It is not fully established whether leukocyte can predict the poor outcome for ruptured cerebral aneurysms (CA) or not. Here, we retrospectively analyzed the clinical data of 428 patients with ruptured CA between 2010 and 2015. Patients' demographic data, including gender, age, history of smoking, alcohol, hypertension, diabetes and hypercholesterolemia, Hunt-Hess and Fisher grade, occurrence of hydrocephalus, aneurysm location, time to surgery, delayed ischemic neurological deficit (DIND) and peak leukocyte of blood test from day 1 to 3 after aneurysmal rupture were recorded and analyzed. In the multivariable analysis model, gender, Fisher grade, time to surgery and hydrocephalus were not relevant to poor outcome. However, Hunt-Hess grade, DIND and preoperative leukocyte count (>13.84 × 109/L) were significantly associated with adverse outcome. The respective increased risks were 5.2- (OR5.24, 95% CI 1.67-16.50, p = 0.005), 6.2-(OR 6.24, 95% CI 3.55-10.99, p < 0.001) and 10.9-fold (OR 9.35, 95% CI 5.98-19.97, p < 0.001). The study revealed that Hunt-Hess grade, DIND and preoperative leukocyte count (>13.84 × 109/L) were independent risk factors for poor outcome of ruptured CA at 3 months. Higher leukocyte count is a convenient and useful marker to predict 3-month poor outcome for ruptured CA.

The dog is frequently used as a model for hematologic human diseases. In this study the suitability of nine potential reference genes for quantitative RT-PCR studies in canine whole blood was investigated.

Synovial fluid analysis for diagnosis of prosthetic joint infections has gained increasing interest in the recent past when markers more specific for these infections than the serum ones have been identified. Despite the important steps forward, identification of a gold standard has not yet been identified. In this study, usefulness of alpha defensin, leukocyte esterase, C-reactive protein (CRP), and white blood cells (WBCs) in synovial fluids alone and in combination for diagnosis of prosthetic joint infection was evaluated. Synovial fluids from 32 infected and 34 not infected patients were analyzed. Sensitivity, specificity, positive and negative predictive values, diagnostic accuracy, and receiver-operating characteristic (ROC) curves were calculated for each parameter. Moreover, combination of coupled variables was also evaluated by logistic regression analysis. Sensitivity of alpha defensin, CRP, leukocyte count, and leukocyte esterase were 84.4%, 87.5%, 93.7%, and 93.8%, respectively. Specificity was 91.2% for leukocyte counts, 94.1% for alpha defensin, 97.0% for CRP, and 97.1% for leukocyte esterase. Diagnostic accuracy was 89.4% for alpha defensin, 92.4% for WBC counts and CRP, and 95.5% for leukocyte esterase. No statistical differences were observed in area under the curve (AUC) of the ROC curves of alpha defensin, CRP, and leukocyte counts. Logistic regression analysis applied to a model comprising all the variables showed an AUC higher than AUC of coupled variables. In conclusion, results of this study confirm the high sensitivity and specificity of synovial leukocyte esterase for diagnosis of prosthetic joint infection, also suggesting the need to assess a panel of markers to optimize diagnosis of these infections.

Ischemic stroke (IS) is a common neurological disease in the elderly, but the relationship between neutrophil/albumin ratio (NAR) and leukocyte count/albumin ratio (LAR) and the severity of neurological function injury and early neurological deterioration (END) occurrence remain elusive in acute IS. A total of 299 patients with acute IS and 56 healthy controls were enrolled. According to the NIHSS score at admission, the disease group was divided into three groups (mild, moderate and severe IS), and the differences in five indexes NAR, LAR, neutrophil count, leukocyte count and albumin among the four groups were analyzed. Furthermore, explore the correlation between the above indicators and the severity of IS and END occurrence. The results showed that higher NAR, LAR, neutrophil count, leukocyte count levels and lower albumin levels were associated with acute IS, and the levels of NAR and LAR increased gradually in three groups of IS. NAR and LAR were positively and albumin was negatively correlated with the severity of IS. Meanwhile, NAR and LAR showed a good predictive value in identifying patients with END after acute IS. NAR and LAR may be predictors of the severity of IS and END occurrence after acute IS.

