Doença de Krabbe da infância é um distúrbio neurodegenerativo autossômico recessivo, com início precoce, caracterizado por perda visual, espasticidade e rigidez de descerebração. A atrofia cerebral difusa e neuropatia periférica são achados comuns, associados a mioclonias e vômitos.
Introdução
O que você precisa saber de cara
Visão geral
A Doença de Krabbe da infância (identificada no sistema MONDO como MONDO:0016089 e classificada sob o código CID-10 E75.2) é uma condição metabólica rara e neurodegenerativa, cuja prevalência global é considerada desconhecida. Possui padrão de herança autossômico recessivo e manifesta seus primeiros sinais caracteristicamente na infância.[1][2]
Sinais e sintomas
O quadro clínico com início na infância pode apresentar manifestações neurológicas complexas, incluindo encefalopatia, atrofia cerebral difusa, neuropatia periférica, morfologia anormal da substância branca periventricular e rigidez de descerebração. Observam-se também alterações motoras como espasticidade, diplegia espástica, clônus do tornozelo, fraqueza muscular generalizada e fraqueza dos músculos do pescoço, além de mioclonias e crises mioclônicas generalizadas.[1][2]
As crianças afetadas podem apresentar ainda perda visual, anormalidade dos potenciais visuais evocados, deficiência auditiva e aumento do perímetro cefálico. Outros achados descritos englobam vômitos, desconforto respiratório, laringomalácia, infecções recorrentes, déficit de crescimento, manchas cutâneas hipopigmentadas e aumento da concentração de proteína no líquido cefalorraquidiano (LCR).[1][2]
Causas genéticas
Diagnóstico
A investigação diagnóstica apoia-se no reconhecimento dos sinais neurológicos, alterações líquicas e nos exames genéticos moleculares. No contexto de testes genéticos, há registros de 9 testes genéticos disponíveis e mais de 655 variantes catalogadas na base ClinVar para a confirmação de variantes patogênicas nos genes relacionados.[1][3][4]
Tratamento e manejo
Tratamentos citados na literatura
Com base em dados minerados de literatura científica pela plataforma PubTator3 (NCBI), foram identificadas coocorrências textuais de biomoléculas e compostos relacionados à doença, sem que isso represente indicação de uso ou recomendação clínica: Psychosine (92 publicações), Galactosylceramides (23 publicações), Sphingolipids (12 publicações), Lipids (10 publicações), Glycosphingolipids (7 publicações), Cerebrosides (6 publicações), CDw17 antigen (5 publicações), galactocerebroside (5 publicações), sphingosyl beta glucoside (5 publicações) e Sulfoglycosphingolipids (3 publicações).[4]
Conteúdo informativo gerado e mantido automaticamente a partir de fontes oficiais (Orphanet, HPO, OMIM, SUS). Não substitui avaliação médica.
A Doença de Krabbe da infância é uma condição genética rara de herança autossômica recessiva que começa a manifestar sintomas nos primeiros meses de vida. Ela costuma provocar irritabilidade, espasticidade muscular, crises mioclônicas e perda progressiva das capacidades psicomotoras. A alteração está ligada principalmente a variantes no gene GALC, que afetam o funcionamento enzimático. No Brasil, a enfermidade não consta na lista oficial de PCDTs de doenças raras do SUS, não havendo remédio específico dispensado em diretriz ministerial própria.
Doença de Krabbe da infância é um distúrbio neurodegenerativo autossômico recessivo, com início precoce, caracterizado por perda visual, espasticidade e rigidez de descerebração. A atrofia cerebral difusa e neuropatia periférica são achados comuns, associados a mioclonias e vômitos.
Tem tratamento?
Escala de raridade
<1/50kMuito rara
1/20kRara
1/10kPouco freq.
1/5kIncomum
1/2k
Encontrou um erro ou informação desatualizada? Sugira uma correção →
Entender a doença
Do básico ao detalhe, leia no seu ritmo
Preparando trilha educativa...
