Reassessing clinical presentations of emamectin benzoate poisoning: A comprehensive study.

BACKGROUND: The mechanism of emamectin benzoate (EMB-a macrocyclic lactone insecticide like abamectin) action involves the disruption of glutamate-gated chloride channels and GABA receptors in insects, leading to paralysis and death. EMB overdose can breach the blood-brain barrier, resulting in severe poisoning and altered consciousness. AIM: Review EMB poisoning presentations in patients and reevaluate clinical manifestations. MATERIALS AND METHODS: This retrospective study reviewed (August 31, 2008-August 31, 2023) medical university hospital records. We analyzed symptoms, patient characteristics, vital signs, Glasgow Coma Scale scores, laboratory findings, and outcomes. RESULTS: Ten patients (males: 6, females: 4, median age = 64.5 years) experienced EMB poisoning. Common symptoms included sore throat, gastrointestinal distress, dyspnea, and altered consciousness; two patients showed laryngeal corrosive injuries. Management involved activated charcoal administration, gastric lavage, and intensive care unit admission. DISCUSSION: Sore throat and corrosive injuries were distinctive presentations of EMB poisoning, warranting vigilance. Potential mechanisms of corrosive injury include skin and eye irritation effects of EMB, the solvents of which might exert corrosive action. CONCLUSION: EMB poisoning manifests as diverse symptoms, including sore throat, gastrointestinal symptoms, central nervous system depression, and potential aspiration pneumonia. Recognizing and promptly managing EMB poisoning are crucial for enhancing patient outcomes and minimizing complications.

Rat Bait, Not Healthy Rice!

Bromadiolone, a potent, long-acting anticoagulant rodenticide is frequently tinted to a red or pink color and mixed with cereals as rat bait. Six peoples working in a small factory suffered from a severe bleeding tendency several weeks after consuming a rice meal that was tainted with bromadiolone mistaken to be healthy food. High serum levels of bromadiolone and excessive bleeding were found in these individuals, and they needed vitamin K1 therapy for weeks. These cases indicated that long-acting anticoagulant rodenticide might induce cumulative toxicity in repeated, low-dose exposure, and the blood levels of bromadiolone might be an indicator for antidote therapy if available.

Oral administration of injectable vitamin K1 in brodifacoum intoxication.

Brodifacoum is a highly potent and long-acting anticoagulant rodenticide (LAAR). LAAR poisoning possibly leads to long term bleeding problems and needs vitamin K1 treatment for several months. Due to economic concern, tablet preparation of vitamin K1 was not available in most of the countries, including Taiwan. In literature, few reports had pointed out that injectable form of vitamin K could be used orally in patients on anticoagulant therapy with supratherapeutic state. Here, we reported a family with 3 members suffering from brodifacoum poisoning with severe coagulopathy needed to prolong hospitalization for intravenous vitamin K1 therapy, and successfully managed with injectable formula orally for about 5 months. Oral administration of injectable vitamin K1 might be a suitable substitute for intravenous route in long-term treatment for LAAR poisonings.

Local Cytotoxic Effects in Cobra Envenoming: A Pilot Study.

The cobra (genus Naja (N.)) is one of the most common venomous snakes. Due to its frequency and deadly complications of muscle paralysis, local necrosis, and chronic musculoskeletal disability, it should not be ignored. The pathology of devastating tissue destruction, even though specific antivenoms exist, is not fully clear. Here, we attempted to dig in envenomed tissues to study the clinical toxicology of cobra venom. Four cases of N. atra snake envenomation, in which the subjects developed advanced tissue injury, were involved in this study. We used enzyme-ligand sandwich immunoassay (ELISA) to assay the whole venom, cytotoxin A3 and short-chain neurotoxin (sNTX) in blood, bullae, wound discharge, and debrided tissue. We found that persistently high concentrations of venom and toxins, especially cytotoxin A3, were detected in bullae, wound discharge fluid and necrotic tissue of these patients even after large doses of specific antivenom treatment, and wide excision and advanced debridement could largely remove these toxins, lessen the size of necrosis, and promote wound healing. We also found that the point-of-care apparatus, ICT-Cobra kit, might be used to promptly monitor the wound condition and as one of the indicators of surgical intervention in cases of cobra envenomation in Taiwan.