The association between sepsis and segmented neutrophil-to-monocyte (SeMo) ratio is unclear. We postulated that an increase in dynamic SeMo ratio measurement can be applied in risk stratification. This retrospective study included 727 consecutive sepsis patients in medical intensive care units (ICUs), including a subpopulation of 153 patients. According to the leukocyte (white blood cell, WBC) count on day 3 (normal range, between 4,000/µL and 12,000/µL) and delta SeMo (value of SeMo ratio on day 3 minus value of SeMo ratio on day 1; normal delta SeMo, <7), patients were grouped into 3 (delta SeMo & WBC tool). The survival lines separated significantly with hazard ratios of 1.854 (1.342-2.560) for the delta SeMo or WBC abnormal group and 2.860 (1.849-4.439) for the delta SeMo and WBC abnormal group compared to the delta SeMo and WBC normal group. Delta SeMo & WBC tool and delta sequential organ failure assessment (SOFA) tool performed better than the other tools (delta SeMo, delta WBC, day 3 WBC, and day 1 WBC). Severity in delta SeMo & WBC tool and delta SeMo tool reflected the immune dysfunction score, cytokine expression, and human leukocyte antigen D-related monocyte expression on day 1 and day 3. There was correspondence between delta SOFA and delta WBC and between delta SeMo and delta cytokine expression. Incorporation of dynamic SeMo ratio with WBC count provides risk stratification for sepsis patients admitted in the ICU.

Coronavirus disease (COVID-19) is an infectious disease caused by a recently discovered coronavirus. Blood test including complete blood count is crucial in diagnosing of several viral and bacterial infection.

The neutrophil-lymphocyte ratio (NLR) is often used as an inflammatory marker in chronic diseases such as cancer or cardiovascular diseases. However, there are few studies about the association between the NLR and diabetes mellitus (DM) or impaired fasting glucose (IFG) patients in Korea. This study investigated the association between the fasting plasma glucose (FPG) level and NLR in Koreans.

The association between peripheral leukocyte count and bleeding events in nonvalvular atrial fibrillation (NVAF) patients treated with dabigatran remains unclear. This study aimed to explore the association between leukocyte count and bleeding events after excluding other confounders in NVAF patients taking dabigatran.

Background: Inflammation is important in the development of atherosclerosis. Research suggested sex-dependent differences for the value of inflammatory markers for risk stratification of stroke patients with internal carotid artery stenosis (ICAS). We investigated whether leukocytes and thrombocytes were associated with ≥50% ICAS in acute stroke and whether this was sex-dependent. Patients included in the Preventive Antibiotics in Stroke Study (PASS) were used. PASS is a randomized controlled trial that randomized between four days of preventive ceftriaxone intravenously or standard stroke care alone. It investigated whether ceftriaxone could improve functional outcome at three months after stroke. Methods: Patients included in PASS were evaluated for the predictive value of leukocytes and thrombocytes for ICAS. Ischemic stroke and TIA patients were selected out of PASS patients. Logistic regression analysis was performed adjusting for NIHSS and other covariates. Results: 2550 patients were included in PASS. 1413 of 2550 patients (55%) were evaluated in this sub study. Female patients showed a mean of 8.55 × 109/L for leukocytes and 259 × 109/L for thrombocytes. Men showed a mean of 8.29 × 109/L for leukocytes and 224 × 109/L for thrombocytes. Multivariate logistic regression analysis showed that leukocytes were independently associated with ICAS ≥ 50% in male patients (OR 1.094, p = 0.008), but not in female patients (OR 1.041, p = 0.360). Thrombocytes were not associated with ICAS. Conclusions: We conclude that blood leukocyte count independently predicts ICAS in men after acute stroke, but not in women. Clinical Trial unique identifier: ISRCTN66140176.

