| The influence of pre-existing diabetes mellitus on the host immune response and outcome of pneumonia: analysis of two multicentre cohort studies. | |
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MedLine Citation:
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PMID: 20861291 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Although diabetes mellitus is implicated in susceptibility to infection, the association of diabetes with the subsequent course and outcome is unclear. METHODS: A retrospective analysis of two multicentre cohorts was carried out. The effect of pre-existing diabetes on the host immune response, acute organ function and mortality in patients hospitalised with community-acquired pneumonia (CAP) in the GenIMS study (n=1895) and on mortality following either CAP or non-infectious hospitalisations in the population-based cohort study, Health ABC (n=1639) was determined. Measurements included the mortality rate within the first year, risk of organ dysfunction, and immune responses, including circulating inflammatory (tumour necrosis factor, interleukin 6, interleukin 10), coagulation (Factor IX, thrombin-antithrombin complexes, antithrombin), fibrinolysis (plasminogen-activator inhibitor-1 and D-dimer) and cell surface markers (CD120a, CD120b, human leucocyte antigen (HLA)-DR, Toll-like receptor-2 and Toll-like receptor-4). RESULTS: In GenIMS, diabetes increased the mortality rate within the first year after CAP (unadjusted HR 1.41, 95% CI 1.12 to 1.76, p=0.002), even after adjusting for pre-existing cardiovascular and renal disease (adjusted HR 1.3, 95% CI 1.03 to 1.65, p=0.02). In Health ABC, diabetes increased the mortality rate within the first year following CAP hospitalisation, but not after hospitalisation for non-infectious illnesses (significant interaction for diabetes and reason for hospitalisation (p=0.04); HR for diabetes on mortality over the first year after CAP 1.87, 95% CI 0.76 to 4.6, p=0.16, and after non-infectious hospitalisation 1.16, 95% CI 0.8 to 1.6, p=0.37). In GenIMS, immediate immune response was similar, as evidenced by similar circulating immune marker levels, in the emergency department and during the first week. Those with diabetes had a higher risk of acute kidney injury during hospitalisation (39.3% vs 31.7%, p=0.005) and they were more likely to die due to cardiovascular and kidney disease (34.4% vs 26.8% and 10.4% vs 4.5%, p=0.03). Conclusions: Pre-existing diabetes was associated with a higher risk of death following CAP. The mechanism is not due to an altered immune response, at least as measured by a broad panel of circulating and cell surface markers, but may be due to worsening of pre-existing cardiovascular and kidney disease. |
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Authors:
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Sachin Yende; Tom van der Poll; Minjae Lee; David T Huang; Anne B Newman; Lan Kong; John A Kellum; Tamara B Harris; Doug Bauer; Suzanne Satterfield; Derek C Angus; |
Publication Detail:
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Type: Journal Article; Multicenter Study; Research Support, N.I.H., Extramural |
Journal Detail:
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Title: Thorax Volume: 65 ISSN: 1468-3296 ISO Abbreviation: Thorax Publication Date: 2010 Oct |
Date Detail:
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Created Date: 2010-09-23 Completed Date: 2010-10-29 Revised Date: 2012-03-21 |
Medline Journal Info:
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Nlm Unique ID: 0417353 Medline TA: Thorax Country: England |
Other Details:
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Languages: eng Pagination: 870-7 Citation Subset: IM |
Affiliation:
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Clinical Research, Investigation, and Systems Modeling of Acute Illness (CRISMA) Laboratory, University of Pittsburgh, Pittsburgh, PA, USA. yendes@upmc.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Aged Aged, 80 and over Biological Markers / blood Blood Glucose / metabolism Cohort Studies Community-Acquired Infections / immunology, mortality Diabetes Complications / immunology*, mortality Female Hospitalization Humans Male Middle Aged Multiple Organ Failure / epidemiology, immunology, microbiology Pneumonia / complications, immunology*, mortality Prognosis Retrospective Studies United States / epidemiology |
| Grant Support | |
ID/Acronym/Agency:
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27913//PHS HHS; 39482//PHS HHS; K23 GM083215-01A1/GM/NIGMS NIH HHS; K23GM083215/GM/NIGMS NIH HHS; N01-AG-6-2101/AG/NIA NIH HHS; N01-AG-6-2103/AG/NIA NIH HHS; N01-AG-6-2106/AG/NIA NIH HHS; R01HL74104/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Biological Markers; 0/Blood Glucose |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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