Acid sphingomyelinase deficiency in France: a retrospective survival study.


Journal

Orphanet journal of rare diseases
ISSN: 1750-1172
Titre abrégé: Orphanet J Rare Dis
Pays: England
ID NLM: 101266602

Informations de publication

Date de publication:
05 Aug 2024
Historique:
received: 06 02 2024
accepted: 27 05 2024
medline: 6 8 2024
pubmed: 6 8 2024
entrez: 5 8 2024
Statut: epublish

Résumé

Acid sphingomyelinase deficiency (ASMD) or Niemann-Pick disease types A, A/B, and B is a progressive, life-limiting, autosomal recessive disorder caused by sphingomyelin phosphodiesterase 1 (SMPD1) gene mutations. There is a need to increase the understanding of morbidity and mortality across children to adults diagnosed with ASMD. This observational retrospective survey analysed medical records of patients with ASMD with retrievable data from 27 hospitals in France, diagnosed/followed up between 1 A total of 118 medical records of patients with ASMD (type B [n = 94], type A [n = 15], and type A/B [n = 9]) were assessed. The majority of patients were males (63.6%); the median [range] age at diagnosis was 8.0 [1.0-18.0] months (type A), 1.0 [0-3] year (type A/B), and 5.5 [0-73] years (type B). Overall, 30 patients were deceased at the study completion date; the median [range] age at death for patients with ASMD type A (n = 14) was 1 [0-3.6] year, type A/B (n = 6) was 8.5 [3.0-30.9] years, and type B (n = 10) was 57.6 [3.4-74.1] years. The median [95% confidence interval (CI)] survival age from birth in patients with ASMD type A and type A/B was 2.0 [1.8-2.7] years and 11.4 [5.5-18.5] years, respectively. Survival analysis in ASMD type B was explored using SMR [95% CI] analysis (3.5 [1.6-5.9]), which showed that age-specific deaths in the ASMD type B population were 3.5 times more frequent than those in the general French population. The causes of death were mostly severe progressive neurodegeneration (type A: 16.7%), cancer (type B: 16.7%), or unspecified (across groups: 33.3%). This study illustrated a substantial burden of illness with high mortality rates in patients with ASMD, including adults with ASMD type B, in France.

Sections du résumé

BACKGROUND BACKGROUND
Acid sphingomyelinase deficiency (ASMD) or Niemann-Pick disease types A, A/B, and B is a progressive, life-limiting, autosomal recessive disorder caused by sphingomyelin phosphodiesterase 1 (SMPD1) gene mutations. There is a need to increase the understanding of morbidity and mortality across children to adults diagnosed with ASMD.
METHODS METHODS
This observational retrospective survey analysed medical records of patients with ASMD with retrievable data from 27 hospitals in France, diagnosed/followed up between 1
RESULTS RESULTS
A total of 118 medical records of patients with ASMD (type B [n = 94], type A [n = 15], and type A/B [n = 9]) were assessed. The majority of patients were males (63.6%); the median [range] age at diagnosis was 8.0 [1.0-18.0] months (type A), 1.0 [0-3] year (type A/B), and 5.5 [0-73] years (type B). Overall, 30 patients were deceased at the study completion date; the median [range] age at death for patients with ASMD type A (n = 14) was 1 [0-3.6] year, type A/B (n = 6) was 8.5 [3.0-30.9] years, and type B (n = 10) was 57.6 [3.4-74.1] years. The median [95% confidence interval (CI)] survival age from birth in patients with ASMD type A and type A/B was 2.0 [1.8-2.7] years and 11.4 [5.5-18.5] years, respectively. Survival analysis in ASMD type B was explored using SMR [95% CI] analysis (3.5 [1.6-5.9]), which showed that age-specific deaths in the ASMD type B population were 3.5 times more frequent than those in the general French population. The causes of death were mostly severe progressive neurodegeneration (type A: 16.7%), cancer (type B: 16.7%), or unspecified (across groups: 33.3%).
CONCLUSIONS CONCLUSIONS
This study illustrated a substantial burden of illness with high mortality rates in patients with ASMD, including adults with ASMD type B, in France.

