Severe bleeding is a leading cause of ICU admission and mortality. Fibrinogen plays a crucial role in prognosis, yet optimal thresholds and supplementation targets remain unclear.

Patients with major bleeding were extracted from the MIMIC-IV database. Restricted cubic splines (RCS) identified the optimal pre-treatment fibrinogen threshold, and propensity score matching adjusted for confounders. Multiple analytical methods, including multivariable regression and machine learning models, were applied. Post-treatment fibrinogen levels were stratified based on guideline recommendations, and Cox regression assessed survival outcomes.

Among 7,063 patients (6,666 survivors, 397 non-survivors), RCS analysis revealed a nonlinear relationship between pre-treatment fibrinogen and ICU mortality (P-non-linear < 0.001), with a threshold at 1.3 g/L. Patients with Fib > 1.3 g/L had a significant 28-day survival benefit (OR = 0.65, 95% CI: 0.48-0.87, p < 0.01). Post-treatment stratification showed that fibrinogen ≥ 1.3 g/L was associated with improved survival (p < 0.01). RCS analysis identified an optimal post-treatment target of 2.0-2.5 g/L.

Fibrinogen levels are predictive of ICU outcomes in massive hemorrhage. A pre-treatment threshold of 1.3 g/L indicates poor prognosis, while post-treatment levels of 2.0-2.5 g/L may optimize survival.

Background: Morbidity and mortality rates in intensive care units (ICUs) reflect the severe health challenges faced by critically ill patients. Nutritional and immune status, as measured by the prognostic nutritional index (PNI), are increasingly recognized as important predictors of intensive care unit outcomes. Objective: We aimed to compare the prognostic nutritional index levels of survived and deceased subjects treated in intensive care units. Methods: This retrospective study examined the association between prognostic nutritional index and mortality among intensive care unit patients treated from June 2023 to June 2024. The prognostic nutritional index was calculated using serum albumin and lymphocyte levels, and patients were categorized into survived and deceased groups. Statistical analyses, including ROC and logistic regression, were used to evaluate prognostic nutritional index's predictive capacity. Results: We revealed that deceased patients had significantly lower prognostic nutritional index values, lower platelet counts, and higher C-reactive protein (CRP) and serum creatinine levels compared to survivors. The prognostic nutritional index was independently associated with mortality, with each unit increase decreasing mortality risk by 6%. Conclusion: These findings highlight the prognostic nutritional index's utility as a prognostic tool in intensive care unit settings, underscoring the need for nutritional assessments and targeted interventions to improve patient outcomes. Further research with larger cohorts is warranted to validate these findings and explore causative mechanisms.

Identification of prognostic biomarkers for critical illness are essential to improving mortality in the context of precision medicine. The purpose of this study was to evaluate the prognostic value of interleukin-6 (IL-6) and platelet-derived growth factor AA(PDGF-AA) in predicting 28-day mortality in critically ill patients.

199 critically ill patients were recruited from the emergency department of the Beijing Chaoyang Hospital, Capital Medical University, between October 2020 and April 2021. IL-6, PDGF-AA and other markers were tested immediately, and the Sequential Organ Failure Assessment (SOFA) and Acute Physiology and Chronic Health Evaluation II (APACHE II) scores were calculated within 24h of admission to the emergency department. Patients were divided into survival and non-survival groups according to clinical outcomes for 28 days. The quantitative detections of IL-6 and PDGF-AA were performed using the Luminex assay. Spearman correlation, logistic regression, and receiver operating characteristic curve (ROC) analyses were conducted for comparison.

Among 199 patients, 139 died and 60 survived within 28 days, IL-6 and PDGF-AA levels were higher in the non-survival group (P<0.05). IL-6 levels correlated with PDGF-AA levels in the non-survival group (P<0.001). IL-6 and PDGF-AA were independent predictors off 28-day mortality in critically ill patients (OR=1.003, 1.002). Combination of IL-6 and SOFA can make an AUROC of 0.892 with a specificity of 91.4%. Combination of IL-6, PDGF-AA and SOFA can make an AUROC of 0.905 with a specificity of 91.5%.

This study highlights the importance of monitoring serum levels of IL-6 and PDGF-AA in critically ill patients. Compared with the marker alone, combinations with other conventional risk factors have better predictive values.

Limited data are available on bicytopenia (BC) in patients with heart failure (HF).

This study evaluated the association between BC and prognosis in patients with HF.

This retrospective cohort study enrolled consecutive hospitalised patients with HF. We compared all-cause and cardiovascular mortality between those with and without BC. BC was defined as the combination of any two conditions among leukopaenia, thrombocytopaenia, and anaemia. Propensity score matching and a Cox proportional hazards model were applied.

Among 935 hospitalised patients, 103 patients had BC. Patients in the BC group were older (80.0 ± 12.0 vs. 73.4 ± 14.7 years; P < 0.0001), including a higher proportion of females (55.3% vs. 41.7%; P = 0.009), had a higher prevalence of atrial fibrillation (51.5% vs 41.1%; P = 0.047), had a lower baseline estimated glomerular filtration rate (50.8 ± 24.1 vs. 56.2 ± 23.9 mL/min/1.73 m2; P = 0.03), and had a higher left ventricular ejection fraction (48.1 ± 16.1 vs. 42.4 ± 15.8%; P = 0.0008). Propensity score matching with a 1:1 ratio produced 63 matched pairs. All-cause mortality was significantly higher in the BC group than in the non-BC group (log-rank P = 0.069 and Wilcoxon P = 0.048); however, cardiovascular mortality and hospitalisation for HF showed no significant differences. In the multivariate Cox proportional hazard model, BC was associated with higher all-cause mortality but not with cardiovascular mortality (hazard ratio, 1.983; 95% confidence interval, 1.008-3.898; P = 0.047).

BC was associated with all-cause mortality but not with cardiovascular mortality in patients with HF. BC is an important risk factor for all-cause mortality in patients with HF.

