Silent existence of eosinopenia in sepsis: a systematic review and meta-analysis.

BACKGROUND: Sepsis is a life-threatening and time-critical medical emergency; therefore, the early diagnosis of sepsis is essential to timely treatment and favorable outcomes for patients susceptible to sepsis. Eosinopenia has been identified as a potential biomarker of sepsis in the past decade. However, its clinical application progress is slow and its recognition is low. Recent studies have again focused on the potential association between Eosinopenia and severe infections. This study analyzed the efficacy of Eosinopenia as a biomarker for diagnosis of sepsis and its correlation with pathophysiology of sepsis. METHOD: The protocol for this meta-analysis is available in PROSPERO (CRD42020197664). We searched PubMed, EMBASE, Web of Science, and Cochrane Central Register of Controlled Trials CENTRAL databases to identify studies that met the inclusion criteria. Two authors performed data extraction independently. The pooled outcomes were calculated by TP (true positive), FP (false positive), FN (false negative), TN (true negative) by using bivariate meta-analysis model in STATA 14.0 software. Meanwhile, possible mechanisms of sepsis induced Eosinopenia was also analyzed. RESULTS: Seven studies were included in the present study with a total number of 3842 subjects. The incidence of Eosinopenia based on the enrolled studies varied from 23.2 to 92.7%. For diagnosis of sepsis, the pooled sensitivity, specificity, positive likelihood ratio, negative likelihood ratio and diagnostic odds ratio of Eosinopenia were 0.66 (95%CI [0.53-0.77]), 0.68 (95%CI [0.56-0.79]), 2.09 (95%CI [1.44-3.02]), 0.49 (95%CI [0.34-0.71]) and 4.23 (95%CI [2.15-8.31]), respectively. The area under the summary receiver operator characteristic curve (SROC) was 0.73 (95%CI [0.68-0.76]). Meta-regression analysis revealed that no single parameter accounted for the heterogeneity of pooled outcomes. For each subgroup of different eosinopenia cutoff values (50, 40, ≤25, 100), the sensitivity was 0.61, 0.79, 0.57, 0.54, and the specificity was 0.61, 0.75, 0.83, 0.51, respectively. CONCLUSIONS: Our findings suggested that Eosinopenia has a high incidence in sepsis but has no superiority in comparison with conventional biomarkers for diagnosis of sepsis. However, eosinopenia can still be used in clinical diagnosis for sepsis as a simple, convenient, fast and inexpensive biomarker. Therefore, further large clinical trials are still needed to re-evaluate eosinopenia as a biomarker of sepsis.

Eosinopenia and neutrophil-to-lymphocyte count ratio as prognostic factors in exacerbation of COPD.

Exacerbations of Chronic Obstructive Pulmonary Disease (AECOPDs) are one of the most important clinical aspects of the disease, and when requiring hospital admission, they significantly contribute to mortality among COPD patients. Our aim was to assess the role of eosinopenia and neutrophil-to-lymphocyte count (NLR) as markers of in-hospital mortality and length of hospitalization (LoH) among patients with ECOPD requiring hospitalization. We included 275 patients. Eosinopenia was associated with in-hospital deaths only when coexisted with lymphocytopenia, with the specificity of 84.4% (95% CI 79.6-88.6%) and the sensitivity of 100% (95% CI 35.9-100%). Also, survivors presented longer LoH (P < 0.0001). NLR ≥ 13.2 predicted in-hospital death with the sensitivity of 100% (95% CI 35.9-100%) and specificity of 92.6% (95% CI 88.8-95.4%), however, comparison of LoH among survivors did not reach statistical significance (P = 0.05). Additionally, when we assessed the presence of coexistence of eosinopenia and lymphocytopenia first, and then apply NLR, sensitivity and specificity in prediction of in-hospital death was 100% (95% CI 35.9-100) and 93.7% (95% CI 90.1-96.3), respectively. Moreover, among survivors, the occurrence of such pattern was associated with significantly longer LoH: 11 (7-14) vs 7 (5-10) days (P = 0.01). The best profile of sensitivity and specificity in the prediction of in-hospital mortality in ECOPD can be obtained by combined analysis of coexistence of eosinopenia and lymphocytopenia with elevated NLR. The occurrence of a such pattern is also associated with significantly longer LoH among survivors.

Hypocalcemia, hypochloremia, and eosinopenia as clinical predictors of leptospirosis: A retrospective study.

BACKGROUND: Underestimation of leptospirosis cases is happening in many countries. The most common factor of underreporting is misdiagnosis. Considering the limitations of direct detection of pathogen and serological diagnosis for leptospirosis, clinical features and blood tests though non-specific are usually referred in making presumptive diagnosis to decide disease management. METHODS: In this single-centre retrospective study, comparative analysis on clinical presentations and laboratory findings was performed between confirmed leptospirosis versus non-leptospirosis cases. RESULTS: In multivariate logistic regression evidenced by a Hosmer-Lemeshow significance value of 0.979 and Nagelkerke R square of 0.426, the predictors of a leptospirosis case are hypocalcemia (calcium <2.10mmol/L), hypochloremia (chloride <98mmol/L), and eosinopenia (absolute eosinophil count <0.040×109/L). The proposed diagnostic scoring model has a discriminatory power with area under the curve (AUC) 0.761 (p<0.001). A score value of 6 reflected a sensitivity of 0.762, specificity of 0.655, a positive predictive value of 0.38, negative predictive value of 0.91, a positive likelihood ratios of 2.21, and a negative likelihood ratios of 0.36. CONCLUSION: With further validation in clinical settings, implementation of this diagnostic scoring model is helpful to manage presumed leptospirosis especially in the absence of leptospirosis confirmatory tests.