Lead poisoning due to incense burning: an outbreak in a family.

BACKGROUND: In Asia and some other regions of the world, incense burning is an important folk and cultural activity. However, this ritual can cause health impacts, such as chronic respiratory diseases and neoplasms. Herein, we describe a family with lead poisoning possibly related to the frequent use of incense sticks at home. CASE REPORT: A 65-year-old homemaker with severe anemia, pitting edema of the lower legs, bone pain, abdominal pain, and exertional dyspnea for several months presented to our clinic. Her blood workup indicated severe anemia with basophilic stippling in red blood cells and blood lead level (BLL) of 59.75 µg/dL. Her husband, three children, and four grandchildren who lived with her also had high BLLs. As a Daoist clergy person, she had been exposed to a large amount of smoke from every day use of incense for >30 years. In the field investigation, the chronic dust deposited in hidden corners of their home had considerably higher lead content and other toxic metals. DISCUSSION: Our observations indicated chronic, frequent exposure to smoke from incense burning may be a cause of lead poisoning. Strict avoidance of incense smoke is a significant step toward preventing lead poisoning in children in societies with the custom of incense burning.

The prevalence of esophageal cancer after caustic and pesticide ingestion: A nationwide cohort study.

Habits such as smoking and alcohol drinking and existing esophageal malfunction are considered the main risk factors for esophageal carcinogenesis. Caustic ingestion of acidic or alkaline agents or strong irritants can induce severe esophageal corrosive injury and increase esophageal cancer risk. We studied the relationship between esophageal carcinoma and acute detergent or pesticide poisoning by using nationwide health insurance data. Methodology/Principle findings: We compared a pesticide/detergent intoxication cohort (N = 21,840) and an age- and gender-matched control cohort (N = 21,840) identified from the National Health Insurance Research Database between 2000 and 2011. We used the multivariable Cox proportional model to determine esophageal carcinoma risk. The overall incidence density of esophageal cancer was 1.66 per 10,000 person-years in the comparison cohort and 4.36 per 10,000 person-years in the pesticide/detergent intoxication cohort. The corresponding adjusted hazard ratio (HR) for esophageal cancer was 2.33 (95% confidence interval [CI] = 1.41-3.86) in the pesticide/detergent intoxication cohort compared with the control cohort. Patients with corrosive and detergent intoxication did not have a higher risk of esophageal cancer (adjusted HR = 0.98, 95% CI = 0.29-3.33) than those without pesticide/detergent intoxication. However, patients with pesticide intoxication had a significantly higher risk of esophageal cancer (adjusted HR = 2.52, 95% CI = 1.52-4.18) than those without pesticide/detergent intoxication. Conclusion: In the present study, after adjusting for conventional risk factors, we observed that pesticide intoxication could exert substantial effects through increased esophageal cancer risk. However, patients with detergent intoxication may not have an increased risk of esophageal cancer.

Presentations of tetramethylammonium hydroxide dermal exposure and the valuable potential of diphoterine solution in decontamination: a retrospective observational study.

BACKGROUND: Tetramethylammonium hydroxide (TMAH) is a quaternary ammonium compound that is both a base corrosive and a cholinergic agonist, and it is widely used in the photoelectric and semiconductor industries. It causes corrosive skin injuries and systemic cholinergic toxicity with death primarily resulting from respiratory failure without efficacious early decontamination. METHODS: A retrospective observational study was performed of all cases of TMAH exposure reported to the Taiwan Poison Control Center between July 2010 and October 2017. Retrieved medical records were independently reviewed by two trained clinical toxicologists. RESULTS: Despite immediate (< 5 min) skin decontamination with copious amounts of tap water, one patient exposed to 25% TMAH involving ≥5% of total body surface area (TBSA) developed significant systemic toxicity. Patients exposed to 25% TMAH involving ≤1% TBSA developed first-degree chemical skin injuries but no systemic toxicity. Among patients exposed to lower concentrations (≤2.38%) of TMAH, the majority only experienced first-degree chemical skin injuries without systemic signs. Patients exposed to 0.5% TMAH involving nearly their entire TBSA developed no chemical skin injuries or systemic toxicity. All patients who had only first-degree chemical skin injuries did not develop systemic toxicity after exposure to either 2.38% or 25% TMAH. CONCLUSIONS: TMAH acts as an alkaline corrosive and cholinergic agonist. Systemic signs attributable to TMA+ can rapidly lead to respiratory failure and death after dermal exposure. We have demonstrated that an amphoteric solution may be efficacious for skin decontamination on-site immediately to prevent or ameliorate such toxicity. This practice especially carries a valuable potential in managing victims (patients) who have been exposed to those chemicals with immediate life-threatening toxicity (e.g. TMAH), suggesting that its early utilization deserves further study.

