Evidence map›Paper›PMID 31555217›Full record

ArticleFrontiers in endocrinology2019

2q37 Deletions in Patients With an Albright Hereditary Osteodystrophy Phenotype and PTH Resistance.

Francesca Marta Elli, Luisa de Sanctis, Bruno Madeo, Maria A Maffini, Paolo Bordogna, Arianna Pirelli, Maura Arosio, Giovanna Mantovani

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 24% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Novel Pathogenetic Variants in PTHLH and TRPS1 Genes Causing Syndromic Brachydactyly.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022
    Article
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

8 authors at 3 institutions in 1 country.

Francesca Marta ElliDepartment of Clinical Sciences and Community Health, University of Milan, Milan, Italy.
Luisa de SanctisDepartment of Public Health and Pediatric Sciences, Regina Margherita Children's Hospital-AOU Città della Salute e della Scienza, University of Torino, Turin, Italy.
Bruno MadeoUnit of Endocrinology, Department of Medical Specialties, Ospedale Civile di Baggiovara, Azienda Ospedaliero-Universitaria di Modena, Modena, Italy.
Maria A MaffiniDepartment of Clinical Sciences and Community Health, University of Milan, Milan, Italy.
Paolo BordognaEndocrinology Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.
Arianna PirelliDepartment of Clinical Sciences and Community Health, University of Milan, Milan, Italy.
Maura ArosioDepartment of Clinical Sciences and Community Health, University of Milan, Milan, Italy.
Giovanna MantovaniDepartment of Clinical Sciences and Community Health, University of Milan, Milan, Italy.
University of Milan · ITFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico · ITAzienda Unita' Sanitaria Locale Di Modena · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pseudohypoparathyroidism (PHP) is a rare endocrine disorder derived from the defective activation of the cAMP pathway by the parathyroid hormone secondary to GNAS molecular defects. PHP subtypes are defined by the presence/absence of specific clinical/biochemical features. PHP1A is characterized by resistance to multiple hormones with features of Albright hereditary osteodystrophy (AHO), while pseudopseudohypoparathyroidism (PPHP) is characterized by AHO in the absence of PTH resistance. Small subsets of PHP and PPHP patients without known molecular defects have been re-diagnosed as being affected by the brachydactyly-mental retardation syndrome (BDMR), also known as the AHO-like syndrome. This study aimed to analyse 24 PHP1A and 51 PPHP patients without a molecular diagnosis for the presence of BDMR-associated 2q37 deletions to improve the differential diagnosis and to identify features that might help to avoid a misdiagnosis. Molecular investigations identified 4 deletions in 4 unrelated patients. The affected patients showed a combination of the most pathognomonic AHO features. Of note, 3 of the patients also displayed mild PTH resistance, and none of the patients developed ectopic ossifications. Our work confirmed the rarity of the misdiagnosis of BDMR in PHP patients through the identification of 4 patients bearing a 2q37 deletion in a cohort of 73 PHP patients (5.3%). Three patients with the deletion presented a PHP1A phenotype in the absence of any BDMR-specific findings. Further studies on larger case series are needed to elucidate the overlap between these clinical entities and to allow the early identification of patients.

Indexed as

2q37 deletionAlbright hereditary osteodystrophybrachydactyly-mental retardation syndromeGNASpseudohypoparathyroidism

Identifiers

PMID31555217
PMCPMC6727065
OpenAlexW2969926565

What OpenQuestion holds

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Registered trials

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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.