive performance of LT4 dose thresholds. The LT4 dose was significantly lower in the TCH group at 6 (3.16±0.83 μg/kg vs. 3.75±0.99 μg/kg, P=0.005), 12 (2.51±0.82 μg/kg vs. 3.37±1.17 μg/kg, P&lt;0.001), and 24 months (2.02±0.61 μg/kg vs. 3.09±1.19 μg/kg, P&lt;0.001). ROC curve analysis showed an area under the curve (AUC) of 0.649, 0.746, and 0.794 at 6, 12, and 24 months, respectively. A logistic regression model incorporating LT4 dose, birth weight, and thyroid-stimulating hormone (TSH) levels improved prediction accuracy (AUC: 0.740, 0.782, 0.833 at 6, 12, and 24 months, respectively). LT4 dose requirements at 6, 12, and 24 months serve as useful indicators for differentiating TCH from PCH. A combined predictive model incorporating LT4 dose, birth weight, and TSH levels may improve diagnostic accuracy, supporting earlier discontinuation of treatment.

#2

Permanent or Transient Congenital Hypothyroidism: A Diagnostic Dilemma.

Acta paediatrica (Oslo, Norway : 1992)2026 Jan

Distinguishing between transient congenital hypothyroidism (TCH) and permanent congenital hypothyroidism (PCH) remains clinically challenging and is typically deferred until the age of 2-3 years, to minimise the potential risk of adverse neurodevelopmental effects due to treatment cessation. However, evidence suggests that earlier discrimination may be feasible, thus avoiding unnecessary, potentially harmful, prolonged levothyroxine (LT4) treatment. This narrative review aims to provide an overview of the current literature regarding potential predictive markers for distinguishing PCH from TCH. A comprehensive search of the PubMed and Google Scholar databases was independently performed by two authors to identify studies that evaluated the utility of several predictive factors. A total of 27 studies were included. The most commonly proposed predictors were thyroid imaging findings, thyroid-stimulating hormone (TSH) levels at diagnosis, LT4 doses at various time points during the treatment period, absolute daily LT4 dose, and episodes of TSH elevation above the reference interval during treatment. Despite these advances, no single marker or combination of markers has yet proven definitive in reliably differentiating PCH from TCH. Further research is needed to establish predictive models that could facilitate the early identification of TCH and the timely and safe treatment withdrawal.

#3

Hearing assessment of Egyptian children with permanent congenital hypothyroidism: A single-center experience.

International journal of pediatric otorhinolaryngology2026 Mar 17
#4

Term birth and levothyroxine dosage are significant factors associated with permanent congenital hypothyroidism: experience from a medical center in Taiwan.

BMC pediatrics2025 Oct 14

Before the introduction of newborn screening, congenital hypothyroidism was the leading cause of intellectual disability in infants and children. Patients with permanent congenital hypothyroidism require lifelong levothyroxine supplementation to prevent intellectual disability and growth failure. With progressively lower thyrotropin (TSH) cutoffs in newborn screening programs, more transient congenital hypothyroidism cases-requiring only temporary treatment-have also been identified. To avoid unnecessary medication use and reduce the burden on healthcare systems, early differentiation is essential. We retrospectively enrolled congenital hypothyroidism patients born between 2004 and 2018 and followed at MacKay Children's Hospital and classified them as permanent congenital hypothyroidism or transient congenital hypothyroidism based on levothyroxine dependence. Basic demographic data, including gender, gestational age, birth weight, newborn screening TSH levels, body height and weight, serum free T4, TSH levels, levothyroxine doses at every clinical visit, and age of TSH normalization were collected and compared between permanent and transient congenital hypothyroidism groups. A total of 152 infants were enrolled in this study, with 73 (48%) classified as permanent congenital hypothyroidism. Term births were more common in permanent than transient congenital hypothyroidism (80% vs. 48%, p < 0.01). TSH normalization took longer in permanent congenital hypothyroidism (75 vs. 45 days, p < 0.01). Serum TSH and levothyroxine doses remained higher in permanent congenital hypothyroidism at 6 months, and at 1, 2, and 3 years. The levothyroxine dose that provided the best discrimination between permanent and transient congenital hypothyroidism was 2.5 𝛍g/kg/d at age 2 years (sensitivity: 73%, specificity: 90%), and 1.8 𝛍g/kg/d at age 3 years (sensitivity: 82%, specificity: 91%). Nearly half of the patients required lifelong levothyroxine supplements under the current newborn screening program. Permanent congenital hypothyroidism patients were more likely term-born, showed delayed TSH normalization, had higher TSH levels, and required higher levothyroxine doses during follow-up. The best cut-off level to discriminate permanent from transient congenital hypothyroidism was 2.5 and 1.8 µg/kg/day at the age of 2 and 3 years, respectively.

