The novel coronavirus, COVID-19, which was first identified in December 2019 rapidly spread worldwide and was declared a global pandemic. Beyond respiratory symptoms, COVID-19 often results in coagulation and vascular endothelium disorders, causing increased clotting and bleeding, which are closely linked to the acute phase of the infection. Factor VIII is a crucial protein in the blood coagulation cascade, and elevated FVIII levels have been linked to thrombotic events in COVID-19, highlighting the need to understand its behavior during treatment. Remdesivir is an antiviral drug that has shown promise in reducing recovery time and mortality rates in COVID-19 patients. This study aims to examine the changes in blood factors and the expression of the factor VIII gene in patients treated with Remdesivir. Blood samples were collected from 30 COVID-19 patients before and after Remdesivir treatment and from 20 healthy individuals. Patients with underlying diseases were excluded from the study. RNA was extracted from these samples, followed by cDNA synthesis. The expression of the factor VIII gene was analyzed using Real-Time PCR. The results indicated that blood factors such as Urea, ALK, AST, WBC, and CRP were elevated in the patient group compared to the control group. At the same time, FBS, Urea, ALK, AST, WBC, RDW, INR, and K levels increased in the Remdesivir treatment group (P < 0.001). Conversely, MCHC, RBC, and Ca levels decreased in both patient and treatment groups compared to the control group (P < 0.001). The expression of the FVIII gene was upregulated approaching 2 times in COVID-19 patients and 1.5-fold in the treatment group compared to the control group (P < 0.001). However, no significant changes were observed in FVIII expression before and after Remdesivir treatment. However, a positive correlation between RBC, FBS, and Urea in the patient group and a negative correlation between RDW and FVIII expression levels was observed. In the treatment group, FVIII expression level correlated negatively with Urea, P, and RDW. These findings suggest that elevated FVIII levels are associated with disease severity and excessive coagulation in COVID-19 patients. Additionally, Remdesivir does not appear to exacerbate the coagulation process.

COVID-19 severity affects liver damage. The utilization of various anti-COVID-19 drugs in non-severe cases related to liver impairment in the short term seemed intriguing.

To assess the dynamic course of liver injury in mild to moderate COVID-19 patients within 10 days of admission and identify risk variables, including medication linkage.

This prospective cohort study of 300 newly diagnosed mild to moderate COVID-19 cases between September 2021 and October 2022. Tertiary center hospitel, field hospital, or cohort ward admissions were made. Patient demographics and treatment were recorded. The drug, liver injury (LI) dynamics, and clinical course were evaluated.

Hospitel/field hospital (188) and cohort wards (112) had 300 individuals. One hundred fifteen participants had liver damage. Favipiravir (45 %), remdesivir (17.4 %), molnupiravir (11.3 %), Andrographis paniculata (ADG) (8.7 %), and favipiravir plus ivermectin (7.7 %) were given to most LI group (n = 104). The baseline AST/ALT levels of 68 (65.4 %) treated patients were abnormal. Favipiravir, remdesivir, and favipiravir + ivermectin increased mean AST/ALT in participants with normal baseline AST/ALT (p = 0.001, 0.003, and 0.016, respectively), but not molnupiravir or Andrographis paniculata. Transaminase levels climbed in untreated patients independent of baseline. The ground-glass imaging pattern was linked to mild LI. Most subjects had transaminase declines after 10 days. Preexisting liver disease did not increase the likelihood of in-hospital LI.

In the real world, a less-than-critical level of liver damage was reported in mild to moderate COVID-19 that allows clinicians to administer a variety of standard medications during short periods of hospital stay.

SARS-CoV-2 and Mycobacterium tuberculosis (Mtb) share similarities in their modes of transmission, pathophysiological symptoms, and clinical manifestations. An imbalance in the immune response characterised by elevated levels of some inflammatory cytokines caused by tuberculosis (TB) and COVID-19 may increase the risk of developing a severe disease-like condition. It has been reported that TB increases the expression levels of Ace2 (angiotensin converting enzyme 2) and Tmprss2 (transmembrane protease serine 2) proteins, which are essential for COVID-19 pathogenesis. Single nucleotide polymorphisms (SNPs) variants of ace2 and tmprss2 genes can impact virus and host-cell interactions and alter immune responses by modulating cytokine production. This may modify the susceptibility and/or severity in COVID-19-infected people. The role of SNPs in ace2 and tmprss2 in relation to Mtb and SARS-CoV-2 co-infection is relatively underexplored.

In this study, genotype frequency of 10 SNPs of ace2 and 03 SNPs of tmprss2 genes in a Cameroonian cohort consisting of COVID-19-positive (n = 31), TB-positive (n = 43), TB-COVID-19 co-infected (n = 21), and a control group (n = 24) were studied. The immune response was estimated by quantitating inflammatory cytokine levels alongside self-reported and clinically diagnosed symptoms. The relationship between specific genetic mutations in these ace2 gene SNPs and their impact on cytokine expression levels in Mtb and SARS-CoV-2 co-infected patients was investigated.

We identified wild-type, heterozygous, and double-mutant genotypes in seven SNPs (rs2285666, rs6632677, rs4646116, rs4646140, rs147311723, rs2074192 and rs4646142) in ace2 gene, which showed significant variations in distribution across the study groups. Our most significant findings include the association of double mutant alleles (AA) of rs4646140 and rs2074192 in the ace2 gene with decreased IL-6 and IL-2 expression levels respectively in TB-COVID-19 participants. Also, the double mutant alleles (AA) of rs4646116 were responsible for increased expression level of IL-2 in TB-COVID-19 patients. Additionally, elevated serum levels of AST, urea, and D-dimer, as well as increased plasma concentrations of IL-10, IFN-γ, and TNF-α, have been associated with co-infections involving Mtb and SARS-CoV-2.

These biomarkers may reflect the complex interplay between the two pathogens and their impact on host immune responses and disease progression. This study highlights the critical role of genetic and immunological factors in shaping altered immune responses during co-infections involving Mtb and SARS-CoV-2. By elucidating these factors, the findings provide a foundation for a deeper understanding of host-pathogen interactions and their implications for disease progression and outcomes. Furthermore, this research has the potential to drive advancements in diagnostic approaches enabling more accurate detection and monitoring of co-infections.

