Background: Tocilizumab, an inhibitor of the interleukin-6 receptor, may decrease the inflammatory response and control the symptoms of severe coronavirus disease 2019 (COVID-19), but the evidence is scarce. Methods: This retrospective study included patients with severe COVID-19 requiring oxygen therapy who received tocilizumab in seven centers across Poland. We assessed on-treatment changes in clinical status and inflammatory markers. Results: Twenty-eight patients were included (19 male), with a mean age of 61.7 ± 12.4 years. The mean time from symptom onset to the first tocilizumab dose was 10.5 ± 5.7 days. Clinical status improved within 24 hours in 11 (39%) patients, within one week in 23 (82%) patients, and within two weeks in 25 (89%); one (4%) patient showed no change and two (7%) patients died. Sixteen patients (57%) no longer needed oxygen therapy within a week (p < 0.001). The serum concentrations of C-reactive protein, procalcitonin, and fibrinogen decreased significantly (p ≤ 0.001). Lung changes improved in 21 (84%) patients within two weeks of treatment; 19 had minimal or no changes upon final examination. Conclusions: Tocilizumab can control the symptoms of severe COVID-19 by reducing the inflammatory response and rapidly improves the clinical status in most patients.

SARS-CoV-2 shows a high affinity for the ACE-2 receptor, present on the epithelial cells of the upper and lower respiratory tract, within the intestine, kidneys, heart, testes, biliary epithelium, and—where it is particularly challenging—on vascular endothelial cells. Liver involvement is a rare manifestation of COVID-19. Material and Methods: We reviewed 450 patients admitted due to the fact of SARS-CoV-2 infection (COVID-19) including 88 with liver injury. Based on medical history and previous laboratory test results, we excluded cases of underlying liver disease. The analysis involved a clinical course of COVID-19 in patients without underlying liver disease as well as the type and course of liver injury. Results: Signs and symptoms of liver injury were present in 20% of patients, mostly presenting as a mixed-type pattern of injury with less common cases of standalone hepatocellular (parenchymal) or cholestatic injury. The liver injury symptoms resolved at the end of inpatient treatment in 20% of cases. Sixteen patients died with no cases where liver injury would be deemed a cause of death. Conclusions: (1) Liver injury secondary to COVID-19 was mild, and in in 20%, the signs and symptoms of liver injury resolved by the end of hospitalization. (2) It seems that liver injury in patients with COVID-19 was not associated with a higher risk of mortality. (3) The underlying mechanism of liver injury as well as its sequelae are not fully known. Therefore, caution and further monitoring are advised, especially in patients whose liver function tests have not returned to normal values.

Hepatocellular carcinoma is the fifth most common malignancy and the third leading mortality cause worldwide. It typically develops secondarily to liver cirrhosis, due to hepatitis B or C infection, alcohol abuse, metabolic disease, and so forth. According to the American Association for the Study of Liver Diseases (AASLD) guidelines, which constitute diagnostic standards, the diagnosis of primary hepatocellular carcinoma (HCC) should be based on contrast-enhanced imaging. Lesion hyperenhancement should be observed throughout the arterial phase, followed by the washout during the venous phase. The diagnosis can also be based on the histopathological evaluation of liver biopsy specimen. Although the standards are clear, we often see patients with advanced HCC in clinical practice, who cannot be offered any effective treatment. Patients with chronic liver disease, presenting with inconclusive and changeable test results, constitute a separate problem. In such cases the diagnostic process is typically long-term and delayed. In this paper we present three case reports where the diagnosis could not be made promptly and the patients died as a result of a delayed diagnostic process.

Ephedrone encephalopathy is referred to as a group of symptoms of manganese deposition within the central nervous system (CNS), resulting from the abuse of ephedrone (methcathinone), obtained in reaction using the excess amount of manganese-containing oxidants. The diagnosis is based on the contrast-enhanced head MRI findings characteristic for this syndrome, clinical manifestation and history of ephedrone use. The syndrome has been reported in recent years in young people from Eastern Europe and Russia with a history of ephedrone overuse. However, no report has ever been published on ephedrone encephalopathy in Polish patients.