Objective: Patients with sepsis often experience reductions or increases in platelet counts, but the implications of these temporal patterns on prognosis remain unclear. The aim of this study was to investigate the impact of changes in platelet trajectories on the clinical prognosis of sepsis. Methods: This study was a retrospective analysis using data from the Medical Information Mart for Intensive Care IV database. Patients with sepsis were identified from the database, and their platelet trajectories were categorized into four distinct models based on the changes in platelet counts over a period of 14 days after diagnosis of sepsis. The effect of these trajectories on patient prognosis was subsequently evaluated. Results: A total of 15,250 patients with sepsis were included to construct a model, and the following four distinct platelet count trajectories were identified: normal platelet levels (phenotype 1); persistently low platelet levels (phenotype 2); gradually increasing platelet levels exceeding the normal range (phenotype 3); and consistently significantly elevated platelet levels (phenotype 4). Statistically significant differences were found in the 28-day mortality, in-hospital mortality, and 90-day mortality among the four phenotypes. Multivariate regression analysis showed that compared to the group with normal platelet levels (phenotype 1), the group with persistently low platelet levels (phenotype 2) had higher in-hospital mortality (odds ratio [OR] = 1.34, 95% confidence interval [CI]: 1.16-1.54), 28-day mortality (OR = 1.69, 95% CI: 1.47-1.94), and 90-day mortality (OR = 1.50, 95% CI: 1.32-1.69). There was no difference in in-hospital mortality between phenotypes 3 and 4 compared to phenotype 1, although phenotype 4 showed an increase in 28-day mortality ( P < 0.05), and phenotype 3 showed a decreasing trend in 90-day mortality ( P < 0.05). The results of inverse probability weighting adjusted by regression were basically consistent with the above findings, except that there was no statistical difference in 28-day mortality between phenotype 4 and phenotype 1. In the subgroups based on age, weight, and antiplatelet drugs or therapies, there was an interaction between platelet levels and these factors. Conclusions: In patients with sepsis, a decrease in platelet count is associated with increased mortality, while a moderate increase in platelet count can reduce 90-day mortality. However, for patients with persistently elevated platelet counts, caution is advised when using antiplatelet drugs or therapies, as it may increase mortality.

This narrative review aims to describe the epidemiology and aetiologies of thrombocytopenia in critically ill patients, the bleeding risk assessment in thrombocytopenic patients, and provide an update on platelet transfusion indications.

Thrombocytopenia is a common disorder in critically ill patients. The classic definition relies on an absolute platelet count below 150 × 109/L. Alternatively, the definition has extended to a relative decrease in platelet count (typically within a range of >30->50% decrease) from baseline, yet remaining above 150 × 109/L. Thrombocytopenia may result from multiple mechanisms depending upon the underlying conditions and the current clinical setting. Regardless of the causes, thrombocytopenia accounts as an independent determinant of poor outcomes in critically ill patients, albeit often of unclear interpretation. Nevertheless, it is well established that thrombocytopenia is associated with an increased incidence of bleeding complications. However, alternative factors also contribute to the risk of bleeding, making it difficult to establish definite links between nadir platelet counts at the expense of potential adverse events. Platelet transfusion represents the primary supportive treatment of thrombocytopenia to prevent or treat bleeding. As randomised controlled trials comparing different platelet count thresholds for prophylactic platelet transfusion in the ICU are lacking, the prophylactic transfusion strategy is largely derived from studies performed in stable haematology patients. Similarly, the platelet count transfusion threshold to secure invasive procedures remains based on a low level of evidence. Indications of platelet transfusions for the treatment of severe bleeding in thrombocytopenic patients remain largely empirical, with platelet count thresholds ranging from 50 to 100 × 109/L. In addition, early and aggressive platelet transfusion is part of massive transfusion protocols in the setting of severe trauma-related haemorrhage.

Thrombocytopenia in critically ill patients is very frequent with various etiologies, and is associated with worsened prognosis, with or without bleeding complications. Interventional trials focused on critically ill patients are eagerly needed to better delineate the benefits and harms of platelet transfusions.

Platelet-to-white blood cell ratio (PWR) as a comprehensive indicator of inflammatory response has been widely used to assess the prognosis of various diseases. However, the relationship between PWR and adverse outcomes in patients with acute decompensated heart failure (ADHF) remains unclear. This study aimed to evaluate the association between PWR and all-cause mortality within 30 days of hospitalization in ADHF patients from Jiangxi, China.

A total of 1,453 ADHF patients from the Jiangxi-ADHF study1 cohort were included. The primary outcome measure was all-cause mortality within 30 days of hospitalization. Multivariable Cox proportional hazards regression, restricted cubic spline regression, and receiver operating characteristic curve analysis were employed to explore the association between the inflammatory marker PWR and all-cause mortality in ADHF patients within 30 days of hospitalization.

During the 30-day observation period, a total of 53 subjects experienced mortality events. Multivariable Cox regression showed a negative correlation between PWR and all-cause mortality within 30 days of hospitalization in ADHF patients. Restricted cubic spline regression demonstrated an L-shaped association between PWR and 30-day mortality risk (p for nonlinear = 0.038). Further threshold analysis revealed a threshold point for PWR at 15.88, where a decrease in PWR below this threshold was significantly associated with increased risk of all-cause mortality (p for log-likelihood ratio test = 0.046). Additionally, the results of receiver operating characteristic curve analysis indicated that PWR had high predictive accuracy for mortality events within 30 days of hospitalization in ADHF patients and is significantly better than the traditional HF marker N-Terminal Pro-Brain Natriuretic Peptide (AUC: NT-proBNP 0.69, PWR 0.76; Delong test P < 0.05). Subgroup analysis showed that compared to subjects with reduced or moderately reduced ejection fraction, ADHF patients with preserved ejection fraction had a lower risk of short-term mortality associated with PWR (HR:0.99 vs. 0.98 vs. 0.87, P for interaction = 0.0067).

This study reveals, for the first time, a negative correlation between the inflammatory marker PWR and all-cause mortality within 30 days of hospitalization in ADHF patients. Based on the threshold analysis findings, patients with ADHF and a PWR below 15.88 had a significantly higher risk of death within 30 days.

While thrombocytopenia's link to mortality is known, the prognostic impact of longitudinal trajectories of platelet indices in combination with analysis of thrombocytopenia's mediating role remains unexplored. This is the first study that addresses this significant gap by investigating the association between seven platelet indices trajectory subphenotypes and ICU mortality, considering thrombocytopenia's mediating influence.

Four hundred and twenty-one adult ICU patients were enrolled in this longitudinal cohort study. Three trajectories were identified for each platelet index, namely: descending, stable, and ascending, and using a regression, receiver-operating characteristic curve, and mediation analysis, their associations with 90-day mortality were evaluated with the mediating effect of thrombocytopenia. The findings were adjusted (prefixed 'a') for covariates.

