Platelet Counts
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Natalia Bednarz-Knoll ◽  
Marta Popęda ◽  
Tomasz Kryczka ◽  
Barbara Kozakiewicz ◽  
Katarzyna Pogoda ◽  

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Birsen Ertekin ◽  
Mehmet Yortanlı ◽  
Ozan Özelbaykal ◽  
Ali Doğru ◽  
A. Sadık Girişgin ◽  

The aim of this study is to investigate the routine blood parameters of COVID-19 patients at the time of admission to the emergency department and their relationship with the severity of the disease and prognosis. A total of 500 patients, who were diagnosed with severe COVID-19 and hospitalized in the intensive care unit between 01.04.2020 and 01.02.2021 in the emergency department of a pandemic hospital, were retrospectively analyzed. Demographic, clinical, and laboratory data of the patients were obtained from the hospital registry system. Neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), and platelet-to-lymphocyte ratio (PLR) were calculated using neutrophil, lymphocyte, monocyte, and platelet counts. These patients were divided into two groups: survivors and deceased. All parameters obtained from routine blood analysis were statistically compared between these two groups. While 280 out of 500 patients survived, 220 died. Of all patients, the mean age was 67 years and 51.8% were males. There was a significant difference between the two groups in terms of age, gender, length of hospital stay, need for mechanical ventilation, white blood cell, neutrophil, lymphocyte, monocyte, eosinophil, platelet counts, CRP, ferritin, procalcitonin values, NLR, MLR, and PLR ( p < 0.001 for all). While NLR alone and MLR + NEU and NLR + PLR + MLR combinations had the highest AUC values (0.930, 0.947, and 0.939, respectively), MLR and PLR alone showed the lowest AUC values (0.875 and 0.797, respectively). The sensitivity, specificity, positive predictive values (PPVs), and negative predictive values (NPVs) in the prediction of death according to the cutoff values of the parameters have been determined. A significant correlation was determined between age, NLR, MLR, and PLR and duration of hospital stay ( p < 0.001 for all). Routine blood parameters and NLR, MLR, and PLR can assist emergency physicians to identify the severity and early prognosis of COVID-19 patients.

Blood ◽  
2021 ◽  
Shen Heazlewood ◽  
Tanveer Ahmad ◽  
Monika Mohenska ◽  
Belinda B Guo ◽  
Pradnya Gangatirkar ◽  

RNA processing is increasingly recognised as a critical control point in the regulation of different haematopoietic lineages including megakaryocytes responsible for the production of platelets. Platelets are anucleate cytoplasts that contain a rich repertoire of RNAs encoding proteins with essential platelet functions derived from the parent megakaryocyte. It is largely unknown how RNA binding proteins contribute to the development and functions of megakaryocytes and platelets. We show that Serine-arginine rich splicing factor 3 (SRSF3) is essential for megakaryocyte maturation and generation of functional platelets. Megakaryocyte-specific deletion of Srsf3 in mice led to macrothrombocytopenia characterised by megakaryocyte maturation arrest, dramatically reduced platelet counts and abnormally large functionally compromised platelets. SRSF3 deficient megakaryocytes failed to reprogram their transcriptome during maturation and to load platelets with RNAs required for normal platelet function. SRSF3 depletion led to nuclear accumulation of megakaryocyte mRNAs demonstrating that SRSF3 deploys similar RNA regulatory mechanisms in megakaryocytes as in other cell types. Our study further suggests that SRSF3 plays a role in sorting cytoplasmic megakaryocyte RNAs into platelets and demonstrates how SRSF3-mediated RNA processing forms a central part of megakaryocyte gene regulation. Understanding SRSF3 functions in megakaryocytes and platelets provides key insights into normal thrombopoiesis and platelet pathologies as SRSF3 RNA targets in megakaryocytes are associated with platelet diseases.

