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Abstract
目的： 探索和分析新型冠状病毒感染肺炎（NCP）患者发生肝损伤的可能机制。 方法： 综合分析已报道文献中NCP患者的丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）等肝酶变化情况与疾病状态的相关性；基于肝组织单细胞测序数据（GSE115469）分析新冠病毒受体血管紧张素转换酶2（ACE2）在肝组织中的表达；采用RNA-seq方法分析半肝切除急性肝损伤小鼠模型肝切除后不同时间点残肝组织中Ace2的表达及与其表达相关的转录因子。统计学方法采用t检验和Spearman秩相关分析。 结果： 部分新冠病毒感染者发生了ALT、AST异常升高，且NCP重症患者ALT、AST升高的比率及程度均高于非重症患者。肝组织单细胞测序和免疫组织化学检测结果显示，ACE2在正常肝组织中只在胆管上皮细胞表达，而在肝细胞中表达极低。在小鼠半肝切除急性肝损伤模型中，Ace2在术后第1天的急性损伤期表达下调，但在术后第3天的肝细胞增殖高峰期表达升高至正常水平的2倍以上，并在肝脏恢复、肝细胞增殖停止的第7天恢复到正常水平。这一现象是否提示ACE2表达阳性的胆管上皮细胞参与了部分肝切除后的肝再生过程，值得进一步的研究。RNA-seq数据中有77个转录因子与Ace2表达呈正相关（r > 0.2，FDR < 0.05），主要富集在腺体腔管表皮细胞的发育、分化、形态生成以及细胞增殖等功能。 结论： 除了NCP患者过度激活的炎症反应可导致肝损伤外，胆管上皮细胞来源肝实质细胞的代偿性增生所致病毒受体ACE2在肝组织中的表达上调，可能是新型冠状病毒感染肝细胞造成肝组织损伤的可能机制。.
... The World Health Organization (WHO) dubbed novel coronavirus disease-2019 (COVID- 19), which causes a severe acute respiratory syndrome, as coronavirus 2 (SARS-CoV-2) infection. It was first diagnosed in Wuhan, China, in December 2019. ...
... 6,7 There are limited studies on this subject in Turkey. This study intended to identify the clinical features of geriatric patients who have COVID- 19 and explore the in-hospital mortality rate and its predictors. ...
... Although the cause of liver damage in COVID-19 is not fully understood, it is suggested that the elevation in liver enzymes is caused by cytokine storm syndrome and drug-induced liver damage. 19 CRP is an acute phase reactant which is synthesized in the liver and increases during inflammation due to infection or tissue damage. In the vast majority of COVID-19 patients, it was found to be high, and it is associated with the disease's severity. ...
... The liver is susceptible to cardiovascular abnormalities because of composite vascular supply and substantial metabolic activity. The condition known as ischemic hepatitis, also referred to as hypoxic hepatitis, is frequently found in critically ill patients and is the consequence of underlying circulatory, cardiac, or respiratory failure that can result in passive congestion or reduced hepatic perfusion [75,76]. Systemic stress causes a compensatory reduction in peripheral and splanchnic blood flow, which in turn, causes a reduction in hepatic blood flow, and as a result, hepatocellular hypoxia, particularly in zone 3 [12,77]. ...
... Additionally, individuals with COVID-19 reported experiencing recurrent gastrointestinal issues [74]. In individuals with severe COVID-19, research found an abnormally high level of aminotransferase that may not have a hepatic origin [76]. The study shows a consistent link between the severity of COVID-19 and liver damage, although the mechanisms behind this damage are still unknown, given the multifaceted nature of the condition. ...
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.
... Through these genes, we can describe possible functions making metabolic hypotheses, aided by GO and KEGG analyses. Many researchers focused on the impact of the disease on evaluating the regeneration of liver epithelial cells [9,10], to create a model of acute liver failure and identify the possible therapeutic effects of inhibitors of some high ranked genes, such as hub genes [11]. Knowledge of hub genes, therefore, represents an indispensable crucial point for characterizing the molecular aspects of a disease, such as cellular stress due to COVID-19 but also for the design of specific drugs. ...
... (www.preprints.org) | NOT PEER-REVIEWED | Posted: 13 February 2024 doi:10.20944/preprints202402.0757.v110 ...
Many metabolic processes at the molecular level support both viral attack strategies and human defenses during Covid-19. This knowledge is of vital importance in the design of antiviral drugs. In this study, we extracted 18 articles (2021-2023) from PubMed reporting the discovery of hub-nodes specific for the liver during covid-19, identifying 142 hub-nodes. They are highly connected proteins from which to get deep functional information on viral strategies when used as functional seeds. Therefore, we evaluated the functional and structural significance of each of them to endorse their reliable use as seeds. After filtering, the remaining 111 hubs were used to get by STRING an enriched interactome of 1111 nodes (13,494 interactions). It shows the viral strategy in the liver is to attack the entire cytoplasmic translational system, including ribosomes, to take control of protein bio-synthesis. We used the SARS2-Human-Proteome Interaction Database (33,791 interactions), de-signed by us with BioGRID data to implement a reverse-engineering process that identified human proteins actively interacting with viral proteins. The results show 57% of human liver proteins di-rectly involved in Covid, a strong impairment of the ribosome and spliceosome, an antiviral defense mechanism against cellular stress of the p53 system, and, surprisingly, a viral capacity for multiple protein attacks against single human proteins that reveal underlying evolutionary-topological molecular mechanisms. Viral behavior over time suggests different molecular strategies for different organs.
... Hepatocytes and bile duct cells over express the ACE2 receptor, which binds to the SARS-CoV-2 virus [66]. This ACE2 receptor could be one of the receptors involved in the liver damage seen in COVID-19 [67]. Similar to our results, a study by Medetalibeyoglu et al. showed that an increase in hepatic aminotransferases such as AST and ALT was associated with a more severe course and an increase in mortality in COVID-19 patients [68]. ...
... Moorthy et al. [74], depicted that the CRP, LDH, eosinophil, and lymphocyte counts serve to predict the severity and prognosis of COVID-19 patients [74]. Some studies have shown that LDH has a poor prognosis with COVID-19 [67,75]. According to the findings of this study, the serum level of LDH in COVID-19 patients related to the severity of the disease had a significant decrease compared to the control group. ...
Introduction
Understanding the mechanisms and identifying effective treatments for the COVID-19 outbreak are imperative. Therefore, this study aimed to assess the antioxidant status and oxidative stress parameters as potential pivotal mechanisms in asymptomatic, non-severe, and severe COVID-19 patients.
Methods
This study is a case–control study that was performed on patients referred to the Persian Gulf Martyrs Hospital of Bushehr University of Medical Sciences, Bushehr, Iran, from May 2021 to September 2021. A total of 600 COVID-19 patients (non-severe and severe group) and 150 healthy volunteers of the same age and sex were selected during the same period. On the first day of hospitalization, 10 ml of venous blood was taken from subjects. Then, hematological, biochemical, serological, antioxidant and oxidative stress parameters were determined.
Results
Our results indicated that ESR, CRP, AST, ALT, and LDH significantly augmented in the severe group as compared to the non-severe and normal groups ( P ≤ 0.05). It was observed that the levels of FRAP, G6PD activity, and SOD activity significantly reduced in the non-severe patients in comparison with the severe and normal groups ( P ≤ 0.05). We found that MDA content and NO metabolite markedly increased in severe patients as compared to the non-severe group.
Conclusions
Taken together, it seems that the balance between antioxidants and oxidants was disturbed in COVID-19 patients in favor of oxidant markers. In addition, this situation caused more aggravation in severe patients as compared to the non-severe group.
... Deaths among dialysis patients have increased during the pandemic [9][10]. CKD is a common comorbidity in elderly patients, associated with higher mortality rates [11][12][13][14]. ...
... . EC: Erythrocyte count (in ×10 12 /l); Gb: Amount of hemoglobin (in g/l); H: Hematocrit fraction (in %); P: Platelet counts (in ×10 9 /l); L: Leukocyte counts (in ×109 /l); MCV: Mean erythrocyte volume values (femtoliters [fl]); MCH: Average hemoglobin in erythrocyte (pg); MCHC: Average Hb concentration index in erythrocyte (g/dL); RDW: Distribution range of red blood cells (in %); N%: Proportion of neutrophils (%); NEU: Neutrophil concentration (in ×10 9 /l); E%: Share of eosinophils (%); EOS: Eosinophils concentration (in %); B%: Presence of basophils (%); BASO: Basophil concentration (%); L%: Share of lymphocytes (%); LYM: Lymphocyte concentration (%); M%: Share of monocytes (%); MONO#: Monocyte concentration (%); & BSR: Blood sedimentation rate (mm/h) Results of a computed tomography (3D) scan in a patient (age 21) (reprinted with permission of the patient) ...
The study’s objective was to comprehensively assess kidney function alterations in patients with COVID-19. The study was carried out in Moscow (Russia) in 2021. 100 patients of 19-30 years old (51 females and 49 males) took part in the survey. The study collected participant data on basal urine, serum creatinine, and estimated glomerular filtration rate from medical histories before COVID-19 infection. COVID-19 diagnosis (delta strain) was confirmed by polymerase chain reaction test. Serum creatinine was measured, considering age and race. Micro-albuminuria levels from daily urine samples were established. Laboratory blood tests included quantitative indices of blood-forming elements, hemoglobin levels, and biochemical parameters. Based on the results, the study observed a slight increase in serum creatinine levels after COVID-19 infection, with concentrations of 78.4±6.4 mmol/L before infection and 87.5±7.7 mmol/L after the disease (p≥0.05). The microalbuminuria-creatinine ratio also showed an increase. The glomerular filtration rate in renal glomeruli declined from 93.3±10.1 mL/min/1.73 m2 before infection to 78.9±8.7 mL/min/1.73 m2 after the disease (p≥0.05). These findings suggest a trend towards decreased kidney function in young patients with moderate COVID-19 severity. However, normoalbuminuric compared to creatinine was significantly higher than normal after COVID-19. Urine tests indicated a trend of decreased renal glomerular filtration rate. Clinical symptoms included high temperature, weakness, cough, and, in some cases, liquid stools. Laboratory findings revealed significant deviations in hematocrit, neutrophil, and eosinophil concentrations. Parallel tests focusing on cystatin C and beta-2 macroglobulin are recommended to assess kidney function and identify potential dysfunction.
