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OBJECTIVE: To analyze the experience of diagnosis and treatment of a case of brodifacoum poisoning. METHODS: The clinical data of a case of unexplained brodifacoum poisoning was retrospectively analyzed. RESULTS: The patient went to the doctor for unexplained bleeding. The bleeding symptoms included nasal o blood ozing, blood in saliva and skin ecchymosis. Blood anticoagulative rodenticide test showed positive with brodifacoum. The results of coagulative function tests showed that the indexes of partial prothrombin time, prothrombin time and fibrinogen were increased. The patient was diagnosed as brodifacoum poisoning based on the clinical symptoms and laboratory test results. The combined use of 40 mg/d of vitamin K_1 and frozen plasma improved the clotting time and quickly alleviated the bleeding symptoms of the patient. However, the patient′s bleeding symptoms recurred when vitamin K_1 was discontinued. The patient was hospitalized for 62 days and then discharged. With follow-up one month after discharge, the patient showed no bleeding symptoms, but brodifacoum could still be detected in the blood. CONCLUSION: The symptoms of brodifacoum poisoning may relapse and the treatment course is long. Vitamin K_1 could be used as the first-choice medicine for the treatment of brodifacoum poisoning, but its usage needs to be optimized.
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OBJECTIVE: To explore the immune cytotoxic effect and the maximum non-effect dose of trichloroethylene( TCE) on Jurkat T cells in vitro. METHODS: i) Naive and activated Jurkat T cells were treated with different concentrations of TCE( 0. 10, 0. 50, 1. 00, 2. 00, 5. 00, 10. 00 mmol / L). Phorbol-12-myristate-13-acetate and ionomycin were used as agonist. No TCE was used in the control group and dimethyl sulfoxide( DMSO) was used as the solvent group. The morphology of Jurkat T cells was observed using a light microscope and the survival rate of Jurkat T cells was investigated using CCK-8 essay after cells were cultured for 24,48 and 72 hours. ii) Nave and activated Jurkat T cells were treated with different concentrations of TCE( 0. 00,0. 02,0. 20,2. 00 mmol / L). The apoptosis of cells was detected using flow cytometry and the level of interleukin-2( IL-2) in supernatant was detected using enzyme linked immunosorbent assay after cells were cultured for 24,48 and 72 hours. RESULTS: i) Cytotoxic effect was observed after cells were exposed to 10. 00 mmol / L TCE for 24 hours. Cells dispersed,cell volume diminished,cell membrane ruptured,cytoplasm condensed and increased outflow of intercellular organelles. The effect of interaction between exposure dose and exposure time was statistically significant on cell survival rate( P < 0. 01). Compared with the control and DMSO groups at the same time points,there were no significant differences in the 0. 10,0. 50,1. 00 and 2. 00 mmol / L TCE treatment groups in cell survival rates in three different time points( P > 0. 05),while the cell survival rates of 5. 00 and 10. 00 mmol / L TCE treatment groups were significantly decreased( P < 0. 01). ii) When TCE concentration was 0. 00-2. 00 mmol / L,there were no significant differences in the main effect of exposure dose and interactions of between exposure dose and cell type or exposure time on cell apoptosis rate( P > 0. 05). Compared with the same time points and groups of naive Jurkat T cells,the levels of IL-2 of activated Jurkat T cells were significantly increased( P < 0. 01). In the three different time points,the level of IL-2 of activated Jurkat T cells increased in accordance with the TCE exposure dose,showing a dose-effect relationship( P < 0. 01). The level of IL-2 of activated Jurkat T cells increased in accordance with TCE exposure time,showing a time-effect relationship( P < 0. 01). CONCLUSION:s TCE at the level of 2. 00 mmol / L had no observed effect in Jurkat T cells. High doses of TCE( ≥5. 00 mmol / L) showed cytotoxic damages to naive and activated Jurkat T cells and low doses of TCE( ≤2. 00 mmol / L) could stimulate activated Jurkat T cells secrete IL-2 in a dosedependent and time-dependent manner.
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OBJECTIVE: To analyze the usage of glucocorticoid in patients who were treated with occupational medicamentose-like dermatitis due to trichloroethylene( OMDT),in order to provide a reference for regulating the glucocorticoid treatment of the disease. METHODS: Using a retrospective survey method,144 OMDT cases of patients who were diagnosed and cured by Guangdong Province Hospital for Occupational Disease Prevention and Treatment from 2001 to2013 were selected. The general information,clinical data and the use of glucocorticoid were collected and analyzed.RESULTS: i) The usage of glucocorticoid. The median and the 0th to 100 th percentile [M( P_0-P_(100)) ] of first dose of methylprednisolone was 100. 00( 40. 00-1 000. 00) mg / d; 58 patients( 40. 3%) using the first dose of treatment were ineffective. The dosage of glucocorticoid was increased one week after admission,the M( P_0-P_(100)) to an initial dose of120. 00( 40. 00-1 000. 00) mg / d; The M( P_0-P_(100)) of maintenance time of initial dose was 5. 5( 1. 0-14. 0) days. After treating effectively,should the decrement to stop using gradually the first glucocorticoid. The dose was gradually cut down to 20-50 mg every 1 to 3 days if the glucocorticoid dose was more than 100 mg / d; it was cut down to 10 mg every 2 to 3days if the glucocorticoid dose was less than 100 mg / d. The M( P_0-P_(100)) of glucocorticoid using time was 66. 0( 22. 0-229. 0) days. The M( P_0-P_(100)) of total amount of glucocorticoid was 3 510. 0( 420. 0 ~ 27 336. 3) mg. ii) The first dose of glucocorticoid in patients of erythema multiforme group were less than those of exfoliative dermatitis group and bullous epidermal necrolysis group( P < 0. 05),the initial dose and total amount of glucocorticoid were less than the other 3 types of rash( P < 0. 05). iii) Compared with the patients with severe impaired liver function,the first dose,the initial dose and the total amount of glucocorticoid were significantly higher than those in mild impaired liver function( P < 0. 05),and the time of using glucocorticoid was longer than that in mild impaired liver function( P < 0. 05). iv) The first dose and the initial dose of glucocorticoid in patients were positively correlated with the total amount of glucocorticoid [Spearmen correlation coefficient( r_S) were 0. 73 and 0. 78 respectively,P < 0. 01). The maintenance time of the initial dose of glucocorticoid was not correlation with the time of patients who were out of contact with trichloroethylene or the urinary level of trichloroacetic acid at admission( r_Swere- 0. 14 and 0. 10 respectively,P > 0. 05). v) Binary Logistic regression analysis showed that,if the patients who had no erythema multiforme,the more severe the degree of liver dysfunction or the white blood cell count higher than 9. 5 × 10~9/ L,the first dose of glucocorticoid used should be more than 120 mg / d( P <0. 05). CONCLUSION: Liver function and type of rash are important factors that affect the usage of glucocorticoid in patients with OMDT. Glucocorticoid therapy should be prescribed in reference to the liver function and skin lesion of patients with OMDT.