Evidence map›Paper›PMID 27523285›Full record

ArticleEuropean journal of medical genetics2016

Long-term clinical follow-up and molecular testing for diagnosis of the first Tunisian family with Alström syndrome.

Amine Chakroun, Mariem Ben Said, Amine Ennouri, Imen Achour, Mouna Mnif, Mohamed Abid, Abdelmonem Ghorbel, Jan D Marshall, Jürgen K Naggert, Saber Masmoudi

Abstract readCase Reports
In one paragraph

Article in European journal of medical genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

4 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Review
  4. 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

10 authors.

Amine ChakrounLaboratory of Molecular and Cellular Screening Processes, Center of Biotechnology of Sfax, Tunisia; Department of Otorhinolaryngology, Habib Bourguiba Teaching Hospital, University of Sfax, Tunisia. Electronic address: amine.chakroun22@gmail.com.
Mariem Ben SaidLaboratory of Molecular and Cellular Screening Processes, Center of Biotechnology of Sfax, Tunisia.
Amine EnnouriDepartment of Ophthalmology, Habib Bourguiba Teaching Hospital, University of Sfax, Tunisia.
Imen AchourDepartment of Otorhinolaryngology, Habib Bourguiba Teaching Hospital, University of Sfax, Tunisia.
Mouna MnifDepartment of Endocrinology, Hedi Chaker Teaching Hospital, University of Sfax, Tunisia.
Mohamed AbidDepartment of Endocrinology, Hedi Chaker Teaching Hospital, University of Sfax, Tunisia.
Abdelmonem GhorbelDepartment of Otorhinolaryngology, Habib Bourguiba Teaching Hospital, University of Sfax, Tunisia.
Jan D MarshallThe Jackson Laboratory, Bar Harbor, ME, USA.
Jürgen K NaggertThe Jackson Laboratory, Bar Harbor, ME, USA.
Saber MasmoudiLaboratory of Molecular and Cellular Screening Processes, Center of Biotechnology of Sfax, Tunisia.

Funding

MOLECULAR GENETIC CHARACTERIZATION OF ALSTROM SYNDROMER01HD036878 · NICHD · JACKSON LABORATORY · PI NAGGERT, JUERGEN K. · 1998 to 2011
$4.2M
NICHD NIH HHS R01 HD036878
6 · The paper itself

Abstract

Alström syndrome is a clinically complex disorder characterized by progressive degeneration of sensory functions, resulting in visual and audiological impairment as well as metabolic disturbances. It is caused by recessively inherited mutations in the ALMS1 gene, which codes for a centrosomal/basal body protein. The purpose of this study was to investigate the genetic and clinical features of two Tunisian affected siblings with Alström syndrome. Detailed clinical examinations were performed including complete ophthalmic examination, serial audiograms and several biochemical and hormonal blood tests. For the molecular study, first genomic DNA was isolated using a standard protocol. Then, linkage analysis with microsatellite markers was performed and DNA array was used to detect known mutations. Subsequently, all ALMS1 exons were simultaneously sequenced for one affected patient with the TaGSCAN targeted sequencing panel. Finally, segregation of the causal variant was performed by Sanger sequencing. Both affected siblings had cone rod dystrophy with impaired visual acuity, sensorineural hearing loss and truncal obesity. One affected individual showed insulin resistance without diabetes mellitus. Other clinical features including cardiac and pulmonary dysfunction, hypothyroidism, hyperlipidemia, acanthosis nigricans, renal and hepatic dysfunction were absent. Genetic analysis showed the presence of a homozygous splice site mutation (c.10388-2A > G) in both affected siblings. Although Alström syndrome is relatively well characterized disease, this syndrome is probably misdiagnosed in Tunisia. Here, we describe the first report of Tunisian patients affected by this syndrome and carrying a homozygous ALMS1 mutation. The diagnosis was suspected after long-term clinical follow-up and confirmed by genetic testing.

Indexed as

AdolescentAdultAlstrom SyndromeCell Cycle ProteinsChild, PreschoolExonsFemaleFollow-Up StudiesHearing Loss, SensorineuralHomozygoteHumansMaleMicrosatellite RepeatsMutationPedigreeProteinsALMS1 protein, humanCell Cycle ProteinsProteinsALMS1Alström syndromeDNA sequencingMicroarray analysisMutation

Identifiers

PMID27523285
PMCPMC5335873

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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.