... The process of regeneration has been studied extensively in preclinical models and factors such as the hepatocyte growth factor (HGF), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and signal transducer and activator of transcription 3 (STAT3), whilst Notch and Yap pathways have been found to be important in the regenerative process. During the era of COVID-19, the role of angiotensin-converting enzyme II receptors (ACEII) has been emphasized [6][7][8][9]. Studies have shown that ACEII is over-expressed early after partial hepatectomy and is sustained until the termination of the regenerative process [6][7][8][9]. ...
... During the era of COVID-19, the role of angiotensin-converting enzyme II receptors (ACEII) has been emphasized [6][7][8][9]. Studies have shown that ACEII is over-expressed early after partial hepatectomy and is sustained until the termination of the regenerative process [6][7][8][9]. Studies regarding the ACEII levels following liver resection in humans are lacking. ...
Background:
Inflammation and the associated immune pathways are among the most important factors in liver regeneration after living donor hepatectomy. Various biomarkers, especially liver function tests, are used to show liver regeneration. The aim of this study was to evaluate the course of liver regeneration following donor hepatectomy (LDH) by routine and regeneration-related biomarkers.
Method:
Data from 63 living liver donors (LLDs) who underwent LDH in Inonu University Liver Transplant Institute were prospectively analyzed. Serum samples were obtained on the preoperative day and postoperative days (POD) 1, 3, 5, 10, and 21. Regenerative markers including alfa-fetoprotein (AFP), des carboxy prothrombin (DCP), ornithine decarboxylase (ODC), retinol-binding protein 4 (RBP4), and angiotensin-converting enzyme isotype II (ACEII) and liver function tests including alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), alkaline phosphatase (ALP) and total bilirubin levels were all analyzed.
Results:
The median age of the LLDs was 29.7 years and 28 LLDs were female. Eight LLDs developed postoperative complications requiring relaparotomy. The routine laboratory parameters including AST (<0.001), ALT (<0.001), ALP (<0.001), and total bilirubin (<0.001) showed a significant increase over time until postoperative day (POD) 3. For the regeneration-related parameters, except for the RBP4, all parameters including ACEII (p = 0.006), AFP (p = 0.002), DCP (p = 0.007), and ODC (p = 0.002) showed a significant increase in POD3. The regeneration parameters showed a different pattern of change. In right-lobe liver grafts, ACEII (p = 0.002), AFP (p = 0.035), and ODC (p = 0.001) showed a significant increase over time. DCP (p = 0.129) and RBP4 (p = 0.335) showed no significant changes in right-lobe liver grafts.
Conclusions:
Regenerative markers are increased in a sustained fashion following LDH. This is more prominent following right-lobe grafts which are indicative of progenitor-associated liver regeneration.
... Previous RNA-seq data in the human protein atlas database demonstrated expression of ACE2 in the liver [20]. In a mouse model of acute liver injury, ACE2 expression in the liver was downregulated on the first day, but it was elevated up to twice the normal level on the third day due to the compensatory proliferation of hepatocytes and liver cells [21,22]. Due to this upregulation, the liver is considered one of the most affected organs in COVID-19 infection. ...
... A recent study by Chai et al., using single cell RNA-seq data of two independent cohorts, reported a predominance of ACE2 expression in cholangiocytes (59%) compared to hepatocytes (2.6%) [68], suggesting a predominant cholestatic pattern. However, based on mice model of liver injury, there was a transient upregulation of ACE2 expression caused by a compensatory differentiation of cholangiocyte epithelial cells into hepatocytes [22]. Although other studies have showed the existence of the viral RNA in liver cells [69], liver histology obtained from positive COVID-19 patients did not show any intracytoplasmic or intranuclear viral inclusion bodies to suggest direct liver damage [70]. ...
BackgroundSARS-CoV-2-induced severe inflammatory response can be associated with severe medical consequences leading to multi-organ failure, including the liver. The main mechanism behind this assault is the aggressive cytokine storm that induces cytotoxicity in various organs. Of interest, hepatic stellate cells (HSC) respond acutely to liver injury through several molecular mechanisms, hence furthering the perpetuation of the cytokine storm and its resultant tissue damage. In addition, hepatocytes undergo apoptosis or necrosis resulting in the release of pro-inflammatory and pro-fibrogenic mediators that lead to chronic liver inflammation.AimsThe aim of this review is to summarize available data on SARS-CoV-2-induced liver inflammation in addition to evaluate the potential effect of anti-inflammatory drugs in attenuating SARS-CoV-2-induced liver inflammation.Methods
Thorough PubMed search was done to gather and summarize published data on SARS-CoV-2-induced liver inflammation. Additionally, various anti-inflammatory potential treatments were also documented.ResultsPublished data documented SARS-CoV-2 infection of liver tissues and is prominent in most liver cells. Also, histological analysis showed various features of tissues damage, e.g., hepatocellular necrosis, mitosis, cellular infiltration, and fatty degeneration in addition to microvesicular steatosis and inflammation. Finally, the efficacy of the different drugs used to treat SARS-CoV-2-induced liver injury, in particular the anti-inflammatory remedies, are likely to have some beneficial effect to treat liver injury in COVID-19.ConclusionSARS-CoV-2-induced liver inflammation is a serious condition, and drugs with potent anti-inflammatory effect can play a major role in preventing irreversible liver damage in COVID-19.
... Дані свідчать, що у 14,8 -53,1 % пацієнтів із COVID-19 має місце підвищення рівня аланінамінотрансферази (АЛТ) і аспар татамінотрансферази (АСТ) та незначне/помірнебілірубіну в сироватці крові. Повідомлено про збільшення вмісту -глутамінтрансферази (ГГТП) у 54 % хворих на COVID-19 [1,9,14,29,31]. За даними епідеміологічного дослідження, більшість № 4 (114) • 2020 | СУЧАСНА ГАСТРОЕНТЕРОЛОГІЯ ОГЛЯДИ уражень печінки були тимчасовими і перебігали у легкій формі, але у деяких пацієнтів відзначене тяжке ураження печінки. Частота уражень печінки була вищою у хворих із тяжким перебігом COVID-19. ...
... Це вказує на можливість прямої дії вірусної інфекції на клітини печінки. Крім того, за даними автопсії, у хворих на ГРВІ мали місце велика кількість мітотичних клітин печінки, балонна дегенерація гепатоцитів, легке запалення, помірна інфільтрація лімфоцитів, стеатоз і центральний часточковий некроз у поєднанні з апоптозом [9]. Є дані, що специфічний для SARS-CoV білок 7a може індукувати клітинний апоптоз у різних органах (зокрема легенях, нирках та печінці) через каспазний шлях, що також підтверджує можливість прямої атаки SARS-CoV на тканини печінки [21]. ...
Коронавірусну хворобу 2019 (COVID‑19) уперше зареєстровано у грудні 2019 р. у м. Ухані (провінція Хубей, КНР). 11 березня 2020 р. COVID‑19 визнано ВООЗ пандемією. Станом на 31 травня 2020 р. зафіксовано понад 6 млн випадків. Етіологічним чинником захворювання є новий коронавірус тяжкого гострого респіраторного синдрому‑2 (SARS‑CoV‑2), який належить до роду β‑коронавірусів, як і відомі збудники цієї родини — SARS і коронавірус близькосхідного респіраторного синдрому (MERS). Унаслідок захворювання близько 350 тис. осіб померли. Понад 2,5 млн осіб одужало. Доведено, що SARS‑CoV‑2 може уражати всі органи та системи організму (легені (пневмонія, респіраторний дистрес‑синдром), головний мозок (енцефаліт), органи серцево‑судинної системи, нирки, органи шлунково‑кишкового тракту (ШКТ)). До основних клінічних симптомів COVID‑19 належать підвищення температури тіла, вияви з боку респіраторної системи (біль у горлі, рідше — нежить, втрата та/або зміна смаку і нюху, сухий кашель, задуха, біль у грудях тощо), а також симптоми з боку ШКТ (погіршення апетиту, нудота та/або блювання, діарея, біль у животі, підвищення рівня печінкових трансаміназ, загострення хронічних захворювань ШКТ (запальних захворювань кишечника тощо)). Дані китайських досліджень засвідчили, що РНК SARS‑CoV‑2 наявна не лише у матеріалі, отриманому з дихальних шляхів, а й у зразках випорожнень заражених пацієнтів. Ці факти демонструють здатність SARS‑CoV‑2 активно впливати на органи ШКТ і реплікуватися в ньому, що має важливе значення для вибору тактики діагностики та лікування захворювання, а також для запобігання поширенню інфекції. Численні дослідження показали різний ступінь ураження печінки у пацієнтів, інфікованих SARS‑CoV‑2. У тематичних дослідженнях COVID‑19 не з’ясовано точну причину ураження печінки, відсутні чіткі докази взаємодії між ушкодженням печінки та COVID‑19. Дослідження тривають. Через низький рівень обізнаності лікарів щодо впливу COVID‑19 на органи ШКТ доцільно розглянути існуючі дані з метою підвищення ефективності діагностики, лікування та динамічної курації пацієнтів. Висвітлено особливості впливу SARS‑CoV‑2 на органи ШКТ. Особливу увагу приділено ураженню печінки при захворюванні на COVID‑19, а також впливу печінкових ускладнень на ефективність лікування та прогноз COVID‑19.
