(1) Background/Aim: People infected with SARS-CoV-2 may develop COVID-19 in a wide range of clinical severity. Pulmonary fibrosis is characterized by several grades of chronic inflammation and collagen deposition in the interalveolar space. SARS-CoV-2 infection has been demonstrated to cause lung fibrosis without a currently elucidated mechanism. Some studies emphasize the role of proinflammatory cytokines. This research studies the correlation of the released cytokines with mortality or lung injury in COVID-19 patients. (2) Methods: Electronic medical record data from 40 patients diagnosed with COVID-19 in the COVID-19 Department, Galilee Medical Center, Nahariya, Israel, were collected. Epidemiological, clinical, laboratory, and imaging variables were analyzed. The cytokine levels were measured upon admission and discharge. A correlation between cytokine levels and severity and mortality or lung involvement was undertaken. (3) Results: IFN-gamma and IL-10 are the most powerful risk factors for mortality in the COVID-19 patient groups in a multivariate analysis. However, in a univariate analysis, TGF-β, CXCL-10, IFN gamma, and IL-7 affected mortality in COVID-19 patients. MMP-7 was significantly correlated with a cytokine storm and a high 4-C (severity) score in COVID-19 patients. MMP-7, TGF-β, IL-10, IL-7, TNF-α, and IL-6 were correlated with high lung involvement in COVID-19 patients. Serum concentrations of IGF-1 were significantly increased upon discharge, but MMP-7 was decreased. (4) Conclusions: Proinflammatory cytokines predict clinical severity, lung fibrosis, and mortality in COVID-19 patients. High concentrations of TGF-β, CXCL-10, IL-10, IL-6, and TNF-α are correlated to severity and lung injury. However, certain cytokines have protective effects and higher levels of these cytokines increase survival levels and lower lung damage. High levels of INF-γ, IL-7, MMP-7, and IGF-1 have protection probabilities against lung injury and severity.

Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide, with a continuously growing prevalence. The pathophysiology of the disease is complex and includes several mechanisms, with metabolic syndrome and insulin resistance playing a major role. It is crucial to diagnose NAFLD before it advances to nonalcoholic steatohepatitis (NASH), which can progress to cirrhosis, presented by its complications which include ascites, portal hypertension, bleeding varices and encephalopathy. Another important complication of NAFLD and cirrhosis is hepatocellular carcinoma (HCC), a cancer with increasing incidence and poor prognosis. Even with the growing prevalence of NAFLD, diagnosis via liver biopsies is unrealistic, considering the costs and complications. Noninvasive tests, including serum biomarkers and elastography, are cost-effective and convenient, thereby replacing liver biopsies in diagnosing and excluding liver fibrosis. However, currently, these noninvasive tests have several limitations, such as variability, inadequate accuracy and risk factors for error. The limitations and variability of these tests comet the investigator to propose combining them in diagnostic algorithms to produce more accurate tools. Identifying patients with significant fibrosis is important for targeted therapies to prevent disease progression. Effective screening using noninvasive tests can be crucial for patient risk stratification and early diagnosis.

Early identification of patients with COVID-19 who will develop severe or critical disease symptoms is important for delivering proper and early treatment. We analyzed demographic, clinical, immunological, hematological, biochemical and radiographic findings that may be of utility to clinicians in predicting COVID-19 severity and mortality. Electronic medical record data from patients diagnosed with COVID-19 from November 2020 to June 2021 in the COVID-19 Department in the Galilee Medical Center, Nahariya, Israel, were collected. Epidemiologic, clinical, laboratory and imaging variables were analyzed. Multivariate stepwise regression analyses and discriminant analyses were used to identify and validate powerful predictors. The main outcome measure was invasive ventilation, or death. The study population included 390 patients, with a mean age of 61 ± 18, and 51% were male. The non-survivors were mostly male, elderly and overweight and significantly suffered from hypertension, diabetes mellitus type 2, lung disease, hemodialysis and past use of aspirin. Four predictive factors were found that associated with increased disease severity and/or mortality: age, NLR, BUN, and use of high flow oxygen therapy (HFNC). The AUC or diagnostic accuracy was 87%, with a sensitivity of 97%, specificity of 60%, PPV of 87% and NPP of 91%. The cytokine levels of CXCL-10, GCSF, IL-2 and IL-6 were significantly reduced upon the discharge of severely ill COVID-19 patients. The predictive factors associated with increased mortality include age, NLR, BUN, and use of HFNC upon admission. Identifying those with higher risks of mortality could help in early interventions to reduce the risk of death.

