ArticleOrphanet journal of rare diseases2026
Family studies in Gaucher Disease: a key resource for early diagnosis and personalized treatment strategies.
Article in Orphanet journal of rare diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gaucher Disease (GD) is an inherited metabolic disorder caused by mutations in the GBA1 gene, which is responsible for the synthesis of the enzyme glucocerebrosidase (GCase). The clinical manifestations, which are extremely heterogeneous, include splenomegaly, hepatomegaly, anaemia and bone complications. GD is an autosomal recessive condition, meaning that the clinical phenotype manifests itself only in the presence of two mutated alleles, which are inherited from both parents, who are generally healthy and asymptomatic. However, other family members (brothers, sisters, grandparents, uncles, aunts, cousins) may be heterozygous carriers or, in some cases, present with undiagnosed forms. In order to identify these individuals and monitor their health, it is essential to conduct family segregation studies. These are often disregarded in clinical practice, despite their crucial role in understanding the distribution of the disease. In this study, a comprehensive diagnostic analysis was conducted on four families, including biochemical and genetic investigations. In the first three families, an affected proband was identified, exhibiting characteristic symptoms, reduced enzyme activity and increased substrate, associated with the presence of two causative mutations. Segregation studies revealed additional affected individuals or carriers, some of whom were completely asymptomatic or had mild manifestations. In the fourth family, the investigation started with a paternal uncle who was found to be a heterozygous carrier. The study was extended to non-direct relatives, which allowed the identification of other affected individuals who would otherwise have remained undiagnosed. These results emphasise the significance of extended family analysis, encompassing second-and third-degree relatives, as a fundamental instrument for comprehension of the hereditary distribution of GD and for the timely identification of individuals at risk. The exclusion of non-direct relatives from genetic screening represents a significant missed opportunity for timely diagnosis, effective clinical management, and family planning.
Indexed as
Identifiers
What OpenQuestion holds
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.