Early Adverse Reactions to Snake Antivenom: Poison Center Data Analysis

Antivenom is an essential treatment for snake envenomation; however, early adverse reactions (EARs) are major limitations to its use. We performed a retrospective cross-sectional study using Ramathibodi Poison Center data (January 2016 to December 2017) to clarify the incidence and severity of EARs following different F(ab’)2 antivenoms. Among 1006 envenomed patients, 684 (68%) received antivenom therapy with a total of 1157 doses, mostly green pit viper antivenom. The overall EAR incidence and rate were 22. 5% (154/684) and 15% (173/1157), respectively. The EAR rate following each type of antivenom was >10%, except for Russell’s viper antivenom (2.9%); the severe reaction rate was 2.6% (30/1157). Malayan pit viper bites caused a high incidence of EARs (37.8%) and the highest EAR rate (22.3%). Fifty-two cases developed anaphylaxis. All EARs occurred within 2 h after treatment initiation. No deaths were attributed to EARs. The duration of administration was significantly different between doses of antivenom that induced EARs and those that did not. In conclusion, all types and every dose of antivenom should be infused for 30–60 min. Preparation of resuscitation equipment and continuous clinical observation are crucial for at least 2 h after administration, and prompt treatment should be provided when EARs occur

Association between Inflammatory Marker, Environmental Lead Exposure, and Glutathione S-Transferase Gene

A number of studies suggested that lead is related to the induction of oxidative stress, and alteration of immune response. In addition, modifying these toxic effects varied partly by GST polymorphism. The objectives of this study were to assess the association between the lead-induced alteration in serum hs-CRP, with GSTM1, GSTT1, and GSTP1 Val105Ile genetic variations and the health consequence from environmental lead exposure. The 924 blood samples were analyzed for blood lead, CRP, and genotyping of three genes with real-time PCR. Means of blood lead and serum hs-CRP were 5.45 μg/dL and 2.07 mg/L. Both CRP and systolic blood pressure levels were significantly higher for individuals with blood lead in quartile 4 (6.48–24.63 μg/dL) compared with those in quartile 1 (1.23–3.47 μg/dL, P6.47 μg/dL the adjusted odds ratio (OR) of CRP levels for individuals with GSTP1 variants allele, GSTM1 null, GSTT1 null, double-null GSTM1, and GSTT1 compared with wild-type allele was 1.46 (95% CI; 1.05–2.20), 1.32 (95% CI; 1.03–1.69), 1.65 (95% CI; 1.17–2.35), and 1.98 (95% CI; 1.47–2.55), respectively. Our findings suggested that lead exposure is associated with adverse changes in inflammatory marker and SBP. GST polymorphisms are among the genetic determinants related to lead-induced inflammatory response

Cyanide poisoning in Thailand before and after establishment of the National Antidote Project^*

<p><b>Context:</b> Antidote shortage is a global problem. In Thailand, the National Antidote Project (NAP) has operated since November 2010 to manage the national antidote stockpile, educate the healthcare providers on appropriate antidote use, and evaluate antidote usage.</p> <p><b>Objective:</b> To evaluate the effect of NAP implementation on mortality rate and antidote use in cyanide poisoning cases arising from ingestion of cyanide or cyanogenic glycoside.</p> <p><b>Methods:</b> This is a retrospective cohort of poisoning cases involving cyanide or cyanogenic glycoside ingestion reported to Ramathibodi Poison Center from 1 January 2007 to 31 December 2015. Mortality rate, antidote use, and appropriateness of antidote use (defined as correct indication, proper dosing regimen, and administration within 90 min) before and after NAP implementation were compared. Association between parameters and fatal outcomes was analyzed.</p> <p><b>Results:</b> A total of 343 cases involving cyanide or cyanogenic glycoside ingestion were reported to Ramathibodi Poison Center. There were 213 cases (62.1%) during NAP (Project group) and 130 cases (37.9%) pre-NAP implementation (Before group). Implementation of NAP led to increased antidote use (39.9% in Project group versus 24.6% in Before group) and a higher rate of appropriate antidote use (74.1% in Project group versus 50.0% in Before group). All 30 deaths were presented with initial severe symptoms. Cyanide chemical source and self-harm intent were associated with death (OR: 12.919, 95% CI: 4.863–39.761 and OR: 10.747, 95% CI: 3.884–28.514, respectively). No difference in overall mortality rate (13 [10.0%] deaths before versus 17 [8.0%] deaths after NAP) was found. In subgroup analysis of 80 cases with initial severe symptoms, NAP and appropriate antidote use reduced mortality (OR: 0.327, 95% CI: 0.106–0.997 and OR: 0.024, 95% CI: 0.004–0.122, respectively). In the multivariate analysis of the cases with initial severe symptoms, presence of the NAP and appropriate antidote use independently reduced the risk of death (OR: 0.122, 95% CI: 0.023–0.633 and OR: 0.034, 95% CI: 0.007–0.167, respectively), adjusted for intent of exposure, cyanide source, age, and sex.</p> <p><b>Conclusions:</b> After NAP implementation, both antidote use and appropriate antidote use increased. In cases presenting with severe symptoms, presence of the NAP and appropriate antidote use independently reduced the risk of mortality.</p