#5

Congenital hypothyroidism in two children affected by Sotos syndrome: a simple association?

Italian journal of pediatrics2025 Sep 29

Congenital hypothyroidism (CH) is the most common congenital endocrine disorder and one of the most preventable causes of intellectual disability. The underlying etiology of CH can be thyroid dysgenesis or dyshormonogenesis, and in rare cases, CH can occur as part of a genetic syndrome. Sotos syndrome is a rare overgrowth disorder caused by pathogenic variants in the NSD1 gene, characterized by excessive growth in infancy, distinctive facial features, and developmental delay. We describe two unrelated children with permanent CH and genetically confirmed Sotos syndrome. Both children were referred to our Pediatric Endocrinology Centre due to abnormal thyroid-stimulating hormone (TSH) values detected through neonatal screening. A permanent CH was confirmed in both cases: one patient had thyroid hypoplasia with the presence of only the right thyroidal lobe; the other one had an in-situ thyroid gland. The diagnosis of Sotos syndrome was made later in infancy. In the first case, auxological parameters at birth were within normal ranges and overgrowth became apparent after six months of age; in the second case, overgrowth was already manifest at birth, but the diagnosis was guided primarily by the neurodevelopmental delay. We describe two cases in which CH occurred with Sotos syndrome, and we hypothesize that this association may not be coincidental. To our knowledge, these are among the few reported cases of genetically confirmed Sotos syndrome associated with permanent congenital hypothyroidism. Further studies are needed to determine whether CH is a clinical feature of Sotos syndrome or an unrelated finding. We recommend early thyroid function testing in patients with Sotos syndrome and suggest suspecting Sotos syndrome in children presenting with CH, cognitive delay and overgrowth or additional congenital anomalies.

Publicações recentes

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📚 EuropePMC46 artigos no totalmostrando 79

2026

Hearing assessment of Egyptian children with permanent congenital hypothyroidism: A single-center experience.

International journal of pediatric otorhinolaryngology
2026

Early prediction of transient versus permanent congenital hypothyroidism: a retrospective cohort study.

Annals of pediatric endocrinology &amp; metabolism
2025

Predictive Factors of Transient Congenital Hypothyroidism among Filipino Children: A Retrospective Study.

Acta medica Philippina
2025

Prematurity Appears to Be the Main Factor for Transient Congenital Hypothyroidism in Greece, a Recently Iodine-Replete Country.

Nutrients
2025

Term birth and levothyroxine dosage are significant factors associated with permanent congenital hypothyroidism: experience from a medical center in Taiwan.

BMC pediatrics
2025

Congenital hypothyroidism in two children affected by Sotos syndrome: a simple association?

Italian journal of pediatrics
2026

Permanent or Transient Congenital Hypothyroidism: A Diagnostic Dilemma.

Acta paediatrica (Oslo, Norway : 1992)
2025

Clinical Outcomes of Congenital Hypothyroidism Due to DUOX2 Biallelic Mutations after Levothyroxine Withdrawal.

Thyroid : official journal of the American Thyroid Association
2025

Differentiating transient and permanent congenital hypothyroidism: predictive clues from Istanbul, Türkiye.

Journal of pediatric endocrinology &amp; metabolism : JPEM
2025

50 YEARS OF NEWBORN SCREENING FOR CONGENITAL HYPOTHYROIDISM: EVOLUTION OF INSIGHTS IN ETIOLOGY, DIAGNOSIS AND MANAGEMENT: Transient or permanent congenital hypothyroidism: from milestones to current and future perspectives.

European thyroid journal
2025

Predicting variables associated with diagnostic reevaluation of transient congenital hypothyroidism.

Annals of pediatric endocrinology &amp; metabolism
2025

Transient vs Permanent Congenital Hypothyroidism: Does Thyroid Volume Tell the Tale?

Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
2025

Permanent Congenital Hypothyroidism due to Rare Thyroglobulin Gene Variant (p.Cys1476Arg): A Delayed Diagnosis of Thyroid Dyshormonogenesis.

Case reports in medicine
2025

Genetic Etiology of Permanent Congenital Hypothyroidism in Korean Patients: A Whole-Exome Sequencing Study.

International journal of molecular sciences
2025

Author Correction: Age of menarche and final height in patients with permanent congenital hypothyroidism.

Annals of pediatric endocrinology &amp; metabolism
2025

Predictive factors of permanent versus transient congenital hypothyroidism: a pragmatic cohort study.

Annals of pediatric endocrinology &amp; metabolism
2024

Age of menarche and final height in patients with permanent congenital hypothyroidism.

Annals of pediatric endocrinology &amp; metabolism
2024

The natural course of newborns with transient congenital hypothyroidism.

Endocrine connections
2025

Comparison Between Ultrasonography and Radiography in the Detection of Epiphyseal Ossification Centers of the Knee in Infants With Permanent Congenital Hypothyroidism.

Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine
2024

Diagnostic options, physiopathology, risk factors and genetic causes of permanent congenital hypothyroidism: A narrative review.

Caspian journal of internal medicine
2024

Patients with Thyroid Dyshormonogenesis and DUOX2 Variants: Molecular and Clinical Description and Genotype-Phenotype Correlation.

International journal of molecular sciences
2025

A practical gestational age-based algorithm for timely detection of hypothyroidism in premature infants.

Journal of perinatology : official journal of the California Perinatal Association
2024

High frequency of transient congenital hypothyroidism among infants referred for suspected congenital hypothyroidism from the Turkish National screening program: thyroxine dose may guide the prediction of transients.

Journal of endocrinological investigation
2023

Comparison between transient and permanent congenital hypothyroidism on a thyroid function test after re-evaluation.

Annals of pediatric endocrinology &amp; metabolism
2023

Evaluation of patients diagnosed with congenital hypothyroidism by newborn screening between 2011-2019 in Diyarbakir, Turkey.

Medicine
2024

Permanent vs Transient Congenital Hypothyroidism in Chinese Children: Physical Growth and Predictive Nomogram.

The Journal of clinical endocrinology and metabolism
2023

Congenital hypothyroidism and thyroid function in a Japanese birth cohort: data from The Japan Environment and Children's Study.

Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology
2023

Evaluation of Transient or Permanent Congenital Hypothyroidism.

Journal of clinical practice and research
2023

Physical Development at School Entry in Children with Congenital Hypothyroidism Diagnosed by the National Program of Newborn Screening in Iran.

International journal of endocrinology and metabolism
2023

Congenital hypothyroidism in children with eutopic gland or thyroid hemiagenesis: prognostic factors for transient vs. permanent hypothyroidism.

Journal of pediatric endocrinology &amp; metabolism : JPEM
2023

Predictive factors for the diagnosis of permanent congenital hypothyroidism and its temporal changes in Sergipe, Brazil - A real-life retrospective study.

Archives of endocrinology and metabolism
2023

Clinical and genetic investigation in patients with permanent congenital hypothyroidism.

Clinica chimica acta; international journal of clinical chemistry
2022

Gene mutations in children with permanent congenital hypothyroidism in Yunnan, China.

Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences
2022

Iatrogenic hyperthyroidism in primary congenital hypothyroidism: prevalence and predictive factors.

Journal of pediatric endocrinology &amp; metabolism : JPEM
2021

Diagnostic Re-Evaluation and Potential Predictor Factors of Transient and Permanent Congenital Hypothyroidism in Eutopic Thyroid Gland.

Journal of clinical medicine
2022

Screening of 23 candidate genes by next-generation sequencing of patients with permanent congenital hypothyroidism: novel variants in TG, TSHR, DUOX2, FOXE1, and SLC26A7.

Journal of endocrinological investigation
2022

Transient vs Permanent Congenital Hypothyroidism in Ontario, Canada: Predictive Factors and Scoring System.

The Journal of clinical endocrinology and metabolism
2021

Congenital Hypothyroidism Can Dictate the Mode of Delivery and Intra-Labor Medication Usage.

Thyroid : official journal of the American Thyroid Association
2021

Congenital hypothyroidism in Indian preterm babies - screening, prevalence, and aetiology.

