Evidence map›Paper›PMID 26862482›Full record

ArticleMeta gene2016

Clinical characteristics and follow-up of 5 young Chinese males with gonadotropin-releasing hormone deficiency caused by mutations in the KAL1 gene.

Juan Li, Niu Li, Yu Ding, Xiaodong Huang, Yongnian Shen, Jian Wang, Xiumin Wang

Open access · hybridAbstract read
In one paragraph

Article in Meta gene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

2 citing papers in PubMed, 8 citations in OpenAlex.

  1. The molecular basis of hypoprolactinaemia.Reviews in endocrine & metabolic disorders · 2024
    Review
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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

7 authors at 1 institution in 1 country.

Juan LiDepartment of Endocrinology, Shanghai Children's Medical Center, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Niu LiInstitute of Pediatric Translational Medicine, Shanghai Children's Medical Center, Shanghai Jiaotong University School of Medicine, Shanghai,China.
Yu DingDepartment of Endocrinology, Shanghai Children's Medical Center, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Xiaodong HuangDepartment of Endocrinology, Shanghai Children's Medical Center, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Yongnian ShenDepartment of Endocrinology, Shanghai Children's Medical Center, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Jian WangInstitute of Pediatric Translational Medicine, Shanghai Children's Medical Center, Shanghai Jiaotong University School of Medicine, Shanghai,China; Department of Laboratory Medicine, Shanghai Children's Medical Center, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Xiumin WangDepartment of Endocrinology, Shanghai Children's Medical Center, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Shanghai Children's Medical Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Isolated gonadotropin-releasing hormone (GnRH) deficiency (IGD) pertains to a group of genetic disorders consisting of anosmic hypogonadotropic hypogonadism (Kallmann syndrome, KS) and normosmic idiopathic hypogonadotropic hypogonadism (nIHH). KS is genetically heterogeneous. We hereby present 5 young male patients with GnRH deficiency caused by mutations in the KAL1 gene. Their ages ranged from 9 months to 16 years. They were referred to our department for an endocrine consultation for micropenis. Hormone assays showed low circulating gonadotropins and testosterone. Molecular studies revealed KAL1 mutations in all cases, three reported nonsense sequence variants in the KAL1 gene were detected in 4 patients, respectively (c.784C > T (p.Arg 262*), c.1267C > T (p.Arg423*), and c.1270C > T (p.Arg424*)), and one patient harbored a novel hemizygous sequence variant [c.227G > A (p.Trp76*)]. Only one patient presented short stature without growth hormone deficiency and anosmia. Another patient had bilateral eyelid ptosis, trichiasis, and refractive error. This is the first report on the co-occurrence of a KAL1 gene mutation and tent-like upper lip in four patients. All of our cases had normal olfactory bulbs and showed no renal agenesis, cleft lip/palate, and hearing impairment. These cases expand our knowledge of the phenotype associated with KAL1 sequence variations, although the precise mechanism by which KAL1 gene influences the development of this phenotype is still unknown.

Indexed as

Clinical phenotypeIsolated gonadotropin-releasing hormone deficiencyKAL1 mutationsKallmann syndrome

Identifiers

PMID26862482
PMCPMC4707242
OpenAlexW2192006568

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.