... Both murine studies and human tissue studies have depicted an increase in ACE2r expression following liver injury and cirrhosis [124,125]. Findings suggest that the upregulation of ACE2r was secondary to compensatory proliferation of hepatocytes that were derived from bile duct epithelial cells [126]. It could be deducted that an initial liver insult results in upregulation of ACE2r, which may subsequently create an environment that supports greater invasion and pronounced hepatocyte injury by the SARVS-CoV2 virus, although such a hypothesis has not been proven. ...
Background
Our study aimed to describe the group of severe COVID-19 patients at an institutional level, and determine factors associated with different outcomes.
Methods
A retrospective chart review of patients admitted with severe acute hypoxic respiratory failure due to COVID-19 infection. Based on outcomes, we categorized 3 groups of severe COVID-19: (1) Favorable outcome: progressive care unit admission and discharge (2) Intermediate outcome: ICU care (3) Poor outcome: in-hospital mortality.
Results
Eighty-nine patients met our inclusion criteria; 42.7% were female. The average age was 59.7 (standard deviation (SD):13.7). Most of the population were Caucasian (95.5%) and non-Hispanic (91.0%). Age, sex, race, and ethnicity were similar between outcome groups. Medicare and Medicaid patients accounted for 62.9%. The average BMI was 33.5 (SD:8.2). Moderate comorbidity was observed, with an average Charlson Comorbidity index (CCI) of 3.8 (SD:2.6). There were no differences in the average CCI between groups(p = 0.291). Many patients (67.4%) had hypertension, diabetes (42.7%) and chronic lung disease (32.6%). A statistical difference was found when chronic lung disease was evaluated; p = 0.002. The prevalence of chronic lung disease was 19.6%, 27.8%, and 40% in the favorable, intermediate, and poor outcome groups, respectively. Smoking history was associated with poor outcomes (p = 0.04). Only 7.9% were fully vaccinated. Almost half (46.1%) were intubated and mechanically ventilated. Patients spent an average of 12.1 days ventilated (SD:8.5), with an average of 6.0 days from admission to ventilation (SD:5.1). The intermediate group had a shorter average interval from admission to ventilator (77.2 hours, SD:67.6), than the poor group (212.8 hours, SD:126.8); (p = 0.001). The presence of bacterial pneumonia was greatest in the intermediate group (72.2%), compared to the favorable group (17.4%), and the poor group (56%); this was significant (p<0.0001). In-hospital mortality was seen in 28.1%.
Conclusion
Most patients were male, obese, had moderate-level comorbidity, a history of tobacco abuse, and government-funded insurance. Nearly 50% required mechanical ventilation, and about 28% died during hospitalization. Bacterial pneumonia was most prevalent in intubated groups. Patients who were intubated with a good outcome were intubated earlier during their hospital course, with an average difference of 135.6 hours. A history of cigarette smoking and chronic lung disease were associated with poor outcomes.
... 24 In animal model, liver injury is associated with upregulation of ACE2 expression in liver. 25 More research is needed to investigate the correlation between SARS-CoV-2 infection and ACE 2 in the liver of COVID-19 patients. ...
Background and Aim
Currently, SARS‐CoV‐2 is still spreading rapidly and globally. A large proportion of patients with COVID‐19 developed liver injuries. The human‐induced pluripotent stem cell (iPSC)‐derived hepatocytes recapitulate primary human hepatocytes and have been widely used in studies of liver diseases.
Methods
To explore the susceptibility of hepatocytes to SARS‐CoV‐2, we differentiated iPSCs to functional hepatocytes and tried infecting them with different MOI (1, 0.1, 0.01) of SARS‐CoV‐2.
Results
The iPSC‐derived hepatocytes are highly susceptible to virus infection, even at 0.01 MOI. Other than the ancestral strain, iHeps also support the replication of SARS‐CoV‐2 variants including alpha, beta, theta, and delta. More interestingly, the ACE2 expression significantly upregulated after infection, suggesting a vicious cycle between virus infection and liver injury.
Conclusions
The iPSC‐derived hepatocytes can support the replication of SARS‐CoV‐2, and this platform could be used to investigate the SARS‐CoV‐2 hepatotropism and hepatic pathogenic mechanisms.
... Computational approaches, such as gene expression analysis, have emerged as valuable tools in understanding COVID-19 pathogenesis and its effects on liver metabolism [9,10]. By evaluating changes in gene expression, researchers have identified hub genes associated with COVID-19 [11], offering insights into disease progression and potential therapeutic targets. ...
Many metabolic processes at the molecular level support both viral attack strategies and human defenses during COVID-19. This knowledge is of vital importance in the design of antiviral drugs. In this study, we extracted 18 articles (2021–2023) from PubMed reporting the discovery of hub nodes specific for the liver during COVID-19, identifying 142 hub nodes. They are highly connected proteins from which to obtain deep functional information on viral strategies when used as functional seeds. Therefore, we evaluated the functional and structural significance of each of them to endorse their reliable use as seeds. After filtering, the remaining 111 hubs were used to obtain by STRING an enriched interactome of 1111 nodes (13,494 interactions). It shows the viral strategy in the liver is to attack the entire cytoplasmic translational system, including ribosomes, to take control of protein biosynthesis. We used the SARS2-Human Proteome Interaction Database (33,791 interactions), designed by us with BioGRID data to implement a reverse engineering process that identified human proteins actively interacting with viral proteins. The results show 57% of human liver proteins are directly involved in COVID-19, a strong impairment of the ribosome and spliceosome, an antiviral defense mechanism against cellular stress of the p53 system, and, surprisingly, a viral capacity for multiple protein attacks against single human proteins that reveal underlying evolutionary–topological molecular mechanisms. Viral behavior over time suggests different molecular strategies for different organs.
... Moreover, abnormalities in coagulation parameters, including D-dimer and fibrinogen levels, have been linked to an increased risk of thromboembolic events and mortality [6,7]. Liver dysfunction, characterized by elevated levels of liver enzymes such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST), has been observed in a subset of COVID-19 patients, indicating potential hepatocellular injury [8,9]. ...
Background: Coronavirus disease 2019 (COVID-19) has had a significant impact on global health and healthcare systems. This retrospective study aimed to assess the association between biochemical parameters and outcomes in COVID-19 patients in Jazan, Saudi Arabia.
Methods: After establishing the inclusion criteria and obtaining ethical approval, data from 156 reverse transcriptase-polymerase chain reaction (RT-PCR)-confirmed COVID-19 patients were collected from electronic medical records from a general hospital in Samtah, Jazan, from April 2020 to October 2021. The collected data included patient demographics and liver, kidney, heart, and electrolyte function marker levels. Descriptive, inferential, and principal component analyses were conducted.
Results: Survival rates varied according to age and body mass index (BMI). Statistical analysis demonstrated that the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), sodium (Na), potassium (K), blood urea nitrogen (BUN), creatinine (Cr), creatine kinase (CK), CK myocardial band (MB), and lactate dehydrogenase (LDH) were significantly higher (P < 0.05) than the reference values, as assessed using the one-sample t-test. Principal component analysis (PCA) also revealed an underlying pattern in the variation of these biochemical markers. These findings suggest that certain biochemical parameters may serve as useful indicators for monitoring the condition of COVID-19 patients.
Conclusion: This retrospective study in Jazan, Saudi Arabia highlights the association between biochemical parameters and outcomes in COVID-19 patients. Elevated levels of markers of liver, kidney, heart, and electrolyte function suggest organ damage and dysregulation. The pattern identified through PCA provides insights into disease severity. Monitoring these parameters may serve as valuable indicators for assessing COVID-19 patients. Further research is needed to validate these findings, explore their potential for personalized treatment strategies, and improve patient outcomes during the ongoing pandemic.
... SARS-CoV-2 may be able to infiltrate the liver via constitutively expressed ACE2, primarily on cholangiocytes and, to a reduced degree, hepatocytes [263,264]. As a result, it has been proposed that liver damage attributed to SATS-CoV-2 is mainly caused by biliary tract infection via cholangiocytes, with secondary damage to and compensatory proliferation of hepatocytes [175,265]. The hepatic sinusoidal endothelium has extremely reduced ACE2 expression compared to the endothelial linings of other organs [258]. ...
... Complicações como estase biliar resultando em lesão hepática e dilatação de vias biliares, lesão celular pancreática direta, efeitos diretos de lesão celular endotelial renal e resposta inflamatória com coagulopatia, cistite intersticial ou hemorrágica e infartos de órgãos sólidos podem ocorrer em pacientes com COVID-19 [11][12][13] . ...
Introdução: A pandemia causada pelo SARS-CoV-2 teve início no ano de 2020 e ocasionou mudanças importantes no número de transplantes realizados nos hospitais e nos protocolos de admissão de candidatos para realização do procedimento. A Associação Brasileira de Transplante de Órgãos (ABTO) recomendava não realizar transplante de doadores com infecção COVID-19 ativa, teste positivo ou com Síndrome Respiratória Aguda Grave. As repercussões hepáticas relacionadas a COVID-19 são apresentadas em alguns relatos presentes na literatura médica. Estão bem documentadas as alterações hepáticas decorrentes de outros coronavírus tais como SARSCoV e MERS-CoV. O Hospital de Clínicas da Universidade Estadual de Campinas é um centro terciário que realiza transplantes de órgãos sólidos. Objetivos: Realizar a análise retrospectiva descritiva perioperatória dos transplantes hepáticos no contexto da pandemia por SARS-CoV-2 realizados no hospital das clínicas da Universidade Estadual de Campinas no período de março de 2020 a julho de 2021. Materiais e Métodos: Estudo retrospectivo, descritivo de coorte longitudinal baseado na revisão dos prontuários dos pacientes submetidos ao transplante hepático no contexto da pandemia por SARS-CoV-2 no período de março de 2020 a julho de 2021 no hospital de clínicas da Universidade Estadual de Campinas. Resultados: A análise retrospectiva foi realizada em 57 pacientes no período. Apenas 1 paciente precisou ser excluído por ter menos de 18 anos. Dos 56 pacientes, 52 realizaram coleta do exame laboratorial RT-PCR e tomografia (TC) de tórax. Desses 52 pacientes apenas 2 positivaram o exame, um pré transplante (TX) e um no pós-operatório (pós-op). Em relação às TC de tórax nenhuma apresentava alterações típicas para COVID pré-TX, no pós-op 4 pacientes apresentaram TC típicas. A média de idade foi de 55,86 anos. A taxa de mortalidade foi de 38% e nenhum óbito foi atribuído ao COVID 19. A escala de MELDNa média foi de 20,94. Conclusão: O presente estudo realizado no Hospital de Clínicas da Unicamp analisou a associação clínica, laboratorial e radiológica para melhor elucidar as variáveis determinadas pela COVID-19 no seu diagnóstico e manejo intra-hospitalar. Conclui-se que a pandemia por SARS-CoV-2 teve impacto na rotina de realização do transplante hepático mundialmente e no serviço no qual o estudo foi realizado.