The heterogeneous trajectories significantly associated with 90-day mortality included: descending platelet count (PC) [aOR, 2.75 (CI, 1.56-4.85), p = 0.0005, aAUC, 0.783], descending plateletcrit (PCT) [aOR, 3.49 (CI, 1.88-6.46), p = 0.0001, aAUC, 0.802], ascending platelet distribution width (PDW) [aOR, 2.04 (CI, 1.13-3.71), p = 0.0188, aAUC, 0.776], and ascending percent-immature platelet fraction (%-IPF) [aOR, 2.25 (CI, 1.29-3.94), p = 0.0045, aAUC, 0.778], with 11.6% (p = 0.027), 12.0% (p = 0.019), 22.1% (p = 0.011), and 15.9% (p = 0.024) effects mediated by thrombocytopenia, respectively. In contrast, ascending mean platelet volume (MPV) was significantly and independently associated with mortality [aOR, 3.04 (CI, 1.45-6.39), p = 0.0033, aAUC, 0.781], without the effect mediated by thrombocytopenia (p = 0.056). The trajectories of platelet-large cell ratio (P-LCR) and absolute-immature platelet count (A-IPF) were not significantly associated with the risk of mortality (p > 0.05).

This study demonstrated that descending PC and PCT and ascending PDW and %-IPF, mediated by thrombocytopenia, and ascending MPV, without mediation by thrombocytopenia, are useful longitudinal trajectories for predicting 90-day mortality in the ICU.

Platelet storage duration may influence transfusion effectiveness and patient outcomes.The present study aimed to evaluate the effect of platelet storage duration on platelet increment and clinical outcomes in patients admitted to the intensive care unit (ICU).

This prospective, open-label, randomized controlled trial, conducted at a single centre, enrolled ICU patients requiring platelet transfusion. Patients were randomly assigned to receive platelet concentrates aged ≤ 3 days (Group 1) or 4-5 days (Group 2). Platelet increments were assessed by Absolute Platelet Count Increment (ACI), Corrected Count Increment (CCI), and Percentage Platelet Recovery (PPR). Clinical outcomes including bleeding, infection rates, ICU stay, red cell transfusion requirements, and mortality were also monitored.

Patients transfused fresher platelets (Group 1) had higher median ACI, CCI and PPR at 1 h compared to those transfused older platelets (Group 2) though the difference was not statistically significant. At 24 h, Group 1 patients had a median ACI of 28,000/µl compared to 14,000/µl in Group 2(p = 0.001). The median CCI was 16,800 in Group 1 versus 8,200 in Group 2(p = 0.001). Group 1 also had a higher median PPR of 45.7% compared to 23.6% in Group 2(p = 0.011).There was no significant difference in clinical outcomes such as bleeding, infection rates, ICU stay, or mortality between the groups. Multivariate analysis indicated that co-morbidities and higher APACHE-III score were associated with increased mortality.

Transfusion of fresher platelets resulted in higher increments and transfusion effectiveness but did not affect clinical outcomes or mortality.

Clinical Trials Registry of India (CTRI/2023/03/050676).

Thrombocytopenia, defined as a platelet count of less than 150 × 109/L, is a frequent condition among hospitalized patients and presents unique challenges in diagnosis and management. Despite its commonality, data on incidence and related risk factors in medical inpatients remain limited, especially in older people.

A 2-year prospective cohort study with a 3-year follow-up was conducted on inpatients aged ≥65 years admitted to a medical ward. Clinical data were collected, including demographics, comorbidities, laboratory results, and outcomes. Multivariate logistic regression analysis assessed risk factors associated with non-resolution of thrombocytopenia and mortality.

The study included 961 older inpatients with a mean age of 82 years. Thrombocytopenia occurred in 22.6% of the study population. The most common causes were infections (57.4%) and drug-induced thrombocytopenia (25.3%). The non-resolution of thrombocytopenia was noted in 59% of patients. In-hospital and 3-year mortality was significantly higher in this subgroup compared to the rest (24.5% vs. 12.7%, p = 0.015) and (72.4% vs. 59.8%, p = 0.04, respectively). In multivariate analysis, nadir platelet count and hematologic disease were independent factors associated with the non-resolution of thrombocytopenia. Furthermore, in individuals with thrombocytopenia, the administration of norepinephrine (p < 0.001) and a higher clinical frailty score (p < 0.001) were observed as independent mortality predictors.

Thrombocytopenia in older medical inpatients is associated with poor prognosis, particularly in those with non-resolution thrombocytopenia. Early identification and targeted management may improve outcomes.

A reduction in platelet count in critically ill patients is a marker of severity of the clinical condition. However, whether this association holds true in acute kidney injury (AKI) is unknown. We analyzed the association between platelet reduction in patients with AKI and major adverse kidney events (MAKE).

In this retrospective cohort, we included AKI patients at the Hospital Civil of Guadalajara, in Jalisco, Mexico. Patients were divided according to whether their platelet count fell >21% during the first 10 days. Our objectives were to analyze the associations between a platelet reduction >21% and MAKE at 10 days (MAKE10) or at 30-90 days (MAKE30-90) and death.

From 2017 to 2023, 400 AKI patients were included, 134 of whom had a > 21% reduction in platelet count. The mean age was 54 years, 60% were male, and 44% had sepsis. The mean baseline platelet count was 194 x 103 cells/µL, and 65% of the KDIGO3 patients met these criteria. Those who underwent hemodialysis (HD) had lower platelet counts. After multiple adjustments, a platelet reduction >21% was associated with MAKE10 (OR 4.2, CI 2.1-8.5) but not with MAKE30-90. The mortality risk increased 3-fold (OR 2.9, CI 1.1-7.7, p = 0.02) with a greater decrease in the platelets (<90 x 103 cells/µL). As the platelets decreased, the incidence of MAKE was more likely to increase. These associations lost significance when accounting for starting HD.

In our retrospective cohort of patients with AKI, a > 21% reduction in platelet count was associated with MAKE. Our results are useful for generating hypotheses and motivating us to continue studying this association with a more robust design.

