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      Do Benefits Outweigh Risks for Corticosteroid Therapy in Acute Exacerbation of Chronic Obstructive Pulmonary Disease in People with Diabetes Mellitus?

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          Chronic obstructive pulmonary disease (COPD) and diabetes mellitus (DM) are chronic health conditions with significant impacts on quality and extent of life. People with COPD and DM appear to have worse outcomes in each of the comorbid conditions. Treatment with corticosteroids in acute exacerbation of COPD (AECOPD) has been shown to reduce treatment failure and exacerbation relapse, and to shorten length of hospital stay, but not to affect the inexorable gradual worsening of lung function. Treatment with corticosteroids can lead to a wide spectrum of side effects and complications, including worsening hyperglycemia and deterioration of diabetes control in those with pre-existing DM. The relationship between COPD and DM is rather complex and accumulating evidence indicates a distinct phenotype of the comorbid state. Several randomized controlled trials on corticosteroid treatment in AECOPD excluded people with DM or did not report on outcomes in this subgroup. As such, the perceived benefits of corticosteroids in AECOPD in people with DM have not been validated. In people with COPD and DM, the detrimental side effects of corticosteroids are guaranteed, while the benefits are not confirmed and only presumed based on extrapolation from the general COPD population. Therefore, the potential for harm when prescribing corticosteroids for AECOPD in people with DM cannot be excluded.

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          Chronic obstructive pulmonary disease (COPD) is associated with important chronic comorbid diseases, including cardiovascular disease, diabetes and hypertension. The present study analysed data from 20,296 subjects aged > or =45 yrs at baseline in the Atherosclerosis Risk in Communities Study (ARIC) and the Cardiovascular Health Study (CHS). The sample was stratified based on baseline lung function data, according to modified Global Initiative for Obstructive Lung Disease (GOLD) criteria. Comorbid disease at baseline and death and hospitalisations over a 5-yr follow-up were then searched for. Lung function impairment was found to be associated with more comorbid disease. In logistic regression models adjusting for age, sex, race, smoking, body mass index and education, subjects with GOLD stage 3 or 4 COPD had a higher prevalence of diabetes (odds ratio (OR) 1.5, 95% confidence interval (CI) 1.1-1.9), hypertension (OR 1.6, 95% CI 1.3-1.9) and cardiovascular disease (OR 2.4, 95% CI 1.9-3.0). Comorbid disease was associated with a higher risk of hospitalisation and mortality that was worse in people with impaired lung function. Lung function impairment is associated with a higher risk of comorbid disease, which contributes to a higher risk of adverse outcomes of mortality and hospitalisations.
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            The National Cholesterol Education Program (NCEP) recently proposed a simple definition for metabolic syndrome. Information on the prospective association of this definition for coronary heart disease (CHD) and type 2 diabetes is currently limited. We used a modified NCEP definition with body mass index in place of waist circumference. Baseline assessments in the West of Scotland Coronary Prevention Study were available for 6447 men to predict CHD risk and for 5974 men to predict incident diabetes over 4.9 years of follow-up. Mean LDL cholesterol was similar but C-reactive protein was higher (P<0.0001) in the 26% of men with the syndrome compared with those without. Metabolic syndrome increased the risk for a CHD event [univariate hazard ratio (HR)=1.76 (95% CI, 1.44 to 2.15)] and for diabetes [univariate HR=3.50 (95% CI 2.51 to 4.90)]. Metabolic syndrome continued to predict CHD events (HR=1.30, 95% CI, 1.00 to 1.67, P=0.045) in a multivariate model incorporating conventional risk factors. Men with 4 or 5 features of the syndrome had a 3.7-fold increase in risk for CHD and a 24.5-fold increase for diabetes compared with men with none (both P<0.0001). C-reactive protein enhanced prognostic information for both outcomes. With pravastatin, men with the syndrome had similar risk reduction for CHD as compared with those without (HR, 0.73 and 0.69; pravastatin versus placebo). A modified NCEP metabolic syndrome definition predicts CHD events, and, more strikingly, new-onset diabetes, and thus helps identify individuals who may receive particular benefit from lifestyle measures to prevent these diseases.
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              Immune dysfunction in patients with diabetes mellitus (DM).

              Patients with diabetes mellitus (DM) have infections more often than those without DM. The course of the infections is also more complicated in this patient group. One of the possible causes of this increased prevalence of infections is defects in immunity. Besides some decreased cellular responses in vitro, no disturbances in adaptive immunity in diabetic patients have been described. Different disturbances (low complement factor 4, decreased cytokine response after stimulation) in humoral innate immunity have been described in diabetic patients. However, the clinical relevance of these findings is not clear. Concerning cellular innate immunity most studies show decreased functions (chemotaxis, phagocytosis, killing) of diabetic polymorphonuclear cells and diabetic monocytes/macrophages compared to cells of controls. In general, a better regulation of the DM leads to an improvement of these cellular functions. Furthermore, some microorganisms become more virulent in a high glucose environment. Another mechanism which can lead to the increased prevalence of infections in diabetic patients is an increased adherence of microorganisms to diabetic compared to nondiabetic cells. This has been described for Candida albicans. Possibly the carbohydrate composition of the receptor plays a role in this phenomenon.

                Author and article information

                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of Chronic Obstructive Pulmonary Disease
                16 March 2020
                : 15
                : 567-574
                [1 ]Dasman Diabetes Institute , Kuwait City, Kuwait
                [2 ]Institute of Cellular Medicine, Newcastle University , Newcastle upon Tyne, UK
                [3 ]Metabolic and Diabetes Unit, Sunderland Royal Hospital, South Tyneside and Sunderland NHS Foundation Trust , Sunderland, UK
                Author notes
                Correspondence: Ali M Aldibbiat Dasman Diabetes Institute , Sharq, Block 3, P.O. Box 1180, Dasman15462, KuwaitTel +965 2224 2999 Ext. 2214Fax +965 2249 2436 Email
                © 2020 Aldibbiat and Al-Sharefi.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (

                Page count
                Figures: 3, References: 87, Pages: 8


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