Lopinavir/ritonavir, an anti-severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) drug, may be associated with the development of liver injury. In this paper, we reported an elderly female patient with drug-induced liver injury secondary to lopinavir/ritonavir, which was evaluated for their causality using the updated Roussel Uclaf Causality Assessment Method (RUCAM) of 2016. She had a RUCAM score of 8 which was equivalent to a probable causality grading. Her clinical course was complicated by persistent hepatocyte secretion failure (PHSF), followed by septic shock and SARS-CoV-2 re-infection during her hospitalization. Her response to any medical intervention, including ursodeoxycholic acid, glutathione, methylprednisolone sodium succinate, rifampicin, artificial liver support, and endoscopic nasobiliary drainage (ENBD) was very poor, and her family members refused liver transplantation. Finally, she died. In summary, this case suggests the possibility that lopinavir/ritonavir can cause DILI and even PHSF in our clinical practice.

Long COVID is characterized by the persistence of symptoms among individuals who are infected with the SARS-CoV-2 virus. The enduring impact of these long-term effects on the health and well-being of those affected cannot be denied.

470 patients with SARS-CoV-2 were consecutively recruited in this longitudinal study. The participants were entered into moderate, severe, and critical groups. 235 out of 470 participants were female. The levels of fasting blood sugar (FBS), alanine transaminase (SGPT), aspartate aminotransferase (SGOT), alkaline phosphatase (ALP), creatinine (Cr), urea, uric acid (UA), and total protein (TP) were measured during hospitalization and again at one and three months after infection. The levels of Zn and hemoglobin A1c (HbA1c) were also measured only during hospitalization.

COVID-19 severity was associated with high levels of glucose, urea, Cr, ALT, AST, ALP, and HbA1c, and low levels of Zn, UA, and TP. There were significant sex differences for these markers at all three-time points. Glucose, urea, Cr, ALT, AST, and ALP all decreased three months after infection, whereas the levels of UA and TP returned towards normal.

COVID-19 infection affects the levels of multiple biochemical factors in a gender-dependent manner. The biochemical changes become more tangible with increasing disease severity, and several of these predict mortality. Levels begin to return to normal after the acute phase of the disease, but in some individuals, at three months, several markers were still not within the normal range. Whether the trajectory of these changes can predict long COVID requires further testing.

Coronavirus disease 2019 is a highly contagious respiratory illness caused by the coronavirus SARS-CoV-2. Symptoms can range from mild to severe and typically appear 2-14 days after virus exposure. While vaccination has significantly reduced the incidence of severe complications, strategies for the identification of new biomarkers to assess disease severity remains a critical area of research. Severity biomarkers are essential for personalizing treatment strategies and improving patient outcomes. This study aimed to identify sex-specific biomarkers for COVID-19 severity in a Chilean population (n = 123 female, n = 115 male), categorized as control, mild, moderate, or severe. Data were collected using clinical biochemistry parameters and mass spectrometry-based metabolomics and lipidomics to detect alterations in plasma cytokines, metabolites, and lipid profiles related to disease severity. Principal component analysis (PCA) and orthogonal partial least squares discriminant analysis (OPLS-DA) were performed to select significant characteristic features for each group. The results revealed distinct biomarkers for males and females. In males, COVID-19 severity of was associated with inflammation parameters, triglycerides content, and phospholipids profiles. For females, liver damage parameters, triglycerides content, cholesterol derivatives, and phosphatidylcholine were identified as severity biomarkers. For both sexes, most of the biomarker combinations evaluated got areas under the ROC curve greater than 0.8 and low prediction errors. These findings suggest that sex-specific biomarkers can help differentiate the levels of COVID-19 severity, potentially aiding in the development of tailored treatment approaches.

Azvudine, a repurposed oral small molecule antiviral drug, has potential effects in combating the SARS-CoV-2 virus. However, studies on its clinical efficacy in patients with COVID-19 are still limited and controversial, and further research and validation are necessary.

A retrospective cohort study was conducted on COVID-19 patients who were hospitalized in the General Hospital of Central Theater Command from 1 December 2022 to 31 January 2023. We included 132 patients treated with Azvudine and 132 controls after screening and propensity score matching. The primary outcomes including all-cause mortality and a composite outcome of disease progression such as non-invasive respiratory support, invasive respiratory support, admission to intensive care unit (ICU), and death were compared.

Azvudine recipients had a much lower incidence rate of composite disease progression outcome than controls (13.9075/1000 person-days versus 25.7731/1000 person-days, P<0.05). Azvudine recipients also possessed a lower all-cause mortality rate than controls (2.6797/1000 person-days versus 8.5910/1000 person-days, P<0.01). Azvudine treatment significantly reduced the risk of composite disease progression (HR: 0.37, 95% CI: 0.16-0.84, P=0.017) and all-cause death (HR: 0.25, 95% CI: 0.08-0.81, P=0.021) after adjusting potential confounding factors such as age, sex, severity of COVID-19, complications, concomitant therapy, time from symptoms to treatment, and important laboratory indicators. The subgroup analyses of composite disease progression outcome and all-cause death indicated robustness of Azvudine's in treating COVID-19 patients in general.

Our study demonstrates that Azvudine has a significant positive impact on the clinical recovery of hospitalized patients with COVID-19. These findings provide important support for the use of Azvudine as a therapeutic option for COVID-19, given the current divergent views on its therapeutic efficacy and its importance in public health and medical care.

Background : The treatment strategy of early nutritional support after cardiac surgery has gradually been adopted. However, there are no scientific guidelines for the timing and specific programs of early nutritional support. Methods: A retrospective, single-center analysis (2021-2023) was carried out including elderly patients who were admitted for valvular heart disease and received open-heart valve replacement surgery. We designated patients who started the optimized nutritional support after surgery as the optimized enteral nutritional support strategy TN (EN) group and those who received traditional nutritional support as the traditional nutritional support strategy (TN) group. The nutritional and immune indexes, postoperative complications, length of hospital stay, and hospitalization cost of the two groups were compared and analyzed. Results: We identified 378 eligible patients, comprising 193 (51%) patients in the EN group and 185 (49%) patients in the TN group. There was no significant difference in hospital mortality between the two groups, but the proportion of nosocomial pneumonia was significantly lower in the EN group than in the TN group ( P < 0.001). In the Poisson regression analysis, EN was not associated with an increase in gastrointestinal complications ( P = 0.549). The EN group also seemed to have shorter hospital stays and lower hospitalization expenses ( P < 0.001). In the comparison of postoperative gastrointestinal complications, fewer patients experienced diarrhea ( P = 0.021) and abdominal distension ( P = 0.033) in the EN group compared with the TN group. Conclusion: The optimal nutritional support strategy could effectively improve the clinical outcome of high-risk patients with valvular heart disease.