Sinais e sintomas
O que aparece no corpo e com que frequência cada sintoma acontece
Partes do corpo afetadas
+ 22 sintomas em outras categorias
Características mais comuns
Os sintomas variam de pessoa para pessoa. Abaixo estão as 71 características clínicas mais associadas, ordenadas por frequência.
Linha do tempo da pesquisa
Encontrou um erro ou informação desatualizada? Sugira uma correção →
Genética e causas
O que está alterado no DNA e como passa nas famílias
Genes associados
2 genes identificados com associação a esta condição. Padrão de herança: Autosomal recessive.
Krabbe disease
An autosomal recessive disorder characterized by insufficient catabolism of several galactolipids that are important for normal myelin production. Four clinical forms are recognized. The infantile form accounts for 90% of cases. It manifests before six months of age with irritability, spasticity, arrest of motor and mental development, and bouts of temperature elevation without infection. This is followed by myoclonic jerks of arms and legs, oposthotonus, hypertonic fits, and mental regression, which progresses to a severe decerebrate condition with no voluntary movements and death from respiratory infections or cerebral hyperpyrexia before 2 years of age. Cases with later onset present with unexplained blindness, weakness and sensorimotor peripheral neuropathy, mental deterioration and death.
Variantes genéticas (ClinVar)
655 variantes patogênicas registradas no ClinVar.
Vias biológicas (Reactome)
15 vias biológicas associadas aos genes desta condição.
Diagnóstico
Os sinais que médicos procuram e os exames que confirmam
Tratamento e manejo
Remédios, cuidados de apoio e o que precisa acompanhar
Onde tratar no SUS
Hospitais de referência no Brasil e o protocolo oficial do SUS (PCDT)
Dado oficial do SIH/SUS · Volume por estado de residência do paciente.
🇧🇷 Atendimento SUS — Doença de Krabbe da infância
Selecione um estado ou use sua localização para ver resultados.
Dados de DATASUS/CNES, SBGM, ABNeuro e Ministério da Saúde. Sempre confirme a disponibilidade diretamente com o estabelecimento.
Pesquisa ativa
Ensaios clínicos abertos e novidades científicas recentes
Pesquisa e ensaios clínicos
Nenhum ensaio clínico registrado para esta condição.
Publicações mais relevantes
Caregiver-reported disease burden in Krabbe disease: evaluating outcomes of hematopoietic stem cell transplantation.
Krabbe disease (KD) is a rapidly progressive neurodegenerative disorder caused by β-galactocerebrosidase deficiency. While KD has been added to the Recommended Uniform Screening Panel (RUSP), only 15 states have an active KD newborn screening (NBS) program. It is uncertain at what rate states will adopt RUSP recommendations, with a frequently cited barrier being the absence of investigations addressing the impact of hematopoietic stem cell transplantation (HSCT) on quality-of-life. We developed a 90-minute caregiver interview to gather qualitative and quantitative data (including the validated Leukodystrophy Quality-of-Life Assessment – LQLA) evaluating patient/family-centered outcomes of HSCT. The interview was designed to explore the following: 1) disease burden on the patient; 2) physical burden on the caregiver; and 3) emotional/social burden on the caregiver. Comparisons were made between children not transplanted/transplanted late and children transplanted early. Infantile KD (IKD) and late infantile KD (LIKD) were analyzed independently. Forty caregivers participated (non-transplanted/transplanted late: IKD = 19, LIKD = 7; transplanted early: IKD = 10, LIKD = 4). Analysis of the LQLA revealed a relative reduction in disease burden in both IKD and LIKD groups who were transplanted early. Specifically, the early transplanted cohorts achieved statistically significant higher overall scores on the LQLA, as well as better scores in various subcategories in comparison to their non-transplanted/transplanted late counterparts. For IKD, analysis of Likert scale and weighted analysis demonstrated a tendency towards decreased physical burden on caregivers of children transplanted early. Although all groups experienced significant social/emotional burdens, caregivers of IKD transplanted early benefitted from improved sleep, mental health, and familial/spousal relationships compared to IKD non-transplanted/transplanted late. This study provides convincing evidence that HSCT improves quality-of-life and reduces caregiver burden in IKD. The evidence is somewhat less clear for LIKD due to the small LIKD sample size. This data will be critical in the decision-making process for states not currently screening for KD but debating the addition of KD to their NBS panels. Lastly, it will allow families to weigh the risks and benefits of HSCT more confidently when contemplating the life-altering decision of whether to proceed with transplantation.
