[Clinical analysis of 22 cases of syndrome caused by acute poisoning].

Objective: To analyze the clinical characteristics, treatment and prognosis of rhabdomyolysis (RM) caused by acute poisoning.Summarize the clinical characteristics and treatment experience, pay attention to the complications and improve the quality of rescue. Methods: We collecte and summarize the clinical data, treatment and prognosis of 22 cases of RM caused by acute poisoning. Results: We found that 21 patients (95.5%) had muscle damage, 13(59.1%) with coma, 8(36.4%) with brown, tea or even soy sauce urine, 6(27.3%) had acute renal injury (AKI), and 4(18.2%) had multiple organ dysfunction syndrome (MODS). After the treatment, 21 cases (95.5%) got better, and one case were discharged. All the patients with AKI were survived, three of them were treated by hemodialysis, and the other recovered gradually after massive fluid replacement. Conclusion: Acute poisoning combined with RM is not uncommon in clinic. We should pay attention to examination of serum enzymes and other indicators, observe the clinical symptoms and make early diagnosis. The key to diagnosis and treatment is early fluid resuscitation, comprehensive treatment, blood purification and maintain the stability of water and electrolyte.

[Analyses on relevant factors of the prognosis of elderly patients with acute poisoning].

Objective: To explore the risk factors influencing the prognosis of elderly patients with acute poisoning. Methods: We retrospected 177 elderly patients with Acute Poisoning who were treated in the emergency department of the first affiliated hospital of wenzhou medical university from July 2009 to May 2015. According to the outcome of patients, we distributed the patients to death group (31 cases) and survival group (146 cases) , compared the clinic data and using multivariate analysis with Logistic regression to prognosis factors. Results: There were 177 cases in total, with 146 survivors (82.5%) and 31 deaths (17.5%) . In which 102 cases (57.6%) had chronic underlying diseases. There were 28 cases of pesticide poisoning in the death group, and the fatality rate of pesticide poisoning was 23.5%. The mortality rate was 12.8% in the 60-69 years-old group (11/86) , 20% (13/65) in the 70-79 years-old group, 26.9% (7/26) in the 80-89 years-old group. The most common reason of poisoning was intentional ingestion, with 100 cases (56.5%) . The tract of the poisoning was mainly in digestive system, including 148 cases (83.6%) . The PSS score and APACHE-II score were 2.97±0.18 and 19.8±2.8 in the death group, 2.27±0.81 and 12.8±5.3 in the survival group. Compared with the survival group, poison (pesticides or non) 、poisoning route、cause of poisoning、PSS score、APACHEⅡ score have significant difference in death group (P<0.05) . Poison (pesticides or non) 、PSS score、APACHEⅡ, were the independent risk factors of poor prognosis. Conclusion: Most of the elderly patients with acute poisoning have one or more chronic underlying diseases, the digestive tract ingestion and pesticide poisoning are more common. The fatality rate of the old patients is significantly higher than that of non elderly poisoning. Type of toxications, PSS score and APACHE-II score are the prognostic factors in elderly patients.

[Mechanism research and effect of ulinastatin in the brain tissue injury of acute hydrogen sulfide intoxicated rats].