Background: Both polycythemia and high leukocyte count are associated with the risk of cardiovascular disease. However, it remains to be determined whether polycythemia and high leukocyte count show synergistic increasing effects on cardiometabolic risk. Methods: Cardiometabolic risk was evaluated by cardiometabolic index (CMI) and metabolic syndrome in a cohort of middle-aged men (n = 11,140) who underwent annual health check-up examinations. The subjects were divided into three tertile groups by hemoglobin concentration or leukocyte count in peripheral blood, and their relations with CMI and metabolic syndrome were investigated. A new index, named hematometabolic index (HMI), was defined as the product of hemoglobin concentration (g/dL)-minus-13.0 and leukocyte count (/μL)-minus-3000. Results: When the subjects were further classified by tertiles for hemoglobin concentration and leukocyte count into nine groups, the odds ratios for high CMI and metabolic syndrome of the group categorized in the highest (third) tertiles for both hemoglobin concentration and leukocyte count versus the group of the lowest (first) tertiles for both of them were highest among the nine groups. In receiver-operating characteristic (ROC) analysis for relationships of HMI with high CMI and metabolic syndrome, areas under the ROC curves (AUCs) were significantly larger than the reference level and tended to be smaller with an increase in age. In subjects from 30 to 39 years of age, the AUC for the relationship between HMI and metabolic syndrome was 0.707 (0.663-0.751) and the cutoff of HMI was 9850. Conclusions: HMI, reflecting hemoglobin concentration and leukocyte count, is thought to be a possible marker for discriminating cardiometabolic risk.

Acute pancreatitis (AP) is associated with high complications. Early, reliable prediction of mortality may improve patient management.

Among patients with peritoneal dialysis-associated peritonitis (PDAP), It has been regarded as an indicator of deterioration of clinical condition that peritoneal dialysis effluent leukocyte count (PDELC) cannot be restored to normal after initial antibiotic therapy. However, the precise relationship between PDELC on day 5 and the clinical outcomes of PDAP episodes remains uncertain.

This study examined the effects of the PI3K/AKT pathway and mitochondrial autophagy in macrophages and the leukocyte count after pulmonary infection. Sprague‒Dawley rats were subjected to tracheal injection of lipopolysaccharide (LPS) to establish animal models of pulmonary infection. By inhibiting the PI3K/AKT pathway or inhibiting/inducing mitochondrial autophagy in macrophages, the severity of the pulmonary infection and the leukocyte count were altered. The PI3K/AKT inhibition group did not show a significant difference in leukocyte counts compared with the infection model group. Mitochondrial autophagy induction alleviated the pulmonary inflammatory response. The infection model group had significantly higher levels of LC3B, Beclin1, and p-mTOR than the control group. The AKT2 inhibitor group exhibited significantly increased levels of LC3B and Beclin1 compared with the control group (P < 0.05), and the Beclin1 level was significantly higher than that in the infection model group (P < 0.05). Compared with the infection model group, the mitochondrial autophagy inhibitor group exhibited significantly decreased levels of p-AKT2 and p-mTOR, whereas the levels of these proteins were significantly increased in the mitochondrial autophagy inducer group (P < 0.05). PI3K/AKT inhibition promoted mitochondrial autophagy in macrophages. Mitochondrial autophagy induction activated the downstream gene mTOR of the PI3K/AKT pathway, alleviated pulmonary inflammatory reactions, and decreased leukocyte counts.

Patients with established Parkinson's disease (PD) display differences in peripheral blood markers of immune function, including leukocyte differential counts, compared with controls. These differences may be useful biomarkers to predict PD and may shed light on pathogenesis. We sought to identify whether peripheral immune dysregulation was associated with increased risk of subsequent PD diagnosis.

To investigate the relationship between white blood cell (WBC) count and incidence of hyper-low-density lipoprotein (LDL) cholesterolemia in a population-based longitudinal study. This is a retrospective study using data of annual health check-ups for residents of Iki City, Japan. A total of 3312 residents (≥ 30 years) without hyper-LDL cholesterolemia at baseline were included in this analysis. Primary outcome was incidence of hyper-LDL cholesterolemia (LDL cholesterol levels ≥ 3.62 mmol/L and/or use of lipid lowering drugs). During follow-up (average 4.6 years), 698 participants development of hyper-LDL cholesterolemia (incidence 46.8 per 1000 person-years). Higher incidence of hyper-LDL cholesterolemia was observed among participants with higher leukocyte count (1st quartile group: 38.5, 2nd quartile group: 47.7, 3rd quartile group: 47.3, and 4th quartile group: 52.4 per 1,000 person-years, P = 0.012 for trend). Statistically significant relation was observed even after adjustment for age, gender, smoking, alcohol intake, leisure-time exercise, obesity, hypertension and diabetes: hazard ratio 1.24 (95% confidence interval 0.99 to 1.54) for 2nd quartile group, 1.29 (1.03-1.62) for 3rd quartile group and 1.39 (1.10-1.75) for 4th quartile group, compared with 1st quartile group (P for trend = 0.006). Increased WBC count was related to incidence of hyper-LDL cholesterolemia in general Japanese population.

