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Thrombocytopenia is a common complication of critical care patients. The rates of bleeding events and mortality are also significantly increased in critical care patients with thrombocytopenia. Therefore, the Critical Care Medicine Committee of Chinese People’s Liberation Army (PLA) worked with Chinese Society of Laboratory Medicine, Chinese Medica...
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Context 1
... platelet function tests analyze platelet adhesion, aggregation, and release during hemostasis [70,71].Viscoelasticity-based tests(thromboelastography, coagulation and platelet function analyzer) can all comprehensively reflect the overall function of coagulation factors, fibrinogen, and platelets; and are used to guide platelet replacement therapy and antiplatelet therapy (Table 3) [72,73]. Viscoelasticity-based tests such as thromboelastography and coagulation and platelet function analyzer indicate the contribution of platelets during coagulation. ...Context 2
... platelet function tests analyze platelet adhesion, aggregation, and release during hemostasis [70,71].Viscoelasticity-based tests(thromboelastography, coagulation and platelet function analyzer) can all comprehensively reflect the overall function of coagulation factors, fibrinogen, and platelets; and are used to guide platelet replacement therapy and antiplatelet therapy (Table 3) [72,73]. Viscoelasticity-based tests such as thromboelastography and coagulation and platelet function analyzer indicate the contribution of platelets during coagulation. ...Citations
... According to the World Health Organization's diagnostic criteria for anemia, hemoglobin (Hb) < 120 g/L in premenopausal women and < 130 g/L in postmenopausal women and men of all ages are called anemia. Thrombocytopenia Platelet (PLT) < 100×10 9 /L were de ned as thrombocytopenia (15). ...
Background: Extrahepatic manifestations of hepatitis E have been extensively reported, yet there is a lack of comprehensive systematic studies on this aspect. This article is to report hematologic systemdamage caused by hepatitis E.
Methods: A retrospective study enrolled 170 patients with acute hepatitis E. The study analyzed the proportion of patients with decreased white blood cell, hemoglobin, and platelet levels in their blood routine, along with their potential clinical significance. 49 patients with HA were also included as controls to compare and analyze the differences in biochemical indicators and hematologic damage.
Results: Among the 170 patients with hepatitis E, 47 cases (27.64%) presented with leukopenia, 94 cases (55.29%) exhibited anemia, and 33 cases (19.41%) experienced thrombocytopenia. The findings indicated that hemoglobin and platelets are lower in patients with hepatitis E than in patients with hepatitis A, and anemia is more common in patients with hepatitis E. The anemia group had significantly lower levels of albumin, alanine aminotransferase, and cholinesterase compared to the normal group (p<0.001, p=0.005, p<0.001). Additionally, total bilirubin and alkaline phosphatase were significantly higher in the anemia group than in the normal group (p=0.031, p=0.003). Moreover, the anemia group showed a higher likelihood of experiencing spontaneous bacterial peritonitis (p=0.025). In comparison to the normal platelet group, the thrombocytopenia group exhibited significantly lower levels of albumin, cholinesterase, and prothrombin activity (p=0.036, p=0.015, p<0.001). Patients with decreased platelet have the higher incidence of death, spontaneous bacterial peritonitis, upper gastrointestinal bleeding and hepatorenal syndrome (p<0.001, p<0.001, p=0.027, p=0.014).
Conclusion: Hepatitis E patients with hematologic system damage are common. Patients with hepatitis Ehave lower levels of hemoglobin and platelets compared to patients with hepatitis A. The presence of anemia and low platelets in patients with hepatitis Eindicates a more severe condition.
... Thrombocytopenia, such as that occurrs in patients with inherited/acquired thrombocytopenia, microbial infection, radiotherapy, or chemotherapy [1], as well as in military personnel and civilians that have encountered chemical, biological, radioactive, and nuclear events [2], will significantly increase hemorrhagic risk. However, spontaneous hemorrhage does not always happen in mammals with thrombocytopenia [3]. ...