Collocation of avian and mammal antibodies to develop a rapid and sensitive diagnostic tool for Russell's Vipers Snakebite.

Russell's vipers (RVs) envenoming is an important public health issue in South-East Asia. Disseminated intravascular coagulopathy, systemic bleeding, hemolysis, and acute renal injury are obvious problems that develop in most cases, and neuromuscular junction blocks are an additional problem caused by western RV snakebite. The complex presentations usually are an obstacle to early diagnosis and antivenom administration. Here, we tried to produce highly specific antibodies in goose yolks for use in a paper-based microfluidic diagnostic kit, immunochromatographic test of viper (ICT-Viper), to distinguish RVs from other vipers and even cobra snakebite in Asia. We used indirect ELISA to monitor specific goose IgY production and western blotting to illustrate the interaction of avian or mammal antibody with venom proteins. The ICT-Viper was tested not only in prepared samples but also in stored patient serum to demonstrate its preliminary efficacy. The results revealed that specific anti-Daboia russelii IgY could be raised in goose eggs effectively without inducing adverse effects. When it was collocated with horse anti-Daboia siamensis antibody, which broadly reacted with most of the venom proteins of both types of Russell's viper, the false cross-reactivity was reduced, and the test showed good performance. The limit of detection was reduced to 10 ng/ml in vitro, and the test showed good detection ability in clinical snake envenoming case samples. The ICT-Viper performed well and could be combined with a cobra venom detection kit (ICT-Cobra) to create a multiple detection strip (ICT-VC), which broadens its applications while maintaining its detection ability for snake envenomation identification. Nonetheless, the use of the ICT-Viper in the South-East Asia region is pending additional laboratory and field investigations and regional collaboration. We believe that the development of this practical diagnostic tool marks the beginning of positive efforts to face the global snakebite issue.

A Rapid and International Applicable Diagnostic Device for Cobra (Genus Naja) Snakebites.

Cobra snakes (genus Naja) are some of the most dangerous snake species in Asia and Africa, as their bites cause severe life-threatening respiratory failure and local tissue destruction, especially in the case of late diagnosis. The differential diagnosis of snakebite envenomation still mainly relies upon symptomatology, the patient's description, and the experience of physicians. We have designed a rapid test, immunochromatographic test of cobra (ICT-Cobra), which obtained fair results in improving the diagnosis and treatment of Naja (N.) atra snakebites in Taiwan. In this study, we further investigated the feasibility of applying the kit for the detection of other cobra venoms based on the potential interspecies similarity. We firstly demonstrated the cross-reactivity between eight venoms of medically important cobra species and the rabbit anti-N. atra IgG that was used in ICT-Cobra by Western blotting and sandwich enzyme-linked immunosorbent assay. Then, ICT-Cobra was used to detect various concentrations of the eight venoms to elucidate its performance. Noticeable correlations between the cross-reactivity of venoms from genus Naja snakes and existing geographical characteristics were found. ICT-Cobra could detect venoms from other Asian cobras with variable detection limits comparable to those observed for N. atra, but the kit was less successful in the detection of venom from African cobras. The similar but slightly different venom components and the interaction between venom and rabbit anti-N. atra IgG led to variations in the detection limits. The transcontinental usage of ICT-Cobra might be possible due to the cross-reactivity of antibodies and similarities among the larger-sized proteins. This study showed that the close immunological relationships in the genus Naja could be used to develop a venom detection kit for the diagnosis of cobra envenomation in both Asian and African regions. Additional clinical studies and technical adjustments are still needed to improve the efficacy and broadening the application of ICT-Cobra in the future.