... Complications such as bile stasis resulting in liver damage and dilated bile ducts, direct pancreatic cell damage, direct effects of renal endothelial cell damage, and inflammatory response with coagulopathy, interstitial or hemorrhagic cystitis or solid organ infarcts can occur in COVID-19 patients [11][12][13] . ...
Introduction
SARS-CoV-2 began in 2020 and caused important changes in the number of transplants performed in hospitals and in the protocols for admitting candidates to perform the procedure. The Brazilian Association of Organ Transplantation (ABTO) recommends not performing transplants from donors with active COVID-19 infection, positive test results or with Severe Acute Respiratory Syndrome. The hepatic repercussions related to COVID-19 are presented in some reports in the medical literature. Liver changes resulting from other corona viruses such as SARS-CoV and MERS-CoV are well documented. The Hospital de Clínicas of the State University of Campinas is a tertiary center that performs solid organ transplants.
Objectives
To carry out a perioperative, retrospective, descriptive analysis of liver transplants in the context of the SARS-CoV-2 pandemic carried out at the Hospital das Clínicas of the State University of Campinas from March 2020 to July 2021.
Materials and Methods
Retrospective, descriptive, longitudinal cohort study based on the review of medical records of patients undergoing liver transplantation in the context of the SARS-CoV-2 pandemic from March 2020 to July 2021 at the clinical hospital of the State University of Campinas.
Results
Retrospective analysis was performed on 57 patients in the period. Only 1 patient needed to be excluded because he was under 18 years old. Of the 56 patients, 52 underwent RT-PCR laboratory testing and chest tomography (CT). Of these 52 patients, only 2 tested positive, one pre-transplant (TX) and one post-operatively (post-op). Regarding chest CT scans, none of them showed typical changes for COVID pre-TX, in the post-op 4 patients presented typical chest CT scans. The average age was 55.86 years. The mortality rate was 38% and no deaths were attributed to COVID 19. The average MELD-Na scale was 20.94.
Conclusion
The present study carried out at the Hospital de Clínicas da Unicamp analyzed the clinical, laboratory and radiological association to better elucidate the variables determined by COVID-19 in its diagnosis and in-hospital management. It is concluded that the SARS-CoV-2 pandemic had an impact on the routine of liver transplantation worldwide and on the service in which the study was carried out.
Descriptors
COVID 19; Chest CT; Liver Transplant; RT-PCR
... One answer is the similarity of COVID-19 and SARS-CoV that can attack the human body by binding to the human angiotensin-converting enzyme 2 receptor. This reaction causes liver tissue injury by upregulation of ACE2 expression in liver tissue caused by a compensatory proliferation of hepatocytes derived from bile duct epithelial cells [14]. The other theory is that COVID-19 causes direct and indirect damages to the digestive system by an inflammatory response. ...
Background: Various digestive symptoms have been frequently reported in a significant portion of patients infected with the virus since the outbreak of Coronavirus Disease 2019 (COVID-19). Most patients with COVID-19 have a fever accompanied by respiratory signs and symptoms, such as cough and dyspnea. We present 36 cases with a chief complaint of Gastrointestinal (GI) symptoms along with respiratory symptoms. In this study, we aimed at investigating the prevalence and outcomes of COVID-19 patients with digestive symptoms. Methods: A variety of observed GI symptoms included nausea and vomiting (72.2%), diarrhea (25%), abdominal pain (19.4%), loss of appetite (14%), and anosmia (14%). The most nonGI symptoms were dyspnea (66.7%), fever (66.7%), dry cough (58.3%), myalgia (52.4%), and others. Six patients (16.6%) were critically ill, 7 (19.4%) were in stable condition, and 23 patients (64%) showed moderate symptoms. Among the patients, 7 (19.5%) needed critical care and were admitted to ICU. Leucopenia, lymphopenia, and elevated acute-phase proteins were other features observed in these patients. The most common antiviral regimen was hydroxychloroquine and oseltamivir. Finally, 32 patients (89%) were discharged, and 4 (11%) died. Conclusion: This case series study highlights that patients with COVID-19 are prone to GI symptoms along with fever and respiratory symptoms. Patients may even present with digestive symptoms and without any respiratory symptoms. Hence, clinicians should pay more attention to these patients and help diagnose COVID-19 earlier to s t
... A retrospective study of patients treated with tocilizumab showed no evidence of adverse liver effects (249). Other studies reported DILI after using tocilizumab and mild to moderate elevations in liver enzyme levels (219,221). ...
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.
... Correspondingly, singlecell lineage tracing technology in combination with immunohistochemistry (IHC) techniques has demonstrated a relatively low expression pattern of ACE2 (0.31%) in biliary duct cholangiocytes of healthy hepatic tissues and slight ACE2 expression in diseased hepatocytes (31). The transgenic mouse models of severe hepatic impairment have also suggested an up-regulation of ACE2 expression in hepatocytes originating from bile duct epithelial cells, which readjusted to normal levels when liver function was restored, and hepatocyte proliferation was blocked (21,32). Hepatic impairment, as the first atypical clinical manifestation of acute COVID-19, is extremely rare. ...
Context: The uninterrupted dissemination and transmission of COVID-19 brought enormous jeopardy and public-health urgency during past three years. Some patients, who recovered from the infection, develop persistent symptoms and organ dysfunction for weeks or even months; conditions that are called long COVID. Among multiple COVID-related complications, positive individuals suffer from lesser to greater degrees of intrahepatic and extrahepatic complications that principally mediated by ACE2 receptors. Evidence acquisition: We reviewed manuscripts from PubMed, Google Scholar and Web of Science on underlying COVID-19-linked clinical relevance and potential pathogenesis of liver complications during short COVID, as well as long COVID with no time limitation. Results: Liver impairment needs a large-scale and persistent follow-up as it may be multivariate in nature. During COVID-19, physicians must assess whether hepatopathy is associated with hepatic disorders, medications utilized for the COVID-19 therapy, viral antigenic outcomes progression to a complicated course. In the context of COVID-19, physicians report that potential pathophysiological approaches to hepatic failure in critical patients further could be leading to deep vein thrombosis, myocardial infarction, venous thromboembolism, and acute kidney injury. These complications might be either reversible, or irreversible with extended manifestations that mostly occur as a consequence of long COVID in the post-COVID era. Moreover, pre-existing cardiovascular and digestive tract problems tend to be highly correlated with adverse clinical outcomes and the highest fatality rate. Potential drug-disease interactions adversely influencing COVID-19 subjects and persistent comorbidities are also getting a major consideration. Conclusion: The assessment of whether the upshot of hepatic-associated co-morbidities in COVID-19 status can improve an acceptable personalized therapeutic strategy considering these specific tropisms.
... An increase in bilirubin levels is less common, and an increase in gamma-glutamyl transferase activity can be detected in 54% of patients with COVID-19. Several authors [25,26,27] suggest the following possible mechanisms of liver damage in COVID-19: -direct cytopathic effect of the SARS-CoV-2 virus on the liver (penetration of the virus into the cell occurs due to the binding of the S-protein of the virus to the ACE2 receptors, a significant increase in the expression of which is manifested in cholangiocytes (59.7% of cells) and hepatocytes (2.6% of cells); -immune inflammation (cytokine 'storm' within the systemic inflammatory response); -drug-induced liver damage due to the use in the treatment of drugs that may potentially have a hepatotoxic effect. ...
Introduction and objective:
Past COVID-19 significantly worsens Chronic viral hepatitis C patients with concomitant NAFLD. The aim of the study was to assess effectiveness of including mineral water in the rehabilitation complex in patients with chronic hepatitis C with concomitant non-alcoholic fatty liver disease who contracted COVID-19.
Material and methods:
71 patients with chronic hepatitis C with concomitant NAFLD wo contracted COVID-19 were examined. Group I (control) - 39 patients prescribed dietary nutrition and exercise therapy. Group II (main) - 32 patients, in addition to the above, received packaged 'Shayanskaya' mineral water. Methodology comprised anamnestic, anthropometric and clinical, general clinical, biochemical, serological, and molecular genetic (markers of hepatitis C virus, HCV RNA PCR (qualitative and quantitative determination, genotyping), enzyme-linked immunosorbent assay, ultrasonographic examination of digestive organs, and statistical methods.
Results:
Due to the treatment, there were significant improvements in carbohydrate and lipid metabolism, as well as the cytokine profile.
Conclusions:
The effectiveness was established of the use of silicon low-mineralized bicarbonate sodium mineral water in the complex rehabilitation of patients with chronic hepatitis C and suputor NAFLD after contracted COVID-19. There was a significant improvement in the clinical course of the disease and improvement in the functional state of the liver.
... And it quickly attracted global attention [1] [2]. With the increase of confirmed cases, the novel coronavirus pneumonia (NCP) epidemic has been listed by the World Health Organization as a "public health emergency of international concern", and it has also attracted great attention from the governments of our country and other countries [3]. According to immunology, the most effective way to control the virus is to vaccinate. ...
