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Background: Aluminum phosphate (ALP) poisoning has a high mortality rate (MR) secondary to cardiogenic shock. Recently, extracorporeal membrane oxygenation (ECMO) showed a successful result in this issue. We conducted a systematic review and meta-analysis to compare the MR of patients with ALP poisoning who underwent ECMO versus those with conventional treatment. Materials and Methods: Two parallel databases' reviews were done to find the ECMO treatment-applied studies or conventional treatment-applied studies according to the PRISMA protocol. All studies in any languages and English conference abstracts were included for ECMO treatment-applied studies. Only English-language human observational studies, which reported MR, were included in conventional treatment-applied studies. All ETAS case reports were summarized and used as a newly generated cross-sectional study (NGCSS) for inclusion in the meta-analysis. Results: Out of 167 and 1043 records, 17 case reports (24 cases), 3 cross-sectional studies, and 9 conventional treatment-applied studies were selected. In meta-analysis NGCSS applied as the fourth cross-sectional ECMO treatment-applied studies. The overall MR of ECMO-treated cases (23% [95% confidence interval (CI): 7%-39%]) was significantly less than conventionally treated cases (60% [95% CI: 39%-63%]; P < 0.001). In ECMO-treated cases, the weighted mean difference (WMD) for age, blood pH, ALP dose, hospitalization, ECMO lag time, and ECMO duration were not statistically significant between survived and nonsurvived cases. However, WMD of cardiac ejection fraction (4.6%; 95% CI: 2.76%-6.39%; P < 0.0001), exposure to hospitalization lag time (-2.05; 95% CI: -4.05-0.14 h; P = 0.06), and length of hospital stay (16; 95% CI: 12.0-20.5 days; P < 0.0001) between survived and nonsurvived ETC were significant. Conclusion: ECMO reduced the MR of ALP-poisoned patients; however, it is a highly invasive and complicated procedure. [ABSTRACT FROM AUTHOR]

Background: Poisoning with Organophosphates (OP) and/or Pyrethroids (PYR) pesticides is common. We present a rare case of OP+PYR poisoned patient who suffered from Atrial Fibrillation (AF) at the beginning of treatment by a low dose of atropine and reviewed the literature. Case Presentation: A 50-year-old man had ingested about 5-10 ml of a mixture of chlorpyrifos/cypermethrin. Half an hour later, he went to the rural hospital and 2 hr later, after gastrointestinal decontamination, he was referred to the clinical toxicology department with normal vital signs except normal sinus tachycardia [Heart rate (HR)]=105. On admission, he had nausea, vomiting, diarrhea, mild sialorrhea, symmetric mid-size pupils, wet skin, and bilateral moist rales in his lungs. His cardiac rhythm changed to rapid AF (HR >140 beats/min) after treatment with 3 mg midazolam followed by 0.3 mg of atropine (0.1 mg every 1-3 min). Atropine administration was discontinued and he was treated with 0.5 mg of digoxin. 6 hr later, his arrhythmia disappeared and all cardiac and laboratory evaluations changed to normal except reduced serum cholinesterase activity. Conclusion: AF may be induced by Organophosphates (OP) and Pyrethroids (PYR) intoxication or during the treatment by atropine. We could not find any known risk factor (cardiac or medical issues) for AF in the current case. It may be suggested that poisoning with OP, PYR (alone or mixed) or atropine (in general or in low dose), or combination is the trigger of AF. However, AF is not life threating and can easily cure by antiarrhythmic therapy. [ABSTRACT FROM AUTHOR]

