Perception of the Role and Potential Side Effects of Inhaled Corticosteroids Among Asthmatic Patients

CHEST Journal ◽  
1998 ◽  
Vol 113 (3) ◽  
pp. 587-592 ◽  
Author(s):  
Louis-Philippe Boulet
2020 ◽  
Vol 9 (1) ◽  
Author(s):  
Marina MB ◽  
Ramli R ◽  
Primuharsa Putra SHA

Introduction: Inhaled steroids such as fluticasone propionate and beclomethasone dipropionate play an important role in the treatment of bronchial asthma. Its usage facilitates disease control in asthmatic patients, resulting in improved quality of life. Because of its benefit, the inhaled steroid is used extensively, at higher doses and for longer duration. However, the localized effects of inhaled corticosteroids on oral/laryngeal mucosa, such as fungal infections can be problematic. Case Report: We report a case of oropharyngeal and laryngeal candidiasis following a long period and high doses of inhaled steroid in a 42-year-old male. He presented with a complaint of increasing tiredness, phlegm, intermittent wheezing and hoarseness for 2-3 months. There was no weight loss or loss of appetite. He has been using inhaled steroids and long acting bronchodilators in increasing doses for his claimed ‘wheezing’ despite the negative history of asthma. The inhaled steroids were fluticasone dipropionate at doses of 500-100 mcg daily for 2-3 months. Results: Examination revealed widespread oral thrush involving the oral cavity, oropharynx and larynx. There was no cushingoid habitus. His muscle power was of 5/5 bilaterally and his lungs were clear. Lung function and chest film were also normal. The steroid was stopped immediately and flucanozole and nystatin syrup were prescribed. The patient made an uneventful and complete recovery. Conclusion: We conclude that patients on inhaled corticosteroids should be monitored for local side effects. Physicians should be aware not only of the systemic but also of the local side effects of inhaled corticosteroids. Patients may increase doses without the knowledge of their physicians and subsequently suffer the adverse effects either local or systemic.


2015 ◽  
Vol 25 (7) ◽  
pp. 334-342 ◽  
Author(s):  
Hun Soo Chang ◽  
Jeong-Seok Heo ◽  
Seung-Woo Shin ◽  
Da-Jeong Bae ◽  
Hyun Ji Song ◽  
...  

2021 ◽  
Vol 32 (4) ◽  
pp. 479-484
Author(s):  
Sura F. Alsaffar ◽  
Haider A. Rasheed ◽  
Jabbar H. Yenzeel ◽  
Haider F. Ghazi

Abstract Objectives Inhaled corticosteroids are the most effective controllers of asthma, although asthmatics vary in their response. FKBP51 is a major component of the glucocorticoid receptor which regulates its responses to corticosteroids. Therefore, the present study aims to identify the role of FKBP5 gene polymorphism in asthma susceptibility and corticosteroid resistance. Methods DNA was extracted from the blood of 68 asthmatic and 40 control subjects. FKBP5 gene fragments were amplified by PCR and sequenced by the Sanger method. The sequencing results were aligned by mapping on the reference sequences of National center of Biotechnology Information (NCBI) and single nucleotide polymorphisms (SNPs) which were checked. Finally, the genotype, allele frequency and odds ratio (OR) were calculated. Results The FKBP5 fragment sequencing revealed the presence of rs1360780 and one novel SNP found in 17 samples taken from asthmatic patients as compared to db SNP data in the NCBI database. The FKBP5 variant (rs1360780) indicated that the allele frequency of risk allele T was 41.18% in patients and 20% in control group members p<0.001 and OR=2.8 when compared to a wild C allele frequency of 58.82% in patients and 64% in the control group members. The novel SNP FKBP5 was compared to the SNP database in the NCBI database in which wild T allele was substituted with G. The novel SNP was submitted to the ClinVar Submission Portal at NCBI with accession number: rs1581842283 and confirmed an asthma susceptibility risk factor with allele G frequency of 11.76% in asthmatics and 2.5% in the control group members (OR=5.2, p<0.05), as compared to a wild T allele frequency of 88.24% in asthmatics and 97.5% in the control group members. Conclusions The risk allele T of rs1360780 and the novel SNP rs1581842283 risk allele G predict asthma susceptibility but show no association with corticosteroid resistant.


2020 ◽  
Vol 55 (5) ◽  
pp. 1902259 ◽  
Author(s):  
Gráinne d'Ancona ◽  
Joanne Kavanagh ◽  
Cris Roxas ◽  
Linda Green ◽  
Mariana Fernandes ◽  
...  