As the new crown virus epidemic becomes more and more intense around the world, more and more people are pinning their hopes of containing the epidemic on the development of new crown virus vaccines. At present, the new crown vaccines developed by countries around the world are gradually being marketed. This article summarizes the development of five major new coronavirus vaccines: inactivated vaccines, live attenuated vaccines, adenovirus vector vaccines, recombinant protein vaccines, and nucleic acid vaccines. It also illustrates relevant assays for the new coronavirus.
... Патофизиологическая основа полиорганного по вреждения может быть связана с органоспецифиче ским иммунным ответом на коронавирус или ответом на гипоксемию, цитокиновый шторм и лекарственные препараты [5]. В ранее проведенных исследованиях было установлено, что вирусы SARS и MERS могут вызывать повреждение печени [6,7,8]. Это соотно сится с информацией о частом повышении активно сти аминотрансфераз у госпитализированных пациен тов с COVID19 [3]. ...
Objective. To identify risk factors for fatal outcome and COVID-19-associated liver damage in hospitalized adult patients with coronavirus infection. Materials and Methods. In a retrospective cohort study, 389 cases of patients with coronavirus infection complicated by bilateral viral pneumonia were studied. Demographic characteristics, clinical features of the course of the disease, anamnestic data, results of laboratory and instrumental methods of examination were analyzed and correlated with mortality. At the time of admission, the following were taken into account: fever, severity of the patient’s condition according to COVID-19 classification of severity, body mass index (BMI), oxygen saturation (SpO2), percentage of lung tissue damage according to computed tomography (CT). Laboratory indices of biochemical blood analysis were assessed in dynamics: alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin, total protein, albumin, C-reactive protein (CRP). Data analysis was performed using the R programming language (ver. 4.1.1.). Results. The following risk factors, assessed at the time of hospitalization, increased the likelihood of death: severe and extremely severe condition of the patient (RR = 4.77; 95% CI: 3.33–6.83); SpO2 less than 93% (RR = 3.76; 95% CI: 2.57–5.49); diabetes mellitus (RR = 2.94; 95% CI: 2.01–4.30); lung tissue damage CT-3 and CT-4 (RR = 2.66; 95% CI: 1.79–3.75); concomitant chronic pyelonephritis and chronic kidney disease (CKD) (RR = 2.59; 95% CI: 1.79–3.74); age 65 years and older (RR = 2.50; 95% CI: 1.70–3.67); ischemic heart disease (IHD) (RR = 2.39; 95% CI: 1.42–4.01); an increase in the level of CRP more than 15 mg/l (RR = 2.22; 95% CI: 1.16–4.24); BMI 35 kg/m2 or more (RR = 1.89; 95% CI: 1.28–2.77); AST level more than 2 upper limit of normal (ULN) (RR = 1.75; 95% CI: 1.20–2.55). Risk factors for an increase in AST more than 2 ULN were: SpO2 less than 93% (RR = 1.53; 95% CI: 1.15– 2.03), severe and extremely severe course of coronavirus infection (RR = 1.83; 95% CI: 1.38–2.43), concomitant chronic liver disease (RR = 1.45, 95% CI: 1.08–1.95). Conclusions. Risk factors for fatal COVID-19 in hospitalized patients are: severe and extremely severe initial condition of the patient, oxygen saturation less than 93%, lung tissue damage more than 50%, age older than 65 years, presence of concomitant diabetes mellitus, chronic pyelonephritis and CHD, CHD, obesity, increased CRP level more than 15 mg/l, and AST more than 70 units/l. Elevation of AST over 2 IU/L can be considered as one of the prognostic laboratory markers of adverse prognosis COVID-19.
... Although the main mechanism of gastrointestinal manifestations caused by the new coronavirus is still unclear, foreign scholars have proposed two possible mechanisms. They believe that SARS-CoV-2, like SARS-CoV, can interact with ACE-2 receptors combined [18]. Pan et al. proposed that SARS-CoV-2 itself can cause a gastrointestinal flora imbalance, which in turn leads to a series of gastrointestinal symptoms in patients [19]. ...
Background: In the face of the COVID-19 pandemic, surgical personnel and patients experience many diagnosis and treatment-related challenges. COVID-19 is highly virulent, and thus, immediate, safe, and effective solutions to the patients’ management are required. Research collaboration and knowledge dissemination are necessary to optimize medical and surgical approaches to the individual patients’ needs. Gastric manifestations of SARS-CoV-2 infection are not uncommon and may even precede respiratory symptoms. Common gastrointestinal symptoms include loss of appetite, diarrhea, nausea, vomiting and abdominal pain. Case Presentation: A 50-year-old male patient complained of "blood in the stool and tenesmus for half a year" and was admitted to the hospital on March 2, 2023. Half a year ago, the patient had blood in the stool without obvious incentives, the bleeding was bright red, the habit of defecation changed, the stool became thinner, and the frequency of defecation increased, 3-5 times a day, and the amount was not much. At that time, he went to a regular medical institution for any treatment measures.
... The exact mechanism of impaired liver function in COVID-19 infection is not fully understood, but it appears that the SARS-CoV-2 virus may cause direct liver damage. Viral hepatotropism can also be attributed to the relatively high expression at this level of the ACE2 receptor, which is the gateway to the cell (in cholangiocytes, rather than in hepatocytes), making them vulnerable to viral attack [17]. This hypothesis is supported by increased circulating serum gamma-glutamyl transferase (GGT) levels in patients with COVID-19. ...
... Despite being frequently overlooked, involvement of the gastrointestinal (GI) tract and the hepatic system is now being increasingly reported (Cha, 2020 3 Liver function tests (LFTs) include measures of hepatocyte injury such as Aspartate aminotransferase (AST) and Alanine aminotransferase (ALT), bile duct injury or cholestasis like alkaline phosphatase, and gamma-glutamyltransferase, (GGT), markers of hepatic clearance/biliary secretion capacity (bilirubin), as well as measures of synthetic capacity (prothrombin time and albumin) (Bertolini, 2020). A varying degree of liver test abnormalities has been described in COVID-19 affected patients (Guan, 2020), elevated markers of liver cell injury (ALT, AST) are more common . ...
The current pandemic caused by SARS-CoV-2 originated in the city of Wuhan, China with an outbreak of pneumonia. The reported symptoms were mostly respiratory, but mounting evidence began to indicate that COVID-19 could reach other organs and systems. Among the gastrointestinal symptoms, liver involvement appears to be more common, with changes in liver enzymes (ALT and AST) being the first sign. Therefore, the present study aims to evaluate and discuss the hepatic manifestations in COVID-19 as the infection, manifestations, and drug effects. The study was based on a literature review, of a qualitative nature and an exploratory type. The mechanism that SARS-CoV-2 uses to reach the liver is still uncertain, there are currently 3 hypotheses: ACE2 receptors in cholangiocytes, cytokine storm, and drug-induced liver injury, due to the increase in the indiscriminate use of hepatotoxic drugs without scientific comprovation, hydroxychloroquine can lead to fulminant hepatic failure and azithromycin potentiates these effects, the role of remdesivir on the liver are still uncertain. Liver damage in mild cases of COVID-19 can be transient, but doctors should monitor and be alert to any changes in liver enzymes. When severe liver damage occurs, liver protective drugs have usually been given to these patients. Thus, this review provides a review of hepatic impairment and the management of patients considering the main studies carried out to date.
... However, it has been recently demonstrated that hypoxia, systemic inflammation, and pre-existing liver disease could induce ACE2 and TMPRSS2 expression in hepatocytes, thus potentiating viral hepatotropism and increasing hepatic susceptibility to SARS-CoV-2 infection [28][29][30]. Moreover, in vitro experiments showed that the spike protein significantly increases the affinity for its receptor when it is pre-incubated with trypsin [18]. ...
The liver is a secondary and often collateral target of COVID-19 disease but can lead to important consequences. COVID-19 might directly cause a high number of complications in patients with pre-existing chronic liver disease, increasing their risk of hepatic decompensation. Moreover, it also determines indirect consequences in the management of patients with liver disease, especially in those suffering from decompensated cirrhosis and HCC, as well as in the execution of their follow-up and the availability of all therapeutic possibilities. Liver imaging in COVID-19 patients proved to be highly nonspecific, but it can still be useful for identifying the complications that derive from the infection. Moreover, the recent implementation of telemedicine constitutes a possible solution to both the physical distancing and the re-organizational difficulties arising from the pandemic. The present review aims to encompass the currently hypothesized pathophysiological mechanisms of liver injury in patients with COVID-19 mediated by both the direct invasion of the virus and its indirect effects and analyze the consequence of the pandemic in patients with chronic liver disease and liver tumors, with particular regard to the management strategies that have been implemented to face this worldwide emergency and that can be further improved.
... (14) La interrelación entre las patologías que comprenden el síndrome metabólico y la COVID-19 se han estado demostrando en varios estudios. (15)(16)(17) El estrés oxidativo es consecuencia del empleo de oxígeno en la respiración aeróbica por organismos vivientes, y es, además, una condición persistente de un desequilibrio entre la generación de especies reactivas de oxígeno (ERO) y la habilidad del sistema endógeno antioxidante para neutralizarlas. La teoría del estrés oxidativo ha estado confirmada en muchos estudios, los cuales han demostrado que el mantenimiento de homeostasis celular, la estabilidad biomolecular y la integridad son cruciales para la longevidad celular y el envejecimiento exitoso. ...
Metabolic syndrome comprises a set of cardiovascular risk factors tightly associated to obesity and insulin resistance that propitiates cardiovascular disease and type 2 diabetes mellitus. Its prevalence raises around the world, causing a pro-thrombotic and pro-inflammatory status which in the current context of the COVID-19 pandemic worsens the clinical characteristics of the patients. The objective was to analyze the current status of the scientific knowledge in the research on the interrelation between the metabolic disorders associated to proinflammatory condition, exacerbated in COVID-19 patients. Several combinations of descriptors were used in the review in PubMed, SciELO, Clinical Key and LILACS database, and the most recent articles were considered for the analysis and redaction. In the scientific literature a relevant role is attributed to the proinflammatory process that characterizes the metabolic syndrome manifestation as a risk factor, and in the complications in COVID-19 patients. The high and increasing prevalence worldwide of obesity, hypertension and type 2 diabetes mellitus-which are part of metabolic syndrome-indicates that they have not been given special attention; moreover, due to the inflammatory processes inherent in it and its lethal effects.
