Point-of-care Glucose Monitoring in COVID-19 Intensive Care Unit: How's It Different?

How to cite this article: Panda R, Hirolli D, Baidya DK. Point-of-care Glucose Monitoring in COVID-19 Intensive Care Unit: How''s It Different? Indian J Crit Care Med 2021;25(12):1465–1466.     

Clinical experiences of LAK therapy in patients with hepatocellular carcinoma

A patient with hepatocellular carcinoma (HCC) was treated with newly established adoptive immunotherapy using LAK cells (LAK therapy) together with transcatheter arterial embolization therapy (TAE). This patient responded well, and the therapeutic efficacy still continues 6 months after the therapy. Since the efficacy of LAK therapy does not last long, it is recommended that LAK therapy should be employed in combination with such therapeutic maneuvers as TAE or anticancer drugs in patients with HCC.     

An experimental study on the severe type of alcoholic liver disease--a pathogenetic role of potentiated activation of complement system by endotoxin after chronic ethanol consumption

Endotoxemia frequently appears in severe type of alcoholic liver disease. However, we have little knowledge how endotoxin influences the progression of alcoholic liver injury. Thus, to study the causal mechanism for the progression to the severe type of alcoholic liver diseases, endotoxin (0.2 mg/100 g BW, E. Coli O26:B6) was intravenously injected in chronic ethanol-fed rats and controls, and then, rats were sacrificed after 16 hours of endotoxin treatment. The elevation of serum GOT and GPT activities induced by endotoxin was significantly higher in chronic ethanol-fed rats than controls, and these biochemical changes were well correlated with the grade of necrosis of liver histology. Furthermore, in chronic ethanol-fed rats, endotoxin treatment tremendously increased blood BUN and creatinine levels and produced the degeneration of renal tubuli with neutrophil infiltration into glomerulus. These experimental findings are very similar to the severe type of alcoholic liver disease. On the other hand, endotoxin significantly decreased serum values of CH50 in chronic ethanol-fed rats, but not in controls. Such alterations of CH50 induced by endotoxin were well correlated with the several parameters indicating the injury of liver and kidney. Therefore, the present study may indicate that chronic ethanol ingestion aggravates endotoxin-induced organ injury, and that the activation of complement system may associate with such progression of organ injury.