COVID-19 has affected millions worldwide, causing significant morbidity and mortality. While predominantly involving the respiratory tract, SARS-CoV-2 has also caused systemic illnesses involving other sites. Liver injury due to COVID-19 has been variably reported in observational studies. It has been postulated that liver damage may be due to direct damage by the SARS-CoV-2 virus or multifactorial secondary to hepatotoxic therapeutic options, as well as cytokine release syndrome and sepsis-induced multiorgan dysfunction. The approach to a COVID-19 patient with liver injury requires a thorough evaluation of the pattern of hepatocellular injury, along with the presence of underlying chronic liver disease and concurrent medications which may cause drug-induced liver injury. While studies have shown uneventful recovery in the majority of mildly affected patients, severe COVID-19 associated liver injury has been associated with higher mortality, prolonged hospitalization, and greater morbidity in survivors. Furthermore, its impact on long-term outcomes remains to be ascertained as recent studies report an association with metabolic-fatty liver disease. This present review provides insight into the subject by describing the postulated mechanism of liver injury, its impact in the presence of pre-existing liver disease, and its short- and long-term clinical implications.

COVID-19 pneumonia is characterized by an increased rate of deep venous thrombosis and pulmonary embolism. To better understand the pathophysiology behind thrombosis in COVID-19, we performed proteomics analysis on SARS-CoV-2 infected lung tissue.

Liquid chromatography mass spectrometry was performed on SARS-CoV-2 infected postmortem lung tissue samples. Five protein profiling analyses were performed: whole slide lung parenchyma analysis, followed by analysis of isolated thrombi and endothelium, both stratified by disease (COVID-19 versus influenza) and thrombus morphology (embolism versus in situ). Influenza autopsy cases with pulmonary thrombi were used as controls.

Compared to influenza controls, both analyses of COVID-19 whole-tissue and isolated endothelium showed upregulation of proteins and pathways related to liver metabolism including urea cycle activation, with arginase being among the top upregulated proteins in COVID-19 lung tissue. Analysis of isolated COVID-19 thrombi showed significant downregulation of pathways related to platelet activation compared to influenza thrombi. Analysis of isolated thrombi based on histomorphology shows that in situ thrombi have significant upregulation of coronavirus pathogenesis proteins.

The decrease in platelet activation pathways in severe COVID-19 thrombi suggests a relative increase in venous thromboembolism, as thrombi from venous origin tend to contain fewer platelets than arterial thrombi. Based on histomorphology, in situ thrombi show upregulation of various proteins related to SARS-CoV-2 pathogenesis compared to thromboemboli, which may indicate increased in situ pulmonary thrombosis in COVID-19. Therefore, this study supports the increase of venous thromboembolism without undercutting the involvement of in situ thrombosis in severe COVID-19.

The coronavirus disease 2019 (COVID-19) pandemic has caused changes in the global health system, causing significant setbacks in healthcare systems worldwide. This pandemic has also shown resilience, flexibility, and creativity in reacting to the tragedy. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection targets most of the respiratory tract, resulting in a severe sickness called acute respiratory distress syndrome that may be fatal in some individuals. Although the lung is the primary organ targeted by COVID-19 viruses, the clinical aspect of the disease is varied and ranges from asymptomatic to respiratory failure. However, due to an unorganized immune response and several affected mechanisms, the liver may also experience liver cell injury, ischemic liver dysfunction, and drug-induced liver injury, which can result in respiratory failure because of the immune system's disordered response and other compromised processes that can end in multisystem organ failure. Patients with liver cirrhosis or those who have impaired immune systems may be more likely than other groups to experience worse results from the SARS-CoV-2 infection. We thus intend to examine the pathogenesis, current therapy, and consequences of liver damage concerning COVID-19.

COVID-19 is a complex disease that can lead to fatal respiratory failure with extrapulmonary complications, either as a direct result of viral invasion in multiple organs or secondary to oxygen supply shortage. Liver is susceptible to many viral pathogens, and due to its versatile functions in the body, it is of great interest to determine how hepatocytes may interact with SARS-CoV-2 in COVID-19 patients. Liver injury is a major cause of death, and SARS-CoV-2 is suspected to contribute significantly to hepatopathy. Owing to the lack of knowledge in this field, further research is required to address these ambiguities. Therefore, we aimed to provide a comprehensive insight into host-virus interactions, underlying mechanisms, and associated risk factors by collecting results from epidemiological analyses and relevant laboratory experiments. Backed by an avalanche of recent studies, our findings support that liver injury is a sequela of severe COVID-19, and certain pre-existing liver conditions can also intensify the morbidity of SARS-CoV-2 infection in synergy. Notably, age, sex, lifestyle, dietary habits, coinfection, and particular drug regimens play a decisive role in the final outcome and prognosis as well. Taken together, our goal was to unravel these complexities concerning the development of novel diagnostic, prophylactic, and therapeutic approaches with a focus on prioritizing high-risk groups.

We aimed to determine the reliability of using the Fibrosis-4 (FIB-4) index in COVID-19 patients without underlying liver illness.

We employed multivariate logistic regression to identify variables that exhibited statistically significant influence on the ultimate outcome. Multilayer perceptron analysis was employed to develop a prediction model for the FIB-4 index concerning ICU admission and intubation rates. However, the scarcity of cases rendered the assessment of the mortality rate unfeasible. We plotted ROC curves to analyze the predictive strength of the FIB-4 index across various age groups.

In univariate logistic regression, only the FIB-4 index and respiratory rate demonstrated statistical significance on all poor outcomes. The FIB-4 index for mortality prediction had an ROC and AUC of 0.863 (95% CI: 0.781-0.9444). It demonstrates predictive power across age groups, particularly for age ≥65 (AUC: 0.812, 95% CI: 0.6571-0.9673) and age <65 (AUC: 0.878, 95% CI: 0.8012-0.9558). Its sensitivity for intubation and ICU admission prediction is suboptimal.

FIB-4 index had promising power in prediction of mortality rate in all age groups.