Novel GALC Deletion and Paradoxical Optic Nerve Hypertrophy in Severe Infantile Krabbe Disease.
Molecular Characterization of the GALC Mutation Thr112Ala Causing Krabbe Disease.
Krabbe disease is a rare and severe lysosomal disorder affecting the white matter of the central and peripheral nervous system. It is characterized by neurodegeneration, with the most common form being infantile Krabbe disease, typically diagnosed within the first year of life. This autosomal-recessive disease is caused by mutations in the GALC gene, which encodes the lysosomal enzyme β-galactocerebrosidase. This study focuses on a β-galactocerebrosidase variant, with Thr112Ala identified as a homozygous mutation in a patient with infantile Krabbe disease. To understand the structural effects of this mutation, we conducted all-atom molecular dynamics simulations of both the mutant and wild-type (wt) enzymes at cytosolic (pH 7.0) and lysosomal pH (pH 4.5), as β-galactocerebrosidase is localized in the lysosome. The results showed differences in protein flexibility, the hydrogen bond network, and the stability of secondary structure elements between the wild type and mutant enzymes. Additionally, the mutation affected the size of the substrate-binding pocket at lysosomal pH, even though the mutation site is not part of the active/binding site of the enzyme. These findings provide valuable insights into how the mutation impacts the structure of β-galactocerebrosidase in the lysosomal environment, contributing to the understanding of Krabbe disease's molecular mechanisms.
Two-tiered newborn screening for infantile Krabbe disease allows timely treatment initiation and avoids false-positive results.
Infantile Krabbe disease (IKD) is a severe, progressive neurological disorder that was recently added to the Recommended Uniform Screening Panel in the United States. IKD is a critical condition that requires a hematopoietic stem cell transplant, preferably by 30 days of age. This study examines whether the 2-tier newborn screening (NBS) strategy (psychosine [PSY] analysis when enzyme activity is low) causes clinically relevant delays compared with PSY measured at a first clinical follow-up visit. We reviewed the PSY analyses performed over a 6-year period on dried blood spots on infants < 28 days old. Results were sorted by the ordering site and final diagnosis. On average, infants with a positive NBS for IKD that included abnormal PSY received their diagnosis 7 days sooner than whose PSY testing was initiated during follow-up. Hematopoietic stem cell transplant occurred by the 36th day of life, on average, for cases with IKD detected by 2-tiered NBS. Effective NBS for Krabbe disease requires the use of PSY as a second-tier test, allowing for timely initiation of treatment while virtually eliminating false-positive results. PSY should be included in NBS algorithms for Krabbe disease, and timeliness metrics need to be adjusted.
Evidence and Recommendation for Infantile Krabbe Disease Newborn Screening.