Septic shock is a life-threatening disease worldwide often associated with thrombocytopenia. Platelets play a crucial role in bridging the gap between immunity, coagulation, and endothelial cell activation, potentially influencing the course of the disease. However, there are few studies specifically evaluating the impact of thrombocytopenia on the prognosis of pediatric patients. Therefore, the study investigates effects of early thrombocytopenia in the prognosis of children with septic shock. Pediatric patients with septic shock from 2015 to 2022 were included monocentrically. Thrombocytopenia was defined as a platelet count of <100 × 109/L during the first 24 hours of septic shock onset. The primary outcome was the 28-day mortality. Propensity score matching was used to pair patients with different platelet counts on admission but comparable disease severity. A total of 419 pediatric patients were included in the analysis. Patients with thrombocytopenia had higher 28-day mortality (55.5% vs. 38.7%, p = .005) compared to patients with no thrombocytopenia. Thrombocytopenia was associated with reduced 28-PICU free days (median value, 0 vs. 13 days, p = .003) and 28-ventilator-free (median value, 0 vs. 19 days, p = .001) days. Among thrombocytopenia patients, those with platelet count ≤50 × 109/L had a higher 28-day mortality rate (63.6% vs. 45%, p = .02). Multiple logistic regression showed that elevated lactate (adjusted odds ratio (OR) = 1.11; 95% confidence interval (CI): 1.04-1.17; P <0.001) and white blood cell (WBC) count (OR = 0.97; 95% CI: 0.95-0.99; p = .003) were independent risk factors for the development of thrombocytopenia. Thrombocytopenia group had increased bleeding events, blood product transfusions, and development of organ failure. In Kaplan-Meier survival estimates, survival probabilities at 28 days were greater in patients without thrombocytopenia (p value from the log-rank test, p = .004). There were no significant differences in the type of pathogenic microorganisms and the site of infection between patients with and without thrombocytopenia. In conclusion, thrombocytopenia within 24 hours of shock onset is associated with an increased risk of 28-day mortality in pediatric patients with septic shock.

The diverse presentation of COVID-19 symptoms and outcomes has revealed a significant gap in understanding the specific risk factors and characteristics of the virus among immunocompromised cancer patients, particularly in the Middle East.

We our study aimed to address this gap by investigating the characteristics and outcomes of COVID-19 in cancer patients compared to non-cancer patients.

We carried out a retrospective analysis, collecting demographic, oncologic, and COVID-19-related data from electronic medical records of 248 patients admitted to our tertiary care center in Lebanon. Statistical analysis was conducted using SPSS to identify patterns. Patients with solid tumors were 3.433 times more likely to die than those who were cancer-free (p = 0.012). Moreover, patients with advancing disease were 2.805 times more likely to be admitted to the ICU (p = 0.03) and 14.7 times more likely to die (p < 0.001) compared with those in remission.

Our findings emphasize the critical need for tailored preventive measures and specialized care for immunocompromised cancer patients, given their heightened vulnerability to severe COVID-19 outcomes. These insights contribute to the development of specific strategies aimed at enhancing the protection and clinical management of this high-risk group.

Bleeding events are common complications in critically ill patients with haematological malignancies. The objective of this study was to assess the incidence and identify determinants of ICU-acquired severe bleeding events in critically ill patients with haematological malignancies. We conducted a single-center retrospective study including all adult patients with a history of haematological malignancy requiring unplanned ICU admission over a 12-year period (2007-2018). The primary endpoint was the occurrence of ICU-acquired (i.e. after the first 24 h in the ICU) severe bleeding events, as defined as grades 3 or 4 of the World Health Organization classification.

A total of 1012 patients were analysed, mainly with a diagnosis of lymphoma (n = 434, 42.9%) and leukaemia or myelodysplastic syndrome (n = 266, 26.3%). Most patients were recently diagnosed (n = 340, 33.6%) and under active cancer treatment within the last 3 months (n = 604, 59.7%). The main cause for admission was infection (n = 479, 47.3%), but a significant proportion of patients were admitted for a primary haemorrhage (n = 99, 10%). ICU-acquired severe bleeding events occurred in 109 (10.8%) patients after 3.0 days [1.0-7.0] in the ICU. The main source of bleeding was the gastrointestinal tract (n = 44, 40.3%). Patients experiencing an ICU-acquired severe bleeding event displayed prolonged in-ICU length of stay (9.0 days [1.0-6.0] vs. 3.0 [3.5-15.0] in non-bleeding patients, p < 0.001) and worsened outcomes with increased in-ICU and in-hospital mortality rates (55% vs. 18.3% and 65.7% vs. 33.1%, respectively, p < 0.001). In multivariate analysis, independent predictors of ICU-acquired severe bleeding events were chronic kidney disease (cause-specific hazard 2.00 [1.19-3.31], p = 0.008), a primary bleeding event present at the time of ICU admission (CSH 4.17 [2.71-6.43], p < 0.001), non-platelet SOFA score (CSH per point increase 1.06 [1.01-1.11], p = 0.02) and prolonged prothrombin time (CSH per 5-percent increase 0.90 [0.85-0.96], p = 0.001) on the day prior to the event of interest.

Major bleeding events are common complications in critically ill patients with haematological malignancies and are associated with a worsened prognosis. We identified relevant risk factors of bleeding which may prompt closer monitoring or preventive measures.

Platelets play a critical role in hemostasis and inflammatory diseases. Low platelet count and activity have been reported to be associated with unfavorable prognosis. This study aims to explore the relationship between dynamics in platelet count and in-hospital morality among septic patients and to provide real-time updates on mortality risk to achieve dynamic prediction.

We conducted a multi-cohort, retrospective, observational study that encompasses data on septic patients in the eICU Collaborative Research Database (eICU-CRD) and the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. The joint latent class model (JLCM) was utilized to identify heterogenous platelet count trajectories over time among septic patients. We assessed the association between different trajectory patterns and 28-day in-hospital mortality using a piecewise Cox hazard model within each trajectory. We evaluated the performance of our dynamic prediction model through area under the receiver operating characteristic curve, concordance index (C-index), accuracy, sensitivity, and specificity calculated at predefined time points.

Four subgroups of platelet count trajectories were identified that correspond to distinct in-hospital mortality risk. Including platelet count did not significantly enhance prediction accuracy at early stages (day 1 C-indexDynamic  vs C-indexWeibull: 0.713 vs 0.714). However, our model showed superior performance to the static survival model over time (day 14 C-indexDynamic  vs C-indexWeibull: 0.644 vs 0.617).

For septic patients in an intensive care unit, the rapid decline in platelet counts is a critical prognostic factor, and serial platelet measures are associated with prognosis.