Pediatric endocrinology, diabetes, and metabolism
2021

Case Report: Expanding the Digenic Variants Involved in Thyroid Hormone Synthesis-10 New Cases of Congenital Hypothyroidism and a Literature Review.

Frontiers in genetics
2021

Sotos syndrome with a novel mutation in the NSD1 gene associated with congenital hypothyroidism.

International journal of pediatrics &amp; adolescent medicine
2021

Thyroid Function in Preterm/Low Birth Weight Infants: Impact on Diagnosis and Management of Thyroid Dysfunction.

Frontiers in endocrinology
2021

Newborn Screening for Congenital Hypothyroidism in Japan.

International journal of neonatal screening
2021

Curating the gnomAD database: Report of novel variants in the thyrogobulin gene using in silico bioinformatics algorithms.

Molecular and cellular endocrinology
2021

Prevalence and predictive factors of transient and permanent congenital hypothyroidism in Fars province, Iran.

BMC pediatrics
2021

Re-Evaluation of the Prevalence of Permanent Congenital Hypothyroidism in Niigata, Japan: A Retrospective Study.

International journal of neonatal screening
2021

Risk factors for transient and permanent congenital hypothyroidism: a population-based case-control study.

Thyroid research
2021

Thyroid imaging study in children with suspected thyroid dysgenesis.

Annals of pediatric endocrinology &amp; metabolism
2020

Intelligence Quotient, Anxiety, and Depression in Congenital Hypothyroid Children at School Age.

International journal of preventive medicine
2021

Development of a risk prediction model for early discrimination between permanent and transient congenital hypothyroidism.

Endocrine
2020

Increase in doses of levothyroxine at the age of 3 years and above is useful for distinguishing transient and permanent congenital hypothyroidism.

Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology
2020

Pearls and Pitfalls in Pediatric Thyroid Imaging.

Seminars in ultrasound, CT, and MR
2020

Complicated Relationship between Genetic Mutations and Phenotypic Characteristics in Transient and Permanent Congenital Hypothyroidism: Analysis of Pooled Literature Data.

International journal of endocrinology
2020

Validity of Six Month L-Thyroxine Dose for Differentiation of Transient or Permanent Congenital Hypothyroidism.

Journal of clinical research in pediatric endocrinology
2020

EPIDEMIOLOGIC CHARACTERISTICS AND RISK FACTORS FOR CONGENITAL HYPOTHYROIDISM FROM 2009 TO 2018 IN XIAMEN, CHINA.

Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
2019

Levothyroxine dosages less than 2.4 μg/kg/day at 1 year and 1.3 μg/kg/day at 3 years of age may predict transient congenital hypothyroidism.

Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology
2019

Prediction of Transient or Permanent Congenital Hypothyroidism.

Indian pediatrics
2019

Levothyroxine Dosage as Predictor of Permanent and Transient Congenital Hypothyroidism: A Multicenter Retrospective Study in Japan.

Hormone research in paediatrics
2019

Congenital hypothyroidism in different cities of the Isfahan province: A descriptive retrospective study.

Journal of education and health promotion
2019

The value of serial newborn screening for congenital hypothyroidism using thyroxine (T4) in the neonatal intensive care unit.

Journal of perinatology : official journal of the California Perinatal Association
2018

Prediction of Transient or Permanent Congenital Hypothyroidism from Initial Thyroid Stimulating Hormone Levels.

Indian pediatrics
2018

Higher prevalence of permanent congenital hypothyroidism in the Southwest of Iran mostly caused by dyshormonogenesis: a five-year follow-up study.

Archives of endocrinology and metabolism
2019

Optimal Timing of Repeat Newborn Screening for Congenital Hypothyroidism in Preterm Infants to Detect Delayed Thyroid-Stimulating Hormone Elevation.

The Journal of pediatrics
2018

A 7-year study on the prevalence of congenital hypothyroidism in northern Iran.

Electronic physician
2018

Intelligence Quotient at the Age of Six years of Iranian Children with Congenital Hypothyroidism.

Indian pediatrics
2017

[Transient congenital hypothyroidism due to biallelic defects of DUOX2 gene. Two clinical cases].

Archivos argentinos de pediatria
2017

Three-year follow-up of children with abnormal newborn screening results for congenital hypothyroidism.

Pediatrics and neonatology
2017

[Genetic analysis of TPO, DUOX2 and DUOXA2 genes in children with permanent congenital hypothyroidism suspected dyshormonogenesis].

