Objective: Identification of the offending agent(s) involved in hazardous materials accidents sometimes presents a challenge both for rescue workers on site as well as for toxicologist on call. The ...advent of new economy in some Eastern and Central European countries adds to the problem. By hiring cheap unskilled and untrained personnel, employers are trying to cut down production costs, but this in turn can lead to inappropriate and/or delayed hazmat response as witnessed in the presented case. Case report: We received a call from an emergency medical team on site in a textile processing plant, on mass poisoning with an unknown agent, affecting ten workers. The circumstances surrounding the event were unclear. The workers fell ill within seconds of inhaling an unknown gas. Four of them were unconscious, six more suffered from dyspnea, dizziness, ataxia, vertigo, headache and near-collapse. The inexperienced plant's safety engineer was not able to provide the toxicologist with adequate information for an extended period of time, misinterpreted the offending agent as sulfur dioxide and directed the medical team which was without any personal protecting equipment into the "hot zone". Clinical presentation and the time-frame of the event clearly suggested that a different agent was involved (1) and the medical team was prevented from entry. We suspected that the agent at hand must have been hydrogen sulfide, and our estimation was later confirmed when the MSDSs of the chemicals used in the plant were sent to the PCU and the events leading to its release were reconstructed. All patients recovered without sequelae after a brief hospital stay. Conclusion: New economy's paradigm of "cutting production costs at all costs" went awry in presented case. A string of events involving untrained workers unfamiliar with hazmat procedures and an inexperienced safety engineer, almost lead to potentially disastrous situation (2).
Gyromitrin, acetaldehyde N-methyl-N-formylhydrazone (ca 90%) and its 8 hydrazone homologues are toxic compounds of Gyromitra esculenta (GE). They hydrolyse in vitro and in vivo (a gastric phase) to ...N-methyl-N-formylhydrazine (MFH) and then to monomethylhydrazine (MH). Acute toxicity of MH and MFH is connected with blocking of the cofactors, containing carbonyl function group. Oxidation and alkylation of MH (and perhaps MFH) in hepatic phase, are responsible for hepatotoxicity and most probably for production of carcinogenic derivatives. Micheloth assumed that toxic substances of GE are heat-sensitive, volatile, water-soluble and they accumulate in the cooking juice or in the preservation liquid. The majority of toxicological textbooks cite, that toxins of GE are water-soluble and volatile; unclear and misleading are data about heat-sensitivity.
Poisoning by Scopolia carniolica Grenc, D; Brvar, M; Sarc, L
Clinical toxicology (Philadelphia, Pa.),
04/2006, Letnik:
44, Številka:
4
Journal Article
Recenzirano
Reports of poisoning by Scopolia carniolica are rare. The plant was named by Carl von Linne in honor of its discoverer, natural historian J. A. Scopoli (1723-1788) and the former province of ...Carniola, and is indigenous to some regions of Slovenia. Like several genera of the Solanaceae (Nightshade) family it contains tropane alkaloids which cause distinctive anticholinergic clinical syndrome in case of poisoning. We report a case of two female patients who consumed a meal containing what they thought were spinach leafs.
A study was performed to evaluate different recommendations about Amanita phalloides (APh) poisoning treatment. In a retrospective study mortality between 3 groups of patients, who underwent ...different therapeutic protocols in the last 30 years, was compared. In the first decade (1976-1985), patients were treated with high doses of crystalline penicillin and glucocorticoids. During the second decade (1986-1995), silibinin was added to the treatment protocol. In the last ten years (1996-2005), both penicillin and glucocorticoids were withdrawn from therapeutic guidelines; treatment relied on early silibinin and adequate symptomatic treatment. Concurrently we looked into possible prognostic value of prothrombin time and/or INR in predicting the severity and outcome of Aph poisoning. Patients were classified in 3 categories according to maximal values of prothrombin time (PT) and/or INR (>20%, 10-20%, <10% for PT and <4,4-5, >5 for INR). Diagnosis relied on mushroom identification the characteristic course of clinical symptoms and signs; in a few cases RIA for amanitine or Aph spore identification were also used.
