Evidence map›Paper›PMID 28228103›Full record

ReviewOrphanet journal of rare diseases2017

Disease manifestations and burden of illness in patients with acid sphingomyelinase deficiency (ASMD).

Margaret M McGovern, Ruzan Avetisyan, Bernd-Jan Sanson, Olivier Lidove

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Orphanet journal of rare diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06258577 (Screening for Gaucher Disease and Acid Sphingomyelinase Deficiency From Taiwanese Candidates With Splenomegaly and/or Thrombocytopenia), which is not on this map. Cited by 98 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT06258577 not yet recruitingnot on this mapstarted 2024, after this paper: background citation

Screening for Gaucher Disease and Acid Sphingomyelinase Deficiency From Taiwanese Candidates With Splenomegaly and/or Thrombocytopenia

TypeobservationalSponsorChung-Hsing WangRan2024 to 2028Enrolled50ConditionsGaucher Disease
3 · Its place in the literature

Who cites it

98 citing papers in PubMed, 1 synthesis or guideline pooled it, 173 citations in OpenAlex.

  1. Guideline
  2. Trial
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  7. Article
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  12. Contradictory Effects on Hepatocytes in ASMD.International journal of molecular sciences · 2026
    Review
  13. Article
  14. Article
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  19. Review
  20. Article

38 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 3 countries.

Margaret M McGovernDepartment of Pediatrics, Stony Brook University School of Medicine, Stony Brook, NY, 11794, USA. Margaret.McGovern@stonybrook.edu.
Ruzan AvetisyanSanofi Genzyme, Cambridge, MA, USA.
Bernd-Jan SansonSanofi Genzyme, Cambridge, MA, USA.
Olivier LidoveDepartment of Internal Medicine-Rheumatology, Hôpital de la Croix Saint Simon, Paris, France.
Sanofi (United States) · USInserm · FRStony Brook University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acid sphingomyelinase deficiency (ASMD), a rare lysosomal storage disease, is an autosomal recessive genetic disorder caused by different SMPD1 mutations. Historically, ASMD has been classified as Niemann-Pick disease (NPD) types A (NPD A) and B (NPD B). NPD A is associated with a uniformly devastating disease course, with rapidly progressing psychomotor degeneration, leading to death typically by the age of 3 years, most often from respiratory failure. In contrast, the clinical phenotype and life expectancy of patients with NPD B may vary widely. Almost all patients have hepatosplenomegaly and an atherogenic lipid profile, and most patients have interstitial lung disease with progressive impairment of pulmonary function and hematologic abnormalities including cytopenias. Other common clinical manifestations include liver dysfunction, heart disease, skeletal abnormalities and growth delays. Some patients with ASMD who survive beyond early childhood have intermediate phenotypes (variant NPD B) characterized by combinations of non-neurologic and mild to severe neurologic symptoms. The physical and psychosocial burden of illness in patients with NPD B is substantial. Common symptoms include shortness of breath, joint or limb pain, abdominal pain, bleeding and bruising. The disease often leads to chronic fatigue, limited physical or social activity and difficulties in performing daily activities or work. Many patients die before or in early adulthood, often from pneumonia/respiratory failure or liver failure. Available treatments are limited to symptom management and supportive care. An enzyme replacement therapy currently in clinical development is expected to be the first treatment addressing the underlying pathology of the disease. Early diagnosis and appropriate management are essential for reducing the risk of complications. While knowledge about ASMD is evolving, more evidence about ASMD and the natural history across the disease spectrum is needed, to improve disease recognition, timely diagnosis and appropriate disease management.

Indexed as

Cause of DeathCost of IllnessHumansIncidenceNiemann-Pick DiseasesRare DiseasesSphingomyelin PhosphodiesteraseSMPD1 protein, humanSphingomyelin PhosphodiesteraseAcid sphingomyelinase deficiencyASMDBurden of illnessDisease manifestationsLysosomal storage disorderNatural historyNiemann-Pick disease types A and B

Identifiers

PMID28228103
PMCPMC5322625
OpenAlexW2591036609

What OpenQuestion holds

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LicenceCC BY
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Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.