To investigate the relationship between peripheral leukocyte dynamics and the outcome of large hemispheric infarction (LHI) patients.

Uromodulin (UMOD) is produced and secreted by tubular epithelial cells. Secreted UMOD polymerizes (pUMOD) in the tubular lumen, where it regulates salt transport and protects the kidney from bacteria and stone formation. Under various pathological conditions, pUMOD accumulates within the tubular lumen and reaches extratubular sites where it may interact with renal interstitial cells. Here, we investigated the potential of extratubular pUMOD to act as a damage associated molecular pattern (DAMP) molecule thereby creating local inflammation. We found that intrascrotal and intraperitoneal injection of pUMOD induced leukocyte recruitment in vivo and led to TNF-α secretion by F4/80 positive macrophages. Additionally, pUMOD directly affected vascular permeability and increased neutrophil extravasation independent of macrophage-released TNF-α. Interestingly, pUMOD displayed no chemotactic properties on neutrophils, did not directly activate β2 integrins and did not upregulate adhesion molecules on endothelial cells. In obstructed neonatal murine kidneys, we observed extratubular UMOD accumulation in the renal interstitium with tubular atrophy and leukocyte infiltrates. Finally, we found extratubular UMOD deposits associated with peritubular leukocyte infiltration in kidneys from patients with inflammatory kidney diseases. Taken together, we identified extratubular pUMOD as a strong inducer of leukocyte recruitment, underlining its critical role in mounting an inflammatory response in various kidneys pathologies.

Polymorphonuclear (PMN) leukoyte function tests and clinical data analyses were performed in 28 chronic renal failure (CRF) patients receiving regular hemodialysis. We divided them into two groups; 12 patients with normal serum ferritin were classified as group 1 and 16 patients with high serum ferritin as group 2. There was no difference in age, BUN, serum creatinine, complement (C3, C4), peripheral white blood cell count and the duration of dialysis between the two groups, but the serum iron level was higher in group 2 (129.1 ± 46.58 μg/dl) than in group 1 (74.3 ± 20.9 μg/dl) (p<0.001). The total iron binding capacity was lower in group 2 (p<0.05) and the number of transfusions was higher in group 2 (25 ± 16.1) than in group 1 (12 ± 8.7) (p<0.05). The nitroblue-tetrazolium (NBT) test showed no difference among groups 1, 2 and the healthy control group. In chemotaxis to fMLP (N-formylmethionylleucylphenylalanine), the mean number of migrated neutrophils to fMLP (10−6 M/L) per high power field was significantly decreased in group 2 (99.5 ± 37.6) compared with the healthy control group (140.1 ± 13.4) (p<0.005), but not in group 1 (155.8 ± 79.4). In the phagocytosis test using Staphylococcus aureus, the phagocytic index ratio compared to the healthy control group was significantly decreased in group 2 (0.59 ± 0.14), but not in group 1 (0.97 ± 0.18). These results suggest that iron overload due to multiple transfusions in patients receiving regular long term hemodialysis may play a part in causing susceptibility to infection by impairing PMN leukocyte functions, especially chemotaxis and phagocytosis.

Earlier studies have suggested that the leukocyte redistribution can be considered as an immunological marker of the clinical response to corticosteroids (CS), representing an easy measurable potential biomarker in severe asthma.

Background. Accumulating evidence supports leukocyte telomere length (LTL) as a biological marker of cellular aging. Poor sleep is a risk factor for age-related disease; however, the extent to which sleep accounts for variation in LTL is unknown. Methods. The present study examined associations of self-reported sleep duration, onset latency, and subjective quality with LTL in a community-dwelling sample of 245 healthy women in midlife (aged 49-66 years). Results. While sleep duration and onset latency were unrelated to LTL, women reporting poorer sleep quality displayed shorter LTL (r = 0.14, P = 0.03), independent of age, BMI, race, and income (b = 55.48, SE = 27.43, P = 0.04). When analyses were restricted to participants for whom sleep patterns were chronic, poorer sleep quality predicted shorter LTL independent of covariates and perceived psychological stress. Conclusions. This study provides the first evidence that poor sleep quality explains significant variation in LTL, a marker of cellular aging.