IntroductionInhaled corticosteroids (ICS) achieve disease control in the majority of asthmatic patients, although adherence to prescribed ICS is often poor. Patients with severe eosinophilic asthma may require treatment with oral corticosteroids (OCS) and/or biologic agents such as mepolizumab. It is unknown if ICS adherence changes on, or alters clinical response to, biologic therapy.MethodsWe examined ICS adherence and clinical outcomes in OCS-dependent severe eosinophilic asthma patients who completed 1 year of mepolizumab therapy. The ICS medicines possession ratio (MPR) was calculated (the number of doses of ICS issued on prescription/expected number) for the year before and the year after biologic initiation. Good adherence was defined as MPR >0.75, intermediate 0.74–0.51 and poor <0.5. We examined outcomes after 12 months of biologic therapy, including OCS reduction and annualised exacerbation rate (AER), stratified by adherence to ICS on mepolizumab.ResultsOut of 109 patients commencing mepolizumab, 91 who had completed 12 months of treatment were included in the final analysis. While receiving mepolizumab, 68% had good ICS adherence, with 16 (18%) having poor ICS adherence. ICS use within the cohort remained similar before (MPR 0.81±0.32) and during mepolizumab treatment (0.82±0.32; p=0.78). Patients with good adherence had greater reductions in OCS dose (median (interquartile range) OCS reduction 100 (74–100)% versus 60 (27–100)%; p=0.031) and exacerbations (AER change −2.1±3.1 versus 0.3±2.5; p=0.011) than those with poor adherence. Good ICS adherence predicted the likelihood of stopping maintenance OCS (adjusted OR 3.19, 95% CI 1.02–9.94; p=0.045).ConclusionICS nonadherence is common in severe eosinophilic asthma patients receiving mepolizumab, and is associated with a lesser reduction in OCS requirements and AER.


2000 ◽  
Vol 100 (1) ◽  
pp. 19-23
Author(s):  
A. J. BROWN ◽  
J. E. NALLY

Angiotensin II potentiates methacholine-evoked bronchoconstriction both in bovine airways in vitro and in asthmatic patients in vivo. Angiotensin II also potentiates endothelin-1-evoked contractions in vitro, but fails to alter such contractions in vivo. One possible confounding factor in patients is their use of inhaled corticosteroids. Accordingly the present study examined the effects of hydrocortisone (cortisol) on contractions evoked by methacholine and endothelin-1 in the presence and absence of angiotensin II. Contractions of rings of isolated bovine airways were measured isometrically in organ baths. Concentration–response curves were obtained for endothelin-1 or methacholine in the presence and absence of angiotensin II, hydrocortisone and a combination of angiotensin II and hydrocortisone. Hydrocortisone abolished the angiotensin II-mediated potentiation of endothelin-1-evoked, but not methacholine-evoked, contractions. Hydrocortisone alone evoked the enhancement of methacholine responses, similar to the effect produced by angiotensin II. While species differences may exist, our present results suggest that the use of corticosteroids can have a profound effect on the interaction between angiotensin II and endothelin-1. Accordingly, the presence of inhaled corticosteroids might explain the differences between the results obtained in vitro and in vivo.


2020 ◽  
Vol 16 (1) ◽  
pp. 43-52 ◽  
Author(s):  
Nese Akcan ◽  
Nerin N. Bahceciler

Asthma is the most common chronic inflammatory disease of children. Inhaled corticosteroids (ICS) are the cornerstone of asthma therapy which are the most effective, commonly used treatment of persistent asthma. Mostly, studies on the relationship between asthma and cortisol have focused on side effects of treatment. Recently, asthmatic patients not treated with ICS have been reported to have an attenuated activity and/or responsiveness of their Hypothalamic-Pituitary- Adrenal (HPA) axis. Moreover, it has been proposed that asthma worsening with stress may be due to a dysfunctional HPA axis, or cortisol insensitivity due to chronic psychological stress through impaired glucocorticoid receptor expression or function. Although long-term ICS treatment might produce adrenal suppression or iatrogenic Cushing syndrome, improvement of adrenal function has also been detected in some of asthmatic cases. Thus, the response scheme of HPA axis still contains undiscovered features in asthma. The management of asthma can be improved by increasing knowledge on the role of HPA axis in asthma pathophysiology. The risk for side effects of ICS can be minimized through increased awareness, early recognition of at-risk patients and regular patient follow-up. This review was written to draw attention to the role of HPA axis in both asthma and its treatment and to illustrate a follow up algorithm of HPA axis in the management of asthma.


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