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Bidirectional ventricular tachycardia is a rare variety of tachycardia with a morphologically distinct presentation. The QRS axis and/or morphology alternate in the frontal plane leads. We report a patient with bidirectional ventricular tachycardia in association with aconitine poisoning., (Copyright © 2016 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.)

Levamisole is a veterinary anthelmintic drug with immunomodulatory properties in humans. It has become increasingly common as a contaminant in cocaine and is now detected in the majority of cocaine seized in the United States. A variety of adverse reactions have been reported in association with levamisole, the most severe being agranulocytosis, vascular occlusive disease, and thrombotic vasculopathy, with or without vasculitis. The combination of rapidly progressive cutaneous ecchymosis and purpura leading to necrosis, often affecting the ears and cheeks; neutropenia or agranulocytosis; serologic autoantibodies; and thrombotic vasculopathy, with or without associated vasculitis, in a patient who has recently used cocaine is characteristic of exposure to contaminant levamisole. We report the case of a 54-year-old man who presented with the clinical findings of levamisole-contaminated cocaine use and review the literature regarding cutaneous reactions associated with levamisole. Our case highlights this important public health issue and represents a clinical course that is unusually severe.

An increasing percentage of US cocaine has been adulterated with levamisole, an immunomodulator associated with agranulocytosis. We describe 3 emergency department patients with hyponatremia and cocaine use. Despite extensive evaluation, the cause of the hyponatremia was not elucidated but resolved during hospitalization. Because hyponatremia has not previously been associated with cocaine, we sought to uncover a plausible explanation that might be contributing to this new finding. Levamisole was detected in all 3 patients. Although we are unable to confirm causality, we propose that levamisole-adulterated cocaine may have contributed to the hyponatremia described in these patients., (Copyright © 2011 American College of Emergency Physicians. Published by Mosby, Inc. All rights reserved.)

Accidental aconitine poisoning is extremely rare in North America. This report describes the confirmation of a case of accidental aconitine poisoning using a liquid chromatography-tandem mass spectrometry (LC-MS/MS) method. The case involved a 25-year-old man who died suddenly following a recreational outing with friends where he consumed a number of wild berries and plants including one that was later identified as Monkshood (Aconitum napellus). Postmortem blood and urine samples were available for analysis. All routine urine and blood toxicology screens were negative. The LC-MS/MS method allowed sensitive quantification of aconitine, the main toxin in A. napellus, and showed 3.6 and 149 microg/L in blood and urine, respectively. These concentrations were similar to that reported in other aconitine-related deaths. This case illustrates the dangers of consuming unidentified plants, and documents concentrations of aconitine in blood and urine in a fatal case of A. napallus-related poisoning.

We describe a homicide complicated by an aconitine poisoning, which was initially thought to be a strangulation case. Routine toxicological analyses demonstrated only a small amount of alcohol in the blood and the urine. The case could not be clarified until 5 years after the event. A new element in the investigation made the wife the prime suspect, and finally, after thorough interrogation, she confessed her crime. She had mixed a decoction of three plants of Aconitum with red wine. Additional toxicological analyses, using the liquid chromatography-tandem mass spectrometry (LC-MS-MS) technique demonstrated 810 ng/ml of aconitine in urine, 6.5 ng/g in liver and 1.3 ng/g in the kidneys. Even though aconitine poisoning is still rare in Europe, it should be taken into account in suicides and homicides, particularly in unclarified cases.

With the increasing trend of cross mixing of populations, aconitine induced poisoning and its related arrhythmias may be more frequently encountered worldwide. However, the clinical experience is often too limited to draw any conclusion on the optimal treatment for tachycardia induced by aconitine intoxication. The clinical presentation, serial electrocardiographic changes, and responses to antiarrhythmic agents are reported in a patient with aconitine induced life threatening ventricular tachyarrhythmia. Amiodarone was effective in suppressing polymorphic ventricular tachycardia, which might provide an example of successful pharmacological intervention in aconitine induced ventricular tachyarrhythmia.

Hexachlorobenzene (HCB) is a persistent environmental pollutant. The toxicity of HCB has been extensively studied after an accidental human poisoning in Turkey and more recently it has been shown that HCB has immunotoxic properties in laboratory animals and probably also in man. Oral exposure of rats to HCB showed stimulatory effects on spleen and lymph node weights and histology, increased serum IgM levels, and an enhancement of several parameters of immune function. Moreover, more recent studies indicate that HCB-induced effects in the rat may be related to autoimmunity. In Wistar rats exposed to HCB, IgM antibodies against several autoantigens were elevated; in the Lewis rat, HCB differently modulated two experimental models of autoimmune disease. Oral exposure of rats to HCB induces skin and lung pathology in the rat. Recently several studies have been conducted to investigate whether these skin and lung lesions can be related to HCB-induced immunomodulation, and these studies will be discussed in this review. HCB-induced skin and lung lesions probably have a different etiology; pronounced strain differences and correlation of skin lesions with immune parameters suggest a specific involvement of the immune system in HCB-induced skin lesions. The induction of lung lesions by HCB was thymus independent. Thymus-dependent T cells were not likely to be required for the induction of skin lesions, although T cells enhanced the rate of induction and the progression of the skin lesions. No deposition of autoantibodies was observed in nonlesional or lesional skin of HCB-treated rats. Therefore, we concluded that it is unlikely that the mechanism by which most allergic or autoimmunogenic chemicals work, i.e., by binding to macromolecules of the body and subsequent T- and B-cell activation, is involved in the HCB-induced immunopathology in the rat. Such a thymus-independent immunopathology is remarkable, as HCB strongly modulates T-cell-mediated immune parameters. This points at a very complex mechanism and possible involvement of multiple factors in the immunopathology of HCB.

The influenza virus envelope glycoproteins hemagglutinin and neuraminidase were administered to the apical or basolateral sides of Caco-2 monolayers either as native protein micelles (mic-ag) or after incorporation into the orally active adjuvant formulation, immune stimulating complexes (iscoms) (isc-ag). Biotin-conjugated isc-ag were localized in intracellular vesicles as early as 2 min after administration to the apical side at 37 degrees C. Ten minutes after administration, both intracellular vesicles and intercellular spaces were labeled, and extracellular labeling was observed on the basolateral side of the cells, indicating that isc-ag were transported across the epithelium within 10 min of exposure. Transport of 125I-labeled isc-ag and mic-ag in the apical-to-basolateral and basolateral-to-apical directions across Caco-2 monolayers was comparable at 37 degrees C. Gel chromatography analysis revealed that only 0.55-3.1% of transported isc-ag and mic-ag had a molecular weight of > 5,000, while 21.0-42.3% was eluted at a position corresponding to peptides of approximately 10 amino acids. Although isc-ag and mic-ag were transported and degraded by Caco-2 monolayers in comparable amounts, only transported isc-ag induced a dose-dependent proliferative response in vitro of T cells primed with influenza virus antigen. High-performance gel chromatography and reverse-phase high-performance liquid chromatography indicated that transported antigenic isc-ag consisted of hydrophobic peptides with a molecular weight of < or = 3,000. These results indicate that antigens incorporated into the orally active adjuvant formulation iscom are degraded to antigenic peptides during transport across the intestinal epithelium.