... Hepatic resection increases the susceptibility to SARS-CoV-2 due to increased expression of ACE-2 demonstrated in mouse models. (17) After hepatectomy, lifethreatening complications like post hepatectomy liver failure can affect the metabolism of drugs used in the treatment of COVID-19, and in turn, COVID-19 infections could be responsible for Post Hepatectomy Liver Failure. Lung injury due to COVID-19 is also an independent risk factor for morbidity and mortality after COVID-19.(18) ...
... First one or two days few patients may remain asymptomatic (Mason, 2020) and doesn't show any symptoms, and some patients show non-respiratory symptoms such as acute liver and heart injury, kidney failure and diarrhea Guan et al., 2020a;Guan et al., 2020b;Wang et al., 2020b). Due to the high concentration of ACE2 in the nasal mucosa, bronchi, lung, heart, esophagus, kidney, stomach, bladder and ileum these human organs are most vulnerable to SARS-CoV-2 infections (Zou et al., 2020). ...
COVID-19 is a pandemic malady caused by SARS-CoV-2, a novel coronavirus. It is a global threat that has affected 223 countries and territories all over the world. According to the WHO report as of April 06, 2022 coronavirus has affected 492,189,439 people globally with 6,159,474 confirmed deaths. The pandemic of COVID-19 has badly affected Bangladesh likewise many other countries of the world. According to Worldometer report on 06 April 2022 the number of confirmed cases of COVID-19 were 1,951,903 with 29,123 deaths, and 1,886,036 COVID-19 recoveries in Bangladesh. After originating from China, this notorious virus has been spread to almost all the countries of the world. Its spike protein aids in binding with the ACE2 receptors of the cell membrane resulting in cell entry, replication, and induction of inflammatory and pro-inflammatory responses leading to the pathogenic condition. The novel COVID-19 virus has structural and genetic similarity with its predecessors specially SARS-CoV and MERS-CoV. This review presents the existing literature on COVID-19 and discusses different aspects of COVID-19 including virology, etiology, epidemiology, pathogenesis, diagnosis, transmission and susceptibility and preventive measures of COVID-19.
... Direct hepatic infection was evidenced by showing SARS-CoV-2 particles in the cytoplasm of hepatocytes of COVID-19 patients [7,8]. Recent evidence suggests upregulated ACE2 expression in hepatocytes, triggered by inflammatory signals, such as type I interferon or IL-6 during SARS-CoV-2 infection [9,10]. SARS-CoV-2 directly contributed to cytopathy by conspicuous mitochondria swelling, endoplasmic reticulum dilatation, decreased glycogen granule, and impaired cell membranes in the hepatocytes [11]. ...
Coronavirus causes an outbreak of viral pneumonia that spread throughout the world. Liver injury is becoming more widely recognized as a component of the clinical picture of COVID-19 infection. Hepatitis with serum ALT elevation has been reported in up to half of patients. Patients with CLD were at a higher risk of decompensation with liver failure, hospitalization, and mortality. The percentage of acute liver injury (ALI) varied from 5 to 28%. COVID-19 hinders HCV elimination by 2030. It is recommended to continue treatment of chronic HCV and chronic HBV if already receiving treatment. Consider using antiviral therapy to prevent viral flare-ups in patients with occult or resolved HBV and COVID-19 who are receiving immunosuppressive agents. Patients with AIH do not have an increased risk of adverse outcomes even in high-risk areas. There is an association between MAFLD and disease progression. Patients with any type of cancer are at a higher risk of infection and are more likely to develop more severe clinical outcomes. Most societies advise against immunosuppressant modifications in patients with mild COVID-19, whereas in rare cases such as severe lymphopenia, worsening pneumonia, or bacterial or fungal superinfection, reduction or discontinuation of antiproliferative agents and lymphocyte-depleting therapies has been suggested.
... Then, it would be essential to explain theoretically that unlike the multisystem inflammatory damage seen in MIS-C, only liver was mainly injured in the Brodin and Arditi hypothesis. We had previously observed the direct cause of hepatic impairment in patients with COVID-19 , and proposed a mechanism of virus direct infection of neonatal hepatocytes via angiotensin converting enzyme (ACE) receptors, following liver damage and regeneration caused by cytokine storm during COVID-19 (Guan et al., 2020;Gao et al., 2020). It would be interesting to investigate the persistence of SARS-CoV-2 residuals in the liver tissue of children suffering sever acute hepatitis with unknown cause. ...
• MIS-C and severe acute hepatitis might share the common pathogenic mechanism. • SARS-CoV-2 persistence throughout multiorgan and tissues. • Relationship between COVID-19 vaccines and severe acute hepatitis worth investigating.
... While the exact cause of hepatic injury is uncertain, several factors have been associated with the cause of elevated serum transaminase levels in SARS-CoV-2-infected patients. Both the liver and bile duct cells express angiotensin-converting enzyme 2 (ACE2) receptors that are the binding site for cellular entry by SARS-CoV-2, resulting in deranged LFTs [16,17]. Another hypothesis points to immune-mediated liver injury that is cytokine storm, causing the release of multiple proinflammatory cytokines, particularly interleukin-6 (IL-6), which causes both pulmonary and extrapulmonary damage. ...
Background and objective
The coronavirus disease 2019 (COVID-19) pandemic has caused one of the most devastating healthcare crises in recent times and presented many diagnostic challenges and uncertainties. COVID-19 complicated by acute hepatic dysfunction is a well-described phenomenon, but its impact on maternal and perinatal outcomes is not well documented. In this study, we aimed to evaluate the maternal and neonatal outcomes in pregnant women with COVID-19 complicated by liver dysfunction and compare those with pregnant women with COVID-19 and normal liver function.
Methodology
This was a retrospective observational cohort study conducted at the Tata Main Hospital, Jamshedpur, a tertiary care hospital in eastern India. All COVID-19-positive pregnant women (n=249) admitted to the hospital from May 15, 2020, to August 15, 2021, were included in this study. Retrospective data collection was done using the medical records of these COVID-19-positive pregnant women and included the baseline characteristics, past medical history, obstetric history, clinical presentation, laboratory results, management modalities, and maternal and neonatal outcomes. Of note, 107 women were found to have acute liver function abnormality on admission and 142 women had normal liver function tests (LFTs). Pregnant women with normal LFTs were classified as group one and those with deranged LFTs as group two. Characteristics such as age, period of gestation, symptoms, associated comorbidities, laboratory results, management, and outcomes were compared across both groups.
Results
Out of the total 249 pregnant women with COVID-19 admitted during the study period, 42.97% (n=107) women had laboratory findings consistent with liver dysfunction and 142 women (57.03%) had a normal liver function. Significantly higher levels of lactate dehydrogenase (LDH), C-reactive protein (CRP), neutrophil-lymphocyte ratio (NLR), alanine transaminase (ALT), aspartate aminotransferase (AST), and total bilirubin levels were seen in pregnant women with hepatic dysfunction when compared to those with normal liver function. Among the 249 patients, the majority were asymptomatic or had mild disease, 12 women had moderate disease, and six women had severe COVID-19. All women with severe COVID-19 had deranged LFTs. There was no statistical difference in terms of obstetric management between pregnant patients with and without liver dysfunction. Out of the 107 women with deranged liver function, 18 women had a preterm birth, four had intrauterine fetal death, and one had neonatal death. Complications such as postpartum hemorrhage, the need for blood transfusions, sepsis and multiorgan failure, and mortality were more commonly seen in the group of pregnant women with hepatic dysfunction associated with COVID-19.
Conclusion
COVID-19 in pregnancy may cause deranged LFTs in these women. Pregnant women with COVID-19 complicated by liver dysfunction have been reported to have worse inflammation, higher disease severity, and more morbidity and mortality when compared to those without liver dysfunction. They are also at a higher risk of complications such as postpartum hemorrhage, the need for blood transfusion, sepsis, and multiorgan dysfunction.
... The virus might directly target the renal or hepatic system or indirectly through the inflammatory cytokine storm that resulted in altered renal and liver serum profiles. [1,4,31] However, serum globulin recorded a significant positive association with SpO 2 that might explain that raised immunoglobulin production as an immune response to defend the virus that would prevent the disease progression toward severity. ...
Background and objective:
This study explored the role of various laboratory biomarkers on inflammatory indices for predicting disease progression toward severity in COVID-19 patients.
Methods:
This retrospective study was conducted on 1233 adults confirmed for COVID-19. The participants were grouped undermild, moderate, and severe grade disease. Serum bio-inflammatory index (SBII) and systemic inflammatory index (SII) were calculated and correlated with disease severity. The study variables, including clinical details and laboratory variables, were analyzed for impact on the inflammatory indices and severity status using a sequential multiple regression model to determine the predictors for mortality. Receiver operating characteristics defined the cut-off values for severity.
Results:
Among the study population, 56.2%, 20.7%, and 23.1% were categorized as mild, moderate, and severe COVID-19 cases. Diabetes with hypertension was the most prevalent comorbid condition. The odds for males to have the severe form of the disease was 1.6 times (95% CI = 1.18-2.18, P = 0.002). The median (inter-quartile-range) of SBII was 549 (387.84-741.34) and SII was 2097.6 (1113.9-4153.73) in severe cases. Serum urea, electrolytes, gamma-glutamyl transferase, red-cell distribution width-to-hematocrit ratio, monocytopenia, and eosinopenia exhibited a significant influence on the SpO2, SBII, and SII. Both SBII (r = -0.582, P < 0.001) and SII (r = -0.52, P < 0.001) strongly correlated inversely with SpO2 values [Figures 3a and 3b]. More than 80% of individuals admitted with severe grade COVID-19 had values of more than 50th percentile of SBII and SII. The sensitivity and specificity of SBII at 343.67 for severity were 81.4% and 70.1%, respectively. SII exhibited 77.2% sensitivity and 70.8% specificity at 998.72.
