Chlorfenapyr is a novel pyrrole insecticide widely used in agricultural production. Due to its broad insecticidal activity, low resistance, rapid action, and long-lasting effects, its use has been increasing. In the past three years, there have been incidents of imidacloprid poisoning in China. We reviewed and analyzed the clinical characteristics of patients treated for chlorfenapyr poisoning at the People's Hospital of Chuxiong Yi Autonomous Prefecture from November 2019 to November 2023. The 23 patients included 15 males and 8 females, with ages ranging from 11 to 71 years. Twenty-two cases were due to gastrointestinal exposure, and one case was due to skin or respiratory tract exposure. Clinical symptoms included nausea, vomiting, fever, profuse sweating, and altered consciousness. Laboratory tests showed elevated levels of aspartate aminotransferase and creatine kinase. There was no specific antidote available, and 10 patients died after treatment, resulting in a mortality rate of 43.5%. Among the deceased, a higher proportion experienced fever, profuse sweating, altered consciousness, and generalized muscle stiffness.

Chlorfenapyr is a novel pyrrole insecticide widely used in agricultural production. Due to its broad insecticidal activity, low resistance, rapid action, and long-lasting effects, its use has been increasing. In the past three years, there have been incidents of imidacloprid poisoning in China. We reviewed and analyzed the clinical characteristics of patients treated for chlorfenapyr poisoning at the People's Hospital of Chuxiong Yi Autonomous Prefecture from November 2019 to November 2023. The 23 patients included 15 males and 8 females, with ages ranging from 11 to 71 years. Twenty-two cases were due to gastrointestinal exposure, and one case was due to skin or respiratory tract exposure. Clinical symptoms included nausea, vomiting, fever, profuse sweating, and altered consciousness. Laboratory tests showed elevated levels of aspartate aminotransferase and creatine kinase. There was no specific antidote available, and 10 patients died after treatment, resulting in a mortality rate of 43.5%. Among the deceased, a higher proportion experienced fever, profuse sweating, altered consciousness, and generalized muscle stiffness.

Objective:To explore the protective effect of astaxanthin on acute liver injury induced by α-amanitin in mice.Methods:In June 2023, 42 healthy SPF male Kunming mice were selected. The mice were divided into blank control group, model (0.45 mg/kg α-amanitin) group, olive oil (10 ml/kg olive oil) group, low dose (20 mg/kg) astaxanthin group, medium dose (40 mg/kg) astaxanthin group, high dose (80 mg/kg) astaxanthin group and silybin (20 mg/kg) group by random number table method. Each group had 6 animals. Mice in the blank control group were intraperitoneally injected with 10 ml/kg normal saline, and mice in the other group were injected with α-amanitin. After that, the blank control group and model group were infused with 10 ml/kg normal saline, olive oil group and astaxanthin groups were given olive oil and astaxanthin according to dose by gavage, and silybin group was injected with silybin by dose. The drug was administered once every 12 h for a total of 4 doses. After 60 h, the mice were killed, the liver weight was weighed, and the liver index was calculated. The contents of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in serum of mice were detected, and the contents of superoxide dismutase (SOD), reduced glutathione (GSH), catalase (CAT), malondialdehyde (MDA) in liver tissues were also detected. One-way analysis of variance (ANOVA) was used to compare the difference of indexes among each group, and pairwise comparison was performed by Dunnett- t test. Results:The mice in the blank control group had smooth hair color, good spirit and normal behavior, while the mice in the other groups showed varying degrees of retardation and decreased diet, and no death occurred in each group. Body mass[ (26.67±1.51) g] and liver mass[ (1.23±0.14) g] in model group were significantly lower than those in blank control group [ (33.50±2.43) g and (1.87±0.16) g], and the differences were statistically significant ( P<0.05). The liver index [ (5.39±0.32) %, (5.83±0.30) %, (5.75±0.24) % and (5.78±0.16) %] in low, medium and high dose astaxanthin groups and silybin group were significantly higher than those in model group [ (4.61±0.12) %], and the differences were statistically significant ( P<0.05). Serum ALT and AST contents in model group [ (153.04±13.96) U/L and (59.08±4.03) U/L] were significantly higher than those in blank control group [ (13.77±1.29) U/L and (10.21±0.35) U/L], and the differences were statistically significant ( P<0.05). The contents of CAT, GSH and SOD in liver tissues of model group [ (9.40±2.23) U/mgprot, (3.09±0.26) μmol/gprot and (48.94±3.13) U/mgprot] were significantly lower than those of blank control group [ (26.36±2.92) U/mgprot, (6.76±0.71) μmol/gprot and (89.89±4.17) U/mgprot], the differences were statistically significant ( P<0.05). MDA content[ (6.33±0.24) nmol/mgprot] in liver tissue of model group was significantly higher than that of blank control group [ (0.91±0.21) nmol/mgprot], and the difference was statistically significant ( P<0.05). The CAT contents[ (18.64±1.76) U/mgprot, (18.20±1.76) U/mgprot, and (15.54±1.36) U/mgprot] in liver tissues of low, medium and high dose astaxanthin groups were significantly higher than those of model group, with statistical significances ( P<0.05). Compared with model group, SOD contents[ (72.16±7.44) U/mgprot, (93.18±5.28) U/mgprot, (103.78±7.07) U/mgprot, and (96.60±7.02) U/mgprot] in liver tissues of mice in low, medium and high dose astaxanthin groups and silybin group were significantly increased ( P<0.05), MDA contents [ (4.30±0.84) U/mgprot, (3.66±0.28) U/mgprot, (2.96±0.29) U/mgprot, and (2.88±0.39) U/mgprot] were significantly decreased ( P<0.05). Compared with model group, GSH content [ (7.90±1.25) μmol/gprot] in high dose astaxanthin group was significantly increased ( P<0.05) . Conclusion:Astaxanthin may alleviate acute liver injury induced by α-amanitin by alleviating oxidative stress in mice liver.

