Neutrophil-to-Lymphocyte Ratio in Acute Cerebral Hemorrhage: a System Review

Lattanzi, Simona; Brigo, Francesco; Trinka, Eugen; Cagnetti, Claudia; Napoli, Mario Di; Silvestrini, Mauro

doi:10.1007/s12975-018-0649-4

Cited by 176 publications

(142 citation statements)

References 52 publications

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“…Decrease of lymphocyte count, resulting in proportional increase of NLR, is a characteristic feature of neurogenic immunodepression and closely related to stroke-associated pneumonia which is one of the major contributors of mortality in this population (14). The second mechanism is early systemic inflammatory response triggered by ICH components (15). The resulting neutrophilia, which will lead to an increase in NLR, can enhance secondary tissue damage in the hemorrhagic brain.…”

Section: Discussionmentioning

confidence: 99%

Neutrophil-to-Lymphocyte Ratio and Prognosis of Spontaneous Intracerebral Hemorrhage

Pektezel¹,

Arsava²,

Öge³

et al. 2019

TÃ¼rk Beyin Damar Hast Derg

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INTRODUCTION: Neutrophil to Lymphocyte Ratio (NLR) is suggested to predict functional outcomes and mortality at admission of patients with intracerebral hemorrhage (ICH). However, effect of timing of NLR measurement on prediction of mortality and expansion in ICH has not been clarified. METHODS: From admission and 24th-hour blood samples, admission NLR (NLR-adm) and 24th-hour NLR (NLR-24th) was calculated as "absolute neutrophil count/lymphocyte count". Hematoma expansion was evaluated with the volume (ABC/2) difference from admission cranial CT to follow-up one. RESULTS: A total of 383 patients (41.7% female, age, 65±13) were assessed. Of them, 251 (65.5%) were discharged. The average hematoma volume was 32.8 cc and 35.3 cc in the first and second CT, respectively. The mean NLR was 8.2±10.3 at admission and 16.6 ± 15.7 at 24th hour. Only NLR-24th (β=0.035, OR: 1.036 (1.002-1.071), p=0.04), hematoma volume at first CT (β=0.012, OR 1.012 (0.999-1.024) p=0.067) and Hemphill score (β=0.689, OR 1.992 (1.402-2.832) p<0.001) were found to be significantly related with mortality after adjusted to age (decade), atrial fibrillation, anticoagulant use and NLR-adm. An exploratory logistic regression analysis indicated that hematoma expansion greater than 12.5 cc correlated to, albeit borderline, NLR-24th (β=0.038, OR=1.038 (95%CI: 1.008-1.069) but not NLR-adm. DISCUSSION and CONCLUSION: We found NLR-24th to be associated with higher mortality and greater hematoma expansion rate. This NLR increment, probably secondary to the stress response, in ICH can be considered as an epiphenomenon of worse prognosis.

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Section: Discussionmentioning

confidence: 99%

Neutrophil-to-Lymphocyte Ratio and Prognosis of Spontaneous Intracerebral Hemorrhage

Pektezel¹,

Arsava²,

Öge³

et al. 2019

TÃ¼rk Beyin Damar Hast Derg

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“…During recent years, neutrophil‐to‐lymphocyte ratio (NLR) has been proved of great value with a significant correlation with systemic inflammation reaction in several autoimmune diseases . Because NLR can be easily obtained at low cost through an automatic hematology analyzer, many research groups have further confirmed the value of NLR in predicting disease severity and worse clinical outcomes in a variety of diseases, including cerebrovascular diseases, cardiovascular diseases, and neoplasm . Besides, cumulative evidence has suggested that NLR was associated with AP and better than other serum markers in predicting severity and prognosis of AP.…”

Section: Introductionmentioning

confidence: 99%

Neutrophil‐to‐lymphocyte ratio can specifically predict the severity of hypertriglyceridemia‐induced acute pancreatitis compared with white blood cell

Huang

Chen

Yang

et al. 2019

Clinical Laboratory Analysis

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Objectives We aimed to evaluate the values of neutrophil‐to‐lymphocyte ratio (NLR) and white blood cell (WBC) in predicting severity of acute pancreatitis (AP) with different etiologies. Methods We compared NLR and WBC levels in patients with different etiologies and AP severity. The optimal cutoff value for them to predict severe acute pancreatitis (SAP) was determined by receiver operating characteristic (ROC) curve analysis. Results Both NLR and WBC were elevated in patients with SAP. After subgrouping AP by etiology, NLR was predictive of SAP only in hypertriglyceridemia‐induced AP (HTG‐AP), while WBC could effectively predict severity in both gallstone and HTG‐AP. The best cutoff value of WBC for predicting SAP in gallstone AP patients was 12.81 × 109/L, with sensitivity and specificity of 78.9% and 70.2%. The best cutoff value for NLR and WBC to differentiate HTG‐SAP was more than 5.88 and 15.89 × 109/L, respectively, with sensitivity and specificity of 87% and 50% for NLR and 56.5% and 75.76% for WBC. Conclusions Our study firstly demonstrated that NLR selectively played a role in HTG‐AP, while WBC could predict the severity of both gallstone and HTG‐AP. Furthermore, we firstly elucidated that NLR was more sensitive and accurate in judging the severity of HTG‐AP compared with WBC.

