COVID-19 is caused by SARS-CoV-2. Although pulmonary manifestations have been identified as the major symptoms, several hematological abnormalities have also been identified. This review summarizes the reported hematological abnormalities (changes in platelet, white blood cell, and hemoglobin, and coagulation/fibrinolytic alterations), explores their patho-mechanisms, and discusses its management. Common hematological abnormalities in COVID-19 are lymphopenia, thrombocytopenia, and elevated D-dimer levels. These alterations are significantly more common/prominent in patients with severe COVID-19 disease, and thus may serve as a possible biomarker for those needing hospitalization and intensive care unit care. Close attention needs to be paid to coagulation abnormalities, and steps should be taken to prevent these occurring or to mitigate their harmful effects. The effect of COVID-19 in patients with hematological abnormalities and recognized hematological drug toxicities of therapies for COVID-19 are also outlined.

: COVID-19, a respiratory viral infection, has affected 388 million individuals worldwide as of the February 4, 2022. In this review, we have outlined the important liver manifestations of COVID-19 and discussed the possible underlying pathophysiological mechanisms and their diagnosis and management. Factors that may contribute to hepatic involvement in COVID-19 include direct viral cytopathic effects, exaggerated immune responses/systemic inflammatory response syndrome, hypoxia-induced changes, vascular changes due to coagulopathy, endothelitis, cardiac congestion from right heart failure, and drug-induced liver injury. The majority of COVID-19-associated liver symptoms are mild and self-limiting. Thus management is generally supportive. Liver function tests and abdominal imaging are the primary investigations done in relation to liver involvement in COVID-19 patients. However, imaging findings are nonspecific. Severe acute respiratory syndrome coronavirus 2 RNA has been found in liver biopsies. However, there is limited place for liver biopsy in the clinical context, as it does not influence management. Although, the management is supportive in the majority of patients without previous liver disease, special emphasis is needed in those with nonalcoholic fatty liver disease, cirrhosis, hepatocellular carcinoma, hepatitis B and C infections, and alcoholic liver disease, and in liver transplant recipients.

Background and objective: Carotid artery intima media thickness (CIMT) is a strong predictor of Coronary Heart Disease (CHD) and independent phenotype of early atherosclerosis. The global variation of CIMT and its demographic association is yet unclear. We evaluated regional variations of CIMT based on WHO regions and assessed the differences by age and sex. Methods: A systematic search was conducted on studies published between 1980 January up to December 2020. PubMed, Oxford Medicine Online, EBSCO, Taylor & Francis, Oxford University Press and Embase data bases were used for searching. Supplementary searches were conducted on the Web of Science and Google Scholar. Grey literature was searched in “Open Grey” website. The two major criteria used were “adults” and “carotid intima media”. The search strategy for PubMed was created first and then adapted for the Oxford Medicine Online, EBSCO, Taylor & Francis, Oxford University Press and Embase databases. Covidence software (Veritas Health Innovation, Melbourne, Australia; http://www.covidence.org) was used to manage the study selection process. Meta-analyses were done using the random-effects model. An I² ≥ 50% or p< 0:05 were considered to indicate significant heterogeneity. Results: Of 2847 potential articles, 46 eligible articles were included in the review contributing data for 49 381 individuals (mean age: 55.6 years, male: 55.8%). The pooled mean CIMT for the non-CHD group was 0.65mm (95%CI: 0.62–0.69). There was a significant difference in the mean CIMT between regions (p = 0.04). Countries in the African (0.72mm), American (0.71mm) and European (0.71mm) regions had a higher pooled mean CIMT compared to those in the South East Asian (0.62mm), West Pacific (0.60mm) and Eastern Mediterranean (0.60mm) regions. Males had a higher pooled mean CIMT of 0.06mm than females in the non CHD group (p = 0.001); there were also regional differences. The CHD group had a significantly higher mean CIMT than the non-CHD group (difference = 0.23mm, p = 0.001) with regional variations. Carotid artery segment-specific-CIMT variations are present in this population. Older persons and those having CHD group had significantly thicker CIMTs. Conclusions: CIMT varies according to region, age, sex and whether a person having CHD. There are significant regional differences of mean CIMT between CHD and non-CHD groups. Segment specific CIMT variations exist among regions. There is an association between CHD and CIMT values.

Dengue infection is caused by the dengue virus (DENV) and is transmitted to humans by infected female Aedes aegypti and Aedes albopictus mosquitoes. There are nearly 100 million new dengue cases yearly in more than 120 countries, with a five-fold increase in incidence over the past four decades. While many patients experience a mild illness, a subset suffer from severe disease, which can be fatal. Dysregulated immune responses are central to the pathogenesis of dengue, and haematologic manifestations are a prominent feature of severe disease. While thrombocytopaenia and coagulopathy are major causes of bleeding in severe dengue, leucocyte abnormalities are emerging as important markers of prognosis. In this review, we provide our perspective on the clinical aspects and pathophysiology of haematologic manifestations in dengue. We also discuss the key gaps in our current practice and areas to be addressed by future research.

Introduction: Due to the shortcomings in the 1997-World Health Organisation (WHO) dengue case classification (DCC), a revised classification was proposed in 2009. This study was aimed to assess the clinical usefulness of the two classifications during a large dengue epidemic. Methodology: Clinical data of dengue patients admitted to selected units at National Hospital of Sri Lanka, Panadura Base Hospital and Nawaloka Hospital Colombo between June and August 2017 were collected prospectively. Cases were classified using the 1997 and 2009 WHO DCCs. Results: 1,878 patients [adult = 1,573 (83.8%)] were studied. Based on 1997-WHO-DCC-DF (Dengue Fever): 1,316 (70.1%), DHF (Dengue Haemorrhagic Fever) -1: 468 (24.9%), DHF-2: 86 (4.6%) and DHF-3: 8 (0.4%). Based on 2009-WHO-DCC-Dengue with warning signs (WS): 1647 (87.7%), Dengue without WS: 231 (12.3%) and severe dengue (SD): 41 (2.18%). A total of 1,088 (82.7%) DF and 559 (99.5%) DHF patients developed WS. Of those without WS, 228 (17.3%) were DF patients and 3 (0.5%) were DHF patients. Three (0.23%) DF and 38 (6.76%) DHF patients had SD. All SD patients had WS. The level of agreement between the two systems of classification was poor (Kappa = - 0.035, p < 0.001). Conclusions: The 2009-WHO-DCC was more useful than 1997-WHO-DCC in predicting dengue disease severity as few DF patients also had SD. Furthermore, the presence of WS identified patients with SD. However, the 2009-WHO-DCC may not suit the resource limited countries as WS are non-specific, and lack of diagnostic tests can result in case overload.