Oxidative storm in a patient with acute rotenone-containing plant poisoning.

A 64-year-old woman presented with coma, seizure, and lactic acidosis after ingesting 80 yam bean seeds. This rotenone-containing seeds cause cellular asphyxia via blockage of the mitochondrial electron transport. Subsequent oxidative stress results in the formation of lipid peroxidation (LPO). Rotenone analysis via liquid chromatography mass spectrometry revealed the following: 31,590 ng/mL in cooked yam bean seed and 100 ng/mL in the blood. We attempted to use N-acetylcysteine to alleviate oxidative stress and documented the continuous decline in the plasma concentration of LPO.

Alcohol use disorder tied to development of chronic kidney disease: A nationwide database analysis.

INTRODUCTION: Alcohol use disorder (AUD) is a spectrum of high risk behaviors including alcohol abuse and dependence. Chronic kidney disease (CKD) is progressive loss of renal function for more or equal to 3 months or presence of any irreversible kidney damage. Common risk factors of CKD have been identified, but the impact of alcohol consumption on kidney function is controversial. The study aims to investigate the relationship between alcohol use disorder and CKD on a national scale. METHODS: This retrospective cohort study was conducted using Taiwan's National Health Insurance research database. Patients aged 20 years or older, without CKD and with the diagnosis of AUD (ICD-9-CM codes 303.X; 305.0, V113) from years 2000 to 2013 were enrolled. Control cohort was selected to match the demographics of the target population. Patients were followed until the end of 2013 or earlier if they developed CKD, died, or lost follow up. Baseline characteristics and comorbidities were identified for risk stratification. RESULTS: We identified 11639 patients in the AUD cohort and 46556 patients in the control cohort. Compared to patients in the control cohort, those in the AUD group were more likely to have multiple comorbidities (p < 0.001 for all comorbidities). After adjustment of age, gender, baseline comorbidities, and nonsteroidal anti-inflammatory drug use, the diagnosis of AUD was associated with an increased risk of CKD development (aHR = 1.62, 95% CI, 1.46-1.81). During the mean follow up periods of 6.47 (standard deviation (SD) = 3.80) years for the AUD cohort and 7.23 (SD = 3.75) years for the control cohort, the overall incidence density of CKD was significantly higher in patients with AUD than those in the control cohort (3.48 vs 6.51 per 1000 person-years, aHR = 1.68, 95% CI, 1.50-1.87). Kaplan-Meier analysis showed that the AUD cohort had a higher cumulative incidence of CKD than the control cohort (log-rank test, p value < 0.001). Patients with AUD had higher risks of CKD in all the stratified groups, except for the subgroup with age over 65 years old. CONCLUSION: Our study suggested that AUD was associated with an increased incidence of newly diagnosed CKD by nearly two folds. Young age, in particular, had a higher association between AUD and CKD. Considering the preventable nature of AUD, establishing effective health policies is imperative to reduce high-risk alcohol behaviors and thereby prevent alcohol-related kidney disease. Further prospective studies are warranted to further elucidate the causation of AUD on kidney function.

Increased risk of pyogenic liver abscess in patients with alcohol intoxication: A population-based retrospective cohort study.

We designed a population-based retrospective cohort study to investigate the association between the event of alcohol intoxication and the risk of pyogenic liver abscess. The present study enrolled 245,076 patients with a history of alcohol intoxication from 2000 to 2010 and matched each of them with four comparison patients, with similar mean age and sex ratios. We determined the cumulative incidences and adjusted hazard ratios (aHRs) of liver abscess. A significant association was observed between alcohol intoxication and liver abscess. The incidence density rate of liver abscess was 3.47-fold greater in the alcohol intoxication (AI) cohort than in the non-AI cohort (12.2 vs. 3.43 per 10,000 person-years), with an adjusted HR (aHR) of 2.64 (95% CI = 2.26 to 3.08). This population-based study positively associated the event of alcohol intoxication with increased risk of liver abscess. Our findings warrant further large-scale and in-depth investigations in this area.