OBJECTIVE: To observe the effect of Ulinastatin (UTI) in the dynamic changes of aquaporin 4 (AQP4) and cyclooxygenase-2 (COX-2) in the brain tissue injury of acute hydrogen sulfide (H2S) intoxicated, to explore the Mechanism of brain tissue injury of acute H2S-intoxicated and the protection effect of UTI. METHODS: A total of 96 SD rats of clean grade were divided randomly into four groups: normal control group (NS group, n=8) , UTI control group (UTI group, n=8) , H2S-intoxicated model group (H2S group, n=40) , UTI treatment group (H2S+UTI group, n=40). The H2S group and H2S+UTI group were exposed to H2S (284 mg/m(3)) by inhalation for 1 h, then H2S+UTI group was intraperitoneally exposed to UTI at the dose of 10(5) U/kg for 2 h, H2S group and H2S+UTI group were sacrificed at 2, 6, 12, 24 and 48 h after exposure, respectively. Remove the brain tissue, observe the rats behavioral changes at each time points. The mRNA expression of AQP4、COX-2 and NSE in the brain tissue were measured by RT-PCR method, and the protein expression of AQP4、COX-2 and NSE in the brain tissue were detected by immunohistochemical Streptavidin-perosidase method. Pathological changes of brain tissue were observed by lightmicroscope. RESULTS: 1、Nerve cells in the H2S group rats had edema, degeneration, focal inflammatory cell infiltrate, capillary hyperplasia, expansion. Compared with NS group, the cerebral NSE mRNA and protein expression at each time point in H2S group after exposure were significantly increased (P<0.01). 2、Compared with NS group, the cerebral AQP4 and COX-2 mRNA and protein expression at each time point in H2S group after exposure were significantly increased (P<0.01). 3、The degree of brain damage was significantly decreased in H2S+UTI group than that in H2S group. Compared with H2S group, the cerebral NSE mRNA and protein expression at 6, 12, 24 and 48 h in H2S+UTI group after exposure were significantly decreased (P<0.01) , no significantly difference at 2h (P>0.05). 4、Compared with the H2S group, the cerebral AQP4 and COX-2 mRNA and protein expression at 6, 12, 24 and 48 h in H2S+UTI group after exposure were significantly decreased (P<0.01) , slightly decreased at 2 h. CONCLUSION: The mechanism of brain injury of acute hydrogen sulfide intoxicated associated with abnormal expression of the cerebral AQP4, COX-2 levels. Intervention of UTI can reduce the cerebral AQP4 and COX-2 levels after hydrogen sulfide intoxicated, reduce the degree of brain injury.

Mifepristone-inducible recombinant adenovirus attenuates paraquat-induced lung injury in rats.

OBJECTIVE: To investigate the effects of overexpression of nuclear factor E2-related factor-2 (NRF2) on lung injury in rats exposed to paraquat (PQ) poisoning. METHODS: A mifepristone (RU486)-inducible recombinant adenoviral vector carrying the human NRF2 gene (Ad-RUNRF2) was constructed and transfected via airway into the rats 7 days before the administration of RU486. Rats were orally challenged with PQ at 20 mg/kg 24 h after the injection of RU486. On days 0.5, 3 and 21 after PQ poisoning, the expressions of NRF2 and cytokines related to inflammation and oxidation in lung tissue were examined. RESULTS: RU486 remarkably enhanced NRF2 mRNA and NRF2 protein levels in Ad-RUNRF2-transfected rats in a dose-dependent manner (p < 0.01). PQ stimulated compensatory overexpression of NRF2, heme oxygenase 1 (HO-1) and NAD(P)H quinone oxidoreductase 1 (NQO-1) in lungs on days 0.5 and 3 after exposure (p < 0.05), but depleted the expression of catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione (GSH), with an increased malondialdehyde (MDA) (p < 0.05). However, pretreatment with Ad-RUNRF2 and RU486 strongly enhanced the expression levels of NRF2, HO-1, NQO-1, CAT and GSH-Px in the lungs of PQ intoxicated rats, with increased GSH and decreased MDA (p < 0.05). Pretreatment with Ad-RUNRF2 and RU486 also strongly suppressed the PQ-induced activation of nuclear factor κB (NF-κB) and decreased the levels of tumour necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß) and interleukin-6 (IL-6). In addition, Ad-RUNRF2 and RU486 induction significantly reduced PQ-induced pathological changes in lungs and attenuated lung oedema and protein leakage caused by PQ (p < 0.05). CONCLUSION: RU486-induced overexpression of NRF2 in lungs transfected with Ad-RUNRF2 can ameliorate PQ-induced lung injury by the activation of the NRF2-antioxidant response element (ARE) pathway.