Vancomycin-associated acute kidney injury (VA-AKI) is the most clinically relevant side effect of vancomycin. The objective of this study was to investigate the association between VTC and VA-AKI as well as 30-day mortality in critically ill elderly adults.

Elderly patients with trough serum vancomycin concentration records(VTC) in the Medical Information Mart-IV (MIMIC-IV) and eICU databases were retrospectively studied.

A total of 3,146 critically ill elderly adults were finally enrolled. The incidence of VA-AKI in the elderly population was 76.5%. Logistic regression analysis revealed significant relationships between VA-AKI and various factors, including VTC, comorbidities, and laboratory indicators, and SOFA, and GCS score. For each mg/L increase, the OR for VA-AKI increased by 2.5%. The association between VTC and 30-day mortality was found to be statistically significant (odds ratio (OR): 1.021, 95% CI: 1.010-1.031), P < 0.001). The Restricted cubic splines (RCS) curves revealed that VTC ranged of 19.67 to 35.72 mg/l for AKI and 19.17 to 42.86 mg/l for 30-day mortality exhibit OR with 95% CI above 1, indicating statistically significant associations with an increased risk of AKI and 30-day mortality, respectively. In the subgroup analysis, VTC was identified as a risk factor for VA-AKI in specific patient groups, including white individuals, female patients, those with shock, patients with SOFA > 6, patients with baseline creatinine > 1.2 mg/dl and patients with or without exposed to other nephrotoxic medications.

This study found the significant association between VTC and the incidence of VA-AKI and 30-day mortality in critically ill elderly adults. The RCS curves indicated concentration ranges for AKI (19.67-35.72 mg/L) and 30-day mortality (19.17-42.86 mg/L), signifying increased risk.

Extracorporeal membrane oxygenation (ECMO) is utilized as a rescue therapy in the management of pediatric patients with refractory septic shock. Multiple studies support the use of a central cannulation strategy in these patients. This study aimed to assess the survival of and identify mortality risk factors in pediatric patients supported with peripheral veno-arterial (VA) ECMO in the setting of septic shock.

We retrospectively reviewed and compared clinical characteristics of 40 pediatric patients supported with peripheral VA ECMO for refractory septic shock, at two tertiary care children's hospitals from 2006 to 2020. Our hypothesis was that peripheral VA ECMO is effective in supporting cardiac function and improving tissue oxygenation in most pediatric patients with refractory septic shock.

The overall rate of survival to discharge was 52.5%, comparable to previously reported survival for pediatric sepsis on ECMO. With the exclusion of patients with an oncologic process, the survival rate rose to 62.5%. There was a statistically significant difference in mean pump flow rates within 2 hours of initiation of ECMO between survivors and non-survivors (98 mL/kg/min vs 76 mL/kg/min, P  =  .050). There was no significant difference between pre-ECMO vasoactive inotropic score (VIS) in survivors and non-survivors. A faster decrease in VIS in the first 24 hours was associated with lower mortality.

From this large case series, we conclude that peripheral VA ECMO is a safe and effective modality to support pediatric patients with refractory septic shock, provided there is establishment of high ECMO pump flows in the first few hours after cannulation and improvement in the VIS.

Bleeding risk evaluation of thrombocytopenic patients admitted in ICU has been poorly investigated.

A prospective observational study conducted in an 18-bed medical ICU. Consecutive patients with thrombocytopenia (<150 Giga/L) and no bleeding at admission were included.

Over one year, 91 patients were included, mainly men (63%), with an age of 61 [46-68] years and a SOFA score of 6 [3-8]. Twenty-three patients (25%) had an hemorrhagic event during ICU stay, mainly digestive (n = 9; 39%) and urological (n = 6; 26%). The time between ICU admission and bleeding was 8 [2-19] days. Almost half of bleeding events required vasopressor infusion and a hemostatic procedure. At admission, two variables were significantly different between the Bleeding and No-Bleeding groups: plasma urea level was significantly higher in the Bleeding group (9 [5.1; 13] vs. 13 [8.9; 31] mmol/L; p < 0.001) and the presence of skin purpura was associated with a 3-fold higher risk for bleeding during ICU stay (HR: 3.4 [1.3-8.3]; p < 0.05). In contrast, admission platelet count was not significantly different between the 2 groups (90 [32; 128] vs 62 [36; 103] G/L; p = 0.26).

Plasma urea levels and the presence of skin purpura are helpful in identifying thrombocytopenic patients at high-risk of bleeding during ICU stay.

Thrombocytopenia in older individuals is a common but diagnostically challenging condition that has variable clinical impact to those who are affected. Diagnostic approach requires evaluation of the preexisting clinical conditions, detailed review of medications, and assessment for disorders that warrant urgent treatment. In this article, we describe a systematic approach to diagnosis of thrombocytopenia and present a schematic review for management strategies. Three clinical scenarios are presented that are relevant for their prevalence and management challenges in an older adult population. The first scenario addresses primary immune thrombocytopenia (ITP) and reviews different treatment options. The second one addresses complications of thrombocytopenia in management of the myelodysplastic syndrome. The last one reviews diagnostic challenges of drug-induced ITP.

Identifying prognosis for patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) is challenging. Eosinophils and platelet are involved in the development of COPD, which may predict adverse events. The objective of this study was to determine the effect of the eosinophil to platelet ratio (EPR) in predicting adverse events in patients with AECOPD who visited the emergency department.

The records of patients with AECOPD treated at Dalian Municipal Friendship Hospital from January 2018 to December 2020 were retrospectively reviewed. The relationship between the clinical characteristics and EPR, as cut-off value of 0.755, was evaluated.

A total of 508 patients with an AECOPD (316 male, 192 female) were included. An optimal AUC cutoff of 0.755 for the EPR segregated the patients into 2 groups with significantly different mortality (25.3% vs 5.5%, P < 0.001). The same mortality risk with lower EPR was observed among the patients with emergency room attendance (35.6% vs 11.1%, P < 0.001). A model including EPR <0.755, exacerbation history, PaO2 <60mmHg, PaCO2 >50 mm Hg, hypoalbuminemia and age ≥80 was developed to predict death risk and showed good performance.

During severe COPD exacerbation, an EPR < 0.755 preceding therapy can predict worse outcomes in patients with an AECOPD.

Thrombocytopenia is common in critically ill patients with cancer. However, the association of platelet count with spontaneous bleeding is controversial in critically ill patients and the association with cancer-related characteristics is unknown.