Association between antiepileptic drugs and hepatocellular carcinoma in patients with epilepsy: a population-based case-control study.

BACKGROUND: This study explored whether antiepileptic drugs (AEDs) use increases the risk of hepatocellular carcinoma (HCC). METHODS: We conducted a case-control study using data from the National Health Insurance system of Taiwan. The case group comprised 1,454 epilepsy patients with newly diagnosed HCC, and the control group comprised 1,448 epilepsy patients without HCC. Both groups had similar distributions of sex and age, and follow-up duration. Possible associations with the AEDs in Taiwan were examined. RESULTS: After adjusted for AEDs (phenobarbital and primidone, clonazepam, clorazepate and diazepam, and other AEDs), and for the comorbidities of diabetes, chronic liver disease and cirrhosis, hepatitis B and C virus infection, and alcoholism, the odds ratio (OR) of HCC was 1.22 (95% confidence interval [CI]: 1.01-1.47) for the group of phenytoin users compared with nonphenytoin users. An annual means of 61-120, 121-180, and >180 of defined daily doses (DDDs) of phenytoin (OR: 4.07, 95% CI: 2.03-8.18; OR: 7.51, 95% CI: 3.03-18.7, and OR: 14.6, 95% CI: 7.88-26.9, respectively) were significantly correlated with the risk of HCC but not with a DDD of ≤60. Compared with nonphenytoin users, HCC patients who had used phenytoin within 1 year of HCC diagnosis were at a greatest risk of HCC (adjusted OR: 2.29, 95% CI: 1.71-3.08), followed by who had used phenytoin within 2 years of diagnosis (adjusted OR: 1.92, 95% CI: 1.44-2.56). CONCLUSION: The results indicate that high dose of phenytoin was associated with a statistically significant increased OR for HCC, which was not demonstrated for low-dose phenytoin.

Etoposide induces pancreatic ß-cells cytotoxicity via the JNK/ERK/GSK-3 signaling-mediated mitochondria-dependent apoptosis pathway.

Etoposide is widely used in the treatment of the different types of tumors such as pancreatic cancer. However, etoposide also causes several unwanted side-effects in normal viable cells, including pancreatic ß-cells, which are vulnerable to chemical-induced injuries, and the molecular mechanisms underlying etoposide-induced apoptosis are still unclear. Here, the results showed that in RIN-m5F cells (a ß-cell-derived cell line), the number of viable cells was significantly decreased after 24h of etoposide treatment and underwent mitochondria-dependent apoptotic signals accompanied by mitochondrial dysfunction, and increases in the population of sub-G1 hypodiploid cells and apoptotic cells, caspase-3 activity, and the activation of caspase cascades. Etoposide also increased the phosphorylation levels of glycogen synthase kinase (GSK)-3α/ß in treated RIN-m5F cells. Pretreatment with LiCl, a GSK-3 inhibitor, prevented etoposide-induced mitochondria-dependent apoptosis and GSK-3 protein phosphorylation in RIN-m5F cells. Furthermore, exposure of the cells to etoposide induced the phosphorylation of c-Jun N-terminal kinase (JNK) and extracellular signal-related kinase (ERK)1/2 but not p38-MAPK, which was suppressed by the specific JNK inhibitor (SP600125) and ERK1/2 inhibitor (PD98059), respectively. Additionally, pretreatment with both SP600125 and PD98059 effectively suppressed etoposide-induced ß-cell cytotoxicity, apoptosis, and GSK-3 protein phosphorylation; however, LiCl did not reverse JNK and ERK1/2 phosphorylation. Taken together, these results suggest that etoposide is capable of causing cytotoxicity on pancreatic ß-cells by inducing apoptosis through the JNK/ERK-mediated GSK-3 downstream-triggered mitochondria-dependent signaling pathway.

Bacteriology of Naja atra Snakebite Wound and Its Implications for Antibiotic Therapy.