Identifiants

pubmed: 39103853
doi: 10.1186/s13023-024-03234-6
pii: 10.1186/s13023-024-03234-6
doi:

Substances chimiques

Sphingomyelin Phosphodiesterase EC 3.1.4.12

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

289

Investigateurs

Marie-Thérèse Abi-Wardé (MT)
Marc Berger (M)
Emilie Berthoux (E)
Aurélie Cabannes-Hamy (A)
Fabrice Camou (F)
Pascal Cathebras (P)
Vincent Grobost (V)
Jérémy Keraen (J)
Alice Kuster (A)
Bertrand Lioger (B)
Anas Mehdaoui (A)
Claire Merlot (C)
Martin Michaud (M)
Martine-Louise Reynaud-Gaubert (ML)
Fréderic Schlemmer (F)
Amélie Servettaz (A)
Chloé Stavris (C)
Sébastien Trouillier (S)

Informations de copyright

© 2024. The Author(s).

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Auteurs

Wladimir Mauhin (W)

Internal Medicine, Reference Center for Lysosomal Diseases (CRML), GH Diaconesses Croix Saint-Simon, Paris, France.

Nathalie Guffon (N)

Reference Center for Inherited Metabolic Diseases, Hospices Civils de Lyon, Bron, France.

Marie T Vanier (MT)

Laboratory Gillet-Mérieux, Centre de Biologie Et de Pathologie Est, INSERM U820, Hospices Civils de Lyon, Bron, France.

Roseline Froissart (R)

Biochemical and Molecular Biology Department, Centre de Biologie Et de Pathologie Est, Hospices Civils de Lyon, Bron, France.

Aline Cano (A)

Paediatric Neurology, Reference Center for Inherited Metabolic Diseases, CHU La Timone Enfants, Marseille, France.

Claire Douillard (C)

Endocrinology, Diabetology, Metabolism Department, Reference Centre for Inherited Metabolic Diseases, Lille University Hospital, Lille, France.

Christian Lavigne (C)

Internal Medicine and Clinical Immunology, Competence Centre for Inherited Metabolic Diseases, Angers University Hospital, Angers, France.

Bénédicte Héron (B)

Pediatric Neurology, Reference Center for Lysosomal Diseases, Armand Trousseau-La Roche Guyon Hospital, Assistance Publique-Hôpitaux de Paris, Fédération Hospitalo-Universitaire, Sorbonne-Université, I2-D2, Paris, France.

Nadia Belmatoug (N)

Reference Center for Lysosomal Diseases, Beaujon Hospital, Assistance Publique Hôpitaux de Paris Nord, Université Paris Cité, Paris, France.

Yurdagül Uzunhan (Y)

Reference Center for Rare Pulmonary Diseases, Avicenne Hospital, Université Sorbonne Paris Nord, INSERM U1272, Assistance Publique-Hôpitaux de Paris, PneumologyBobigny, France.

Didier Lacombe (D)

Medical Genetics Unit, University Hospital of Bordeaux, INSERM U1211, Bordeaux, France.

Thierry Levade (T)

Cancer Research Center of Toulouse (CRCT) and Clinical Biochemistry Laboratory, Reference Center for Inherited Metabolic Diseases, INSERM UMR1037 Paul Sabatier University Federative Institute of Biology, CHU Toulouse, Toulouse, France.

Aymeric Duvivier (A)

Sanofi, Gentilly, France.

Ruth Pulikottil-Jacob (R)

Sanofi, Reading, UK.

Fernando Laredo (F)

Sanofi, São Paulo, Brazil.

Samia Pichard (S)

Reference Center for Inherited Metabolic Diseases, Hôpital Necker Enfants Malades, Paris, 75015, France.

Olivier Lidove (O)

Internal Medicine, Reference Center for Lysosomal Diseases (CRML), GH Diaconesses Croix Saint-Simon, Paris, France. OLidove@hopital-dcss.org.

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