Incidence of thromboembolism in patients with COVID-19: a systematic review and meta-analysis.

BACKGROUND: Since the beginning of the coronavirus disease 2019 (COVID-19) pandemic, the incidence of thromboembolism has been increasingly reported. The aim of this systematic review was to explore the incidence of venous and arterial thromboembolism among COVID-19 patients requiring hospitalization. METHODS: Medline, Embase, Scopus, and grey literature were searched until June 2020. Observational studies reported on the incidence of venous thromboembolism (VTE), including pulmonary embolism (PE) and deep vein thrombosis (DVT) or arterial thromboembolism (ATE) were included. The pool incidences and their 95% confidence intervals (CI) were calculated using the random-effects model. RESULTS: A total of 36 studies were included. In the intensive care unit (ICU) setting, the pooled incidence of VTE was 28% (95% CI, 22-34%). Subgroups based on compression ultrasound (CUS) screening revealed a higher incidence of DVT in the CUS screening group than in the no CUS screening group (32% [95% CI, 18-45%] vs. 6% [95% CI, 4-9%]). The pooled incidence of ATE in ICU was 3% (95% CI, 2-5%). In the non-ICU setting, the pooled incidence of VTE was 10% (95% CI, 6-14%,). CONCLUSIONS: The incidence of VTE in COVID-19 patients was higher in the ICU setting than in the non-ICU setting, and also significantly higher in studies that incorporated the CUS screening protocol. The incidence of ATE in the ICU setting was low. VTE prophylactic measures should be given to all hospitalized patients diagnosed with COVID-19.

Increased platelet activation and lower platelet-monocyte aggregates in COVID-19 patients with severe pneumonia.

BACKGROUND: The increased procoagulant platelets and platelet activation are associated with thrombosis in COVID-19. In this study, we investigated platelet activation in COVID-19 patients and their association with other disease markers. METHODS: COVID-19 patients were classified into three severity groups: no pneumonia, mild-to-moderate pneumonia, and severe pneumonia. The expression of P-selectin and activated glycoprotein (aGP) IIb/IIIa on the platelet surface and platelet-leukocyte aggregates were measured prospectively on admission days 1, 7, and 10 by flow cytometry. RESULTS: P-selectin expression, platelet-neutrophil, platelet-lymphocyte, and platelet-monocyte aggregates were higher in COVID-19 patients than in uninfected control individuals. In contrast, aGPIIb/IIIa expression was not different between patients and controls. Severe pneumonia patients had lower platelet-monocyte aggregates than patients without pneumonia and patients with mild-to-moderate pneumonia. Platelet-neutrophil and platelet-lymphocyte aggregates were not different among groups. There was no change in platelet-leukocyte aggregates and P-selectin expression on days 1, 7, and 10. aGPIIb/IIIa expression was not different among patient groups. Still, adenosine diphosphate (ADP)-induced aGPIIb/IIIa expression was lower in severe pneumonia than in patients without and with mild-to-moderate pneumonia. Platelet-monocyte aggregates exhibited a weak positive correlation with lymphocyte count and weak negative correlations with interleukin-6, D-dimer, lactate dehydrogenase, and nitrite. CONCLUSION: COVID-19 patients have higher platelet-leukocyte aggregates and P-selectin expression than controls, indicating increased platelet activation. Compared within patient groups, platelet-monocyte aggregates were lower in severe pneumonia patients.

Progression of non-anemic macrocytosis to anemia in HIV-positive persons receiving zidovudine-containing regimens in a resource-limited setting.

BACKGROUND: Non-anemic macrocytosis is frequently observed among HIV-positive persons treated with zidovudine in resource-limited settings. Although zidovudine-associated anemia is well recognized, the probability and predictors of progression from non-anemic macrocytosis to anemia are still unknown. METHODS: A retrospective cohort study was conducted among HIV-positive persons receiving zidovudine-containing antiretroviral therapy (ART) with non-anemic macrocytosis. Kaplan-Meier and Cox regression analyses were used to determine the probability and predictive factors of progression from non-anemic macrocytosis to anemia, respectively. RESULTS: Of 318 HIV-positive persons, 59.4% were male; mean age was 44.3 years. The median follow-up duration was 5.8 years. The probabilities of progression to anemia at 1, 3 and 4 years were estimated at 9.4, 17.3 and 21.3%, respectively. Almost all anemia was mild asymptomatic. Duration of zidovudine use [hazard ratio (HR) = 1.141; 95% confidence interval (CI),1.036-1.256; p = .007], CD4 count prior to start zidovudine [HR = 0.991; 95%CI,0.982-0.999; p = .038], and hematocrit level at development of macrocytosis [HR = 0.683; 95%CI,0.541-0.861; p = .001] were significant factors to predict progression to anemia. CONCLUSION: Non-anemic macrocytosis in HIV-positive persons receiving zidovudine-containing ART can progress to anemia. Longer duration of zidovudine use, lower CD4 cell counts at ART initiation, and lower hematocrit level at development of macrocytosis are predictive factors for progression to anemia.

Spontaneous tension hemothorax in a severe COVID-19 patient receiving ECMO therapy: The other side of COVID-19-associated coagulopathy.