Purpose: We aimed to investigate the impact of Omicron variant infection on the perioperative organ function in patients undergoing elective surgery. Methods: A total of 5029 patients who underwent elective surgery between October 2022 and January 2023 at our hospital were enrolled. Among them, the patients who underwent elective surgery between October 2022 and November 2022 composed Group 1 (not infected with the Omicron variant) the control group; those who underwent elective surgery between December 2022 and January 2023 composed Group 2 (one month after Omicron variant infection) the experimental group. We further divided the patients into two subgroups for analysis: the tumor subgroup and the nontumor subgroup. Data on organ system function indicators, including coagulation parameters, liver function, complete blood count (CBC), and kidney function, were collected before and after surgery. Differences between the two groups were subsequently analyzed via binary logistic regression analysis. Results: Compared with those in the uninfected patient group, the following changes were observed in patients with Omicron variant infection who underwent elective surgery one month after infection: prothrombin activity (PTa), prothrombin time (PT), fibrinogen, albumin/globulin, alanine aminotransferase (ALT), mean corpuscular hemoglobin concentration (MCHC), platelet (PLT), and anemia were increased AST/ALT, indirect bilirubin (IBILI), eosinophils, and uric acid were decreased before surgery; and lung infection/pneumonia and fibrinogen were increased, while AST/ALT, globulin, total bilirubin (TBIL), white blood cell count (WBC), and uric acid were decreased after surgery. There was no significant difference in the mortality rate or length of hospital stay (LOS) between the two groups. Subgroup analysis revealed elevated monocyte, PLT, and fibrinogen classification, levels and decreased globulin, prealbumin (PBA), eosinophil, and uric acid levels in the tumor subgroup of patients who underwent elective surgery one month after Omicron infection compared with those in the uninfected patients. Compared with the nontumor subgroup, fibrinogen levels, lung infection/pneumonia, TBIL, and PLT count were increased in the uninfected patients, while the globulin and eosinophil levels were decreased. Conclusion: Compared with uninfected patients, patients who underwent elective surgery one month after Omicron variant infection exhibited minimal changes in perioperative coagulation parameters, liver function, CBC counts, and kidney function. Additionally, no significant differences in postoperative mortality or LOS were observed between the two groups.

This study aimed to explore the effectiveness and safety of azvudine, nirmatrelvir/ritonavir, and molnupiravir in adult patients with mild-to-moderate COVID-19. This retrospective cohort study included patients with mild-to-moderate COVID-19 (asymptomatic, mild, and common types) at the First Hospital of Changsha (Hunan Province, China) between March and November 2022. Eligible patients were classified into the azvudine, nirmatrelvir/ritonavir, or molnupiravir groups according to the antiviral agents they received. The outcomes were the times to nucleic acid negative conversion (NANC). This study included 157 patients treated with azvudine (n = 66), molnupiravir (n = 66), or nirmatrelvir/ritonavir (n = 25). There were no statistically significant differences in the time from diagnosis to NANC among the azvudine, molnupiravir, and nirmatrelvir/ritonavir groups [median, 9 (95% CI 9-11) vs. 11 (95% CI 10-12) vs. 9 (95% CI 8-12) days, P = 0.15], time from administration to NANC [median, 9 (95% CI 8-10) vs. 10 (95% CI 9.48-11) vs. 8.708 (95% CI 7.51-11) days, P = 0.50], or hospital stay [median, 11 (95% CI 11-13) vs. 13 (95% CI 12-14) vs. 12 (95% CI 10-14) days, P = 0.14], even after adjustment for sex, age, COVID-19 type, comorbidities, Ct level, time from diagnosis to antiviral treatment, and number of symptoms. The cumulative NANC rates in the azvudine, molnupiravir, and nirmatrelvir/ritonavir groups were 15.2%/12.3%/16.0% at day 5 (P = 0.858), 34.8%/21.5%/32.0% at day 7 (P = 0.226), 66.7%/52.3%/60.0% at 10 days (P = 0.246), and 86.4%/86.2%/80.0% at day 14 (P = 0.721). No serious adverse events were reported. Azvudine may be comparable to nirmatrelvir/ritonavir and molnupiravir in adult patients with mild-to-moderate COVID-19 regarding time to NANC, hospital stay, and AEs.

COVID-19 is still a world disaster; however, its vaccination is globally available. Liver and gastrointestinal disturbances occur in patients infected with COVID-19 at varying incidences. Aging decreases the functions of the liver. Thus, the elderly have a weaker response to the COVID-19 virus. The COVID-19 virus affects the liver directly through direct and indirect mechanisms. It directly affects the renin-angiotensin system or indirectly causes sepsis, uncontrolled immune reactions, drug-related hepatic injury, and cytokine storm. Also, COVID-19 vaccines and anti-drugs have adverse effects on the liver too. Thus, this review explores the effect of enhancing aerobic capacity as a nonpharmacological intervention on decreasing COVID- 19-induced liver injury. Enhancing aerobic capacity decreases COVID-19-induced liver injury through the following: 1) downregulating systemic and tissue ACE/ANG II/AT1R axis, upregulating ACE2/ANG 1-7/Mas axis, and moving the renin-angiotensin system to the direction of the ACE2/ANG (1-7)/Mas axis, 2) Improving mitochondrial function and oxygenation to body and lung tissues, causing a decrease in harmful oxidative reactions, 3) Increasing the processing of accumulated free radicals and inhibiting the acute respiratory distress syndrome, 4) Acting as an antioxidant to protect the liver from oxidative stress, 5) Increasing the effect of antiviral drugs and COVID-19 vaccines, which improves the function of immune biomarkers, decreases the viral load, and increases the body's defense against the virus, 6) Decreasing coagulation abnormalities and thrombosis. In conclusion, enhancing aerobic capacity may be an efficient nonpharmacological intervention to decrease COVID-19-induced liver injury in elderlies and regenerate the liver to its normal status after being infected by the COVID-19 virus. It also helps to strengthen the body's immunity for better effects of both COVID-19 vaccination and drugs.

COVID-19 is a global health emergency that requires worldwide collaboration to control its spread. The scientific community is working to understand the different aspects of the post-COVID-19 syndrome and potential treatment strategies. Interestingly, there have been reports of gastrointestinal tract (GIT) involvement in the post-COVID-19 syndrome, suggesting the presence of both severe and mild GIT disorders. The development of the post-COVID-19- GIT syndrome involves various factors, such as impaired GIT mucosa cells, disruptions in the feeling of satiety, reduced blood supply due to the formation of small blood clots, and increased prostaglandin secretion caused by an excessive immune response. GIT symptoms have been observed in around 16% of COVID-19 patients. Other complications include kidney damage and prolonged impairment in the filtration and excretion functions of the glomeruli and tubules. The pathogenesis of post-COVID-19 renal syndrome involves factors, like an overactive immune response, reduced lung perfusion and oxygenation, viral infection in kidney tissues, endothelial dysfunction, and decreased blood volume. Roughly 20% of hospitalized patients experience renal manifestations after recovering from COVID-19.

