A 23-year-old male patient received moxifloxacin, recombinant human interferon α-2b for injection, and lopinavir and ritonavir for 7 days for novel coronavirus pneumonia. There was no abnor-malityof serum potassium. Moxifloxacin was stopped, Qingfei Paidu decoction(清肺排毒汤) was given, and then the patient′s serum potassium began to rise. On day 10 after taking the decoction, laboratory tests showed serum potassium 5.7 mmol/L and the patient was diagnosed with hyperkalemia. Insulin injection 4 U diluted to 5% glucose injection 250 ml was given once by IV infusion, and then the serum potassium decreased to 5.0 mmol/L 6 hours later and 4.6 mmol/L 2 days later. After 5 days, the serum potassium rose again and finally to 5.4 mmol/L on day 17 after taking the decoction. Insulin was given once that day and 2 days later once daily according to the previous method. Then the serum potassium decreased and did not rise again. The patient recovered from novel coronavirus pneumonia and was discharged on day 28 after hospitalization.

A 62-year-old male patient received propacetamol hydrochloride for analgesia, cefuroxime sodium for anti-infection, adenosine cobalamin for nutrition of nerve, and low molecular weight heparin calcium for anticoagulation for burst fracture of the third lumbar vertebra and multiple fractures of transverse process of lumbar spine caused by traffic accident. The patient′s liver function was normal before medication. He underwent the operation under general anesthesia 2 days later. Low molecular weight heparin calcium was stopped before the operation. On day 3 after the operation (on day 5 of medication), the patient developed abdominal distension and pain. The results of laboratory tests showed alanine aminotransferase (ALT) 9 315 U/L, aspartate aminotransferase (AST) 10 760 U/L, gamma glutamyltransferase (γ-GT) 47 U/L, alkaline phosphatase (ALP) 101 U/L, total bilirubin (TBil) 71.3 μmol/L, direct bilirubin (DBil) 48.5 μmol/L, and indirect bilirubin (IBil) 22.8 μmol/L. Drug-induced liver injury was considered. Propacetamol hydrochloride was discontinued and liver-protective drugs were given. The next day, the patient developed yellow staining of his sclera and whole body skin, then followed by confusion, decreased blood oxygen saturation, low blood pressure, and hypoglycemia. The results of reexamination showed ALT 5 975 U/L, AST 3 659 U/L, γ-GT 100 U/L, ALP 141 U/L, TBil 175.2 μmol/L, DBil 101.4 μmol/L, IBil 73.8 μmol/L, and prothrombin time 21.2 s. The patient was diagnosed as acute liver failure. Cefuroxime sodium and adenosine cobalamin were discontinued and symptomatic and supportive treatments such as increasing blood pressure, fluid supplement, and correction of acidosis were given. However, the patient′s condition was not improved. He was transferred to other hospital on the same day. On the 4th day, he died of multiple organ failure.

A 23-year-old male patient received moxifloxacin, recombinant human interferon α-2b for injection, and lopinavir and ritonavir for 7 days for novel coronavirus pneumonia. There was no abnor-malityof serum potassium. Moxifloxacin was stopped, Qingfei Paidu decoction(清肺排毒汤) was given, and then the patient′s serum potassium began to rise. On day 10 after taking the decoction, laboratory tests showed serum potassium 5.7 mmol/L and the patient was diagnosed with hyperkalemia. Insulin injection 4 U diluted to 5% glucose injection 250 ml was given once by IV infusion, and then the serum potassium decreased to 5.0 mmol/L 6 hours later and 4.6 mmol/L 2 days later. After 5 days, the serum potassium rose again and finally to 5.4 mmol/L on day 17 after taking the decoction. Insulin was given once that day and 2 days later once daily according to the previous method. Then the serum potassium decreased and did not rise again. The patient recovered from novel coronavirus pneumonia and was discharged on day 28 after hospitalization.

A 62-year-old male patient received propacetamol hydrochloride for analgesia, cefuroxime sodium for anti-infection, adenosine cobalamin for nutrition of nerve, and low molecular weight heparin calcium for anticoagulation for burst fracture of the third lumbar vertebra and multiple fractures of transverse process of lumbar spine caused by traffic accident. The patient′s liver function was normal before medication. He underwent the operation under general anesthesia 2 days later. Low molecular weight heparin calcium was stopped before the operation. On day 3 after the operation (on day 5 of medication), the patient developed abdominal distension and pain. The results of laboratory tests showed alanine aminotransferase (ALT) 9 315 U/L, aspartate aminotransferase (AST) 10 760 U/L, gamma glutamyltransferase (γ-GT) 47 U/L, alkaline phosphatase (ALP) 101 U/L, total bilirubin (TBil) 71.3 μmol/L, direct bilirubin (DBil) 48.5 μmol/L, and indirect bilirubin (IBil) 22.8 μmol/L. Drug-induced liver injury was considered. Propacetamol hydrochloride was discontinued and liver-protective drugs were given. The next day, the patient developed yellow staining of his sclera and whole body skin, then followed by confusion, decreased blood oxygen saturation, low blood pressure, and hypoglycemia. The results of reexamination showed ALT 5 975 U/L, AST 3 659 U/L, γ-GT 100 U/L, ALP 141 U/L, TBil 175.2 μmol/L, DBil 101.4 μmol/L, IBil 73.8 μmol/L, and prothrombin time 21.2 s. The patient was diagnosed as acute liver failure. Cefuroxime sodium and adenosine cobalamin were discontinued and symptomatic and supportive treatments such as increasing blood pressure, fluid supplement, and correction of acidosis were given. However, the patient′s condition was not improved. He was transferred to other hospital on the same day. On the 4th day, he died of multiple organ failure.