Zhonghua er ke za zhi = Chinese journal of pediatrics
2016

Transient versus Permanent Congenital Hypothyroidism after the Age of 3 Years in Infants Detected on the First versus Second Newborn Screening Test in Oregon, USA.

Hormone research in paediatrics
2016

Can One Predict Resolution of Neonatal Hyperthyrotropinemia?

The Journal of pediatrics
2016

High prevalence of DUOX2 mutations in Japanese patients with permanent congenital hypothyroidism or transient hypothyroidism.

Journal of pediatric endocrinology &amp; metabolism : JPEM
2016

Next-generation sequencing analysis of DUOX2 in 192 Chinese subclinical congenital hypothyroidism (SCH) and CH patients.

Clinica chimica acta; international journal of clinical chemistry
2018

Permanent congenital hypothyroidism with blood spot thyroid stimulating hormone <10 mU/L.

Archives of disease in childhood
2016

Feasibility of an Early Discontinuation of Thyroid Hormone Treatment in Very-Low-Birth-Weight Infants at Risk for Transient or Permanent Congenital Hypothyroidism.

Hormone research in paediatrics
2016

Thyroid dysfunction and developmental anomalies in first degree relatives of children with thyroid dysgenesis.

World journal of pediatrics : WJP
2015

The evaluation of transient hypothyroidism in patients diagnosed with congenital hypothyroidism.

Turkish journal of medical sciences
2015

Mutation screening of DUOX2 in Chinese patients with congenital hypothyroidism.

Journal of endocrinological investigation
2015

Early Discrimination between Transient and Permanent Congenital Hypothyroidism in Children with Eutopic Gland.

Hormone research in paediatrics
2015

Hypothyroidism caused by the combination of two heterozygous mutations: one in the TSH receptor gene the other in the DUOX2 gene.

Journal of pediatric endocrinology &amp; metabolism : JPEM

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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. Early prediction of transient versus permanent congenital hypothyroidism: a retrospective cohort study.
    Annals of pediatric endocrinology &amp; metabolism· 2026· PMID 41787711mais citado
  2. Permanent or Transient Congenital Hypothyroidism: A Diagnostic Dilemma.
    Acta paediatrica (Oslo, Norway : 1992)· 2026· PMID 40976938mais citado
  3. Hearing assessment of Egyptian children with permanent congenital hypothyroidism: A single-center experience.
    International journal of pediatric otorhinolaryngology· 2026· PMID 41863870mais citado
  4. Term birth and levothyroxine dosage are significant factors associated with permanent congenital hypothyroidism: experience from a medical center in Taiwan.
    BMC pediatrics· 2025· PMID 41088038mais citado
  5. Congenital hypothyroidism in two children affected by Sotos syndrome: a simple association?
    Italian journal of pediatrics· 2025· PMID 41024235mais citado
  6. Predictive Factors of Transient Congenital Hypothyroidism among Filipino Children: A Retrospective Study.
    Acta Med Philipp· 2025· PMID 41393913recente
  7. Prematurity Appears to Be the Main Factor for Transient Congenital Hypothyroidism in Greece, a Recently Iodine-Replete Country.
    Nutrients· 2025· PMID 41097117recente

Bases de dados e fontes oficiais

Identificadores e referências canônicas usadas para montar este verbete.

  1. ORPHA:226292(Orphanet)
  2. MONDO:0016408(MONDO)
  3. Hipotiroidismo Congenito(PCDT · Ministério da Saúde)
  4. GARD:20560(GARD (NIH))
  5. Variantes catalogadas(ClinVar)
  6. Busca completa no PubMed(PubMed)
  7. Q55786203(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

Hipotireoidismo congênito permanente
Compêndio · Raras BR

Hipotireoidismo congênito permanente

ORPHA:226292 · MONDO:0016408
🇧🇷 Brasil SUS
Triagem
TSH neonatal em sangue seco
PNTN
Fase 1 · Nacional
Incidência BR
1:3.500
Geral
Prevalência
Unknown
Herança
Autosomal recessive, Not applicable
CID-11
Ensaios
1 ativos
Início
Infancy, Neonatal
Prevalência
0.0 (Worldwide)
MedGen
UMLS
C5680893
Repurposing
1 candidato
liothyroninethyroid hormone stimulant
EuropePMC
Wikidata
Papers 10a
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