Conclusion:
Serial monitoring of the routinely available biomarkers would provide considerable input regarding inflammatory status and severity progression in COVID-19.
... Abnormal liver biochemistry has likewise been described in individuals with Sars and Mers [20][21], hinting that the corona virus infection can lead to liver damage. However, it's uncertain if the coronavirus is directly responsible for the liver damage. ...
The coronavirus disease 2019 (COVID-19) is a viral respiratory illness which was first detected in Wuhan, Hubei Province, China. A few case studies demonstrated that 14–53% of the cases of COVID-19 reported abnormal levels of liver enzymes during disease progression. Patients with severe Hepatic injury is dysfunction.19 seem to have higher rates of hepatic -COVIDcommon in severe COVID-19 patients, which may be caused by direct injury to the bile duct cells by a virus or indirectly by a cytokine storm. The liver function should be evaluated in all symptomatic COVID-19 patients. In patients with pre-existing liver diseases, special attention should be paid to with severe liver persons Immunocompromised. monitoring and treatment illness, hepatocellular carcinoma, as well as liver transplant patients should have more intense surveillance and personalized therapy methods. Despite the fact that there has been little investigation on patients infected by covid-19 with pre-existing liver illness, the present extensive study casts light on liver disease care during Covid-19.
... Active replication of the virus in the human respiratory system leads to nonspecific symptoms, such as fever, myalgia, headache, and the major pathogeneses created by SARS-COV-2 are anaemia and pneumonia combined with acute cardiac injury. Many people infected by SARS-CoV-2 were found to be asymptomatic with respect to respiratory functions and suffered from other symptoms, such as kidney failure, heart injury, liver damage, and multiple organ failure [13][14][15][16][17]. SARS-CoV-2 replication rate is usually high in the upper respiratory tract (nasal cavity and pharynx) and low in the lower respiratory tract and gastrointestinal mucosa, which create low viremia [18,19]. ...
COVID-19, a dreaded and highly contagious pandemic, is flagrantly known for its rapid prevalence across the world. Till date, none of the treatments are distinctly accessible for this life-threatening disease. Under the prevailing conditions of medical emergency, one creative strategy for the identification of novel and potential antiviral agents gaining momentum in research institutions and progressively being leveraged by pharmaceutical companies is target-based drug repositioning/repurposing. A continuous monitoring and recording of results offer an anticipation that this strategy may help to reveal new medications for viral infections. This review recapitulates the neoteric illation of COVID-19, its genomic dispensation, molecular evolution via phylogenetic assessment, drug targets, the most frequently worldwide used repurposed drugs and their therapeutic applications, and a recent update on vaccine management strategies. The available data from solidarity trials exposed that the treatment with several known drugs, viz. lopinavir-ritonavir, chloroquine, hydroxychloroquine, etc had displayed various antagonistic effects along with no impactful result in diminution of mortality rate. The drugs like remdesivir, favipiravir, and ribavirin proved to be quite safer therapeutic options for treatment against COVID-19. Similarly, dexamethasone, convalescent plasma therapy and oral administration of 2DG are expected to reduce the mortality rate of COVID-19 patients.
... Some neonatal hepatocytes expressed ACE2 and were susceptible to SARS-CoV-2 infection during this compensatory process. 290 Pathological and electron microscopic findings revealed typical coronavirus particles in the cytoplasm of hepatocytes from two cases of COVID-19. 291 Histologically, the predominant histological features of SARS-CoV-2-infected liver were massive apoptosis and binuclear hepatocytes. ...
The coronavirus disease 2019 (COVID-19) is a highly transmissible disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that poses a major threat to global public health. Although COVID-19 primarily affects the respiratory system, causing severe pneumonia and acute respiratory distress syndrome in severe cases, it can also result in multiple extrapulmonary complications. The pathogenesis of extrapulmonary damage in patients with COVID-19 is probably multifactorial, involving both the direct effects of SARS-CoV-2 and the indirect mechanisms associated with the host inflammatory response. Recognition of features and pathogenesis of extrapulmonary complications has clinical implications for identifying disease progression and designing therapeutic strategies. This review provides an overview of the extrapulmonary complications of COVID-19 from immunological and pathophysiologic perspectives and focuses on the pathogenesis and potential therapeutic targets for the management of COVID-19.
... Guan et al. proved that COVID-19 is associated with microvascular steatosis and mild lobular activity in COVID-19 infection [9]. ...
Background
Clinically most apparent symptoms of COVID-19 include fever and cough, which in some patients show a worsening trend but are completely non-apparent in patients who present with an asymptomatic course of the disease. The aim of this study was to identify clinical and biochemical differences among polymerase chain reaction (PCR) positive patients who are either febrile or afebrile.
Methods
This study was conducted in Rawalpindi Medical University and Allied Hospitals between September and December 2020. All patients who tested positive for reverse transcription polymerase chain reaction (RT-PCR) COVID-19 were included in the study. After evaluation of 146 patients, 100 were selected, and with a response rate of 97%, a total of 97 patients were included in the final analysis. Depending on the presence of fever, the participants were divided into two groups. Both groups were then compared for baselines vitals and laboratory investigations. Data was entered and analyzed in SPSS v23.0 (IBM Inc., Armonk, New York).
Results
Among the 97 patients, 66 (68%) of the participants were male, and 31 (32%) were females. The mean age of the study participants was 45.23±18.08 years. Fever was present in 39 (40.2%) of the participants. When compared with patients with no fever, the patients with fever had greater severity of disease (p<0.001), higher heart rate (p<0.001), decreased oxygen saturation (p<0.001). Among the laboratory investigations, the fever group had a greater tendency of having deranged alanine aminotransferase (ALT) (70.82±29.23 vs. 32.83±16.22, p=0.010), Lymphocytes (1.56±0.54 vs. 2.12±0.94, p=0.003) and serum total bilirubin (1.06±0.36 vs. 0.55±0.21, p=0.009). Based on multiple regression analysis, the presence of fever is a predictor of derangement in ALT (OR=1.034, CI=1.001-1.068 p=0.025) and total bilirubin (OR=4.38, CI=2.14-6.78, p=0.021).
Conclusion
Fever may not be present among all patients presenting with COVID-19 infection, but those who have a fever have a greater risk of having deranged liver function tests. Hence, it is important to monitor liver function tests (LFTs) in COVID-19 patients presenting with fever.
... Several organ damage, have been reported in COVID-19 infection, including kidney failure, liver and heart injury, implying multiple organ involvement [2,3,4]. ...
Several degrees of Atrio-Ventricular Block, have been reported, in some patients with corona virus disease 2019 (COVID-19) infection, we report three cases of female patients referred to our center for implantation of pacemaker, because of Atrio Ventricular block. The diagnostic of COVID-19 infection has been made before the diagnostic of Atrio Ventricular block for one patient, and after implantation for the two others.
... It was established that Bats have the most variety of coronaviruses in their bodies and are the hosts of many kinds of coronaviruses, such as the SARS-CoV-2 and the MERS-CoV (Cui et al., 2020). The SARS-CoV-2 and the MERS-CoV are considered highly pathogenic, and it is very likely that the SARS-CoV-2 was transmitted from bats to palm civets and the MERS-CoV was transmitted from bats to dromedary camels and finally to humans (Guan et al.,2020). Given the high sequence similarity between the SARS-CoV-2 and the SARS-like bat CoVs from Hipposideros bats in China, the natural host of the SARS-CoV-2 may be the Hipposideros bat. ...
The purpose of this phenomenological study was to clearly describe coronavirus concepts, and address misconceptions that abound about it in Uganda. A qualitative review of more than 40 articles on coronavirus, published between 2019 and 2021 was done. Results showed that the different myths and misconceptions about coronavirus are not true and misleading. The coronavirus concepts are scientifically testable and can be formulated with reasonable clarity. The contribution of this study is: better understanding of conceptions and misconceptions about coronavirus in Uganda. The government of Uganda, through the ministry of health can plan awareness campaigns and interventions to prevent or change peoples' attitude and behaviour towards coronavirus, given the gravity of its impact. However, the findings of this study should be interpreted in the context of the potential limitations such as potential publication bias and inadequate capture of perspectives of the people about misconceptions surrounding the Covid-19 pandemic.
The acute manifestations of coronavirus disease 2019 (COVID-19) exhibit the hallmarks of sepsis-associated complications that reflect multiple organ failure. The inflammatory cytokine storm accompanied by an imbalance in the pro-inflammatory and anti-inflammatory host response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection leads to severe and critical septic shock. The sepsis signature in severely afflicted COVID-19 patients includes cellular reprogramming and organ dysfunction that leads to high mortality rates, emphasizing the importance of improved clinical care and advanced therapeutic interventions for sepsis associated with COVID-19. Phytochemicals of functional foods and nutraceutical importance have an incredible impact on the healthcare system, which includes the prevention and/or treatment of chronic diseases. Hence, in the present review, we aim to explore the pathogenesis of sepsis associated with COVID-19 that disrupts the physiological homeostasis of the body, resulting in severe organ damage. Furthermore, we have summarized the diverse pharmacological properties of some potent phytochemicals, which can be used as functional foods as well as nutraceuticals against sepsis-associated complications of SARS-CoV-2 infection. The phytochemicals explored in this article include quercetin, curcumin, luteolin, apigenin, resveratrol, and naringenin, which are the major phytoconstituents of our daily food intake. We have compiled the findings from various studies, including clinical trials in humans, to explore more into the therapeutic potential of each phytochemical against sepsis and COVID-19, which highlights their possible importance in sepsis-associated COVID-19 pathogenesis. We conclude that our review will open a new research avenue for exploring phytochemical-derived therapeutic agents for preventing or treating the life-threatening complications of sepsis associated with COVID-19.