Objective:To explore the protective effect of astaxanthin on acute liver injury induced by α-amanitin in mice.Methods:In June 2023, 42 healthy SPF male Kunming mice were selected. The mice were divided into blank control group, model (0.45 mg/kg α-amanitin) group, olive oil (10 ml/kg olive oil) group, low dose (20 mg/kg) astaxanthin group, medium dose (40 mg/kg) astaxanthin group, high dose (80 mg/kg) astaxanthin group and silybin (20 mg/kg) group by random number table method. Each group had 6 animals. Mice in the blank control group were intraperitoneally injected with 10 ml/kg normal saline, and mice in the other group were injected with α-amanitin. After that, the blank control group and model group were infused with 10 ml/kg normal saline, olive oil group and astaxanthin groups were given olive oil and astaxanthin according to dose by gavage, and silybin group was injected with silybin by dose. The drug was administered once every 12 h for a total of 4 doses. After 60 h, the mice were killed, the liver weight was weighed, and the liver index was calculated. The contents of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in serum of mice were detected, and the contents of superoxide dismutase (SOD), reduced glutathione (GSH), catalase (CAT), malondialdehyde (MDA) in liver tissues were also detected. One-way analysis of variance (ANOVA) was used to compare the difference of indexes among each group, and pairwise comparison was performed by Dunnett- t test. Results:The mice in the blank control group had smooth hair color, good spirit and normal behavior, while the mice in the other groups showed varying degrees of retardation and decreased diet, and no death occurred in each group. Body mass[ (26.67±1.51) g] and liver mass[ (1.23±0.14) g] in model group were significantly lower than those in blank control group [ (33.50±2.43) g and (1.87±0.16) g], and the differences were statistically significant ( P<0.05). The liver index [ (5.39±0.32) %, (5.83±0.30) %, (5.75±0.24) % and (5.78±0.16) %] in low, medium and high dose astaxanthin groups and silybin group were significantly higher than those in model group [ (4.61±0.12) %], and the differences were statistically significant ( P<0.05). Serum ALT and AST contents in model group [ (153.04±13.96) U/L and (59.08±4.03) U/L] were significantly higher than those in blank control group [ (13.77±1.29) U/L and (10.21±0.35) U/L], and the differences were statistically significant ( P<0.05). The contents of CAT, GSH and SOD in liver tissues of model group [ (9.40±2.23) U/mgprot, (3.09±0.26) μmol/gprot and (48.94±3.13) U/mgprot] were significantly lower than those of blank control group [ (26.36±2.92) U/mgprot, (6.76±0.71) μmol/gprot and (89.89±4.17) U/mgprot], the differences were statistically significant ( P<0.05). MDA content[ (6.33±0.24) nmol/mgprot] in liver tissue of model group was significantly higher than that of blank control group [ (0.91±0.21) nmol/mgprot], and the difference was statistically significant ( P<0.05). The CAT contents[ (18.64±1.76) U/mgprot, (18.20±1.76) U/mgprot, and (15.54±1.36) U/mgprot] in liver tissues of low, medium and high dose astaxanthin groups were significantly higher than those of model group, with statistical significances ( P<0.05). Compared with model group, SOD contents[ (72.16±7.44) U/mgprot, (93.18±5.28) U/mgprot, (103.78±7.07) U/mgprot, and (96.60±7.02) U/mgprot] in liver tissues of mice in low, medium and high dose astaxanthin groups and silybin group were significantly increased ( P<0.05), MDA contents [ (4.30±0.84) U/mgprot, (3.66±0.28) U/mgprot, (2.96±0.29) U/mgprot, and (2.88±0.39) U/mgprot] were significantly decreased ( P<0.05). Compared with model group, GSH content [ (7.90±1.25) μmol/gprot] in high dose astaxanthin group was significantly increased ( P<0.05) . Conclusion:Astaxanthin may alleviate acute liver injury induced by α-amanitin by alleviating oxidative stress in mice liver.