This observational study includes patients with active cancer and severe thrombocytopenia. A logistic regression model adjusted for confounders was used to evaluate the association of daily platelet count and cancer-related characteristics (type of cancer and presence of metastasis) with spontaneous bleeding. Confounders were identified using directed acyclic graphs.

We screened 5822 patients, 255 (4.4%) met eligibility criteria resulting in 1401 daily observations. Fifty-three patients (20.8%) had spontaneous bleeding during the intensive care unit stay, 64% presenting minor, and 36% major bleeding. The adjusted odds ratio (OR) for spontaneous bleeding with platelet count between 49 and 20 × 109 /L was 4.6 (1.1-19.6), with platelet count between 19 and 10 × 109 /L was 14.2 (3.1-66.2), and with platelet count below 10 × 109 /L was 39.6 (6.9-228.5). The adjusted OR for spontaneous bleeding in patients with hematologic malignancies was 0.6 (0.4-1.2), and 4.3 (2.0-9.0) for patients with metastatic tumor.

In critically ill patients with active cancer and severe thrombocytopenia, lower counts of platelets and presence of metastasis are associated with increased risk of spontaneous bleeding, while hematologic malignancy is not associated with increased risk of spontaneous bleeding.

Thrombocytopenia (platelet count < 150 × 109/L) is common in intensive care unit (ICU) patients and is likely associated with worse outcomes. In this study we present international contemporary data on thrombocytopenia in ICU patients.

We conducted a prospective cohort study in adult ICU patients in 52 ICUs across 10 countries. We assessed frequencies of thrombocytopenia, use of platelet transfusions and clinical outcomes including mortality. We evaluated pre-selected potential risk factors for the development of thrombocytopenia during ICU stay and associations between thrombocytopenia at ICU admission and 90-day mortality using pre-specified logistic regression analyses.

We analysed 1166 ICU patients; the median age was 63 years and 39.5% were female. Overall, 43.2% (95% confidence interval (CI) 40.4-46.1) had thrombocytopenia; 23.4% (20-26) had thrombocytopenia at ICU admission, and 19.8% (17.6-22.2) developed thrombocytopenia during their ICU stay. Absence of acquired immune deficiency syndrome (AIDS), non-cancer-related immune deficiency, liver failure, male sex, septic shock, and bleeding at ICU admission were associated with the development of thrombocytopenia during ICU stay. Among patients with thrombocytopenia, 22.6% received platelet transfusion(s), and 64.3% of in-ICU transfusions were prophylactic. Patients with thrombocytopenia had higher occurrences of bleeding and death, fewer days alive without the use of life-support, and fewer days alive and out of hospital. Thrombocytopenia at ICU admission was associated with 90-day mortality (adjusted odds ratio 1.7; 95% CI 1.19-2.42).

Thrombocytopenia occurred in 43% of critically ill patients and was associated with worse outcomes including increased mortality. Platelet transfusions were given to 23% of patients with thrombocytopenia and most were prophylactic.

Acute myocardial infarction (AMI) is one of the major cardiac complications in patients hospitalized in the intensive care unit (ICU) for non-cardiac disease. A better knowledge of ischemic and bleeding risks in these patients is needed to identify those most likely to benefit from specific cardiac management. We therefore assessed the incidence and predictors of a composite outcome of severe ischemic event (AMI recurrence, ischemic stroke), major bleeding, or all-cause death in this setting.

In this multicenter retrospective study, all consecutive adult patients admitted for non-cardiac disease to four French university hospital ICUs between January 2012 and December 2018 who had an AMI with obstructive coronary artery disease (OCAD) during the ICU stay were considered for inclusion. AMI with OCAD was defined as an elevated cardiac troponin value associated with at least one sign (clinical, electrocardiographic, or echocardiographic) suggestive of myocardial ischemia and presence of OCAD on coronary angiography. The primary endpoint was in-hospital occurrence of the composite outcome.

Ninety-six patients [median age 69 years, 22 women (23%), 59 with sepsis (61%), 35 with ST elevation (37%), median sequential organ failure assessment (SOFA) of 8 on the day of AMI] were included. The median peak cardiac troponin value was 131 (IQR 44-303) times the upper reference limit. Dual antiplatelet, therapeutic anticoagulation, and early mechanical reperfusion therapies were administered in 61 (64%), 68 (71%), and 47 (49%) patients, respectively. The composite outcome occurred in 48 (50%) patients. Severe ischemic events occurred in 17 (18%) patients and major bleeding in 26 (27%) patients; 26 patients (27%) died in the hospital. AMI management was not significantly different in patients with and without the composite outcome. A history of arterial hypertension (HR 2.05, 95% CI 1.01-4.16) and high SOFA score at the time of AMI (HR 1.07, 95% CI 1.00-1.15) were independent risk factors for the composite outcome.

Patients who have an AMI with OCAD during an ICU stay for non-cardiac disease are at risk of a composite outcome of severe ischemia, major bleeding, and death. A history of arterial hypertension and high SOFA scores were independent hazards for poor prognosis.

Heparin-induced thrombocytopenia (HIT) is a life-threatening, immune-mediated complication following heparin exposure and is considered to be the most severe adverse reaction to heparin treatment that is not associated with bleeding. Development of autoantibodies against platelet factor 4 (PF4) - heparin complex constitutes the basis of the pathophysiological changes in patients suffering from HIT, which then binds to the surface of platelets and monocytes, thus provoking their activation and subsequent aggregation, ultimately leading to the formation of thrombosis. Formation of arterial and venous thrombosis is aggravated by the simultaneous activation of platelets and monocytes with a substantial mortality rate. The incidence of HIT is reported to be significantly lower in pediatric patients compared with adults. Diagnosis of HIT in pediatric population remains a clinical entity supplemented by laboratory evaluation. The positive predictive value of laboratory evaluation is further elevated by the use of scoring systems and predictive models used for hastening the diagnosis of HIT. Use of alternative anticoagulants like direct thrombin inhibitors and factor Xa inhibitors form the mainstay of treatment in cases of HIT, however, more prospective studies would be required in the pediatric population to delineate definitive guidelines for proper management of patients in this age-group. This article delivers diagnostic and treatment approach in case of patients with HIT, wherein the pathophysiology, clinical manifestations, diagnostic approach and the management of patients with HIT has been described.