This study compared the effects of toxicity of ethanol and its first metabolite acetaldehyde in rat astrocytes through cell viability and cell proliferation. The cells were treated with different ...concentrations of ethanol in the presence or absence of a catalase inhibitor 2-amino-1,2,4 triazole (AMT) or with different concentrations of acetaldehyde. Cell viability was assessed using the trypan blue test. Cell proliferation was assessed after 24 hours and after seven days of exposure to either ethanol or acetaldehyde.We showed that both ethanol and acetaldehyde decreased cell viability in a dose-dependent manner. In proliferation studies, after seven days of exposure to either ethanol or acetaldehyde, we observed a significant dose-dependent decrease in cell number. The protein content study showed biphasic dose-response curves, after 24 hours and seven days of exposure to either ethanol or acetaldehyde. Co-incubation in the presence of AMT significantly reduced the inhibitory effect of ethanol on cell proliferation.We concluded that long-term exposure of astrocytes to ethanol is more toxic than acute exposure. Acetaldehyde is a much more potent toxin than ethanol, and at least a part of ethanol toxicity is due to ethanol's first metabolite acetaldehyde.
V študiji smo primerjali toksi _nost etanola in njegovega prvega metabolita acetaldehida za podganje astrocite z dolo _itvijo celi _ne viabilnosti in proliferacije. Celi _ne kulture smo tretirali z razli _nimi koncentracijami etanola, etanola v prisotnosti inhibitorja katalaze 2-amino-1,2,4 triazol-a (AMT) ali z razli _nimi koncentracijami acetaldehida. Celi _no viabilnost smo vrednotili s pomo _jo testa s tripanskim modrilom, celi _no proliferacijo pa s štetjem celic in dolo _itvijo koncentracije proteinov po 24-urni, kot tudi 7-dnevni izpostavljenosti.S študijo smo pokazali, da tako etanol kot tudi acetaldehid v odvisnosti od njune koncentracije zmanjšata celi _no viabilnost. V študiji proliferacije sta etanol in acetaldehid, v odvisnosti od njunih koncentracij, zna _ilno zmanjšala število celic po 7-dnevni izpostavljenosti. Pri ugotavljanju vsebnosti proteinov smo dobili bifazno krivuljo tako po 24-urni, kot tudi po 7-dnevni izpostavljenosti razli _nim koncentracijam etanola oziroma acetaldehida. Prisotnost AMT je signifikantno zmanjšala u _inek etanola na celi _no proliferacijo.Zaklju _imo lahko, da je dolgotrajna izpostavljenost astrocitov etanolu bolj toksi _na kot akutna. Acetaldehid je mo _nejši toksin kot etanol in vsaj del toksi _nosti etanola je posledica delovanja njegovega prvega metabolita, acetaldehida.
Toxic water soluble polymeric 3-alkylpyridinium salts isolated from the sponge Raniera sarai strongly inhibited AChE in vitro. In vivo, experimental animals died due to plugs formed in ...microcirculation. The mechanism of this plug formation is unknown. In vitro, the toxin did not affect the coagulation rate, but the rate of platelet aggregation was accelerated in a dose-dependent manner. The hemolytic activity of poly-APS was diminished by the addition of serum proteins in a dose-dependent manner. These results support the conclusion that non-specific binding to proteins is the underlying mechanism of the lethality of poly APS.
Aggressive fibromatoses (AF; desmoid tumors) are rare clonal neoplastic proliferations of connective tissues that can be locally aggressive despite wide surgical resection and/or radiation therapy. ...The Sarcoma Alliance for Research through Collaboration (SARC) initiated a prospective phase II trial to investigate the outcome of patients treated with imatinib, a multiple tyrosine kinase inhibitor, in patients with AF, or 1 of 10 sarcoma subtypes. Here, we report specifically on the outcome of patients with AF as well as evaluations undertaken to examine the mechanism of imatinib.
Patients ≥10 years old with desmoid tumors that were not curable by surgical management or in whom curative surgery would lead to undesirable functional impairment were eligible. Imatinib was prescribed at 300 mg twice daily body surface area (BSA) ≥ 1.5 m(2), 200 mg twice daily (BSA = 1.0-1.49 m(2)), or 100 mg twice daily (BSA < 1.0 m(2)). Response outcomes at 2 and 4 months were assessed. Tissue specimens were analyzed by immunohistochemistry for expression of cKIT, platelet-derived growth factor receptor α (PDGFRα), PDGFRβ, AKT, PTEN, FKHR, and β-catenin. Tumor DNA was analyzed for PDGFRα exon 18 and APC mutations by allelic discrimination PCR.
Fifty-one patients were enrolled. The median number of prior regimens was 1. Kaplan-Meier estimates of 2- and 4-month progression-free survival rates were 94% and 88%, respectively, and 1-year progression-free survival was 66%. Objective response rate was 6% (3 of 51). Expression and polymorphisms of target proteins were identified in tissue samples, but no significant correlation with outcome was observed using the samples available.
Imatinib may have a role in the management of unresectable or difficult to resect desmoid tumors.
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