The novel disease produced by SARS-CoV-2 mainly harms the respiratory tract, but it has shown the capacity to affect multiple organs. Epidemiologic evidence supports the relationship between Coronavirus Disease 2019 (COVID-19) and pancreatic and hepatic injury development, identified by alterations in these organ function markers. In this regard, it is important to ascertain how the current prevalence of non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) might affect COVID-19 evolution and complications. Although it is not clear how SARS-CoV-2 affects both the pancreas and the liver, a multiplicity of potential pathophysiological mechanisms seem to be implicated; among them, a direct viral-induced injury to the organ involving liver and pancreas ACE2 expression. Additionally, immune system dysregulation, coagulopathies, and drugs used to treat the disease could be key for developing complications associated with the patient’s clinical decline. This review aims to provide an overview of the available epidemiologic evidence regarding developing liver and pancreatic alterations in patients with COVID-19, as well as the possible role that NAFLD/NASH might play in the pathophysiological mechanisms underlying some of the complications associated with COVID-19. This review employed a comprehensive search on PubMed using relevant keywords and filters. From the initial 126 articles, those aligning with the research target were selected and evaluated for their methodologies, findings, and conclusions. It sheds light on the potential pathophysiological mechanisms underlying this relationship. As a result, it emphasises the importance of monitoring pancreatic and hepatic function in individuals affected by COVID-19.
The present worldwide pandemic of coronavirus disease 2019 (COVID‐19) has highlighted the important function of angiotensin‐converting enzyme 2 (ACE2) as a receptor for severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) entry. A deeper understanding of ACE2 could offer insights into the mechanisms of SARS‐CoV‐2 infection. While ACE2 is subject to regulation by various factors in vivo, current research in this area is insufficient to fully elucidate the corresponding pathways of control. Posttranslational modification (PTM) is a powerful tool for broadening the variety of proteins. The PTM study of ACE2 will help us to make up for the deficiency in the regulation of protein synthesis and translation. However, research on PTM‐related aspects of ACE2 remains limited, mostly focused on glycosylation. Accordingly, a comprehensive review of ACE2 PTMs could help us better understand the infection process and provide a basis for the treatment of COVID‐19 and beyond.
While the world grappled with the pandemic of coronavirus disease 2019 (COVID-19), medical fraternity and policy makers tried desperately to control its spread in the absence of any definite treatment protocol. The scope of homoeopathy, which has been historically found effective in epidemics, has been investigated in the present study. This study was conducted to evaluate the effect of individualised homoeopathic medicine on mild cases of COVID-19 under home isolation. A retrospective, single-arm, non-randomised, open-label, observational trial was conducted on 185 laboratory confirmed mild cases of COVID-19 at Nehru Homoeopathic Medical College and Hospital, Delhi, during September to December 2020. Complete symptom resolution days was the primary outcome (from baseline to total zero symptom score); while assessment of severity of each symptom and sign on a scale of 0-3 ( 0- absent, 1-mild. 3- severe), at baseline and Day 14 comprised of the secondary outcome. Intention-to-treat sample (n = 185) was analysed with SPSS IBM version 20. Of all the patients (n = 185), 165 (90%) successfully completed the follow-up period. The mean (interquartile range [IQR]) age was 35 (26–45) years; the male: female ratio was 11:9.2. Fever (56%), cough (54%), fatigue (45%) and sore throat (36%) were the most common symptoms reported. Median (IQR) time for resolution of symptoms was 4 (3–8) days. Sixty-eight per cent patients recovered within 6 days and rest within 7 to 14 days. The most prescribed medicines were Bryonia alba (30%), Arsenicum album (25%) and Pulsatilla nigricans (12%) accounting for 67% of the total medicines. This study, though preliminary, revealed a positive treatment effect of individualised homoeopathic medicines in promptly alleviating the symptoms of mild COVID-19. Randomised controlled trials with greater scientific rigour are warranted.
An outbreak of a respiratory sickness started in Wuhan, China in December 2019 and the causative agent was found be a novel betacoronovirus of the same subgenus as SARSCoV and named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Coronavirus disease 2019 (COVID-19) quickly spread around the world, with clinical signs ranging from mild respiratory symptoms to severe pneumonia and a fatality rate estimated around 2%. Lower respiratory tract infections can occur in immunocompromised subjects and the elderly persons. Respiratory droplets are the causative agent for the person-to-person spread of the disease resembling the spread of influenza. Individual to individual spread turned into the primary mode of transmission. The transmission of the disease might be more likely in the earlier stage of infection as the viral RNA levels appear to be higher. Accurate diagnosis in the early stages of the epidemic helps control the spread of the disease.
Aims:
COVID-19 patients with type 2 diabetes mellitus (T2DM) show both poorer clinical outcomes and have an increased risk of death. SARS-CoV-2 virus infection requires simultaneous expression of the SARS-CoV-2 cell entry factors angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine type2 (TMPRSS2) in the same cell. The aim of the study was to explore the underlying mechanisms of a COVID-19 infection in patients with T2DM.
Methods:
The distribution and expression of AEC2 and TMPRSS2 in different pancreatic cell types in clinical samples of T2DM patients and diabetic mouse models were analyzed by single-cell sequencing, bioinformatics analysis, and basic experiments.
Results:
The results showed that ACE2 and TMPRSS2 are expressed in the ducts of the human pancreas. These findings suggest that SARS-CoV-2 can infect ductal cells in vivo through ACE2 and TMPRSS2. T2DM can promote the co-expression of ACE2 and TMPRSS2 in exocrine ducts, including in the human pancreas. We hypothesize that ACE2 expression levels are associated with increased numbers of lymphocytes in vivo.
Conclusions:
Increased blood glucose levels are associated with increased ACE2 expression and an increased number of lymphocytes. At the same time, lymphocytes can promote ACE2 expression.
In December 2019, the onset of an unidentified disease known as pneumonia for an unknown reason occurred in Wuhan city, China. Liver dysfunction has occurred in COVID-19-infected patients. The current study investigated liver function abnormalities in COVID-19 infected patients and their relationship with age and sex. A cross-section study was designed and conducted at Al-Hakeem hospital in Al-Najaf city in Iraq. This study comprised 167 patients with SARS-CoV-2 confirmation using real-time polymerase chain reaction. Liver function test results were compared among different age groups and the two genders. The analysis of categorical variables was achieved via the Chi-square test. The differences in the continuous variables between both sexes were detected via Mann-Whitney U test. A statistically significant p-value was determined to be less than 0.05. IBM SPSS software (version 26) was utilized for data analysis. Among 167 patients with COVID-19 infection, 82 (49.1 %) had abnormal liver test and 85 (50.9%) were normal (P=0.816). No significant differences were noted in liver test abnormalities among the various age groups (P=0.784). The percentages of liver function abnormalities in males and females were (68.3 %) and (37.5 %) respectively. Significant differences were detected between males and females (P=0.001). The distribution of AST and ALT between males and females was shown to be significantly different (P=0.012) and (P=0.009), respectively. The ALP (U/L) and total bilirubin (mg/dL) median values between males and females were shown to be statistically insignificant. In our study, we estimated that the risk of liver function abnormalities was not significantly different among all age groups and infected males had a higher incidence of liver dysfunction with significant differences in serum AST and ALT levels between both sexes.
Coronavirus disease 2019 (COVID-19) pneumonia outbreak started in December 2019. On March 12, 2020, the World Health Organization (WHO) declared that the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) constitutes a pandemic, and as of May 2021, SARS-CoV-2 has infected over 167.3 million patients, including 3.4 million deaths, reported to WHO. In this review, we will focus on the relationship between SARS-CoV-2 infection and the liver. We will discuss how chronic liver diseases affect the COVID-19 disease course and outcomes. We will also discuss the SARS-CoV-2 effects on the liver, mechanisms of acute liver injury, and potential management plans.
Objective: We aimed to examine the effects of COVID-19 on biochemical and hematological parameters such as liver and kidney function tests, electrolyte levels and inflammatory markers.
Methods: The research was carried out on 10269 patients who applied to Eskişehir City Hospital between 01.03.2020 and 01.10.2020 with positive and negative COVID-19 test results. Included patients were diagnosed with COVID-19 by real-time polymerase chain reaction and computed tomography Biochemical parameters were examined in the samples of two groups with positive and negative COVID-19 test results. In addition, hematological parameters were obtained retrospectively.
Results: BASO%, EOS#, EOS%, HCT, HGB, LYM#, LYM%, MCHC, MCV, MONO#, MONO%, MPV, NEU#, NEU%, PCT and PLT (p<0.05). There was no statistical difference in BASO# and MCH parameters. BASO%, EOS%, HCT, LYM#, LYM%, MCHC, MONO%, NEU%, PCT and RBC parameters in COVID-19 positive patients were higher than in COVID-19 negative patients. Other parameters were lower in positive patients than in negative patients (p<0.05). There was a statistical difference between the groups in all biochemistry test results except potassium and procalcitonin parameters (p<0.05). ALP, ALT, AST, Direct Bilirubin, Total Bilirubin, BUN, CRP, D-Dimer, Ferritin, GGT, Creatinine, LDH and Troponin data obtained from COVID-19 positive patients were higher than control group. Albumin, Chlorine, Iron, Sodium and total protein levels were lower in positive patients than in negative patients (p<0.05).
Conclusion: Biochemical variants found in COVID-19 positive patients that may indicate multi-organ dysfunction. Abnormalities in some biochemical indices, such as liver and kidney function tests, may reflect the severity of the disease to some degree. These comprehensive biochemical and hematological indicators can be used to create indexes and panels, taking into account the clinical management of the disease.
Keywords: COVID-19; SARS-CoV-2; biochemical biomarkers; hematological parameters.
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