Corticosteroid Therapy for Patients With Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Singh, Jeffrey M.; Palda, Valerie A.; Stanbrook, Matthew B.; Chapman, Kenneth R.

doi:10.1001/archinte.162.22.2527

Cited by 97 publications

(67 citation statements)

References 57 publications

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“…In the current study, we demonstrated for the first time that dexamethasone given at non-ulcerogenic doses 0.1 or 0.2 mg/kg/day relevant to those used in different clinical conditions ranging from 0.05 to 0.2 mg/kg/day or its equivalent dose (Vecht, 1998;Chatham and Kimberly, 2001;Singh et al, 2002;Yang and Lichtenstein, 2002), delayed gastric ulcer healing. To further explore this problem, we used the gastric ulcer model to investigate the pathological mechanism of dexamethasone on ulcer healing.…”

Section: Discussionmentioning

confidence: 60%

Non-Ulcerogenic Dose of Dexamethasone Delays Gastric Ulcer Healing in Rats

Luo

Shin²,

Liu³

et al. 2003

J Pharmacol Exp Ther

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Although the ulcerogenic action of corticosteroids in the stomach is controversial, its action on ulcer healing has not been defined. In this study, we used non-ulcerogenic doses of dexamethasone (0.1 or 0.2 mg/kg/day) to explore the adverse effect on ulcer healing as well as its pathological mechanisms in rat stomach. In this regard, we measured ulcer size, mucus thickness, epithelial cell proliferation and apoptosis, and angiogenesis at the ulcer site at different time points after ulcer induction. Protein expressions of cyclooxygenase-1 and -2 (COX-1 and COX-2) and cytosolic phospholipase A 2 (cPLA 2 ) over the ulcer margin were evaluated, and the mucosal prostaglandin E 2 (PGE 2 ) level was also determined. Dexamethasone treatment in the current doses did not produce mucosal damage in intact animals. However, the drug dose-dependently delayed gastric ulcer healing. It also decreased mucus content and epithelial cell proliferation at the ulcer margin as well as angiogenesis at the ulcer margin and base. These were associated with a significant decrease of COX-2 expression and PGE 2 level but not COX-1 at the ulcer margin. The drug only marginally reduced the cPLA 2 expression without affecting the apoptosis at the ulcer margin. PGE 2 treatment reversed the adverse effects of dexamethasone on ulcer healing. It is concluded that nonulcerogenic doses of dexamethasone can delay ulcer repair via depression of COX-2 expression and PGE 2 formation in the gastric mucosa.

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Section: Discussionmentioning

confidence: 60%

Non-Ulcerogenic Dose of Dexamethasone Delays Gastric Ulcer Healing in Rats

Luo

Shin²,

Liu³

et al. 2003

J Pharmacol Exp Ther

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“…In chronic obstructive pulmonary disease (COPD), exacerbations are observed 1-3 times per year despite optimal medical treatment (1). Acute exacerbations adversely affect the prognosis of the disease and increase morbidity and mortality (2).…”

Section: Introductionmentioning

confidence: 99%

Does eosinophilia and neutrophil to lymphocyte ratio affect hospital re-admission in cases of copd exacerbation?

et al. 2017

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“…Systemic corticosteroids have been shown to improve pulmonary function, shorten hospitalizations, improve dyspnea, and decrease relapse rate in the treatment of exacerbations (52)(53)(54)(55)(56)(57)(58). Three prospective, randomized controlled trials have looked at the use of systemic steroids in the treatment of inpatients with COPD exacerbations (52,55,56).…”

Section: Exacerbations Of Copdmentioning

confidence: 99%

Inhaled and Systemic Corticosteroids in Chronic Obstructive Pulmonary Disease

Falk

Minai²,

Mosenifar³

2008

Proceedings of the American Thoracic Society

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Systemic and local inflammation is central to the pathophysiology of chronic obstructive pulmonary disease (COPD). Increased levels of inflammation have been linked to a more progressive course in COPD and have been shown to be present during an exacerbation. Decreases in inflammatory cytokines, C-reactive protein, and inflammatory cells have been observed with corticosteroid use, suggesting a possible mechanism for a therapeutic benefit of steroids. No available data support the routine use of systemic corticosteroids in stable COPD; however, short courses during exacerbations are likely to improve length of hospitalization, lung function, and relapse rate. Inhaled corticosteroids (ICS) decrease the rate of exacerbation and may improve the response to bronchodilators and decrease dyspnea in stable COPD. No study shows that ICS reduce the loss of lung function; however, recent data suggest a possible survival benefit when combined with long-acting b agonists. There are limited data on the use of ICS in the treatment of acute exacerbations of COPD, and its role in this setting must be more clearly defined. The empiric use of systemic corticosteroids perioperatively represents another area of uncertainty. The role of pharmacogenetics in the metabolism of corticosteroids in COPD is evolving but may be partially responsible for the observed variability in patient responsiveness. The potential benefits of systemic or inhaled corticosteroid use must be weighed against the risk of known toxicities.

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Corticosteroid Therapy for Patients With Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Abstract: Short courses of systemic corticosteroids in acute exacerbations of COPD have been shown to improve spirometric outcomes (good-quality evidence) and clinical outcomes (good-quality evidence).

Cited by 97 publications

References 57 publications

Non-Ulcerogenic Dose of Dexamethasone Delays Gastric Ulcer Healing in Rats

Non-Ulcerogenic Dose of Dexamethasone Delays Gastric Ulcer Healing in Rats

Does eosinophilia and neutrophil to lymphocyte ratio affect hospital re-admission in cases of copd exacerbation?

Inhaled and Systemic Corticosteroids in Chronic Obstructive Pulmonary Disease

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