Objective:To investigate and analyze the safety of empirical or experimental medication (EEM) for adult-onset Still disease (AOSD) before diagnosis.Methods:The AOSD inpatients admitted to the Second Hospital of Jilin University from January 1, 2019 to December 31, 2023 were collected through hospital information system, and those who were misdiagnosed on admission were screened out. The main clinical characteristics, laboratory tests, misdiagnosis situation, the use of EEM and their adverse drug reactions (ADR), and the potential drug-drug interactions in the misdiagnosed patients were analyzed by descriptive statistics.Results:During the set time period, a total of 49 patients with AOSD were admitted to the hospital, of which 16 (32.7%) were misdiagnosed with other diseases on admission. Among the 16 patients, 10 were male and 6 were female, with a median age of 53 years. The main clinical manifestations were fever (in 15 patients), arthralgia/arthritis (in 10 patients), lymphadenopathy (in 10 patients), rash (in 9 patients), pleural or pericardial effusion (in 6 patients), pneumonia (in 5 patients), splenomegaly (in 4 patients) and sore throat (in 4 patients). Abnormalities in laboratory tests included white blood cell count elevation (in 13 patients), platelets count elevation (in 8 patients), serum ferritin elevation (>500 μg/L, in 12 patients), and abnormal liver function (in 9 patients). The median time of treatment before admission was 5.5 months (11 days to 27.0 months), and the median time from admission to diagnosis of AOSD was 12 days. Before the diagnosis of AOSD, all patients received a long time of EEM, including antibiotics, traditional Chinese medicine preparations, liver-protection drugs, anti-allergic drugs and antiviral drugs in 15, 12, 11, 3 and 2 patients, respectively. Four patients experienced ADRs related to EEM, all of which were caused by antibiotics. There were potential interactions in the therapeutic drugs in 4 patients.Conclusion:The misdiagnosis rate of AOSD was high. Patients might had accepted multiple EEMs before the definite diagnosis, which posed risks of ADRs and drug interactions.

Objective:To investigate and analyze the safety of empirical or experimental medication (EEM) for adult-onset Still disease (AOSD) before diagnosis.Methods:The AOSD inpatients admitted to the Second Hospital of Jilin University from January 1, 2019 to December 31, 2023 were collected through hospital information system, and those who were misdiagnosed on admission were screened out. The main clinical characteristics, laboratory tests, misdiagnosis situation, the use of EEM and their adverse drug reactions (ADR), and the potential drug-drug interactions in the misdiagnosed patients were analyzed by descriptive statistics.Results:During the set time period, a total of 49 patients with AOSD were admitted to the hospital, of which 16 (32.7%) were misdiagnosed with other diseases on admission. Among the 16 patients, 10 were male and 6 were female, with a median age of 53 years. The main clinical manifestations were fever (in 15 patients), arthralgia/arthritis (in 10 patients), lymphadenopathy (in 10 patients), rash (in 9 patients), pleural or pericardial effusion (in 6 patients), pneumonia (in 5 patients), splenomegaly (in 4 patients) and sore throat (in 4 patients). Abnormalities in laboratory tests included white blood cell count elevation (in 13 patients), platelets count elevation (in 8 patients), serum ferritin elevation (>500 μg/L, in 12 patients), and abnormal liver function (in 9 patients). The median time of treatment before admission was 5.5 months (11 days to 27.0 months), and the median time from admission to diagnosis of AOSD was 12 days. Before the diagnosis of AOSD, all patients received a long time of EEM, including antibiotics, traditional Chinese medicine preparations, liver-protection drugs, anti-allergic drugs and antiviral drugs in 15, 12, 11, 3 and 2 patients, respectively. Four patients experienced ADRs related to EEM, all of which were caused by antibiotics. There were potential interactions in the therapeutic drugs in 4 patients.Conclusion:The misdiagnosis rate of AOSD was high. Patients might had accepted multiple EEMs before the definite diagnosis, which posed risks of ADRs and drug interactions.

A 32-year-old female patient received anti-virus treatment with tenofovir alafenamide one month after regular hemodialysis due to stage 5 chronic kidney disease complicated with chronic hepatitis B. At the same time, recombinant human erythropoietin injection and iron sucrose injection was periodically used to correct anemia. Her hemoglobin was about 96 g/L without clinical manifestations of anemia such as nausea and fatigue. Eight months after tenofovir alafenamide treatment, she developed dizziness, headache, nausea, fatigue, and lethargy. Laboratory tests showed hemoglobin 94 g/L and serum creatinine 856 μmol/L; blood gas analysis showed pH 7.05, lactate 3.3 mmol/L, arterial partial pressure of oxygen 80 mmHg, arterial partial pressure of carbon dioxide 23 mmHg, base excess -7.4 mmol/L, and bicarbonate 15.6 mmol/L. It was considered that the patient had lactic acidosis, which might be associated with tenofovir alafenamide. The drug was stopped and replaced by entecavir and symptomatic treatments such as fluid rehydration and liver protection were given. One day later, symptoms of dizziness and headache, etc. in the patient were improved and blood gas analysis showed pH 7.25, lactate 2.9 mmol/L, base excess -3.0 mmol/L; 5 days later, the above symptoms basically disappeared and blood gas analysis showed pH 7.45, lactate 1.5 mmol/L, base excess -2.0 mmol/L.