As opposed to widely recognized Coronavirus Disease 2019 (COVID-19)-associated thrombotic events, the unusual but serious bleeding complications in COVID-19 patients are worth-mentioned. Here, we describe a 44-year-old man afflicted by COVID-19 pneumonia with acute respiratory distress syndrome (ARDS) and submassive pulmonary embolism. The patient's condition initially improved with the prescription of ECMO, tocilizumab, and hemoadsorption, however, he later developed spontaneous tension hemothorax, which is considered rare but devastating in the setting of COVID-19. While the exact pathogenesis of COVID-19-associated bleeding events remains poorly understood, we aim to highlight the other aspect of coagulation dysfunction potentially caused by COVID-19.

The association between body mass index and severity of Coronavirus Disease 2019 (COVID-19): A cohort study.

OBJECTIVES: The coronavirus disease 2019 (COVID-19) has become a worst pandemic. The clinical characteristics vary from asymptomatic to fatal. This study aims to examine the association between body mass index (BMI) levels and the severity of COVID-19. METHODS AND STUDY DESIGN: A cohort study included 147 adult patients with confirmed COVID-19 were categorized into 4 groups by BMI levels on admission: <18.5 (underweight), 18.5-22.9 (normal weight), 23.0-24.9 (overweight), and ≥25.0 kg/m2 (obese). Rates of pneumonia, severe pneumonia, acute kidney injury (AKI), and ICU stay during hospitalization across BMI group was determined. Logistic regression analysis was used to determine the association between BMI and severe pneumonia. RESULTS: Of the totals, patients having a BMI <18.5, 18.5-22.9, 23.0-24.9, and ≥25.0 kg/m2 were 12.9%, 38.1%, 17.7%, and 31.3%, respectively. The rates of pneumonia and severe pneumonia tended to be higher in patients with higher BMI, whereas the rates of AKI and ICU stay were higher in patients with BMI <18.5 kg/m2 and ≥ 25 kg/m2, when compared to patients with normal BMI. After controlling for age, sex, diabetes, hypertension and dyslipidemia in the logistic regression analysis, having a BMI ≥25.0 kg/m2 was associated with higher risk of severe pneumonia (OR 4.73; 95% CI, 1.50-14.94; p = 0.003) compared to having a BMI 18.5-22.9 kg/m2. During admission, elevated hemoglobin and alanine aminotransferase levels on day 7 and 14 of illness were associated with higher BMI levels. In contrast, rising of serum creatinine levels was observed in underweight patients on days 12 and 14 of illness. CONCLUSIONS: Obesity in patients with COVID-19 was associated with severe pneumonia and adverse outcomes such as AKI, transaminitis and ICU stay. Underweight patients should be closely monitored for AKI. Further studies in body composition are warranted to explore the links between adiposity and COVID-19 pathogenesis.

Left ventricular thrombus and pulmonary embolism: A case series of thrombosis in COVID-19 in Thai patients.

Thrombosis in COVID-19 is increasingly recognized and is generally associated with a high mortality rate. The key clinical question of this report was whether COVID-19 could be complicated with cardiac thrombus and pulmonary embolism in Asian population. We demonstrated the case series of thrombosis in Thai patients with confirmed severe acute respiratory syndrome coronavirus 2 infection. One patient had the first case of a large left ventricular thrombus, and three other patients had pulmonary embolism. All patients were male and had low absolute lymphocyte count, while lactate dehydrogenase level and d-dimer were markedly elevated, especially at the time when the thrombosis was diagnosed. All patients had severe COVID-19 with pneumonia. Two patients who needed mechanical ventilation were successfully extubated. After hospitalization for 13-49 days, pneumonia and thrombosis improved and all of them could be discharged from the hospital. Thrombosis is common in COVID-19 and could present in both arterial and venous sites even in Asian populations. d-dimer is a strong marker to predict thrombosis and could be a prognostic predictor for severity of COVID-19.

Leukocyte telomere length in patients with transfusion-dependent thalassemia.

BACKGROUND: Thalassemia is a hereditary hemolytic anemia with a severity ranging from mild, non-transfusion dependent to severe chronic anemia requiring lifelong transfusion. Transfusional iron overload is a major complication in patients with transfusion-dependent thalassemia (TDT). Telomeres are sequences of nucleotides forming the end caps of chromosomes that act as a DNA repair system. Iron overload in thalassemia can cause increased oxidative stress which leads to cellular damage and senescence. This may result in telomere length shortening. The degree of telomere length shortening may reflect the severity of thalassemia. METHODS: This research aimed to study the leukocyte telomere length in patients with TDT in comparison to non-thalassemic individuals and to identify the clinical and laboratory parameters that are associated with telomere length. We conducted a cross-sectional study in patients with TDT aged ≥18 years. Leukocyte telomere length was measured by real-time quantitative PCR. RESULTS: Sixty-five patients with TDT were enrolled onto the study. There were 37 female patients (54.4%). The median age was 27 (18-57) years, and mean pre-transfusion hemoglobin level was 7.1 (± 1.07) g/dL. The mean telomere to single copy gene (T/S) ratios of patients with TDT and the controls were 0.72 ± 0.18 and 0.99 ± 0.25, respectively (p < 0.0001). There was a significant correlation between the T/S ratio and age (p = 0.0002), and hemoglobin level (p = 0.044). There was no correlation between telomere length and other factors. CONCLUSIONS: Our study showed that TDT patients had shorter leukocyte telomere length compared with controls. Leukocyte telomere shortening in TDT was an aging-dependent process and associated with lower hemoglobin level.