Aluminium phosphide poisoning with esophageal stricture and tracheoesophageal fistula

Agrawal, D. P.; Kumar, Anand; Ansari, Mumtaz Ahmad; Srivastava, Vivek; Lahiri, T. K.

doi:10.1007/s12055-010-0040-x

Cited by 5 publications

(3 citation statements)

References 6 publications

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“…Several patients have gone on to develop esophageal strictures (Nijhawan et al, 2006). A few cases have been reported with trachea-esophageal fistulae (Agrawal et al, 2010;Jain et al, 2010).…”

Section: Gastrointestinal Toxicitymentioning

confidence: 99%

Aluminum phosphide poisoning: an unsolved riddle

Anand

Binukumar

Gill

2011

J of Applied Toxicology

105

107

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Aluminum phosphide (ALP), a widely used insecticide and rodenticide, is also infamous for the mortality and morbidity it causes in ALP-poisoned individuals. The toxicity of metal phosphides is due to phosphine liberated when ingested phosphides come into contact with gut fluids. ALP poisoning is lethal, having a mortality rate in excess of 70%. Circulatory failure and severe hypotension are common features of ALP poisoning and frequent cause of death. Severe poisoning also has the potential to induce multi-organ failure. The exact site or mechanism of its action has not been proved in humans. Rather than targeting a single organ to cause gross damage, ALP seems to work at the cellular level, resulting in widespread damage leading to multiorgan dysfunction (MOD) and death. There has been proof in vitro that phosphine inhibits cytochrome c oxidase. However, it is unlikely that this interaction is the primary cause of its toxicity. Mitochondria could be the possible site of maximum damage in ALP poisoning, resulting in low ATP production followed by metabolic shutdown and MOD; also, owing to impairment in electron flow, there could be free radical generation and damage, again producing MOD. Evidence of reactive oxygen species-induced toxicity owing to ALP has been observed in insects and rats. A similar mechanism could also play a role in humans and contribute to the missing link in the pathogenesis of ALP toxicity. There is no specific antidote for ALP poisoning and supportive measures are all that are currently available.

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Section: Gastrointestinal Toxicitymentioning

confidence: 99%

Aluminum phosphide poisoning: an unsolved riddle

Anand

Binukumar

Gill

2011

J of Applied Toxicology

105

107

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“…Aluminum phosphide (AlP), known as a highly lethal solid pesticide, is commonly used to preserve the quality and quantity of agricultural products from pests and insects, especially in developing countries. 1,2 High efficiency, cost-effectiveness, ease of use, and not affecting seed viability and stored food are the essential reasons for extensive use of AlP. Although it has numerous advantages, its improper use can lead to severe poisoning of humans and other non-targeted species.…”

Section: Introductionmentioning

confidence: 99%

Electrocardiographic, hemodynamic, and biochemical evidence on the protective effects of exenatide against phosphine-induced cardiotoxicity in rat model

et al. 2021

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Aluminum phosphide (AlP) poisoning can be deadly in most cases targeting the heart. To overcome AlP toxicity, exenatide has been studied in the present study due to its pleiotropic effects on cardiac damages. In this study, the rats were exposed to LD50 of AlP (10 mg/kg) by gavage, and exenatide at doses (0.05, 0.1, and 0.2 mg/kg) injected intraperitoneally 30 min after poisoning. The cardiac parameters including heart rate (HR), blood pressure (BP), QRS, corrected QT (QTc), and ST were monitored for 180 min. Blood glucose level was measured in the study groups 30 min after exenatide injection. Evaluation of biochemical parameters including mitochondrial complexes I, II, and IV activities, adenosine diphosphate (ADP)/adenosine triphosphate (ATP) ratio, malondialdehyde (MDA), apoptosis, lactate, troponin I, and brain natriuretic peptide (BNP) was done on heart tissues after 12 and 24 h. Additionally, the tissues were analyzed for any pathological damages including necrosis, hemorrhage, or hyperemia 24 h post-treatment. Our results showed that AlP-induced HR, BP, and electrocardiographic changes were improved by exenatide at all doses. The blood glucose levels of poisoned animals reached control levels after exenatide treatment. Besides, treatment with exenatide at all doses improved complexes I and IV activity, ADP/ATP ratio, and apoptosis. Malondialdehyde, lactate, troponin I, and BNP levels were also diminished after exenatide co-treatment in poisoned animals. On the other hand, administration of exenatide doses improved the histopathology of AlP-induced tissues. Based on our findings, exenatide has a protective effect against phosphine-induced cardiotoxicity in an almost dose-dependent way. However, further investigations are needed on the potential clinical use of exenatide in this poisoning.

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“…Poisoning by deliberate self-ingestion of AlP is a common cause of death and socioeconomic loss worldwide, especially in developing countries [2,13,26]. AlP is sold as pallet, tablet, porous blister pack, sachets, and as dusts [43].…”

Section: Introductionmentioning

confidence: 99%