The SARS-COV2 (COVID-19) Pandemic: What Clinicians should Know

In late 2019, a novel coronavirus, now designated SARS-CoV-2, emerged and was identified as the cause of an outbreak of acute respiratory illness in Wuhan, a city in China, named as COVID-19. Since then the waves of the virus exponentially hit many countries around the globe with high rates of spread associated with variable degrees of morbidity and mortality. The WHO announced the pandemic state of the infection in March 2020 and by June 1st 2020 more than 6 million individuals and more than 370 thousands case fatalities were documented worldwide. In this article, we discussed many aspects regarding this emerged infection based on the available evidence aiming to help clinician to improve not only their knowledge but also their practices toward this infection.

The SARS-COV2 (COVID-19) Pandemic: What Clinicians should Know

In late 2019, a novel coronavirus, now designated SARS-CoV-2, emerged and was identified as the cause of an outbreak of acute respiratory illness in Wuhan, a city in China, named as COVID-19. Since then the waves of the virus exponentially hit many countries around the globe with high rates of spread associated with variable degrees of morbidity and mortality. The WHO announced the pandemic state of the infection in March 2020 and by June 1st 2020 more than 6 million individuals and more than 370 thousands case fatalities were documented worldwide. In this article, we discussed many aspects regarding this emerged infection based on the available evidence aiming to help clinician to improve not only their knowledge but also their practices toward this infection.

Early prediction of acute kidney injury in patients with acute on chronic liver failure by measuring kidney injury Molecule-1 level in Urine at Zagazig University Hospitals

Background and study aim: Some of patients with decompensated cirrhosis will exhibit newly developed acute liver failure. This condition is called acute-on-chronic liver failure (ACLF). Acute kidney injury (AKI) is common with ACLF. Kidney injury Molecule-1 (KIM-1) is an ideal biomarker of AKI. The aim of this study was to evaluate role of KIM-1 in prediction of AKI in ACLF patients. Patients and Methods: Eighty four patients were included in this study. They were selected from hospitalized patients with acute decompensated cirrhosis. They were allocated into two groups; group I: patients with no acute-on-chronic liver failure (ACLF), group II: patients with ACLF. Results: KIM-1 was significantly higher in the ACLF (group II). KLM-1 median was 2.4 in group I vs 7.35 in group II with p value <0.001. We found that at cut off value of ≥0.5 KLM-1 can predict the presence of AKI with sensitivity of 85.7%, specificity 88.1%, positive predictive value 87.8%, negative predictive value 86%, accuracy 86.9% and AUC= 0.867 p <0.001. Conclusion: KLM-1 rises significantly in patients with ACLF. KLM-1 can be reliable in prediction of the presence of acute kidney injury in decompensated cirrhosis

Effect of Toxoplasma co-inefected with intestinal helminthes on cell mediated immunity to tuberculosis patients.

The effect of intestinal helminthes (IH) and Toxoplasma gondii (Tox) co-infection on anti-mycobacterium tuberculosis (MTB) immunity in patients with active pulmonary tuberculosis was studied in 96 patients of 4 groups. Thirteen patients had TB+IH+Tox (G1), 15 had TB+IH (G2), 21 had TB+Tox (G3) and 47 had TB (G4). The mean diameter of tuberculin and toxoplasmin tests was measured to assess cell mediated immunity. Anti-Toxoplasma IgG1 & IgG4 antibodies were sought in toxoplasmic patients by ELISA for Thelper1 (Th1) and Th2 cytokine responses respectively. All patients were treated by 6 months anti-MTB therapy. Specific anti-IH therapies were given for patients with concomitant IH. Sputum examination for acid fast bacilli was done 2 weeks post-treatment and duration of sputum clearance was recorded. The results showed that IH co-infection had significant negative effect on mean diameter of tuberculin test compared to G4 (5.87 +/- 0.08 vs 8.65 +/- 0.05 mm; P < 0.01). Concurrent Tox with TB significantly increased tuberculin test mean diameter (10.89 +/- 0.11 vs 8.65 +/- 0.05 mm; P < 0.05). Mean level of anti-Tox IgG1 among G3 was significantly higher than in G1 (0.88 +/- 0.05 vs 0.55 +/- 0.02; P < 0.001), but vice versa was with IgG4. Mean tuberculin diameter increased significantly post-treatment in all Gs except G3. Anti-Tox IgGC1 showed significant increase (0.55 +/- 0.02 to 0.82 +/- 0.03; P < 0.001) but IgG4 showed significant decrease (0.62 +/- 0.07 to 0.45 +/- 0.06, P < 0.01) post-treatment in G1, but G3 was insignificantly affected. The duration of sputum clearance was significantly longer in patients with IH co-infection compared to G4 (29 +/- 1 vs 21.8 +/- 4.6 days; P < 0.001).