Gentianopsis is a small gentianaceous genus with a known ethnopharmacological focus as hepatoprotectors containing two underestimated species that are scientifically unexplored: Gentianopsis komarovii (Grossh.) Toyok., which is typical of the Far East, and Gentianopsis stricta (Klotzsch) Ikonn., which is grown in Central Asia. Application of the HPLC-PDA-ESI-tQ-MS/MS technique led to the identification of 28 compounds, such as iridoid glycosides, flavones and xanthones, with loganic acid, sweroside, loganin, secologanin, isoorientin-7-O-glucoside, luteolin-7-O-gentiobioside, chrysoeriol-7-O-glucoside and acacetin-7-O-glucoside being found in the genus for the first time. The extracts of G. komarovii and G. stricta demonstrated choleretic potential, strengthening the bile flow and the total content of bile acids, bilirubin and cholesterol in the bile. The most pronounced effects were observed for luteolin-7-O-glucoside and gentiabavaroside (gentiacaulein-1-O-primveroside), establishing them as the principle choleretics of both herbs. Based on the results, G. komarovii, G. stricta and some phenolic metabolites are prospective new choleretic drugs.

Introduction: In COVID-19 patients, acute kidney injury (AKI) is recognized as a cause of high mortality. The aim of our study was to assess the rate and the predictors of AKI as well as survival among COVID-19 patients. Methods: We analyzed clinical and laboratory admission data, predictors of AKI and outcomes including the need for renal replacement therapy (RRT) and mortality at 30 days. Results: Out of 115 patients, 62 (53.9%) presented with AKI: 21 (33.9%) at stage 1, 7(11.3%) at stage 2, and 34 (54.8%) at stage 3. RRT was required in 22.6% of patients and was resolved in 76%. Pre-existing CKD was associated with a 13-fold risk of AKI (p= 0.0001). Low albumin (p = 0.017), thrombocytopenia (p = 0.022) and increase of creatine kinase over 350UI (p = 0.024) were independently associated with a higher risk for AKI. Mortality rates were significantly higher among patients who developed AKI compared to those without (59.6% vs 30.2%, p= 0.003). Low oxygen blood saturation at admission and albumin were found as powerful independent predictors of mortality (OR 0.937; 95%CI: 0.917 - 0.958, p = 0.000; OR 0.987; 95%CI: 0.885-0.991, p= 0.024, respectively). Longer survival was observed in patients without AKI compared to patients with AKI (22.01± 1.703 vs 16.69 ± 1.54, log rank p= 0.009). Conclusion: Renal impairment is significant in hospitalized COVID-19 patients. The severity of the disease itself is emphasized as main contributing mechanism in the occurrence of AKI, and lower blood saturation at admission is the strongest mortality predictor, surpassing the significance of the AKI itself.

Excessive release of interleukin-6 (IL-6) during the progression of coronavirus disease 2019 (COVID-19) induces cytokine storms, resulting in multi-organ damages including liver injury, similar in nature with mechanism of viral hepatitis. Systemic IL-6 has been associated with the incidence of liver injury among COVID-19 patients; however, studies on IL-6 expression in the liver tissue are completely lacking. The aim of this study was to measure the IL-6 expression in the liver tissues and to determine its correlation with the degree of liver injury in fatal COVID-19 patients. Through this first cross-sectional study, IL-6 expression was measured through immunohistochemical staining and the degree of liver injury was identified based on level of serum alanine aminotransferase (ALT). The Spearman correlation test was used to identify the correlation between IL-6 expression and the degree of liver injury. A total of 47 deceased COVID-19 patients were included and IL-6 expression was observed in all post-mortem liver specimens, ranging from mild to strong expression. Liver injury at various degrees (mild to severe) was found in more than half (59.5%) of the cases. The Spearman correlation analysis suggested a statistically insignificant correlation between liver IL-6 expression and the degree of liver injury (r=0.152; p=0.309). In conclusion, even IL-6 expression was observed in all post-mortem liver specimens, there was an insignificant correlation between IL-6 expression in the liver tissue with the degree of liver injury among fatal COVID-19 patients, suggesting that IL-6 was not the only main factor contributing to liver damage in COVID-19 patients.

With evolving pandemic, a substantial proportion of patients are presenting with liver dysfunction as an extra-pulmonary manifestation of COVID-19 illness. We planned this study to evaluate the incidence of liver dysfunction in COVID-19 pneumonia and find an association between abnormal liver function and the severity of the disease.

We retrospectively analysed the hospital records of 344 patients with moderate to severe COVID-19 illness admitted to a Dedicated COVID Hospital in North India.

Out of 344 patients included in the study, 59.9% were males. The abnormal liver functions were present in 78.49% of patients at admission. Mean age of the patient with liver dysfunction was 53.41 ± 15.71 years. The incidence of elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT), and hypoalbuminemia was 82.96%, 74.91%, and 69.7%, respectively, in patients with COVID-19 at admission. A positive correlation was found between the levels of AST, ALT and hypoalbuminemia with severity of disease. Mortality was 33% in patients with liver dysfunction in comparison to 18.9% in patients with normal liver functions.

More than 75% of the patient had abnormal liver functions at admission, and mortality was also high in this group. Mortality can be effectively reduced if laboratory parameters such as elevated AST and ALT and hypoalbuminemia are closely monitored at admission and during hospital stay in patients with risk factors like male, age <55 years and HTN.

Since 2019, the COVID-19 pandemic wreaked havoc all over the world. Early in the course of the pandemic, multiple hepatic manifestations of COVID-19 were noted. We aim to categorize hepatic dysfunction and its outcome in COVID-19 infection.

This is a review article based on a literature search in PubMed and Medline databases for articles detailing short-term and long-term outcomes of COVID-19 related liver dysfunction.

The most common hepatic manifestation of COVID-19 was aspartate amino transferase (AST) predominant transaminase elevation. Transaminases improve once the COVID-19 infection resolves. In addition, COVID-19 cholangiopathy, autoimmune hepatitis associated COVID-19, and splanchnic venous thrombosis triggered by COVID-19 are other manifestations. Patients with preexisting liver disease, especially those with cirrhosis, have poor prognosis with COVID-19 infections compared to the general population. Elevations in liver tests were associated with severe COVID-19 infections. Patients with chronic liver disease have a higher risk of morbidity and mortality from COVID-19 infection. Among patients with chronic liver disease, decompensated liver cirrhosis, hepatocellular carcinoma and alcohol-associated liver disease were associated with an increased risk of severity and mortality from COVID-19 infection. Interactions between antiviral therapy for COVID-19 and hepatitis B/hepatitis C medications must be considered in patients with chronic viral hepatitis and COVID-19 infection. COVID-19 vaccination-related hepatic dysfunction has been reported.