Influenza virus causes significant global annual morbidity and mortality. Thrombocytopenia is recognized as a poor prognostic factor in sepsis and is associated with mortality, while lymphopenia has been established as a poor prognostic factor in other viral infections. We aimed to assess the incidence of thrombocytopenia and lymphopenia in seasonal influenza and their effect on clinical outcomes.

This single-center, retrospective, cohort study included consecutive adult patients, hospitalized in Rabin Medical Center between October 2017 and April 2018, with laboratory-confirmed influenza. Patients were grouped according to blood counts on admission: (1) thrombocytopenia (<150 K/mL), (2) lymphopenia (<0.5 K/mL), and (3) both thrombocytopenia and lymphopenia. Patients without thrombocytopenia and lymphopenia were designated as controls. The primary outcome was 30-day all-cause mortality. Risk factors were identified by univariable and multivariable analyses, using logistic regression and reported as odds ratios (ORs) and 95% confidence intervals (CIs).

A total of 625 patients were included, 112 (18%) had thrombocytopenia, 98 (15.6%) had lymphopenia, and 107 (17%) had both. The crude 30-day all-cause mortality was 7.6% (48/625). Mortality rates were 7.1% (8/112) for the thrombocytopenia group, 11.2% (11/98) for the lymphopenia group, and 14.9% (16/107) for patients with both versus 4.2% (13/308) in the control (p = 0.000 for all). In a multivariable regression model, significant thrombocytopenia (<100 K/μL) [OR 5.07 (95% CI 1.5-16.2)], age [OR 1.07 (95% CI 1.02-1.11)], time to oseltamivir [OR 1.006 (95% CI 1.002-1.11)], and significant respiratory support [OR 8.85 (3.4-22.6)] were associated with 30-day all-cause mortality.

Patients hospitalized with seasonal influenza and thrombocytopenia <100 K/mL on admission, have an increased 30-day all-cause mortality.

The number of patients with thrombocytopenia (TCP) is relatively high in intensive care units (ICUs). It is therefore necessary to evaluate the prognostic risk of such patients.

This study investigated the risk factors affecting the survival of patients with TCP in the ICU. Using the findings of this investigation, we developed and validated a risk prediction model.

We evaluated patients admitted to the ICU who presented with TCP. We used LASSO regression to identify important clinical indicators. Based on these indicators, we developed a prediction model complete with a nomogram for the development cohort set. We then evaluated the mode's accuracy using a receiver operating characteristic (ROC) curve, calibration curves, and decision curve analysis (DCA) in a validation cohort.

A total of 141 cases of ICU TCP were included in the sample, of which 47 involved death of the patient. Clinical results were as follows: N (HR 0.91, 95% CI 0.86-0.97, P=0.003); TBIL (HR 1.98, 95% CI 1.02-1.99, P=0.048); APACHE II (HR 1.94, 95% CI 1.39, 2.48, P=0.045); WPRN (HR 6.22, 95% CI 2.86-13.53, P<0.001); WTOST (HR 0.56, 95% CI 0.21-1.46, P<0.001); and DMV [HR1.87, 95% CI 1.12-2.33]. The prediction model yielded an area under the curve (AUC) of 0.918 (95% CI 0.863-0.974) in the development cohort and 0.926 (95% CI 0.849-0.994) in the validation cohort. Application of the nomogram in the validation cohort gave good discrimination (C-index 0.853, 95% CI 0.810-0.922) and good calibration. DCA indicated that the nomogram was clinically useful.

The individualized nomogram developed through our analysis demonstrated effective prognostic prediction for patients with TCP in ICUs. Use of this prediction metric may reduce TCP-related morbidity and mortality in ICUs.

HIV infection is associated with increased infections.

To (1) compare patients with sepsis with and without HIV, (2) assess whether HIV is associated with mortality in sepsis, and (3) identify factors associated with mortality in patients with HIV and sepsis.

Patients who met Sepsis-3 criteria were studied. HIV infection was defined as administration of highly active antiretroviral therapy, a diagnosis of AIDS encoded by the International Classification of Diseases, or a positive HIV blood test result. Propensity scores were used to match patients with HIV to similar patients without HIV, and mortality was compared with χ2 tests. Logistic regression was used to determine factors independently associated with mortality.

Sepsis developed in 34 673 patients without HIV and 326 patients with HIV. Of these, 323 (99%) patients with HIV were matched to similar patients without HIV. The 30-60- and 90-day mortality was 11%, 15%, and 17%, respectively, in patients with sepsis and HIV, which was similar to the 11% (P > .99), 15% (P > .99), and 16% (P = .83) in patients without HIV. Logistic regression to adjust for confounders showed that obesity (odds ratio, 0.12; 95% CI, 0.03-0.46; P = .002) and high total protein on admission (odds ratio, 0.71; 95% CI, 0.56-0.91; P = .007) were associated with lower mortality. Mechanical ventilation at sepsis onset, renal replacement therapy, positive blood culture, and platelet transfusion were associated with increased mortality.

HIV infection was not associated with increased mortality in patients with sepsis.

Sepsis-induced hemostatic disturbances are common and are associated with poor outcomes. Additionally, conventional coagulation tests (CCTs) overdiagnose hypocoagulation and cannot detect hypercoagulation and hyperfibrinolysis. The aim of this study was to describe the coagulation profiles of patients with sepsis/septic shock using rotational thromboelastometry (ROTEM) and to compare coagulation states between sepsis and septic shock groups and between surviving and non-surviving groups.

This prospective, observational, single-center study was conducted in the intensive care unit (ICU) of the University Medical Center Ho Chi Minh City, from 6/2020-12/2021. Patients aged ≥18 years with sepsis or septic shock according to the Sepsis-3 criteria were included. ROTEM and CCTs were concurrently performed within the first 24 h of ICU admission.

In total, 161 patients were enrolled. Based on ROTEM, 72.7 % of patients with sepsis/septic shock had coagulation disorders, including 25.5 % hypercoagulation, 54.7 % hypocoagulation, 13.6 % mixed hypo-hypercoagulation patterns, and 18.6 % hyperfibrinolysis. A common mixed disorder subtype was characterized by prolonged initial clotting time (CT) with subsequently increased clot firmness. Fibrinogen levels and maximum clot formation (MCF)-fibtem were strongly correlated (rho = 0.73, p < 0.05). Hypocoagulation was observed more in the septic shock group than in the sepsis group. Compared to survivors, non-survivors had more prolonged CT-extem.