... Especially, in some cases such as ionizing radiation (IR) exposure [4][5][6], chemotherapy [7], and microbial infections including coronavirus disease 2019 [8], and gram-negative bacterial septicemia [9,10], thrombocytopenia is unexpectedly associated with increased thrombotic risk, against the background of a hemorrhagic tendency. Meanwhile, thrombosis is increasingly being considered a major cause of mortality from thrombocytopenia [1], especially from that induced by radiation injury [6]. These lines of evidence imply that other yet to be defined factors such as the alteration of platelet function may be competent to maintain hemostasis or even favor thrombosis, unmasking which could open new opportunities to treat platelet disorders. ...
... Relative to the pathogenesis of thrombocytopenia, the functions of residual platelets during thrombocytopenia progress always get less attention. Thrombosis and hemorrhage usually co-exist in military personnel and civilians who have encountered chemical, biological, radioactive, and nuclear events [1,2], while the underlying mechanism remains elusive. We in this study uncover that the surviving mMKs produce large and hyperreactive platelets post IR. ...
Background
The essential roles of platelets in thrombosis have been well recognized. Unexpectedly, thrombosis is prevalent during thrombocytopenia induced by cytotoxicity of biological, physical and chemical origins, which could be suffered by military personnel and civilians during chemical, biological, radioactive, and nuclear events. Especially, thrombosis is considered a major cause of mortality from radiation injury-induced thrombocytopenia, while the underlying pathogenic mechanism remains elusive.
Methods
A mouse model of radiation injury-induced thrombocytopenia was built by exposing mice to a sublethal dose of ionizing radiation (IR). The phenotypic and functional changes of platelets and megakaryocytes (MKs) were determined by a comprehensive set of in vitro and in vivo assays, including flow cytometry, flow chamber, histopathology, Western blotting, and chromatin immunoprecipitation, in combination with transcriptomic analysis. The molecular mechanism was investigated both in vitro and in vivo, and was consolidated using MK-specific knockout mice. The translational potential was evaluated using a human MK cell line and several pharmacological inhibitors.
Results
In contrast to primitive MKs, mature MKs (mMKs) are intrinsically programmed to be apoptosis-resistant through reprogramming the Bcl-xL-BAX/BAK axis. Interestingly, mMKs undergo minority mitochondrial outer membrane permeabilization (MOMP) post IR, resulting in the activation of the cyclic GMP-AMP synthase-stimulator of IFN genes (cGAS-STING) pathway via the release of mitochondrial DNA. The subsequent interferon-β (IFN-β) response in mMKs upregulates a GTPase guanylate-binding protein 2 (GBP2) to produce large and hyperreactive platelets that favor thrombosis. Further, we unmask that autophagy restrains minority MOMP in mMKs post IR.
Conclusions
Our study identifies that megakaryocytic mitochondria-cGAS/STING-IFN-β-GBP2 axis serves as a fundamental checkpoint that instructs the size and function of platelets upon radiation injury and can be harnessed to treat platelet pathologies.
... She also developed thrombocytopenia (platelet count at 94 x 10 9 /L), a complication that was not present on the initial detection of the splenic cyst. Thrombocytopenia in Chinese, as defined by national guidelines, is the condition when the platelet count is lower than 100 x 10 9 /L [9]. She did not receive any treatment. ...
An asymptomatic splenic cyst smaller than 50 mm was detected incidentally at a routine health checkup. Management of the cyst, affected and determined by multiple factors, including force majeure, became difficult and thrombocytopenia developed during watchful waiting. Spontaneous recovery of the spleen did not occur with continued watchful waiting, and thrombocytopenia worsened. However, when a three-month dietary intervention was subsequently implemented, the initiation of recovery was observed. The diet modification was adding to regular meals a daily serving of vegetables prepared following traditional Chinese culinary style. A second course of dietary intervention was undertaken, and accelerated recovery was detected thereafter, with eventual complete resolution of the splenic cyst and thrombocytopenia. This case demonstrates the feasibility and potential benefits of lifestyle intervention for the management of small splenic cysts, including those complicated with thrombocytopenia. Lifestyle intervention, such as dietary intervention, is particularly suitable for the watchful waiting phase since disease management during this time is non-pharmaceutical and non-surgical by nature.
... Studies have shown that the value of the TEG MA reflects PLT function. [5,6] Therefore, this study utilized the MA as a parameter of PLT function. The prepartum fibrinogen level, PLT count, and TEG MA before delivery, and the prepartum and postpartum hemoglobin (Hb) levels were analyzed. ...
