Purpose: The aim of this study was to investigate ocular side effects in children with allergic rhinitis taking chronic intermittent nasal corticosteroids.
Methods: The study group included 150 children who had used intermittent intranasal budesonide for more than 2 years for allergic rhinitis. Ninety patients who were newly diagnosed as having allergic rhinitis without any treatment comprised the control group. Central corneal thickness, Schirmer test results, visual acuity, intraocular pressure, cataract formation, keratometry, and tear break-up time were compared in the two groups.
Results: The ages of the 150 study patients (85 boys) were between 8 and 15 years. The average age (± standard error of the mean [SEM]) was 11.7 ± 0.7 years and the mean (± SEM) steroid dosage used was 93.3 ± 7.0 μg daily with 42.2 ± 3.2 g total steroid use during treatment. The ages of the 90 control patients (54 boys) were between 7 and 15 years. There was no statistically significant difference between the study and control groups according to ocular findings (P > .05). Eye functions including cataract formation, corneal ectasia, ocular hypertension or glaucoma, and dry eye were not observed in any of the patients in the study group and were not correlated with total steroid dosage (r = 0.125, P = .447).
Conclusion: A 2-year treatment of children with allergic rhinitis prescribed intermittent intranasal budesonide at an average daily dose of approximately 100 μg is not associated with ocular side effects such as cataract, glaucoma, corneal ectasia, and abnormal tear function.
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http://dx.doi.org/10.3928/01913913-20101018-03 | DOI Listing |
Front Allergy
January 2025
Department of Biomedical Science and Technology, School of Biological Sciences, Ramakrishna Mission Vivekananda Educational and Research Institute (RKMVERI), Kolkata, India.
Increasing evidence demonstrates a robust link between environmental pollutants and allergic reactions, with air and indoor pollution exacerbating respiratory allergies and climate change intensifying seasonal allergies. Comprehensive action, including government regulations, public awareness, and individual efforts, is essential to mitigate pollution's impact on allergies and safeguard public health and ecological balance. Recent findings indicate a strong correlation between environmental pollutants and allergic reactions, with air pollution from vehicular emissions and industrial activities exacerbating respiratory allergies like asthma and allergic rhinitis.
View Article and Find Full Text PDFFront Immunol
January 2025
Central Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, China.
Background: Uncontrolled severe eosinophilic chronic rhinosinusitis (eCRS) is associated with elevated levels of Th2 cells and raised immunoglobulin concentrations in nasal polyp tissue. eCRS is characterized by high eosinophilic infiltration and type 2 inflammation. Gαi1/3 proteins participate in allergic inflammation by regulating immune cells.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Physiology and Immunology, Faculty of Medicine, University of Prishtina "Hasan Prishtina", Bulevardi I Deshmoreve P.N., Prishtina, Kosovo.
Allergic rhinitis and asthma are common respiratory conditions with complex etiologies involving genetic, environmental, and physiological factors. In these conditions, the role of thyroid function remains underexplored. This study enrolled 116 participants with a mean age of 29.
View Article and Find Full Text PDFOral Oncol
January 2025
Department of Otolaryngology, The Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou 646000 Sichuan, China. Electronic address:
Tissue Cell
December 2024
Department of Facial Features, 970 Hospital, Joint Service Support Force of the Chinese People's Liberation Army, Yantai, Shandong, China. Electronic address:
Allergic rhinitis (AR), common in children and adolescents, involves Lysophosphatidylcholine acyltransferase 1 (LPCAT1) catalyzing surfactant lipid biosynthesis and suppressing endoplasmic reticulum expression. However, the precise mechanism underlying the impact of LPCAT1 on epithelial cell damage in AR remains elusive. Hence, the present investigation elucidated the potential effect of LPCAT1 on epithelial cell damage in AR by inhibiting endoplasmic reticulum stress.
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