Elevated lactate dehydrogenase predicts pneumonia in spontaneous intracerebral hemorrhage.

Background: 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: 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: 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: 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.

A potential immunotherapeutic and prognostic biomarker for multiple tumors including glioma: SHOX2.

BACKGROUND: Short stature homeobox 2 (SHOX2) is significant gene in the development and progression of multiple types of tumors. Nonetheless, the biological role of SHOX2 within pan-cancer datasets has not been investigated. Thus, comprehensive bioinformatics analyses of pan-cancer datasets were conducted to explore how SHOX2 regulates tumorigenesis. METHODS: A variety of tumor datasets and online analytical tools, including SangerBox, TIMER2, LinkedOmic, GEPIA2 and cBioPortal, were applied to explore SHOX2 expression in various tumors. To ascertain the connections between SHOX2 expression and genetic alterations, SHOX2-related genes and tumor immunity, the pan-cancer datasets were examined. In vitro assays were applied to verify the biological functions of SHOX2 in glioma cells via CCK-8, wound healing, Transwell and colony formation assays. RESULTS: Analyses found that SHOX2 was overexpressed in multiple cancer types. SHOX2 expression level was significantly correlated with isocitrate dehydrogenase (IDH), 1p/19q, O6-methylguanine DNA methyltransferase (MGMT) status and new types of glioma patients. High mRNA expression levels of SHOX2 were associated with a poor prognosis in multiple tumor patients. KEGG enrichment analysis showed that SHOX2-related genes were associated with cell cycle and DNA damage repair. Genetic alterations of SHOX2 were identified in multiple types of cancers, including duplications and deep mutations. Immune analysis showed that SHOX2 was closely correlated with the tumor mutation burden (TMB), microsatellite instability (MSI), neoantigen and neoantigens and immune checkpoint (ICP) in a variety of tumors and could influence the immunotherapy sensitivity of cancers. CCK-8, wound healing, Transwell and colony formation experiments showed that SHOX2 knockdown inhibited glioma cell proliferation, migration, invasion and colony formation abilities. CONCLUSION: SHOX2 was overexpressed in multiple cancer types in TCGA cohort. SHOX2 knockdown inhibited glioma cell proliferation, migration and colony formation ability. Our study showed that SHOX2 may be an immunotherapeutic and promising prognostic biomarker in certain types of tumors.

Cerebral hemorrhage after thrombolysis in stroke patients with unruptured intracranial aneurysms: a systemic review and meta-analysis.

BACKGROUND: For ischemic stroke patients with concomitant unruptured aneurysm, intravenous thrombolysis therapy (IVT) remains a disputable decision. We hence performed a meta-analysis to identify the related brain hemorrhage rate of unruptured aneurysms and the risk ratio for their rupture comparing to stroke patients who do not have aneurysms. METHODS: A comprehensive search was conducted to identify the studies from the online database from 2000 to September 1st, 2022. Cohort studies were included and assessed by Newcastle-Ottawa Scale (NOS) for quality. The research procedures were subjected to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Fixed-effects model was used based on the heterogeneity tests. RESULTS: In 10 eligible studies, 7238 ischemic stroke patients were screened, a total of 302 patients with 348 aneurysms were included. 10 studies were eligible for ICH rate analysis, 8 for SAH rate analysis and 7 for risk ratio of stroke patients with unruptured aneurysms. The pooled any ICH rate was 16% (95% CI 11-21%), symptomatic ICH rate was 4% (95% CI 1-7%, I2 = 0.00%, p = 0.90), and 0% (95% CI 0-1%) for aneurysm-related ICH. Subarachnoid hemorrhage was as low as 2% (95% CI 0-5%), while 0% (95% CI 0-2%) directly related to the aneurysm rupture. The risk ratio of ICH in stroke patients with aneurysms was 1.18 (95% CI 0.79-1.77). Additionally, the hemorrhage rate difference was not evident between saccular and fusiform aneurysms due to a lack of details. CONCLUSIONS: IVT is unlikely to induce hemorrhage of pre-existing unruptured aneurysms in stroke patients. Further randomized control studies are warranted to validate these conclusions.