... In recent years, TEG has been increasingly used for the assessment of the coagulation function. [5,6] In our retrospective analysis, there were 199 pregnant women who underwent an emergency cesarean section but did not receive PLT transfusions as a result of supply and time restrictions. No fatal hemorrhage occurred in all 199 pregnant women. ...
... This may be one of the reasons that these people are prone to Mucor infection. Excessive thrombosis also leads to thrombocytopenia [63,64]. Despite this, antithrombotic therapy is not universally mentioned in International treatment guidelines [1,9,10]. ...
Mucormycosis was an acute and invasive fungal infection with a high mortality rate. The treatment of mucormycosis was challenging. And the incidence of the mucormycosis seems to be increasing. The key to Mucormycosis therapy not only depend on anti-Mucor infection, but also included the management of some risk factors. Liposomal amphotericin B (L-AMB) was the first line drug to treat mucormycosis. The dosage regimen recommended by the guideline was often associated with higher nephrotoxicity and morbidity. A pharmacokinetic/pharmacodynamic (PKPD) model was conducted to evaluate suitable dosage regimens in Mucormycosis patients. 10mg/kg/day LAMB recommended in the guidelines might not be needed. 5mg/kg/day LAMB might be sufficient to achieve the target value of PKPD and indicated a good anti-Mucor effect. Successful management of mucormycosis was also based on suitable management of several risk factors which played a very important role in the progression of mucormycosis, such as iron factor, diabetes mellitus with acidosis and thrombosis. Application of deferasirox, statins and keep platelet level might be promising approaches in mucormycosis therapy.
... Thrombocytopenia can cause substantial morbidity and mortality in critically ill patients. The incidence of thrombocytopenia in adult critically ill patients can reach 8.3% to 67.6% (2). Meanwhile, thrombocytopenia is associated with significantly increased bleeding and blood transfusion and even mortality events (3,4). ...
Thrombocytopenia can cause substantial morbidity and mortality in critically ill patients. There are multiple etiology factors and various mechanisms associated with thrombocytopenia, of which drug-induced thrombocytopenia (DITP) deserves attention. Herein, we describe a case of severe thrombocytopenia during intensive care unit (ICU) hospitalization that was likely to be associated with vancomycin. By revealing the process of identifying this case of DITP and reviewing relevant clinical studies, a risk alert of vancomycin-related severe hematotoxicity should be considered.
Background: This study aims to investigate the relevance of platelet aggregation markers, specifically arachidonic acid (AA) and adenosine diphosphate (ADP), in relation to the prognosis of sepsis patients. Methods: A cohort of 40 sepsis patients was included and stratified, based on their 28-day post-treatment prognosis, into two groups: a survival group (n = 31) and a severe sepsis group (n = 9. Then, their various clinical parameters, including patient demographics, platelet counts (PLT), inflammatory markers, and platelet aggregation rates (PAR) induced by AA and ADP between the two groups, were compared. Long-term health implications of sepsis were assessed using the Acute Physiologic Assessment and Chronic Health Evaluation II (APACHE II) score, and logistic regression analysis was conducted to evaluate the prognostic significance of PAR in sepsis patients. Results: Patients with severe sepsis exhibited significantly elevated levels of procalcitonin (PCT), platelet adhesion rates, and PAR induced by ADP (P < 0.05), but having lower PLT (P < 0.05), compared to those in the survival group. Logistic regression analysis demonstrated that PAR induced by ADP was a protective factor in predicting prognosis in sepsis patients (P < 0.01). Conclusions: Activation of platelets in sepsis intensifies inflammatory response. Patients with sepsis whose ADP-induced PAR was <60% displayed significant impairment in platelet aggregation function, and had higher mortality rate. Monitoring ADP-induced PAR is crucial for management of sepsis.