Objective(s): A narrow margin between the therapeutic and toxic doses of digoxin can result in an increased incidence of toxicity. Since digoxin has an enterohepatic cycle, multiple oral doses of absorbents like montmorillonite may be useful in the treatment of digoxin toxicity. Materials and Methods: In this study, 4 groups of 6 rats received intraperitoneal digoxin (1 mg/kg), and half an hour later, distilled water (DW) or oral adsorbents, including montmorillonite (1 g/kg), activated charcoal (1 g/kg) (AC) alone or in combination in the ratio of 70:30. Half of the mentioned doses were also gavaged at 3 and 5.5 hr after digoxin injection. The serum level of digoxin, biochemical factors, and activity score were assessed during the experiment. Three control groups only received DW, montmorillonite, or AC. Results: All adsorbents were able to significantly decrease the serum level of digoxin compared to the digoxin+DW group (P<0.01). Only montmorillonite reversed the digoxin-induced hyperkalemia (P<0.05). Multiple dose administration of adsorbents also significantly reduced the digoxin area under the curve and half-life and increased digoxin clearance (P<0.05). However, there was no significant difference in the kinetic parameters between groups that received digoxin plus adsorbents. Conclusion: Multiple-dose of montmorillonite reversed digoxin toxicity and reduced serum digoxin levels by increasing the excretion and reducing the half-life. Montmorillonite has also corrected digoxin-induced hyperkalemia. Based on the findings, a multiple-dose regimen of oral montmorillonite could be a suitable candidate for reducing the toxicity issue associated with drugs like digoxin that undergo some degree of enterohepatic circulation. [ABSTRACT FROM AUTHOR]

Objective(s): Acute kidney injury can be associated with serious consequences and therefore early treatment is critical to decreasing mortality and morbidity rate. We evaluated the effect of montmorillonite, the clay with strong cation exchange capacity, on the AKI model in rats. Materials and Methods: Glycerol (50% solution, 10 ml/kg) was injected in the rat hind limbs to induce AKI. 24 hr after induction of acute kidney injury, the rats received oral doses of montmorillonite (0.5 g/kg or 1 g/kg), or sodium polystyrene sulfonate (1 g/kg) for three consecutive days. Results: Glycine induced acute kidney injury in rats with high levels of urea (336.60± 28.19 mg/dl), creatinine (4.10± 0.21 mg/dl), potassium (6.15 ± 0.28 mEq/L), and calcium (11.52 ± 0.19 mg/dl). Both doses of montmorillonite (0.5 and 1 g/kg) improved the serum urea (222.66± 10.02 and 170.20±8.06, P<0.05), creatinine (1.86±0.1, 2.05± 0.11, P<0.05), potassium (4.68 ± 0.4, 4.73 ± 0.34, P<0.001) and calcium (11.15 ± 0.17, 10.75 ± 0.25, P<0.01) levels. Treatment with montmorillonite especially at a high dose reduced the kidney pathological findings including, tubular necrosis, amorphous protein aggregation, and cell shedding into the distal and proximal tubule lumen. However, administration of SPS could not significantly decrease the severity of damages. Conclusion: According to the results of this study, as well as the physicochemical properties of montmorillonite, such as high ion exchange capacity and low side effects, montmorillonite can be a low-cost and effective treatment option to reduce and improve the complications of acute kidney injury. However, the efficacy of this compound in human and clinical studies needs to be investigated. [ABSTRACT FROM AUTHOR]

SV (sodium valproate) is an antiepileptic drug that is often prescribed for epilepsy, bipolar disorders, and migraine. We reported an SV intoxicated case that cardiac and neurologic abnormalities were promptly responded to hemodialysis (HD). She ingested a large amount of SV (150 pills of SV 200mg) for a suicide attempt. She was initially alert but her Glasco coma scale (GCS) decreased to 6 thought 11 hours. However, valproate (>150mg/l) and ammonia serum (164µg/dL) levels were not excessively elevated. The serial electrocardiography (ECG) showed QT prolongation and a signs of sodium channel block such as dominant R wave in AVR lead and T-wave inversion in the precordial leads. She had low level of calcium and potassium serum levels. Supportive treatment, charcoal, and L-carnitine, were not effective and HD was started due to the resistant cardiac and neurologic symptoms. After a 3-hour HD session, decreased GCS, pathological ECG findings, and laboratory abnormalities dramatically disappeared. In conclusion, HD is an effective and rapid response treatment for Valproate-induced loss of consciousness and life-threatening cardiac abnormality. [ABSTRACT FROM AUTHOR]