2021 ◽  
pp. jim-2021-001986
Kavitha Subramoney ◽  
Omar Elsheikh ◽  
Saira Butt ◽  
Daniel Romano ◽  
Lindsey Reese ◽  

Hospitalized patients with COVID-19 must have a safe discharge plan to prevent readmissions. We assessed patients with COVID-19 admitted to hospitals belonging to a single health system between April 2020 and June 2020. Demographics, vitals and laboratory data were obtained by electronic data query and discharge processes were reviewed by manual abstraction. Over the study period, 94 out of 912 (10.3%) patients were readmitted within 14 days of discharge. Readmitted patients were older and spent more time in the intensive care unit (p<0.01). Statistical differences were noted in discharge-day heart rates, temperatures, platelet counts, and neutrophil and lymphocyte percentages between the readmitted and non-readmitted groups. Readmitted patients were less likely to be discharged home and to receive complete discharge instructions or home oxygen (p<0.01). Age, duration of intensive care unit stay, disposition destinations other than home, incomplete discharge planning and no arrangement for home oxygen may be associated with 14-day readmissions in patients with COVID-19. Certain clinical parameters on discharge day, while statistically different, may not reach clinically discriminant thresholds. Structured discharge processes may improve outcomes.

2021 ◽  
pp. 1-10
Nicole L. Spartano ◽  
Jayandra J. Himali ◽  
Ludovic Trinquart ◽  
Qiong Yang ◽  
Galit Weinstein ◽  

Background: One of the mechanisms suggested to link physical activity (PA) to favorable brain health is through stimulation of neural growth factors such as brain-derived neurotrophic factor (BDNF). Acute bouts of PA stimulate circulating BDNF levels. Objective: In this investigation, we assessed whether habitual, accelerometer-measured PA levels were related to circulating BDNF levels in a middle-aged cohort. Methods: In the Framingham Heart Study Third Generation cohort, 1,769 participants provided reliable accelerometry data and were not missing BDNF measurement and platelet counts. In a cross-sectional analysis, using multivariable regression, we related PA measures to serum BDNF levels, adjusting for age, sex, smoking status, platelet count, depression status, and accelerometer wear time. Results: Our study participants (mean age 47±9 years, 50.8% women) spent an average of 22.3 mins/day moderate-to-vigorous (MV)PA. Most PA variables (steps, MVPA, light activity, and sedentary time) were not related to BDNF levels (p > 0.05). We observed a non-linear trend, where 15–50 mins/week vigorous activity was associated with lower BDNF compared to those with 0 min vigorous activity (β= –0.049±0.024, p = 0.05), but with no significant associations at lower or higher vigorous activity levels. In smokers, MVPA was also associated with lower BDNF levels (β= –0.216±0.079, p = 0.01). Conclusion: Our study reveals that circulating BDNF is not chronically elevated in individuals with higher levels of habitual PA in middle-aged adults from the community and may even be chronically suppressed with higher PA in subgroups, including current smokers. These results do not contradict previous studies demonstrating that circulating BDNF rises acutely after PA.

Biomedicines ◽  
2021 ◽  
Vol 9 (12) ◽  
pp. 1791
Krzysztof Laudanski ◽  
Jihane Hajj ◽  
Mariana Restrepo ◽  
Kumal Siddiq ◽  
Tony Okeke ◽  

The balance between neurodegeneration, neuroinflammation, neuroprotection, and COVID-19-directed therapy may underly the heterogeneity of SARS-CoV-2′s neurological outcomes. A total of 105 patients hospitalized with a diagnosis of COVID-19 had serum collected over a 6 month period to assess neuroinflammatory (MIF, CCL23, MCP-1), neuro-injury (NFL, NCAM-1), neurodegenerative (KLK6, τ, phospho τ, amyloids, TDP43, YKL40), and neuroprotective (clusterin, fetuin, TREM-2) proteins. These were compared to markers of nonspecific inflammatory responses (IL-6, D-dimer, CRP) and of the overall viral burden (spike protein). Data regarding treatment (steroids, convalescent plasma, remdasavir), pre-existing conditions, and incidences of strokes were collected. Amyloid β42, TDP43, NF-L, and KLK6 serum levels declined 2–3 days post-admission, yet recovered to admission baseline levels by 7 days. YKL-40 and NCAM-1 levels remained elevated over time, with clusters of differential responses identified among TREM-2, TDP43, and YKL40. Fetuin was elevated after the onset of COVID-19 while TREM-2 initially declined before significantly increasing over time. MIF serum level was increased 3–7 days after admission. Ferritin correlated with TDP-43 and KLK6. No treatment with remdesivir coincided with elevations in Amyloid-β40. A lack of convalescent plasma resulted in increased NCAM-1 and total tau, and steroidal treatments did not significantly affect any markers. A total of 11 incidences of stroke were registered up to six months after initial admission for COVID-19. Elevated D-dimer, platelet counts, IL-6, and leukopenia were observed. Variable MIF serum levels differentiated patients with CVA from those who did not have a stroke during the acute phase of COVID-19. This study demonstrated concomitant and opposite changes in neurodegenerative and neuroprotective markers persisting well into recovery.