ROTEM could identify hypocoagulability, hypercoagulability, mixed hypo-hypercoagulability patterns, and hyperfibrinolysis in patients with sepsis/septic shock. Elevated MCF-fibtem and elevated fibrinogen levels were notably common and strongly correlated. The septic shock group had more hypocoagulation than the sepsis group. Lastly, non-survivors had more prolonged CT-extem than survivors.

The rate of intensive care unit (ICU) mortality in patients with hematologic malignancies is high. The risk factors for this were inconsistent across several previous studies, and there is currently no accepted consensus around risk factors for these patients. We aimed to identify which prognostic factors were associated with ICU mortality in critically ill patients with hematologic malignancies, nearly half of which were allogeneic hematopoietic stem cell transplantation (allo-HSCT) recipients. In addition, we aimed to compare the characteristics and clinical outcomes of patients with and without allogenic allo-HSCT. In total, 217 patients with hematologic malignancies were enrolled consecutive, 119 (54.8%) of whom underwent HSCT (allo-HSCT: n = 115). All survivors were followed up with until August 1, 2022. The rate of ICU mortality in this cohort was 54.4%: 55.5 and 53.1% for the patients with and without HSCT, respectively (p = 0.724). The probabilities of survival after ICU admission were also comparable between the patients who had allo-HSCT and those who did not. A multivariable analysis revealed that cerebrovascular disease, hyperlactic acidemia on the day of ICU admission, lower platelet count, use of vasoactive drugs, and absence of noninvasive ventilation on the day of ICU admission were independent risk factors for ICU mortality. For patients with three to five of these risk factors, the rate of ICU mortality was as high as 84.6%, which was significantly higher than that of other patients. In this study, the ICU mortality rate in patients with hematologic malignancies was still high, particularly for those with multiple risk factors. However, allo-HSCT was not found to be a risk factor for ICU mortality.

Cryptococcus neoformans sequence type 5 (ST5) lineage could infect immunocompetent hosts and cause a significant medical burden. We sought to identify characteristics and prognostic risk factors of ST5 lineage-associated cryptococcosis.

Multilocus sequence typing and antifungal susceptibility testing were conducted for Cryptococcus isolates. The clinical and laboratory characteristics of cryptococcosis patients were investigated. The multivariable logistic regression identified variables independently associated with 30-day mortality in patients with ST5 lineage-associated cryptococcosis without HIV.

The infection rate of the ST5 isolates was 89.4% (370/414) in China. The proportion of ST5 isolates with nonwild-type minimum inhibitory concentrations to amphotericin B, 5-flucytosine, voriconazole, posaconazole, itraconazole, and fluconazole were 0%, 5.4%, 0.3%, 1.4%, 0.3%, and 8.1%, respectively. The ST5 lineage-infected group exhibited significantly higher blood platelet count, lower blood cryptococcal antigen (CrAg) titer, lower cerebrospinal fluid (CSF) CrAg titer than the non-ST5 lineage-infected group, and lower hemoglobin and lower CSF CrAg titer than the Cryptococcus gattii isolates-infected group. Seven baseline parameters, including underlying disease, dyskinesia, anemia, high peripheral blood neutrophils, low platelet count, high CSF fungal burden, and high CSF opening pressure, were associated independently with the 30-day mortality of patients with ST5 lineage-associated cryptococcosis without HIV.

Our study has provided an understanding of the ST5 lineage associated with cryptococcosis.

Beta-lactam antibiotics commonly cause immune thrombocytopenia. Cross-reactivity in patients with drug-induced immune thrombocytopenia has rarely been reported. In this study, we describe the case of a 79-year-old man who developed thrombocytopenia after receiving piperacillin-tazobactam for an acute exacerbation of chronic obstructive pulmonary disease, and he was successfully treated with meropenem and cefotiam. However, thrombocytopenia recurred after cefoperazone-sulbactam administration. This indicated that cross-reactivity of platelet-specific antibodies occurred between piperacillin-tazobactam and cefoperazone-sulbactam. However, the responsible drug structures remain unknown, requiring further investigation. Likewise, chemical structure similarities among beta-lactam antibiotics must be examined to determine the risk of immune thrombocytopenia in the clinical setting.

Sepsis is a life-threatening hyperreaction to infection in which excessive inflammatory and immune responses cause damage to host tissues and organs. The glycosaminoglycan heparan sulphate (HS) is a major component of the cell surface glycocalyx. Cell surface HS modulates several of the mechanisms involved in sepsis such as pathogen interactions with the host cell and neutrophil recruitment and is a target for the pro-inflammatory enzyme heparanase. Heparin, a close structural relative of HS, is used in medicine as a powerful anticoagulant and antithrombotic. Many studies have shown that heparin can influence the course of sepsis-related processes as a result of its structural similarity to HS, including its strong negative charge. The anticoagulant activity of heparin, however, limits its potential in treatment of inflammatory conditions by introducing the risk of bleeding and other adverse side-effects. As the anticoagulant potency of heparin is largely determined by a single well-defined structural feature, it has been possible to develop heparin derivatives and mimetic compounds with reduced anticoagulant activity. Such heparin mimetics may have potential for use as therapeutic agents in the context of sepsis.

Platelets are affected by many factors, such as infectious or aseptic inflammation, and different inflammatory states may induce either thrombocytopenia or thrombocytosis. Tumor necrosis factor α (TNFα) is an important inflammatory cytokine that has been shown to affect the activity of hematopoietic stem cells. However, its role in megakaryocyte (MK) development and platelet production remains largely unknown. This study aimed to investigate the effects of TNFα on MK and platelet generation.

The ex vivo study with human CD34+ cells demonstrated that TNFα differentially modulated commitment toward the MK lineage. Specifically, a low concentration of 0.5 ng/ml TNFα promoted MK maturation, proplatelet formation, and platelet production, whereas a high concentration of 10 ng/ml or more TNFα exhibited a substantial inhibitory effect on MK and platelet production. The distinct effect of TNFα on MKs was mainly dependent on TNFα receptor 1. TNFα differentially regulated the MAPK-ERK1/2 signaling pathway and the cytoskeletal proteins cofilin and MLC2. The in vivo study with Balb/c mice indicated that low-dose or high-dose TNFα administration differentially affected short-term platelet recovery after bone marrow transplantation.

Our study revealed distinct roles for TNFα in megakaryopoiesis and thrombopoiesis and may provide new insights regarding the treatment for platelet disorders.