Evidence map›Paper›PMID 33453710›Full record

ArticleTurkish journal of medical sciences2021

Clinical and molecular findings in 37 Turkish patients with isolated methylmalonic acidemia

Berna Şeker Yılmaz, Deniz Kor, Fatma Derya Bulut, Sebile Kılavuz, Serdar Ceylaner, Halise Neslihan Önenli Mungan

Open access · greenAbstract read
In one paragraph

Article in Turkish journal of medical sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.4field-weighted citation impact, top 43% 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

0 citing papers in PubMed, 3 citations in OpenAlex.

No citing paper in PubMed yet.

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

6 authors at 3 institutions in 2 countries.

Berna Şeker YılmazDepartment of Pediatric Metabolism, University of Mersin, Faculty of Medicine, Mersin, TurkeyORCID 0000-0003-0425-0341
Deniz KorDepartment of Pediatric Metabolism, University Hospital Çukurova, Adana, TurkeyORCID 0000-0002-4362-3107
Fatma Derya BulutDepartment of Pediatric Metabolism, Adana City Research and Training Hospital, Adana, TurkeyORCID 0000-0003-0529-2404
Sebile KılavuzDepartment of Pediatric Metabolism, University Hospital Çukurova, Adana, TurkeyORCID 0000-0002-7527-2620
Serdar CeylanerIntergen Genetics Laboratories, Ankara, TurkeyORCID 0000-0003-2786-1911
Halise Neslihan Önenli MunganDepartment of Pediatric Metabolism, University Hospital Çukurova, Adana, TurkeyORCID 0000-0001-7862-3038
Cukurova University · TRGenomics (United Kingdom) · GBIntergen (Turkey) · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background/aim: Isolated methylmalonic acidemia (MMA) is caused by complete or partial deficiency of the enzyme methylmalonyl- CoA mutase (mut0 or mut– enzymatic subtype), a defect of its cofactor adenosyl-cobalamin (cblA, cblB, or cblD-MMA), or deficiency of the enzyme methylmalonyl-CoA epimerase. While onset of the disease ranges from the neonatal period to adulthood, most cases present with lethargy, vomiting and ketoacidosis in the early infancy. Major secondary complications are; growth failure, developmental delay, interstitial nephritis with progressive renal failure, basal ganglia injury and cardiomyopathy. We aimed to demonstrate clinical and molecular findings based on long-term follow up in our patient cohort. Materials and methods: The study includes 37 Turkish patients with isolated MMA who were followed up for long term complications 1 to 14 years. All patients were followed up regularly with clinical, biochemical and dietary monitoring to determine long term complications. Next Generation Sequencing technique was used for mutation screening in five disease-causing genes including; MUT, MMAA, MMAB, MMADHC, MCEE genes. Mutation screening identified 30 different types of mutations. Results: While 28 of these mutations were previously reported, one novel MMAA mutation p.H382Pfs*24 (c.1145delA) and one novel MUT mutation IVS3+1G>T(c.752+1G>T) has been reported. The most common clinical complications were growth retardation, renal involvement, mental motor retardation and developmental delay. Furthermore, one of our patients developed cardiomyopathy, another one died because of hepatic failure and one presented with lactic acidosis after linezolid exposure. Conclusion: We have detected two novel mutations, including one splice-site mutation in the MUT gene and one frame shift mutation in the MMAA gene in 37 Turkish patients. We confirm the genotype-phenotype correlation in the study population according to the long-term complications.

Indexed as

Amino Acid Metabolism, Inborn ErrorsMitochondrial Membrane Transport ProteinsAdultHumansMethylmalonic AcidMethylmalonyl-CoA MutaseMutationMethylmalonic AcidMethylmalonyl-CoA MutaseMitochondrial Membrane Transport ProteinscomplicationsMethylmalonic acidemianovel mutationsoutcome

Identifiers

PMID33453710
PMCPMC8283478
OpenAlexW3123787115

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.