Elevated lactate dehydrogenase predicts pneumonia in spontaneous intracerebral hemorrhage.

Complication Inflammatory marker Intracerebral hemorrhage Lactate dehydrogenase Pneumonia

Journal

Heliyon
ISSN: 2405-8440
Titre abrégé: Heliyon
Pays: England
ID NLM: 101672560

Informations de publication

Date de publication:
29 Feb 2024
Historique:
received: 04 08 2023
revised: 12 01 2024
accepted: 07 02 2024
medline: 26 2 2024
pubmed: 26 2 2024
entrez: 26 2 2024
Statut: epublish

Résumé

Although a variety of risk factors for pneumonia after spontaneous intracerebral hemorrhage have been established, an objective and easily obtainable predictor is still needed. Lactate dehydrogenase is a nonspecific inflammatory biomarker. In this study, we aimed to assess the association between lactate dehydrogenase and pneumonia in spontaneous intracerebral hemorrhage patients. Our study was a retrospective, multicenter cohort study, undertaken in 7562 patients diagnosed with spontaneous intracerebral hemorrhage from 3 hospitals. All serum Lactate dehydrogenase was collected within 7 days from admission and divided into four groups as quartile(Q). We conducted a multivariable logistic regression analysis to assess the association of Lactate dehydrogenase with pneumonia. Among a total of 7562 patients, 2971 (39.3%) patients were diagnosed with pneumonia. All grades of elevated lactate dehydrogenase were associated with increased raw and risk-adjusted risk of pneumonia. Multiple logistic regression analysis showed odds ratios for Q2-Q4 compared with Q1 were 1.21 (95% CI, 1.04-1.42), 1.64(95% CI, 1.41-1.92), and 1.92 (95% CI, 1.63-2.25) respectively. The odds ratio after adjustment was 4.42 (95% CI, 2.94-6.64) when lactate dehydrogenase was a continuous variable after log-transformed. Elevated lactate dehydrogenase is significantly associated with an increase in the odds of pneumonia and has a predictive value for severe pneumonia in patients with pneumonia. Lactate dehydrogenase may be used to predict pneumonia events in spontaneous intracerebral hemorrhage patients as a laboratory marker.

Sections du résumé

Background UNASSIGNED
Although a variety of risk factors for pneumonia after spontaneous intracerebral hemorrhage have been established, an objective and easily obtainable predictor is still needed. Lactate dehydrogenase is a nonspecific inflammatory biomarker. In this study, we aimed to assess the association between lactate dehydrogenase and pneumonia in spontaneous intracerebral hemorrhage patients.
Methods UNASSIGNED
Our study was a retrospective, multicenter cohort study, undertaken in 7562 patients diagnosed with spontaneous intracerebral hemorrhage from 3 hospitals. All serum Lactate dehydrogenase was collected within 7 days from admission and divided into four groups as quartile(Q). We conducted a multivariable logistic regression analysis to assess the association of Lactate dehydrogenase with pneumonia.
Results UNASSIGNED
Among a total of 7562 patients, 2971 (39.3%) patients were diagnosed with pneumonia. All grades of elevated lactate dehydrogenase were associated with increased raw and risk-adjusted risk of pneumonia. Multiple logistic regression analysis showed odds ratios for Q2-Q4 compared with Q1 were 1.21 (95% CI, 1.04-1.42), 1.64(95% CI, 1.41-1.92), and 1.92 (95% CI, 1.63-2.25) respectively. The odds ratio after adjustment was 4.42 (95% CI, 2.94-6.64) when lactate dehydrogenase was a continuous variable after log-transformed.
Conclusions UNASSIGNED
Elevated lactate dehydrogenase is significantly associated with an increase in the odds of pneumonia and has a predictive value for severe pneumonia in patients with pneumonia. Lactate dehydrogenase may be used to predict pneumonia events in spontaneous intracerebral hemorrhage patients as a laboratory marker.

Identifiants

pubmed: 38404841
doi: 10.1016/j.heliyon.2024.e26109
pii: S2405-8440(24)02140-6
pmc: PMC10884414
doi:

Types de publication

Journal Article

Langues

eng

Pagination

e26109

Informations de copyright

© 2024 The Authors.

Déclaration de conflit d'intérêts

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Yangchun Xiao (Y)

Department of Neurosurgery, Clinical Medical College and Affiliated Hospital of Chengdu University, Chengdu, Sichuan, China.

Shuanghong He (S)

Health Management Center, West China Hospital, Sichuan University, Chengdu, Sichuan, China.

Xin Cheng (X)

Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu, Sichuan, China.

Liyuan Peng (L)

Department of Neurosurgery, Clinical Medical College and Affiliated Hospital of Chengdu University, Chengdu, Sichuan, China.

Yixin Tian (Y)

Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu, Sichuan, China.

Tiangui Li (T)

Department of Neurosurgery, The First People's Hospital of Longquanyi District Chengdu, Sichuan, China.

Jialing He (J)

Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Department of Neurosurgery, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.

Pengfei Hao (P)

Department of Neurosurgery, Shanxi Provincial People's Hospital, Taiyuan, Shanxi, China.

Weelic Chong (W)

Department of Medical Oncology, Thomas Jefferson University, Philadelphia, PA, USA.

Yang Hai (Y)

Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA, USA.

Chao You (C)

Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu, Sichuan, China.

Fang Fang (F)

Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu, Sichuan, China.

Zongjun Peng (Z)

Department of Neurosurgery, Sichuan Friendship Hospital, China.

Yu Zhang (Y)

Department of Neurosurgery, Clinical Medical College and Affiliated Hospital of Chengdu University, Chengdu, Sichuan, China.

Classifications MeSH