Krabbe disease (KD), which affects 0.3-2.6 per 100 000 live births, is an autosomal recessive lysosomal disorder caused by variants in the GALC gene that reduce galactosylceramidase (GALC) activity, leading to psychosine accumulation, cerebral white matter degeneration, and peripheral neuropathy. The most common form, infantile KD (IKD), has onset by 12 months with irritability, feeding difficulty, neurologic regression, and, when untreated, death in early childhood. Hematopoietic stem cell transplantation (HSCT) for IKD approximately 1 month after birth can improve long-term survival but has about a 10% risk of mortality within 100 days, and affected individuals can still have significant functional impairment. Newborn screening for KD is based on low GALC levels in dried-blood spots. Second-tier testing to assess whether an elevated psychosine concentration is present in the same dried-blood spot improves the specificity of screening for IKD. Without newborn screening, diagnosis of IKD is generally made after significant clinical symptoms develop, past when HSCT can be effective. The benefit of newborn detection of later-onset phenotypes of KD is uncertain. In 2024, the US Secretary of Health and Human Services added IKD to the Recommended Uniform Screening Panel after a recommendation by the Advisory Committee on Heritable Disorders in Newborns and Children. For IKD newborn screening to be as effective as possible, it is important to have systems in place to support families in making challenging decisions soon after diagnosis about whether to pursue HSCT and to ensure rapid access to HSCT if chosen.
Publicações recentes
Novel GALC Deletion and Paradoxical Optic Nerve Hypertrophy in Severe Infantile Krabbe Disease.
Caregiver-reported disease burden in Krabbe disease: evaluating outcomes of hematopoietic stem cell transplantation.
Molecular Characterization of the GALC Mutation Thr112Ala Causing Krabbe Disease.
Two-tiered newborn screening for infantile Krabbe disease allows timely treatment initiation and avoids false-positive results.
Peripheral Neuropathy as an Early Marker in Newborn-Screened Krabbe Disease: The Value of Pre-Confirmatory Neurophysiological Testing.
📚 EuropePMC38 artigos no totalmostrando 34
Novel GALC Deletion and Paradoxical Optic Nerve Hypertrophy in Severe Infantile Krabbe Disease.
NeuropediatricsCaregiver-reported disease burden in Krabbe disease: evaluating outcomes of hematopoietic stem cell transplantation.
Orphanet journal of rare diseasesMolecular Characterization of the GALC Mutation Thr112Ala Causing Krabbe Disease.
International journal of molecular sciencesTwo-tiered newborn screening for infantile Krabbe disease allows timely treatment initiation and avoids false-positive results.
Genetics in medicine : official journal of the American College of Medical GeneticsPeripheral Neuropathy as an Early Marker in Newborn-Screened Krabbe Disease: The Value of Pre-Confirmatory Neurophysiological Testing.
Journal of the peripheral nervous system : JPNSEvidence and Recommendation for Infantile Krabbe Disease Newborn Screening.
PediatricsInfantile Krabbe disease (0-12 months), progression, and recommended endpoints for clinical trials.
Annals of clinical and translational neurologyUpregulation of non-canonical and canonical inflammasome genes associates with pathological features in Krabbe disease and related disorders.
Human molecular geneticsImproved Brain Pathology and Progressive Peripheral Neuropathy in a 15 Year Old Survivor of Infantile Krabbe Disease Treated With Umbilical Cord Transplantation.
Frontiers in molecular neuroscienceCarrier screening for Krabbe disease in an isolated inbred community.
American journal of medical genetics. Part AEvidence of seeding capacity of α-synuclein assemblies in infantile Krabbe disease.
Brain : a journal of neurologyBenefits of newborn screening and hematopoietic cell transplant in infantile Krabbe disease.
Blood advancesNewborn Screening for Krabbe Disease-Illinois Experience: Role of Psychosine in Diagnosis of the Disease.
International journal of neonatal screeningLong-term neurodevelopmental outcomes of hematopoietic stem cell transplantation for late-infantile Krabbe disease.
BloodSpontaneous Third Ventriculostomy in Krabbe Disease.
Pediatric neurologyRare Saposin A deficiency: Novel variant and psychosine analysis.
Molecular genetics and metabolismEthical issues with testing and treatment for Krabbe disease.
Developmental medicine and child neurologyReport of a Case that Expands the Phenotype of Infantile Krabbe Disease.
The American journal of case reportsHealth utilities and parental quality of life effects for three rare conditions tested in newborns.
Journal of patient-reported outcomesDiffuse Cranial Nerve Involvement in a Patient With Early Infantile Krabbe Disease.