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“…In the hyperacute phase, PHE involves clot retraction, trans‐capillary efflux of electrolytes, water and osmotically active serum proteins, and cytotoxic edema from neuronal energy failure. In the acute phase, during the first few days, PHE is sustained by coagulation cascade, thrombin production, immune reaction, and inflammatory cells . Finally, beginning from approximately 72 hours after ICH, PHE formation involves erythrocyte lysis and hemoglobin‐induced toxicity .…”

Section: Primary and Secondary Brain Injury Following Cerebral Hematomamentioning

confidence: 99%

Managing blood pressure in acute intracerebral hemorrhage

Lattanzi

Brigo

Silvestrini

2019

J of Clinical Hypertension

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| INTRODUC TI ONIntracerebral hemorrhage (ICH) results from the rupture of cerebral vessels leading to the development of a hematoma in the brain. It comprises approximately 15%-30% of all strokes and affects more than 1 million people every year worldwide. 1 Hypertension is the most common cause of ICH, and less frequent etiologies include coagulopathies, cerebral amyloid angiopathy, vascular abnormalities, brain trauma or tumors, and infections.Cerebral hemorrhage is the stroke subtype characterized by the highest mortality and morbidity: the fatality rate is about 40% at 1 month from bleeding and most survivors retain a severe residual disability, with only 20%-40% of patients living independently at 1 year. 2 Currently, medical and surgical strategies have substantially failed to improve outcome, and the management of ICH consists mainly of supportive therapies. The understanding of the mechanisms underlying the course of hematoma and the progression of the injury in surrounding parenchyma is, hence, of paramount relevance to identify therapeutic targets and effective treatment approaches. | PRIMARY AND S ECONDARY B R AIN INJ URY FOLLOWING CEREB R AL HEMATOMASeveral mechanisms are involved in brain injury related to ICH. Primary brain injury, which occurs at the time of hemorrhage, is due to the mass effect caused by extravasation of blood, physical disruption of adjacent tissue and mechanical compression of local structures. The hematoma can also increase the intracranial pressure, impair cerebral blood flow, and lead to brain herniation. 3 Although damage occurring immediately after ICH is untreatable, it is worth noticing that around one third of patients undergo hematoma expansion (HE) within the first days after stroke. 4 Hematoma growth contributes to midline shift and early neurological deterioration, and is consistently associated with higher fatality and poorer clinical outcome. 5 Remarkably, the intensive blood pressure reduction in acute cerebral hemorrhage trial (INTERACT-1) demonstrated that each 1 mL increase in HE is associated with a raise in the risk of death and dependency by 5%. 6 Secondary brain injury is due either to the body and tissue response to the hematoma or to the toxic effects of clot components, and includes a cascade of events, as inflammation, iron-mediated oxidative stress, apoptosis, necrosis, and autophagy, which mainly result in the development of peri-hemorrhagic edema (PHE). 7Cerebral edema occurs within hours of ICH, peaks several days later and can last for weeks. 5 In the hyperacute phase, PHE involves clot retraction, trans-capillary efflux of electrolytes, water and osmotically active serum proteins, and cytotoxic edema from neuronal energy failure. In the acute phase, during the first few days, PHE is sustained by coagulation cascade, thrombin production, immune reaction, and inflammatory cells. 8,9 Finally, beginning from approximately 72 hours after ICH, PHE formation involves erythrocyte lysis and hemoglobin-induced toxicity. 10 PHE may contribute to an overall ...

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Neutrophil-to-Lymphocyte Ratio in Acute Cerebral Hemorrhage: a System Review

Cited by 176 publications

References 52 publications

Neutrophil-to-Lymphocyte Ratio and Prognosis of Spontaneous Intracerebral Hemorrhage

Neutrophil-to-Lymphocyte Ratio and Prognosis of Spontaneous Intracerebral Hemorrhage

Neutrophil‐to‐lymphocyte ratio can specifically predict the severity of hypertriglyceridemia‐induced acute pancreatitis compared with white blood cell

Managing blood pressure in acute intracerebral hemorrhage

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