ArticleCureus2023
Primary Ciliary Dyskinesia and Type 1 Diabetes: True Association or Circumstantial?
Article in Cureus, 2023. 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
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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, 1 citations in OpenAlex.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary ciliary dyskinesia (PCD) is a rare autosomal recessive inherited heterogeneous respiratory disorder. The diagnosis of PCD is challenging and necessitates a multi-test diagnostic approach because there are no gold standard diagnostic tests available to confirm PCD. However, rapid advancement in understanding the molecular genetic basis of PCD has greatly improved PCD diagnosis. Studies have reported that PCD may increase the risk of rheumatoid arthritis, congenital heart disease, severe esophageal diseases, and others. Therefore, the present study aimed to assess the risk of type 1 diabetes mellitus (T1DM) in a genetically confirmed PCD patient. In this case study, an 11-year-old girl with autosinopulmonary infections and her younger brother were diagnosed with PCD. The patient's DNA was extracted for next-generation exome sequencing. Our analysis of the exome sequencing data revealed the PCD-causing genetic variant p.Glu286del in the RSPH9 gene on chromosome 6p21.1. In addition, the biochemical findings at the time of patient's admission showed elevated glutamic acid decarboxylase antibodies, HbA1c, and ketone levels, with impaired glucose tolerance, which indicated the presence of T1DM. In conclusion, the clinical features, biochemical reports, and genetic testing confirmed PCD in this patient and the possible association between PCD and T1DM.
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Registered trials
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