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Childhood-onset hypophosphatasia

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Disease definition

A rare, moderate form of hypophosphatasia (HPP) characterized by onset after six months of age and widely variable clinical features from low bone mineral density for age, to unexplained fractures, skeletal deformities, and rickets with short stature and waddling gait.

ORPHA:247667

Classification level: Subtype of disorder

Synonym(s):
  • Childhood-onset phosphoethanolaminuria
  • Childhood-onset Rathbun disease

Prevalence: Unknown

Inheritance: Autosomal dominant, Autosomal recessive

Age of onset: Childhood, Infancy

ICD-10: E83.3

ICD-11: 5C64.3

OMIM: 241510

UMLS: C0220743

MeSH: C562440

GARD: 8735

Summary
Epidemiology

The prevalence is unknown. About 130 cases have been reported to date.

Clinical description

Patients develop manifestations after six months of age and generally before five years of age. Clinical manifestations cover a wide spectrum. Commonly, patients have rickets leading to short stature, with delay in walking and a waddling gait, and bone and joint pain. Skeletal deformities may include dolichocephalic skull and enlarged joints. Other common features are signs of intracranial hypertension and failure to thrive. Diaphyseal and metaphyseal fractures are common. Some affected children have premature loss of deciduous teeth, starting with incisors and then loss of other teeth with intact roots, before five years of age. The disease may follow an intermittent course with remission and recurrence in later life. There may be some clinical overlap between childhood-onset HPP and moderately severe infantile HPP.

Etiology

Mutations in the ALPL gene (1p36.12) are known to cause hypophosphatasia.

Diagnostic methods

Diagnosis is based on clinical presentation, alkaline phosphatase assay and confirmed by genetic testing.

Differential diagnosis

Osteogenesis imperfecta is the most common differential diagnosis of HPP.

Genetic counseling

Autosomal recessive and autosomal dominant patterns of inheritance are reported, potentially explaining clinical variability. Genetic counseling is recommended for affected individuals.

Management and treatment

Treatment has traditionally been supportive rehabilitative strategies to minimize functional limitations, and surgery to manage some fractures. However, there is evidence that enzyme replacement therapy with asfotase alfa, approved for pediatric onset HPP (Europe and USA), improves function in childhood-HPP.

Prognosis

Affected individuals may have significant disease, with poor mobility, chronic pain, and short stature. In addition, significant rickets, long bone deformity, and non-traumatic fractures are possible. Fractures may heal poorly and can reoccur.

Last update: February 2020 - Expert reviewer(s): Dr Severine BACROT - Dr Etienne MORNET
A summary on this disease is available in Français, Español, Deutsch, Italiano, Português, Nederlands Polski
Detailed information

Logo ERN: produced/endorsed by ERN(s) Logo FSMR: produced/endorsed by FSMR(s)

General public
Article for general public
Svenska (2016) - Socialstyrelsen
Guidelines
Emergency guidelines
Français (2021.pdf) - Orphanet Urgences
Clinical practice guidelines
Disease review articles
Review article
English (2007) - Orphanet J Rare Dis
Clinical genetics review
English (2025) - GeneReviews
Genetic testing
Guidance for genetic testing
English (2010) - Eur J Hum Genet
Diagnostic Keys
Français (2024) - Les clés du diagnostic Logo FSMR
Français (2024) - Les clés du diagnostic Logo FSMR
Français (2024) - Les clés du diagnostic Logo FSMR
Français (2024) - Les clés du diagnostic Logo FSMR
Français (2024) - Les clés du diagnostic Logo FSMR
Patient-Centered Outcome Measures (PCOMs)
Access questionnaires assessing quality of life in this disease (English)
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