A total of 112 cases of Naja atra envenomation were examined at two referring hospitals: Taichung Veterans General Hospital in central Taiwan and Taipei Veterans General Hospital (VGH-TP) in northern Taiwan. Overall, 77% (86/112) of cases developed clinically suspected wound infections and 54% (61/112) required surgery secondary to tissue necrosis, finger or toe gangrene, and/or necrotizing fasciitis. Morganella morganii was the most abundant gram-negative bacterial strain isolated from bite wounds, followed by Proteus spp., Aeromonas hydrophila, Pseudomonas aeruginosa, and Providencia spp. in descending order; Enterococcus spp. were the most common gram-positive bacteria and Bacteroides spp. were the only anaerobic bacteria. A few episodes of bacteremia were caused by Bacteroides and Shewanella spp. There were no significant variations in the distribution of bacterial species between these two hospitals except for a higher incidence of M. morganii, Enterococcus spp., and polymicrobial infection observed at VGH-TP, which may have been related to variations in the fecal flora of prey and oral flora of individual snakes in different geographic areas in Taiwan. According to the susceptibility test involving various pathogens, first-line drug options for the management of N. atra snakebite wound infections may include monotherapy with ureidopenicillin or combination therapy with aminopenicillin and a third-generation cephalosporin or fluoroquinolone. A prospective evaluation of empiric antibiotic therapy for the management of N. atra snakebite should be considered.

Increased Risk of Mesenteric Ischemia in Patients With Alcohol Use Disorder: A Population-Based Retrospective Cohort Study.

OBJECTIVE: To investigate the association between alcohol use disorder and the risk of mesenteric ischemia by conducting a population-based retrospective cohort study. PATIENTS AND METHODS: The present study enrolled 62,115 patients hospitalized for alcoholic intoxication between January 1, 1999, and December 31, 2009, and matched each of them with 4 comparison patients with similar mean age and sex ratios. We determined the cumulative incidences and adjusted hazard ratios (aHRs) of mesenteric ischemia. RESULTS: A significant association was observed between alcoholic intoxication and mesenteric ischemia (aHR, 5.21; 95% CI, 4.36-6.23; P<.0001) after adjustment for age, sex, and comorbidity history of hypertension, hyperlipidemia, diabetes, atrial fibrillation, stroke, heart failure, chronic renal disease, ischemic heart disease, chronic obstructive pulmonary disease, and cirrhosis. After less than 1 year of follow-up, the incidence rate of mesenteric ischemia in the alcoholic intoxication group was approximately 9.38-fold higher than that in the comparison patients (aHR, 9.38; 95% CI, 5.52-15.9; P<.0001). CONCLUSION: Physicians should carefully consider the alcohol history of patients who complain of abdominal pain and respond poorly to treatment, because alcohol use disorder is a risk factor for mesenteric ischemia, a surgical emergency.

Association between ischemic stroke and carbon monoxide poisoning: A population-based retrospective cohort analysis.

BACKGROUND: The long-term consequence of cardiovascular health has not been evaluated for patients with carbon monoxide (CO) poisoning. This study evaluated the risk of ischemic stroke using population-based data. METHODS: We identified 8705 inpatients with CO intoxication diagnosed from 2000 to 2011 from the Taiwan National Health Insurance Research Database. The control cohort consisted of 34,820 persons randomly identified from patients without exposure frequency matched by age, sex, and the year of hospitalization. Incidence and hazard ratio (HR) of ischemic stroke were evaluated by sociodemographic factors and comorbidities by the end of 2011. RESULTS: The incidence of ischemic stroke revealed a significant increase in the CO-poisoning cohort over the follow-up period (p<0.001). The overall incidence of ischemic stroke was near 2.5-fold greater in the CO-poisoned cohort than in controls (5.49 versus 2.02 per 1000 person-years), with an adjusted HR of 2.60 (95% confidence interval (CI)=2.15-3.15). The adjusted HR for those without comorbidities was slightly higher (2.76, 95% CI=2.13-3.58). The age-specific CO-poisoning to non-CO-poisoning relative risk was greatest in the youngest group (20-34years) (adjusted HR=6.45; 95% CI=3.30-12.6). CONCLUSION: CO poisoning is associated with a long-term risk of increased incident ischemic stroke. Further study on the mechanism of ischemic stroke for CO poisoning affects is needed.