A 32-year-old female patient received anti-virus treatment with tenofovir alafenamide one month after regular hemodialysis due to stage 5 chronic kidney disease complicated with chronic hepatitis B. At the same time, recombinant human erythropoietin injection and iron sucrose injection was periodically used to correct anemia. Her hemoglobin was about 96 g/L without clinical manifestations of anemia such as nausea and fatigue. Eight months after tenofovir alafenamide treatment, she developed dizziness, headache, nausea, fatigue, and lethargy. Laboratory tests showed hemoglobin 94 g/L and serum creatinine 856 μmol/L; blood gas analysis showed pH 7.05, lactate 3.3 mmol/L, arterial partial pressure of oxygen 80 mmHg, arterial partial pressure of carbon dioxide 23 mmHg, base excess -7.4 mmol/L, and bicarbonate 15.6 mmol/L. It was considered that the patient had lactic acidosis, which might be associated with tenofovir alafenamide. The drug was stopped and replaced by entecavir and symptomatic treatments such as fluid rehydration and liver protection were given. One day later, symptoms of dizziness and headache, etc. in the patient were improved and blood gas analysis showed pH 7.25, lactate 2.9 mmol/L, base excess -3.0 mmol/L; 5 days later, the above symptoms basically disappeared and blood gas analysis showed pH 7.45, lactate 1.5 mmol/L, base excess -2.0 mmol/L.

A 66-year-old female patient received gabapentin 0.3 g once daily for restless legs syndrome. After 3 days of medication, she developed muscle soreness, weakness of both legs, and dark brown urine. Laboratory tests showed myoglobin 2 855.0 μg/L, creatine kinase (CK) 3 009 U/L, CK-MB 61 U/L, serum creatinine (Scr) 542 μmol/L, urine protein (+++), and urine occult blood (+). Her lower limb muscle strength was grade 1. Rhabdomyolysis caused by gabapentin was considered. Then the drug was stopped, and the symptomatic treatments including rehydration, alkalized urine, diuresis, etc. were given. After 5 days of treatments, the patient′s dark brown urine and muscle soreness disappeared, weakness of both lower limbs was improved, and lower limb muscle strength returned to grade 3. Laboratory tests showed ALT 35 U/L, AST 55 U/L, myoglobin 929.0 μg/L, CK 325 U/L, Scr 557 μmol/L, urine protein (+), and urine occult blood ( -). At a 1-month follow-up, the symptoms above-mentioned did not recur. Laboratory tests showed ALT 30 U/L, AST 38 U/L, myoglobin 135.0 μg/L, and CK 187 U/L.

A 44-year-old male patient received moxifloxacin 0.4 g orally once daily for pulmonary infection. He had normal renal function with serum creatinine (Scr) 67 μmol/L before treatment. Three days after medication, the patient developed abdominal pain, vomiting, oliguria, and 5 days later, laboratory tests showed Scr 1 372 μmol/L, blood urea nitrogen (BUN) 30.5 mmol/L, and estimated glomerular filtration rate (eGFR) 3.3 ml/(min·1.73 m 2). Acute tubulointerstitial nephritis was diagnosed by renal puncture and pathological examination. Drug-induced kidney injury was considered, which might be related to moxifloxacin. Moxifloxacin was discontinued and hemodialysis, anti-infection, and symptomatic treatments were given. The patient′s urine volume gradually recovered and renal function was improved. Fifteen days later, his Scr was 293 μmol/L and BUN was 10.5 mmol/L. One and a half months later, the Scr was 185 μmol/L and BUN was 9.8 mmol/L.

A 66-year-old female patient received gabapentin 0.3 g once daily for restless legs syndrome. After 3 days of medication, she developed muscle soreness, weakness of both legs, and dark brown urine. Laboratory tests showed myoglobin 2 855.0 μg/L, creatine kinase (CK) 3 009 U/L, CK-MB 61 U/L, serum creatinine (Scr) 542 μmol/L, urine protein (+++), and urine occult blood (+). Her lower limb muscle strength was grade 1. Rhabdomyolysis caused by gabapentin was considered. Then the drug was stopped, and the symptomatic treatments including rehydration, alkalized urine, diuresis, etc. were given. After 5 days of treatments, the patient′s dark brown urine and muscle soreness disappeared, weakness of both lower limbs was improved, and lower limb muscle strength returned to grade 3. Laboratory tests showed ALT 35 U/L, AST 55 U/L, myoglobin 929.0 μg/L, CK 325 U/L, Scr 557 μmol/L, urine protein (+), and urine occult blood ( -). At a 1-month follow-up, the symptoms above-mentioned did not recur. Laboratory tests showed ALT 30 U/L, AST 38 U/L, myoglobin 135.0 μg/L, and CK 187 U/L.