COVID-19 is here to stay. Hepatic dysfunction in COVID-19 signals severe COVID-19 infections. Patients with chronic liver disease have higher mortality from COVID-19 than general population. It is important to remember the lessons learned throughout the covid pandemic to take care of patients with COVID-19 now and in the future. Further studies are needed to document long-term outcomes in patients with COVID-19 who developed hepatic dysfunction.

High interleukin (IL)-6 levels are associated with greater COVID-19 severity. IL-6 receptor blockade by tocilizumab (anti-IL6R; Actemra) is used globally for the treatment of severe COVID-19, yet a molecular understanding of the therapeutic benefit remains unclear. We characterized the immune profile and identified cellular and molecular pathways modified by tocilizumab in peripheral blood samples from patients enrolled in the COVACTA study, a phase 3, randomized, double-blind, placebo-controlled trial of the efficacy and safety of tocilizumab in hospitalized patients with severe COVID-19. We identified markers of inflammation, lymphopenia, myeloid dysregulation, and organ injury that predict disease severity and clinical outcomes. Proteomic analysis confirmed a pharmacodynamic effect for tocilizumab and identified novel pharmacodynamic biomarkers. Transcriptomic analysis revealed that tocilizumab treatment leads to faster resolution of lymphopenia and myeloid dysregulation associated with severe COVID-19, indicating greater anti-inflammatory activity relative to placebo and potentially leading to faster recovery in patients hospitalized with COVID-19.

COVID-19 associated severe acute liver injury in a young healthy patient has not been reported much in the literature. And currently, there are no standard management guidelines. We want to report a case of acute liver injury of mixed pattern in a young healthy female with asymptomatic COVID-19 infection. She presented with abdominal pain, nausea, vomiting and yellowish discoloration of her skin. Further laboratory investigations revealed mixed pattern liver injury with highly raised liver enzymes. She was managed with N-acetyl cysteine protocol and monitoring of her liver enzymes. Other causes of acute liver injury were ruled out. She remained stable during her hospital stay and follow up. Our aim is to highlight the significance of acute liver injury in COVID 19 patients that may lead to fatal outcomes if not managed and monitored accordingly.

Coronavirus disease 2019 (COVID-19) has been associated with various liver injury cases worldwide. To date, the prevalence, mechanism, clinical manifestations, diagnosis, and outcomes of COVID-19-induced liver injury in various at-risk groups are not well defined. Liver injury may arise in the prevention and treatment of COVID-19 from direct causes such as viral infection and indirect causes such as systemic inflammation, hypoxic changes, and drugs that exacerbate any pre-existing liver disease. Studies have found that patients with underlying liver disease are at higher risk of COVID-19-induced liver injury. Certain condition of cardiopulmonary and metabolic diseases and vulnerable stages in lifespan may also involve in the development of COVID-19-induced liver injury. This review summarized studies of COVID-19-induced liver injury in different at-risk groups regarding their clinical characteristics, parameters, and correlations of the severity with these indicators and signs as well as potential treatment suggestions, to increase attention to physiological and pathological conditions and continue liver function monitoring as they can help in strengthening early supportive treatment and reducing the incidence of adverse outcomes.

Teicoplanin, a glycopeptide antibiotic commonly used to treat bacterial infections, was discovered to be active in vitro against SARS-CoV-2. The aim of this study was to assess the levels of teicoplanin and its components in a cohort of adult and pediatric SARS-CoV-2 patients, evaluating the effect of sex and age on analyte concentrations. The levels of AST, ALT and leukocytes were shown to be higher in females, while the C reactive protein was higher in males. Evaluating the absence/presence of teicoplanin isoforms, we observed that A2-2_3 is the only one consistently present in pediatrics and adults. In adult men and all pediatrics, A2-4_5 is always present. In pediatrics, except for A3-1, median isoform concentrations were higher in females; on the contrary, in adult patients, males showed higher levels. This is the first study to describe levels of teicoplanin isoforms in SARS-CoV-2 infected patients in males and females, and pediatrics and adults, despite the small sample size of our cohort. The observed results imply that additional testing, via therapeutic drug monitoring, may be helpful to more effectively manage infections, particularly those caused by the most recent viruses.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is potentially pathogenic and causes severe symptoms; in addition to respiratory syndromes, patients might experience other severe conditions such as digestive complications and liver complications injury. The abnormality in the liver is manifested by hepatobiliary dysfunction and enzymatic elevation, which is associated with morbidity and mortality. The direct cytopathic effect, immune dysfunction, cytokine storm, and adverse effects of therapeutic regimens have a crucial role in the severity of liver injury. According to aging and immune system alterations, cytokine patterns may also change in the elderly. Moreover, hyperproduction of cytokines in the inflammatory response to SARS-CoV-2 can lead to multi-organ dysfunction. The mortality rate in elderly patients, particularly those with other comorbidities, is also higher than in adults. Although the pathogenic effect of SARS-CoV-2 on the liver has been widely studied, the impact of age and immune-mediated responses at different ages remain unclear. This review discusses the association between immune system responses in coronavirus disease 2019 (COVID-19) patients of different ages and liver injury, focusing on cytokine alterations.

This study aimed to investigate the relationship between blood types and COVID-19 susceptibility and explore changes in blood variables, as well as their relationship with the occurrence of COVID-19. SARS-CoV-2 is a pandemic that has affected people's health and the global financial system. Since the initial confirmed case of COVID-19, people have been influenced worldwide with varying manifestations. Moreover, researchers have illustrated a link between ABO blood types and COVID-19 susceptibility and incidence. Research has also shown that ABO blood groups might play a role in estimating COVID-19 susceptibility and death. Our analysis revealed that blood type O might probably reduce vulnerability to the SARS-CoV-2 illness. On the contrary, people with blood type A are at a higher risk of SARS-CoV-2 infection. This study also evaluated liver biomarkers among COVID-19 patients, revealing significant abnormalities in the levels of alanine amino transferees, aspartate amino transferees, gamma-glutamyl transferees, and total bilirubin.

The COVID-19 pandemic has been a burden to the global community as a whole but the healthcare community had bore the brunt of it. The pandemic resulted in policy changes that interfered with effective healthcare delivery. The healthcare community attempted to cope with the pandemic by triaging and prioritizing emergency conditions especially COVID related, ahead of elective conditions like cancer care. There was also fear that patients with cancer were at an increased risk of sever COVID-19 with increased mortality. Hepatocellular carcinoma (HCC) was also affected by these policies.

