ArticleFrontiers in immunology2021
Altered Functions of Neutrophils in Two Chinese Patients With Severe Congenital Neutropenia Type 4 Caused by
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Molecular and Clinical Characterization of a Founder Mutation Causing G6PC3 Deficiency.Journal of clinical immunology · 2024Article
- Molecular and clinical characterization of a founder mutation causing G6PC3 deficiency.Research square · 2024Article
- Molecular and clinical characterization of a founder mutation causing G6PC3 deficiency.medRxiv : the preprint server for health sciences · 2024Article
- Revisiting the immunopathology of congenital disorders of glycosylation: an updated review.Frontiers in immunology · 2024Review
- Precision medicine in monogenic inflammatory bowel disease: proposed mIBD REPORT standards.Nature reviews. Gastroenterology & hepatology · 2023Review
- Severe congenital neutropenia due to G6PC3 deficiency: early and delayed phenotype of a patient.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2023Article
- A metabolic perspective of the neutrophil life cycle: new avenues in immunometabolism.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: SCN4 is an autosomal recessive disease caused by mutations in the Methods: Two Chinese pediatric patients with Results: Both patients had histories of pneumonia, inguinal hernia, cryptorchidism, and recurrent oral ulcers. Patient 1 also had asthma and otitis media, and patient 2 presented with prominent ectatic superficial veins and inflammatory bowel disease. DNA sequencing demonstrated that both patients harbored heterozygous Conclusion: G-CSF treatment is insufficient for patients with SCN4 patients, who remain at risk of infection. Where possible, regular G-CSF treatment, long-term prevention of infection, are the optimal methods for cure of SCN4 patients. It is important to monitor closely for signs of leukemia in SCN4 patients. Once leukemia occurs in SCN4 patients, hematopoietic stem cell transplantation is the most important choice of treatment.
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Registered trials
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