A 44-year-old male patient received moxifloxacin 0.4 g orally once daily for pulmonary infection. He had normal renal function with serum creatinine (Scr) 67 μmol/L before treatment. Three days after medication, the patient developed abdominal pain, vomiting, oliguria, and 5 days later, laboratory tests showed Scr 1 372 μmol/L, blood urea nitrogen (BUN) 30.5 mmol/L, and estimated glomerular filtration rate (eGFR) 3.3 ml/(min·1.73 m 2). Acute tubulointerstitial nephritis was diagnosed by renal puncture and pathological examination. Drug-induced kidney injury was considered, which might be related to moxifloxacin. Moxifloxacin was discontinued and hemodialysis, anti-infection, and symptomatic treatments were given. The patient′s urine volume gradually recovered and renal function was improved. Fifteen days later, his Scr was 293 μmol/L and BUN was 10.5 mmol/L. One and a half months later, the Scr was 185 μmol/L and BUN was 9.8 mmol/L.

OBJECTIVE: To investigate the effect of chronic emotional stimulation induced by empty bottle stimulation on CXCL12/CXCR4-mediated inflammatory response in rats with acute myocardial infarction (AMI). METHODS: Rat models of anxiety were established by a 21-day stimulation with uncertain empty bottle drinking water, and myocardial infarction was induced by ligating the left anterior descending branch of the coronary artery; compound models were established by performing myocardial infarction operation on the 15th day of anxiety modeling. The rats were randomly divided into 4 groups: shamoperated group (=6), myocardial infarction group (=6), compound model group (with myocardial infarcted and anxiety; = 6), and inhibitor group (compound models treated daily with 1 mg/kg AMD3100 for 6 days; =7). Echocardiography was used to examine the LVEF and LVFS to evaluate the cardiac function of the rats. Elevated maze test and open field test were used to evaluate the behaviors of the rats. The expressions of CXCL12, CXCR4, IL-1β, IL-18 and neutrophil active protease (NE) in the myocardial tissues and blood samples were detected with ELISA and immunohistochemistry. RESULTS: The LVEF and LVFS were lower in the compound model group than in the sham group and myocardial infarction group ( < 0.05), and were higher in inhibitor group than in the compound model group ( < 0.05). LVID; d and LVID; s were lower in the inhibitor group than in the compound model group ( < 0.05). Compared to those in the sham group and myocardial infarction group, the rats in the compound model group more obviously preferred to stay in the closed arm ( < 0.05) in EPM; the rats in the inhibitor group had more times of entering and staying in the open arm than the compound model rats ( < 0.05); the horizontal and vertical movements were less in the compound model rats than in those in the sham group and the myocardial infarction group ( < 0.05) in OFT, and the vertical movement of the rats in inhibitor group was higher than those in the compound model group ( < 0.05). The expression of CXCR4 in the marginal zone of myocardial infarction was significantly higher in the compound model group than in the sham-operated group, myocardial infarction group and inhibitor group ( < 0.05). The expressions of IL-1β, IL-18 and NE in the inhibitor group were significantly lower than those in the compound model group ( < 0.05). Compared with at in the sham-operated group, the number of Nissl bodies in the compound model group decreased significantly ( < 0.01). CONCLUSIONS Chronic emotional stress induced by empty bottle stimulation can lead to dysfunction of the CXCL12/CXCR4 axis, which causes inflammatory cascade after myocardial infarction to worsen myocardial cell necrosis, cardiac function and hippocampal neuronal damage after the infarction.
Animals ; Chemokine CXCL12 ; Coronary Vessels ; Emotions ; Myocardial Infarction ; Myocardium ; Psychological Distress ; Rats ; Receptors, CXCR4 ; Signal Transduction

A 39-year-old male patient took orlistat 0.12 g thrice daily for weight loss. More than 4 months after medication, he developed muscle soreness of limbs and weakness of both lower limbs, with lower limb muscle strength at grade 3. Laboratory tests showed alanine aminotransferase (ALT) 65 U/L, aspartate aminotransferase (AST) 125 U/L, myoglobin>3 997 μg/L, creatine kinase (CK) 2 889 U/L, CK-MB (CK-MB) 71 U/L, serum creatinine (Scr) 1 418 μmol/L, urine protein (+++), and urine occult blood (+). Rhabdomyolysis caused by orlistat was considered. Orlistat was stopped and symptomatic treatments such as rehydration, alkaline urine, and diuretics were given. Seven days later, the patient′s symptoms were improved and the muscle strength of his lower limbs returned to grade 4. Laboratory tests showed ALT 52 U/L, AST 68 U/L, myoglobin 1 737 μg/L, CK 475 U/L, Scr 657 μmol/L, urine protein (+), and urine occult blood (-). One month later, the muscle strength of his lower limbs returned to grade 6. Laboratory tests showed ALT 35 U/L, AST 38 U/L, myoglobin 624 μg/L, and CK 192 U/L. The symptoms of myalgia and weakness of lower limbs did not recur.