Pediatric neurologyLong-Term Functional Outcomes after Hematopoietic Stem Cell Transplant for Early Infantile Krabbe Disease.
Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow TransplantationConsensus guidelines for newborn screening, diagnosis and treatment of infantile Krabbe disease.
Orphanet journal of rare diseasesPrecision newborn screening for lysosomal disorders.
Genetics in medicine : official journal of the American College of Medical GeneticsDevelopmental outcomes of cord blood transplantation for Krabbe disease: A 15-year study.
NeurologyPsychosine, a marker of Krabbe phenotype and treatment effect.
Molecular genetics and metabolismKrabbe Disease: Report of a Rare Lipid Storage and Neurodegenerative Disorder.
CureusNeuroradiological, neurophysiological and molecular findings in infantile Krabbe disease: two case reports.
Balkan journal of medical genetics : BJMGPredominant Corticospinal Tract Involvement in a Late Infant with Krabbe Disease.
Japanese clinical medicineInsights into the Pathogenesis and Treatment of Krabbe Disease.
Pediatric endocrinology reviews : PERCompound Galactosylceramidase Gene (GALC) Heterozygosity in a Boy with Infantile Krabbe Disease (KD).
Prilozi (Makedonska akademija na naukite i umetnostite. Oddelenie za medicinski nauki)Clinical outcomes of children with abnormal newborn screening results for Krabbe disease in New York State.
Genetics in medicine : official journal of the American College of Medical GeneticsShould states adopt newborn screening for early infantile Krabbe disease?
Genetics in medicine : official journal of the American College of Medical GeneticsMidbrain morphology reflects extent of brain damage in Krabbe disease.
NeuroradiologyRegional differences in fiber tractography predict neurodevelopmental outcomes in neonates with infantile Krabbe disease.
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Doença com base genética
Um médico geneticista pode ajudar no diagnóstico de Doença de Krabbe da infância e no aconselhamento genético da família.
Doenças relacionadas
Doenças com sintomas parecidos — ajudam quem ainda está buscando diagnóstico
Perguntas frequentes
O que as famílias mais perguntam sobre esta doença — cada resposta com a fonte de onde saiu
É uma doença genética rara com início típico nos primeiros meses de vida. Ela é transmitida de forma autossômica recessiva e catalogada sob o código CID-10 E75.2.
Referências
Fontes citadas no texto, publicações do grafo e bases de dados usadas neste verbete
5 fontes citadas no texto · 6 publicações do grafo RarasNet (PubMed) · 5 bases de dados. Títulos, periódicos e PMIDs vêm direto da fonte, sem intermediação de IA.
Dados compilados pelo RarasNet a partir de fontes abertas (Orphanet, OMIM, MONDO, PubMed/EuropePMC, ClinicalTrials.gov, DATASUS, PCDT/MS). Este conteúdo é informativo e não substitui avaliação médica.
Citar este verbete
Raras. (2026). Doença de Krabbe da infância. Em Raras — Enciclopédia de Doenças Raras do Brasil. https://raras.org/doenca/doenca-de-krabbe-da-infancia
Formato APA. Conteúdo sob CC BY 4.0 — reuso livre com atribuição.
Conteúdo mantido por Agente Raras · Médicos e pesquisadores podem colaborar
Doença de Krabbe da infância
📋 Origem dos dados
Esta página agrega dados de fontes públicas e oficiais. Dados sobre cobertura no SUS (PCDT, CEAF) são verificados ativamente por agente proativo (ver badge no infobox). Demais dados têm atribuição de fonte + data da última sincronização — clique para abrir o original.
- Doença rara (ontologia)
- fonte: Orphanet
- Identificador unificado
- fonte: MONDO
- Codificação WHO/SUS
- fonte: WHO ICD-10 / DATASUS
- CID-11 (futuro)
- fonte: WHO ICD-11
- NIH/GARD
- fonte: GARD (NIH)
- Dado público estruturado
- fonte: Wikidata