Background: Litarge (Lead II oxide) is named Murder-sang, Murdar Singh or Mordab-Sangh (MS) in person, is applied to reduce body odor in the axillary and legs. Several other indications were mentioned in ancient medicine such as syphilitic chancre wound healing, bed sore, and so forth. We reported lead intoxication by eating a few MS. Case: A 34-year-old man was visited due to accidentally consuming his wife's MS powder by adding to his food instead of spices, 10 days earlier. He experienced acute abdominal pain and non-bloody diarrhea 6 hours after ingestion. His symptoms were finally treated by supportive therapy despite their persisted. Ten days later, his blood lead level was 1250 µg/L. His hemoglobin level reduced and transaminase raised to 1.5 times more than the upper limit. He was treated with oral Succimer 10 mg/kg three times a day in the first 5 days and continued by 10mg/kg twice a day up to 21 days. On the 5th day of treatment, his symptoms improved. His blood lead level was 545.5 µg/L on the 8th day of treatment and reduced to 254 µg/L and 245 µg/L one and two months later. Discussion: Mordab-Sangh could induce lead toxicity if ingested. However, other metal poisoning should be considered in MS ingestion. [ABSTRACT FROM AUTHOR]

Paraquat (PQ), one of the most frequently used herbicides, can cause serious health problems in an exposed individual. In the present study, we investigated the protective effect of verbascoside (VB), a phenylpropanoid glycoside from lemon verbena, against PQ-induced A549 cell injury with a particular focus on the possible molecular pathways involved. A549 cells were exposed to PQ (300 µM) and different concentrations of VB (12.5, 25, and 50 µM). Cell viability, ROS content, the level of antioxidant enzymes (SOD, CAT and GPx) and inflammatory markers (IL-6 and TNF-α), as well as 8-OHdG, were detected using MTT assay and an ELISA kit. Western blotting and qRT-PCR were performed to measure the levels of caspase3 and NF-κB mRNA and protein expression. Exposure of cells to PQ caused viability loss and ROS increase. PQ also increased the levels of IL-6, TNF-α and 8-OHdG and decreased the antioxidant enzymes content. PQ treatment resulted in cell death by increasing the gene and protein expression level of caspase 3 and NF-κB. Treatment with VB notably increased cell survival, antioxidant enzymes activity, which concomitantly attenuated ROS, NF-κB and inflammatory mediator production. VB also inhibited apoptosis expression markers. These results indicated that VB could protect A549 cells against PQ induced cell injury by attenuation of ROS and inflammatory marker production and modulation of antioxidant enzymes. VB efficiently suppressed increased NF-κB and caspase-3 activity and formation of 8-OHdG and ultimately improved cell viability. Therefore, VB may be useful in the development of a new therapy for PQ-induced pulmonary toxicity. [ABSTRACT FROM AUTHOR]

Objective(s): The goal of this study was to evaluate the neuroprotective effects of vit B12 on paraquatinduced neurotoxicity. Materials and Methods: Thirty-six male mice were randomly divided into six groups. Three groups were treated intraperitoneally with paraquat (10 mg/kg) twice a week (with a 3-day interval) for 3 weeks. Normal saline, vit B12 (1 mg/kg), or vit C (50 mg/kg) was injected 30 min before paraquat administration. Other groups only received normal saline (control), vit B12, or vit C in the same protocol. Motor performance and coordination were assayed by challenging beam traversal, pole, open field, and rotarod tests. The hippocampus and serum samples were isolated to evaluate the oxidative stress (GSH and ROS), apoptosis (caspase 3), and inflammatory markers (TNF-α and IL-1β). Results: Administration of paraquat leads to induction of motor deficits, which were improved by treatment with vit B12. In addition, vit B12 could prevent oxidative damage, apoptosis, and inflammation caused by paraquat. Conclusion: It seems that vit B12 could be a novel therapeutic agent in the management of paraquat induced-neurotoxicity. [ABSTRACT FROM AUTHOR]