Disease relevance of Poisoning

• Activated charcoal is widely used as an adsorbent for the management of patients with drug overdoses and poisonings [1].
• The diuretic properties of mannitol are also useful in patients with refractory edema or intoxications by aspirin, barbiturates, or bromide [2].
• Lithium alters renal physiology (e.g. polyuria) and is nephrotoxic in severe intoxications [3].
• Of the 45 potential uses of acetylcysteine that were identified for the treatment of poisonings or adverse drug reactions, 14 of the toxic effects have little support for its use while promising results have been demonstrated for 27 toxicities [4].
• In the past, lipoic acid has been administered to patients and test animals as therapy for diabetic neuropathy and various intoxications [5].

Psychiatry related information on Poisoning

• So far, lithium intoxications following excessive intake by patients with manic disorders have not been reported [6].
• These laboratory measures and the clinical signs of vomiting, lethargy, and increased frequency of drinking might complicate the diagnosis or monitoring of some intoxications (such as ethylene glycol) in dogs that have previously received AC suspension containing propylene glycol, glycerol, or both as vehicles [7].

High impact information on Poisoning

• Current concepts about the treatment of selected poisonings: nitrite, cyanide, sulfide, barium, and quinidine [8].
• The Elixir Sulfanilamide disaster of 1937 was one of the most consequential mass poisonings of the 20th century [9].
• These properties of PON1 account for its ability to protect against pesticide poisonings and atherosclerosis [10].
• The pseudo first-order passage of DT intoxications through antitoxin and NH4Cl- or monensin-sensitive stages are shown to have the same cellular basis as the pseudo first-order decrease in protein synthesis [11].
• Both the intoxications caused a progressive decrease in hepatic glutathione content [12].

Chemical compound and disease context of Poisoning

• Acute and chronic intoxications of rhesus monkeys with methylmercury produced lesions in the central nervous system (CNS) with different distributions [13].
• The mechanisms of action of acute carbon monoxide and hydrogen cyanide poisonings are reviewed, with cases presented to illustrate how each chemical can be a major contributor or how they may interact [14].
• Aldicarb is the most potent of the commercially available carbamate pesticides and is an unusual source of acute human poisonings [15].
• Polychlorinated and polybrominated biphenyls are industrial chemical mixtures which have been implicated in numerous human poisonings in Taiwan and Japan (PCBs) and Michigan (PBBs) [16].
• However, ganglionic vessels lack an efficient vascular barrier to many substances which is important in intoxications caused by, e.g., doxorubicin, lead, mercury, and cadmium [17].

Biological context of Poisoning

• The intensity of ESR spectrum associated with ascorbyl free radical (A.) was found to be sensitive to various pathologies and intoxications connected with oxidative stress [18].
• Since phenytoin has a narrow therapeutic index and genotyping may be carried out rapidly and at low cost, dosage adjustment based on CYP2C9 genotype, especially at the induction of therapy, would be of value in order to lower the risk of concentration dependent drug intoxications in carriers [19].
• We also observed a steady increase in carbon monoxide inhalation and alcohol poisonings, mostly among teenagers [20].
• Adult toxicology in critical care: Part II: specific poisonings [21].
• Meprobamate kinetics during and after terminated hemoperfusion in acute intoxications [22].

Anatomical context of Poisoning

• RESULTS: Of the 89 methyl bromide intoxications studied, there were two cases of chronic exposure: two workers presented with neurological signs of cerebello-vestibular and pyramidal deficits, visual troubles and peripheral neuropathy of the lower limbs at the end of a season of exposure during which no acute incident involved [23].
• It has been seen, too, in cerebellar Purkinje cells after acrylamide intoxication and in hippocampal pyramidal neurons and in neurons of the pyriform cortex after triethyllead and trimethyltin intoxications [24].
• Urinary A1M provides a non-invasive, inexpensive diagnostic alternative for the diagnosis and monitoring of urinary tract disorders (early detection of tubular disorders such as heavy metal intoxications, diabetic nephropathy, urinary outflow disorders and pyelonephritis) [25].
• The observed dose range for the inhibition of the cAP of rat phrenic nerve includes that observed after intoxications with dextropropoxyphene (0.004-0.06 mM) in the clinic [26].

Gene context of Poisoning

• The polymorphic CYP2D6 and CYP2C19 genes encode enzymes participating in the metabolism of several potentially toxic drugs, and mutations in these genes may lead to adverse drug reactions, possibly even intoxications [27].
• Pyrazolone intoxication accounts for most (52 percent) mild analgesic poisonings in West Germany. Severe and fatal intoxication with pyrazolones is, however, rare [28].
• Small incremental intravenous doses of 0.1 to 0.2mg of flumazenil are useful in benzodiazepine intoxications, in differential diagnosis of coma, excessive postoperative sedation and possibly in reversing paradoxical reactions of benzodiazepines [29].
• Secondary mania may be caused by metabolic derangements, intoxications, and/or structural lesions, as well as by epilepsy [30].
• OBJECTIVE: Intoxications with organophosphorous compounds such as paraoxon, an inhibitor of serine hydrolases, mainly butyrylcholinesterase and acetylcholinesterase, are frequent [31].

Analytical, diagnostic and therapeutic context of Poisoning

• Conventional management of these intoxications consists of ethanol and hemodialysis [32].
• Eight subjects developed a complication requiring admission to an intensive care unit: six acute cocaine intoxications due to packet rupture and two intestinal occlusions [33].
• Combination therapy of olanzapine and fluvoxamine should be used cautiously, and therapeutic drug monitoring should be instituted to avoid olanzapine-induced adverse effects or intoxications [34].
• In view of the potential interest in an objective parameter for the depth of coma in intoxications with the recreational drug gamma-hydroxybutyrate (GHB), we have studied the relationship between the plasma concentrations and the electroencephalographic (EEG) changes induced by GHB in the rat [35].
• A five-year retrospective study of pediatric salicylate intoxications (serum level greater than 300 micrograms/ml) revealed that 2/20 patients developed salicylate induced pulmonary edema [36].

References