We reviewed the modified measures adopted in screening, surveillance, and management of HCC during the pandemic using PubMed, Medline, Index Medicus, EMBASE, SCOPUS, and Google Scholar databases.

The main modification in surveillance and screening for HCC during the pandemic includes limiting the surveillance to those with very high risk of HCC. The interval between surveillan was also delayed by few months in some cases. The adoption of teleconferencing for multidisciplinary team meetings and patient consultation is one of the highlights of this pandemic all in an effort to reduce contact and spread of the virus. The treatment of early-stage HCC was also modified as needed. The role of ablative therapy in the management of early HCC was very prominent during the pandemic as the surgical therapy was significantly affected by the lacks of ventilators and intensive care unit space resulting from the pandemic. Transplantation, especially living donor liver transplantation, was suspended in few centers because of the risk of infection to the living donors.

As we gradually recover from the pandemic, we should prepare for the fallout from the pandemic as we may encounter increased presentation of those patients deferred from screening during the pandemic.

Predictors of mortality that indicate disease severity plays an important role in COVID-19 management and treatment decisions. This study aimed to investigate the association between fibrosis-4 (FIB-4) score, aspartate aminotransferase-to-platelet ratio index (APRI), and novel biomarker-based score (SAD-60) with mortality in COVID-19 patients treated in a tertiary hospital.

In this single-center retrospective study, patients ≥18 years of age who were admitted to our hospital for COVID-19 between December 1 and 31, 2021, were included. Patients were divided into two groups as deceased and survived. A comparative analysis was applied. Predictive abilities of the FIB-4, APRI, and SAD-60 scores for in-hospital mortality were evaluated.

Of the 453 patients enrolled in the study, 248 (54.6%) were male, and the mean age was 52.2±14.7 years. Mortality was recorded in 39 (8.5%) of the patients. The median values of APRI (0.43 and 0.58; p=0.001), FIB-4 score (1.66 and 2.91; p<0.001), and SAD-60 (2 and 8.25; p<0.001) were higher in deceased patients than in survivors. The optimal cut-off value for predicting mortality in the receiver operating characteristic (ROC) curve analysis was 0.58 for APRI (sensitivity=56.4%, specificity=63.6%); 2.14 for FIB-4 score (sensitivity=79.5%, specificity=68.2%); 4.25 for SAD-60 (sensitivity=90%, specificity=73.8%). In Cox regression analysis with a model that included gender, chronic obstructive pulmonary disease (COPD), and coronary artery disease (CAD), FIB-4 (hazard ratio [HR]=4.013, 95% confidence interval [CI]=1.643-9.803; p=0.002), and SAD-60 (HR=8.850, 95% CI=1.035-75.696; p=0.046) were independent risk factors for mortality.

SAD-60 and FIB-4 scores are easily applicable and may be used to predict mortality in COVID-19 patients.

Hypocalcemia is a common condition in liver cirrhosis and is associated with the severity of SARS-CoV-2 infection. However, there is a lack of data demonstrating the prognostic value of hypocalcemia in COVID-19 patients with cirrhosis. This study aimed to evaluate the prognostic value of hypocalcemia for COVID-19 severity, mortality and its associations with abnormal liver function parameters. We selected 451 COVID-19 patients in this retrospective study and compared the laboratory findings of 52 COVID-19 patients with cirrhosis to those of 399 COVID-19 patients without cirrhosis. Laboratory tests measuring albumin-corrected total serum calcium were performed on admission, and the levels were monitored during hospitalization. The total serum calcium levels were significantly lower in cirrhosis cases (2.16 mmol/L) compared to those without cirrhosis (2.32 mmol/L). Multivariate analysis showed that hypocalcemia in COVID-19 patients with cirrhosis was a significant predictor of in-hospital mortality, with an OR of 4.871 (p < 0.05; 95% CI 1.566-15.146). ROC analysis showed the AUC value of total serum calcium was 0.818 (95% CI 0.683-0.953, p < 0.05), with a sensitivity of 88.3% and a specificity of 75%. The total serum calcium levels showed a significant negative correlation with the Child-Turcette-Pugh score (r = -0.400, p < 0.05). Hypocalcemia on admission was a significant prognostic factor of disease progression in COVID-19 patients with cirrhosis.

As of June 2022, more than 530 million people worldwide have become ill with coronavirus disease 2019 (COVID-19). Although COVID-19 is most commonly associated with respiratory distress (severe acute respiratory syndrome), meta-analysis have indicated that liver dysfunction also occurs in patients with severe symptoms. Current studies revealed distinctive patterning in the receptors on the hepatic cells that helps in viral invasion through the expression of angiotensin-converting enzyme receptors. It has also been reported that in some patients with COVID-19, therapeutic strategies, including repurposed drugs (mitifovir, lopinavir/ritonavir, tocilizumab, etc.) triggered liver injury and cholestatic toxicity. Several proven indicators support cytokine storm-induced hepatic damage. Because there are 1.5 billion patients with chronic liver disease worldwide, it becomes imperative to critically evaluate the molecular mechanisms concerning hepatotropism of COVID-19 and identify new potential therapeutics. This review also designated a comprehensive outlook of comorbidities and the impact of lifestyle and genetics in managing patients with COVID-19.

In patients with severe COVID-19, acute respiratory distress syndrome (ARDS), multiple organ dysfunction syndrome (MODS), and even mortality can result from cytokine storm, which is a hyperinflammatory medical condition caused by the excessive and uncontrolled release of pro-inflammatory cytokines. High levels of numerous crucial pro-inflammatory cytokines, such as interleukin-1 (IL-1), IL-2, IL-6, tumor necrosis factor-α, interferon (IFN)-γ, IFN-induced protein 10 kDa, granulocyte-macrophage colony-stimulating factor, monocyte chemoattractant protein-1, and IL-10 and so on, have been found in severe COVID-19. They participate in cascade amplification pathways of pro-inflammatory responses through complex inflammatory networks. Here, we review the involvements of these critical inflammatory cytokines in SARS-CoV-2 infection and discuss their potential roles in triggering or regulating cytokine storm, which can help to understand the pathogenesis of severe COVID-19. So far, there is rarely effective therapeutic strategy for patients with cytokine storm besides using glucocorticoids, which is proved to result in fatal side effects. Clarifying the roles of key involved cytokines in the complex inflammatory network of cytokine storm will help to develop an ideal therapeutic intervention, such as neutralizing antibody of certain cytokine or inhibitor of some inflammatory signal pathways.

While severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) quickly spread across the globe, our understanding of its pathogenic mechanisms evolved. Importantly, coronavirus disease 2019 (COVID-19) is now considered a syndromic multisystem inflammatory disease involving not only the respiratory system but also the cardiovascular, excretory, nervous, musculoskeletal, and gastrointestinal systems. Moreover, a membrane-bound form of angiotensin-converting enzyme 2, the entry receptor for SARS-CoV-2, is expressed on the surface of cholangiocytes and hepatocytes, suggesting the potential of COVID-19 to involve the liver. With the widespread distribution of SARS-CoV-2 throughout the population, infection during pregnancy is no longer a rare occurrence; however, little is known about the course of hepatic injuries and related outcomes in pregnant SARS-CoV-2-positive women. Thus, the understudied topic of COVID-related liver disease during pregnancy poses a great challenge for the consulting gynecologist and hepatologist. In this review, we aim to describe and summarize potential liver injuries in pregnant women with COVID-19.

There have been numerous concerns about the disease and how it affects the human body since the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic began in December 2019. The impact of SARS-CoV-2 on the liver is being carefully investigated due to an increase in individuals with hepatitis and other liver illnesses, such as alcoholic liver disease. Additionally, the liver is involved in the metabolism of numerous drugs used to treat comorbidities and coronavirus disease 2019 (COVID-19). Determining how SARS-CoV-2 affects the liver and what factors place individuals with COVID-19 at a higher risk of developing liver problems are the two main objectives of this study. This evaluation of the literature included research from three major scientific databases. To provide an update on the current impact of COVID-19 on the liver, data was collected and relevant information was incorporated into the review. With more knowledge about the effect of the disease on the liver, better management and therapeutics can be developed, and education can ultimately save lives and reduce the long-term impact of the pandemic on our population.

Development and worsening of most common neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis, have been associated with COVID-19 However, the mechanisms associated with neurological symptoms in COVID-19 patients and neurodegenerative sequelae are not clear. The interplay between gene expression and metabolite production in CNS is driven by miRNAs. These small non-coding molecules are dysregulated in most common neurodegenerative diseases and COVID-19.

We have performed a thorough literature screening and database mining to search for shared miRNA landscapes of SARS-CoV-2 infection and neurodegeneration. Differentially expressed miRNAs in COVID-19 patients were searched using PubMed, while differentially expressed miRNAs in patients with five most common neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, and multiple sclerosis) were searched using the Human microRNA Disease Database. Target genes of the overlapping miRNAs, identified with the miRTarBase, were used for the pathway enrichment analysis performed with Kyoto Encyclopedia of Genes and Genomes and Reactome.

In total, 98 common miRNAs were found. Additionally, two of them (hsa-miR-34a and hsa-miR-132) were highlighted as promising biomarkers of neurodegeneration, as they are dysregulated in all five most common neurodegenerative diseases and COVID-19. Additionally, hsa-miR-155 was upregulated in four COVID-19 studies and found to be dysregulated in neurodegeneration processes as well. Screening for miRNA targets identified 746 unique genes with strong evidence for interaction. Target enrichment analysis highlighted most significant KEGG and Reactome pathways being involved in signaling, cancer, transcription and infection. However, the more specific identified pathways confirmed neuroinflammation as being the most important shared feature.

Our pathway based approach has identified overlapping miRNAs in COVID-19 and neurodegenerative diseases that may have a valuable potential for neurodegeneration prediction in COVID-19 patients. Additionally, identified miRNAs can be further explored as potential drug targets or agents to modify signaling in shared pathways. Graphical AbstractShared miRNA molecules among the five investigated neurodegenerative diseases and COVID-19 were identified. The two overlapping miRNAs, hsa-miR-34a and has-miR-132, present potential biomarkers of neurodegenerative sequelae after COVID-19. Furthermore, 98 common miRNAs between all five neurodegenerative diseases together and COVID-19 were identified. A KEGG and Reactome pathway enrichment analyses was performed on the list of shared miRNA target genes and finally top 20 pathways were evaluated for their potential for identification of new drug targets. A common feature of identified overlapping miRNAs and pathways is neuroinflammation. AD, Alzheimer's disease; ALS, amyotrophic lateral sclerosis; COVID-19, coronavirus disease 2019; HD, Huntington's disease; KEGG, Kyoto Encyclopedia of Genes and Genomes; MS, multiple sclerosis; PD, Parkinson's disease.

Liver injury occurs frequently as a consequence of SARS-CoV-2 infection. Direct infection of the liver leads to hepatic impairment with elevated transaminases. In addition, severe COVID-19 is characterized by cytokine release syndrome, which may initiate or exacerbate liver injury. In patients with cirrhosis, SARS-CoV-2 infection is associated with acute-on-chronic liver failure. The Middle East and North Africa (MENA) region is one of the world's regions characterized by a high prevalence of chronic liver diseases. Both parenchymal and vascular types of injury contribute to liver failure in COVID-19, with a myriad of pro-inflammatory cytokines playing a major role in perpetuating liver injury. Additionally, hypoxia and coagulopathy complicate such a condition. This review discusses the risk factors, and the underlying causes of impaired liver functions in COVID-19, with a focus on key players in the pathogenesis of liver injury. It also highlights the histopathological changes encountered in postmortem liver tissues as well as potential predictors and prognostic factors of such injury, in addition to the management strategies to ameliorate liver damage.

The coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2, has quickly spread over the world since December 2019. COVID-19 is a systemic disease that can affect various organs throughout the body. Gastrointestinal (GI) symptoms have been reported in 16% to 33% of all patients with COVID-19 and in 75% of critically ill patients. This chapter reviews the GI manifestations of COVID-19 as well as their diagnostic and treatment modalities.

Since the first identification in December of 2019 and the fast spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, it has represented a dramatic global public health concern. Though affecting mainly the respiratory system, SARS-CoV-2 disease, defined as coronavirus disease 2019 (COVID-19), may have a systemic involvement leading to multiple organ dysfunction. Experimental evidence about the SARS-CoV-2 tropism for the liver and the increasing of hepatic cytolysis enzymes during infection support the presence of a pathophysiological relationship between liver and SARS-CoV-2. On the other side, patients with chronic liver disease have been demonstrated to have a poor prognosis with COVID-19. In particular, patients with liver cirrhosis appear extremely vulnerable to infection. Moreover, the etiology of liver disease and the vaccination status could affect the COVID-19 outcomes. This review analyzes the impact of the disease stage and the related causes on morbidity and mortality, clinical outcomes during SARS-CoV-2 infection, as well as the efficacy of vaccination in patients with chronic liver disease.