2021 ◽  
Vol 9 ◽  
Hiroyuki Kitano ◽  
Keisuke Hieda ◽  
Hiroki Kitagawa ◽  
Yusuke Nakaoka ◽  
Yumiko Koba ◽  

A 14-year-old girl noticed malodorous urine and experienced left flank pain. The patient was presented to our hospital with gradually increasing pain. She had no underlying disease but had a history of pain on micturition for several days. Hematologic examination indicated low white blood cell and platelet counts and a high serum lactate level. Computed tomography showed that a part of the parenchyma of the left kidney had poor contrast and was deteriorated, with fluid and gas retention from the perirenal region to the retroperitoneal cavity. A left hydroureter and large ureterocele were observed in the bladder. She was diagnosed with emphysematous pyelonephritis (EPN) with a giant congenital ureterocele. Vasopressors and blood transfusion failed to maintain normal circulatory dynamics, and an open left nephrectomy and transurethral ureterocele fenestration were performed. The excised outer portion of the left kidney was dissolved by the infection and replaced with blood clots and necrotic tissue. Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry identified the inflammatory, gas-producing bacteria Actinotignum schaalii, Peptoniphilus asaccharolyticus, and Actinomyces odontolyticus. Meropenem was administered for 4 days postoperatively and then de-escalated to sulbactam/ampicillin for another 10 days. The patient was discharged on day 17 of hospitalization, and the postoperative course remained favorable. EPN is extremely rare in pediatric patients, and it is believed that nephrectomy is sometimes necessary if the patient does not have normal circulatory dynamics despite the use of catecholamines.

2021 ◽  
Vol 12 ◽  
Bruno Fattizzo ◽  
Raffaella Pasquale ◽  
Valentina Bellani ◽  
Wilma Barcellini ◽  
Austin G. Kulasekararaj

The complex pathophysiologic interplay between SARS-CoV-2 infection and complement activation is the subject of active investigation. It is clinically mirrored by the occurrence of exacerbations of complement mediated diseases during COVID-19 infection. These include complement-mediated hemolytic anemias such as paroxysmal nocturnal hemoglobinuria (PNH), autoimmune hemolytic anemia (AIHA), particularly cold agglutinin disease (CAD), and hemolytic uremic syndrome (HUS). All these conditions may benefit from complement inhibitors that are also under study for COVID-19 disease. Hemolytic exacerbations in these conditions may occur upon several triggers including infections and vaccines and may require transfusions, treatment with complement inhibitors and/or immunosuppressors (i.e., steroids and rituximab for AIHA), and result in thrombotic complications. In this manuscript we describe four patients (2 with PNH and 2 with CAD) who experienced hemolytic flares after either COVID-19 infection or SARS-Cov2 vaccine and provide a review of the most recent literature. We report that most episodes occurred within the first 10 days after COVID-19 infection/vaccination and suggest laboratory monitoring (Hb and LDH levels) in that period. Moreover, in our experience and in the literature, hemolytic exacerbations occurring during COVID-19 infection were more severe, required greater therapeutic intervention, and carried more complications including fatalities, as compared to those developing after SARS-CoV-2 vaccine, suggesting the importance of vaccinating this patient population. Patient education remains pivotal to promptly recognize signs/symptoms of hemolytic flares and to refer to medical attention. Treatment choice should be based on the severity of the hemolytic exacerbation as well as of that of COVID-19 infection. Therapies include transfusions, complement inhibitor initiation/additional dose in the case of PNH, steroids/rituximab in patients with CAD and warm type AIHA, plasma exchange, hemodialysis and complement inhibitor in the case of atypical HUS. Finally, anti-thrombotic prophylaxis should be always considered in these settings, provided safe platelet counts.