Eosinopenia as an Adverse Marker of Clinical Outcomes in Patients Presenting with Acute Myocardial Infarction.

BACKGROUND: Eosinopenia is considered a surrogate of inflammation in several disease settings. Following ST-segment elevation myocardial infarction, eosinopenia is presumed to be a marker of infarct severity. We sought to study the relationship between eosinopenia and infarct severity and how this relationship determined the long-term outcomes following ST-segment elevation myocardial infarction. METHODS: Six hundred and six consecutive patients undergoing primary percutaneous coronary interventions from a large volume single center were enrolled. Low eosinophil count was defined as < 40 cells/mL from samples within 2 hours after reperfusion. Primary endpoint was defined as composite of death, myocardial infarction, stroke, unplanned revascularization, and readmission for heart failure over 3.5 years' follow-up. RESULTS: Sixty-five percent of the patients had eosinopenia. Patients in the low eosinophil group had larger infarct size as measured by troponin value (2934 vs 1177 ng/L, P < .001) and left ventricle systolic function on echocardiography (48% vs 50%, P = 0.029). There was a weak correlation between eosinophil count and both troponin (r = -0.25, P < 0.001) and ejection fraction (r = 0.10, P = .017). The primary endpoint was higher in eosinopenic patients (28.8% vs. 20.4%; hazard ratio [HR] 1.49, 95% confidence interval [CI] 1.05 to 2.13, P = .023). A discordance between eosinopenia and severe left ventricle systolic dysfunction was observed in 55.6% of cases. Compared with normal count, eosinopenia was associated with worse clinical outcomes in patients with non-severe left ventricle dysfunction (24.1% vs 16.2%; HR 1.58, 95% CI 1.01 to 2.45, P = .044) but not in those with severe left ventricle dysfunction (42.3% vs. 38.9%; HR 1.10, 95% CI 0.59 to 2.03, P = .77) (P < .01 for interaction). CONCLUSIONS: Eosinopenia is an easily determined marker that reflects worse clinical outcomes over long-term follow-up.

Agranulocytosis Induced by Vancomycin. Case Report and Literature Review.

BACKGROUND Vancomycin has been used for decades to treat infections by Gram-positive bacteria, particularly those caused by methicillin-resistant staphylococci. Agranulocytosis is an infrequent complication of this antibiotic, postulated in its genesis a mechanism immune-mediated by antineutrophil antibodies and antineutrophil cytoplasm antibodies (ANCA). Treatment includes discontinuing vancomycin, and granulocyte colony-stimulating factor administration. CASE REPORT We present the case of a patient who developed agranulocytosis secondary to vancomycin during the treatment of an infectious endocarditis, which was reversed when the antibiotic was stopped. Concomitantly to neutropenia, he had ANCA positivity, which subsequently became negative. CONCLUSIONS Agranulocytosis induced by vancomycin is infrequent and generally occurs after day 12 of treatment. In most cases, like in our case, it is caused by an immune-mediated mechanism. More studies are needed to determine the pathogenic mechanism and the ANCA role in this adverse effect.

[Case Report - Metamizole-Induced Agranulocytosis]. / Kasuistik: Metamizol-induzierte Agranulozytose.

Metamizole is primarily used for severe perioperative pain, acute injury and colic, and cancer pain. For other acute/chronic forms of pain and high fever, it should only be used if unresponsive to other agents. Metamizole should not be used for middle and low pain. Oral application should be preferred. A contraindication for metamizole is leukopenia. Clinical signs for agranulocytosis are fever, tonsillitis and aphthous stomatitis.

Decreased miR-17-92 cluster expression level in serum and granulocytes preceding onset of antithyroid drug-induced agranulocytosis.

PURPOSE: We aimed to determine changes in miR-17-92 cluster expression in serum and granulocytes from patients with antithyroid drug (ATD)-induced agranulocytosis. METHODS: In this study, real-time polymerase chain reaction (PCR) was used to detect serum miR-17-92 expression levels in 20 ATD-induced agranulocytosis and 16 control patients. Importantly, dynamic changes in neutrophil counts from granulocytopenia to agranulocytosis were observed in 6 of the 20 patients. miR-17-92 expression levels in granulocytes of those six patients under the granulocytopenia condition were measured and compared with corresponding granulocyte samples after recovery. Additionally, the expression levels of these miRNAs in patients with type I or type II bone marrow characteristics were analyzed, and the correlation between miR-17-92 and serum free thyroxine level was analyzed. RESULTS: We found that levels of miR-17-92 expression decreased in both serum and pre-agranulocytosis granulocytes from patients with ATD-induced agranulocytosis compared with those in serum and granulocytes from both recovered patients and control patients. However, no difference among patients with either type of bone marrow characteristics was observed, and no correlation between serum miR-17-92 and free thyroxine levels was found. CONCLUSION: In ATD-induced agranulocytosis, expression of the miR-17-92 cluster is reduced in both serum and granulocytes, though this alteration does not correlate with bone marrow characteristics or thyroid function.