COVID-19 is an infectious disease caused by the SARS-CoV-2 virus. The clinical presentations of the SARS-CoV-2 infection are widely variable and treatment strategies for COVID-19 are dependent on the infection phase. Timing the right treatment for the right phase of this disease is paramount, with correlations detected between the phase of the infection and the type of drug used to treat. The immune system activation following COVID-19 infection can further develop to a fulminant cytokine storm which can progress to acute respiratory distress syndrome. The inflammatory phase, or the hyperinflammation phase, is a later stage when patients develop acute respiratory distress syndrome (ARDS), sepsis, and kidney and other organ failure. In this stage, the virus is probably not necessary and all the damage is due to the immune system’s cytokine storm. Immunosuppressive or immunomodulatory agent administration is the major strategy in treating COVID-19 patients at this stage. On the other hand, immunodeficient patients who are treated with immunomodulator agents have attenuated immune systems that do not produce enough cytokines. Current data do not show an increased risk of severe COVID-19 in patients taking biologic therapies or targeted disease-modifying antirheumatic drugs. However, more comprehensive studies are needed to assess the effect of these medications, and whether they may actually be protective of the severe type of disease. Although medications for COVID-19 and for the cytokine storm are important, the main breakthrough in slowing down the pandemic was developing effective vaccines. These vaccines showed a dramatic result in reducing morbidity and mortality up to the Delta variant’s spread. However, the emergence of the new variant, Omicron, influenced the successful results we had before. This variant is more contagious but less dangerous than Delta. The aim now is to develop vaccines based on the Omicron and Delta immunogens in the future for broad protection against different variants.

Humans infected with SARS-CoV-2 may develop COVID-19, which manifests across a wide spectrum of clinical severity ranging from mild upper respiratory tract illnesses to diffuse viral pneumonia, causing acute respiratory failure. Many therapies have been tested for their efficacy in treating COVID-19. Controversy surrounds convalescent plasma transfusions as an effective treatment for COVID-19. This study discusses the efficacy of this treatment on COVID-19 patients. Electronic medical record data were collected from patients diagnosed with COVID-19, from November 2020 to August 2021, in the Galilee Medical Center’s COVID-19 departments. Epidemiological, clinical, laboratory and imaging variables were analyzed. Multivariate stepwise regression and discriminant analyses were used to identify and validate the correlation between convalescent treatment and either death or time to negative PCR and hospitalization length. The study population included 270 patients, 100 of them treated with convalescent plasma. The results show that convalescent plasma therapy significantly prevented mortality in moderate patients, reduced hospitalization length and time to negative PCR. Additionally, high BMI, elderly age, high CRP and 4C-scores correlated with the severity and mortality of COVID-19 patients. Convalescent plasma also significantly reduced inflammatory markers, especially in moderate COVID-19 patients. In non-critical hospitalized patients, convalescent plasma therapy reduces morbidity and mortality in moderate COVID-19 patients and hospitalization length. Identifying patients who could benefit from this treatment could reduce the risk of death and shorten their hospitalization stay.

Introduction: Increased red blood cell distribution width (RDW) has been reported to be related to underlying chronic inflammation. Our aim is to investigate the relationship of different complete blood count (CBC) parameters such as hemoglobin level, mean corpuscular volume (MCV), mean platelet volume (MPV) or RDW with COPD exacerbation severity. Methods: In the present retrospective analysis, consecutive patients admitted with the diagnosis of “COPD Exacerbation” between 1 January 2012 and 31 December 2015 were evaluated. Results: The study population included 804 patients with COPD exacerbation. The maximal partial pressure of carbon dioxide in the arterial blood (PaCO₂) during hospital stay was significantly higher in patients with high MCV (p < 0.001), and in patients with a high RDW (p < 0.001). The hospitalization duration was significantly longer in patients with high RDW (p < 0.001) and in patients with elevated C-reactive protein (CRP) levels (p < 0.001). CRP levels strongly correlated to RDW (p = 0.001). Conclusions: Our study demonstrated that different CBC parameters, such as MCV and RDW, are in correlation with the severity of acute exacerbation of COPD reflected by the PaCO₂ level and the duration of hospitalization. Furthermore, we also found a positive correlation between RDW and CRP levels. This finding supports the hypothesis that RDW is a good biomarker of acute inflammation.