Jianqin Li ◽  
Yalin Xia ◽  
Xiaoru Fan ◽  
Xiaofang Wu ◽  
Feiyun Yang ◽  

Background: Immune thrombocytopenic purpura (ITP) is an autoimmune bleeding disorder and the decreased number and immunosuppressive dysfunction of Treg cells are key promoters of ITP. However, their mechanisms in ITP development have not been fully clarified.Methods: HUWE1 mRNA and protein levels in CD4+ T cells in peripheral blood from ITP patients were assessed by quantitative real-time PCR and Western blot. HUWE1 function in ITP was estimated using flow cytometry, enzyme-linked immunosorbent assay and immunosuppression assay. Besides, the HUWE1 mechanism in reducing the number and function of Treg cells in ITP was investigated by immunoprecipitation, cycloheximide-chase assay, ubiquitin experiment and immunofluorescence assay.Results: HUWE1 expression was elevated in CD4+ T cells in peripheral blood from ITP patients and HUWE1 mRNA level was negatively correlated with platelet counts and Treg cell percentage. Moreover, the interference with HUWE1 increased the number of Treg cells and enhanced its immunosuppressive function, and the HUWE1 overexpression produced the opposite results. For the exploration of mechanism, HUWE1 interacted with E26 transformation-specific-1 (Ets-1) and this binding was dependent on the negative regulation of the phosphorylation level of Ets-1 (Thr38) and HUWE1 facilitated the ubiquitin degradation of Ets-1 protein to restrain Treg cell differentiation and weaken their immunosuppressive functions. The in vivo assay confirmed that the HUWE1 inhibitor alleviated ITP in mice.Conclusion: HUWE1 induced the immune imbalance in ITP by decreasing the number and weakening the function of Treg cells through the ubiquitination degradation of Ets-1.

2021 ◽  
Vol 9 ◽  
Longli Yan ◽  
Zhuxiao Ren ◽  
Jianlan Wang ◽  
Xin Xia ◽  
Liling Yang ◽  

Background: Platelets play an important role in the formation of pulmonary blood vessels, and thrombocytopenia is common in patients with pulmonary diseases. However, a few studies have reported on the role of platelets in bronchopulmonary dysplasia.Objective: The objective of the study was to explore the relationship between platelet metabolism and bronchopulmonary dysplasia in premature infants.Methods: A prospective case-control study was performed in a cohort of premature infants (born with a gestational age &lt;32 weeks and a birth weight &lt;1,500 g) from June 1, 2017 to June 1, 2018. Subjects were stratified into two groups according to the diagnostic of bronchopulmonary dysplasia: with bronchopulmonary dysplasia (BPD group) and without bronchopulmonary dysplasia (control group). Platelet count, circulating megakaryocyte count (MK), platelet-activating markers (CD62P and CD63), and thrombopoietin (TPO) were recorded and compared in two groups 28 days after birth; then serial thrombopoietin levels and concomitant platelet counts were measured in infants with BPD.Results: A total of 252 premature infants were included in this study. Forty-eight premature infants developed BPD, 48 premature infants without BPD in the control group who were matched against the study infants for gestational age, birth weight, and admission diagnosis at the age of postnatal day 28. Compared with the controls, infants with BPD had significantly lower peripheral platelet count [BPD vs. controls: 180.3 (24.2) × 109/L vs. 345.6 (28.5) × 109/L, p = 0.001]. Circulating MK count in the BPD group was significantly more abundant than that in the control group [BPD vs. controls: 30.7 (4.5)/ml vs. 13.3 (2.6)/ml, p = 0.025]. The level of CD62p, CD63, and TPO in BPD group was significantly higher than the control group [29.7 (3.1%) vs. 14.5 (2.5%), 15.4 (2.0%) vs. 5.8 (1.7%), 301.4 (25.9) pg/ml vs. 120.4 (14.2) pg/ml, all p &lt; 0.05]. Furthermore, the concentration of TPO was negatively correlated with platelet count in BPD group with thrombocytopenia.Conclusions: Our findings suggest that platelet metabolism is involved in the development of BPD in preterm infants. The possible mechanism might be through increased platelet activation and promoted TPO production by feedback.

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