Platelet counts reduction occurs throughout pregnancy, with 5-12% of pregnancies being diagnosed with gestational thrombocytopenia (GT), characterized by a decrease in platelet count during pregnancy. However, the underlying biological mechanism behind this altered platelet count phenomenon and GT remains unclear. Here, we utilized sequencing data from non-invasive prenatal test (NIPT) among 100,186 Chinese pregnancies and conducted the hitherto largest-scale genome-wide association studies (GWAS) on platelet counts at five periods of pregnancy (the first, second, and third trimesters, delivery, and the postpartum period), as well as two GT statuses (GT: platelet count < 150 × 109/L and severe GT: platelet count < 100 × 109/L). Our analysis revealed 138 genome-wide significant loci, explaining 10.4 to 12.1% of the observed variation. Attractively, we identified previously unknown changes in genetic effects on platelet counts during pregnancy for variants present in PEAR1 and CBL, with PEAR1 variants specifically associated with a faster decline in platelet counts. Furthermore, we found that variants present in PEAR1 and TUBB1 increased susceptibility to GT and severe GT. Our study provides the first insight into the genetic basis of platelet counts and GT in pregnancy, highlighting the critical role of PEAR1 in decreasing platelet counts during pregnancy and the occurrence of GT. Pregnancies carrying specific variants associated with declining platelet counts may experience a more pronounced decrease, thereby elevating the risk of GT. These findings lay the groundwork for further investigation into the biological mechanisms and causal implications of GT.
Background
Early recognition of the risk factors is important for acute pancreatitis management. The aim of this study is to investigate the relationship between platelet count and clinical outcomes in patients with acute pancreatitis.
Methods
The data are collected from a university-affiliated hospital between January 2013 and December 2020. A generalized additive model and a two-piecewise linear regression model are used to estimate the association between platelet count and the risks of intra-abdominal infection, surgical intervention, in-hospital mortality, and length of hospital stay.
Results
Among the 1,363 patients, 99 (7.3%) patients suffered intra-abdominal infection, 190 (13.9%) patients underwent surgical intervention, and 38 (2.8%) patients died in the hospital. The median length of hospital stay is 21 days. Generalized additive model and two-piecewise linear regression analysis show that the risk of intra-abdominal infection decreases as the platelet count increases to 160 × 10 ⁹ /L (OR: 0.991, 95% CI: 0.984–0.998, p = 0.015) and then increases as the platelet count levels up (OR: 1.007, 95% CI: 1.004–1.010, p < 0.001). The trend is similar to the risk of surgical intervention and length of hospital stay. Even though there seems a declining trend in mortality, no significant association is found after adjustment for potential confounders. Further analysis shows that changes in platelet count within the first 3 days after admission have no obvious association with clinical outcomes.
Conclusion
A platelet count of approximately 160 × 10 ⁹ /L on admission is associated with the lowest risk of intra-abdominal infection, surgical intervention, and shortest hospital stay in patients with acute pancreatitis.
Iron deficiency anemia (IDA) affects more than 1.2 billion individuals globally. In addition to anemia, reactive thrombocytosis is also a common clinical hematological condition in patients with IDA. However, some case reports have described the thrombotic complications in association with IDA-induced thrombocytosis. Patients with a high risk of thrombosis need prompt identification and effective treatment to prevent thrombotic complications. While iron replacement treatment has been shown to decrease platelet count in this context, there is limited published evidence on how iron supplementation affects the thrombocytosis caused by IDA. We retrospectively examined the clinical records of 440 patients with IDA from an RCT completed from 1 January 2016, to 30 December 2017, and data obtained from this study was used for post hoc analysis to examine the effect of iron on platelet count in IDA-induced thrombocytosis. The mean ± standard deviation (SD) platelet counts of the 440 patients with IDA was 310.23 ± 98.72 × 109/L. With baseline platelet counts>450 × 109 /L as the cutoff for thrombocytosis, patients were divided into 2 groups: 36 (8.1%) in the IDA with thrombocytosis group (mean ± SD platelet count, 521.67 ± 73.85 × 109/L) and the remaining 404 in the IDA without thrombocytosis group (mean ± SD platelet count, 291.39 ± 76.11 × 109/L). Differences were found in baseline characteristics including white blood cell (WBC) count, hemoglobin (Hb) level, mean corpuscular volume (MCV), transferrin saturation (TSAT), serum iron (SI) level, and total iron-binding capacity (TIBC) between the two groups (P