Objective To analyze the epidemiological characteristics,clinical manifestations and treatment of hallucinogenic boletus poisoning patients,and to provide reference for clinical diagnosis and treatment.Methods We retrospectively analyzed the epidemiological data,clinical manifestations,laboratory tests,treatment and outcomes of 36 patients with hallucinogenic boletus poisoning in our hospital from 2015 to 2022,and identified the species of mushrooms responsible for poisoning the patients.Results Of the 36 cases,32 cases were poisoned from June to September,24 cases were poisoned in towns and 12 cases in the countryside.Twenty-three patients were poisoned after eating multiple meals.Thirty-five patients ate Boletus lanmao identified by using genetic fingerprint and 7 ate Lanmaoa asiatica by using genetic sequence comparison.The incubation period of poisoning ranged from 1 to 48 h,with a median(quartile)of 19.0(12.0,24.8)h.All 36 cases had hallucinatory symptoms.Other symptoms were agitation and irritability in 21 cases,consciousness disorders in 29 cases,motor disorders in 21 cases,speech disorders in 19 cases and gastrointestinal symptoms in 18 cases.Laboratory tests showed that 16 patients had increased white blood cells(WBC)and percentage of neutrophils(NEUT%)and decreased percentage of lymphocyte(LY%).After fluid resuscitation combined with sedation and antipsychotic medication,all patients were cured and discharged from the hospital,of which 33 cases were discharged within 7 days.Conclusion Hallucinogenic boletus mushroom poisoning mainly occurs in summer and fall,the poisoned mushrooms are mainly Lanmaoa asiatica mushrooms,the incidence of poisoning is high in patients eating multiple meals,and the typical symptom is hallucination,and the patients can be cured through active symptomatic supportive treatment.

Mushroom poisoning with amatoxins can cause liver dysfunction in patients, and death in severe cases. The amatoxins detection by enzyme-linked immunosorbent assay (ELISA) can help early clinical diagnosis. Three patients were identified as α-amatoxin containing mushroom poisoning by ELISA. The first symptoms of patients was gastrointestinal symptoms, and liver function damage occured later. One patient gave up treatment and died. After received supportive treatments such as adsorption of toxins, catharsis, fluid supplementation to promote toxin metabolism and liver protection, 2 patients were recovered and discharged.

Mushroom poisoning with amatoxins can cause liver dysfunction in patients, and death in severe cases. The amatoxins detection by enzyme-linked immunosorbent assay (ELISA) can help early clinical diagnosis. Three patients were identified as α-amatoxin containing mushroom poisoning by ELISA. The first symptoms of patients was gastrointestinal symptoms, and liver function damage occured later. One patient gave up treatment and died. After received supportive treatments such as adsorption of toxins, catharsis, fluid supplementation to promote toxin metabolism and liver protection, 2 patients were recovered and discharged.