Serum Cholinesterase Level in Aluminum Phosphide Poisoning, the Possible Proposing Role of Atropin & Pralidoxime

Assessment of Serum Cholinesrtrase Level in Aluminum Phosphide Poisoning Cases, the Possible Proposing Role of Atropine and Pralidoxime in Saving the Cases: Clinical and

Status

UNKNOWN

Phases

Unknown

Study type

Observational

Source

ClinicalTrials.gov

Registry ID

NCT04192526

Acronym

ALPH

Enrollment

Registered

2019-12-10

Start date

2019-12-01

Completion date

2020-07-30

Last updated

2020-05-13

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Toxicity;Chemical

Keywords

serum cholinestrase, atropin, aluminum phosphide

Brief summary

Metal phosphides are widely used as a rodenticide and insecticide and poisoning with these substances has a very high mortality. The aim of this study was to evaluate the butyrylcholinesterase (BuCh) level in poisoning with metal phosphides.

Detailed description

Today, the use of pesticides in the world is considered as a recognized health It is estimated that around 30% of global suicides are due to pesticide self-poisoning . Metal phosphides pesticides are highly toxic, low cost, and are easily accessible as rodenticide agents and used for self-poisoning . aluminum phosphide (ALP) are among the most important metal phosphides. Poisoning with these agents is frequently seen in India, Srilanka and Iran. In a recent study, the incidence of fatal aluminum phosphide poisoning cases referred for phosphine analysis was 5.22 and 37.02 per million of population of Tehran, Iran in 2006 and 2013, respectively (9).The mechanism of toxicity is not clearly defined. ALP toxicity is related to the production of phosphine gas. Phosphine inhibits cytochrome c oxidase and causes mitochondrial destruction and inhibits oxidative respiration which leads to anaerobic metabolism, severe metabolic acidosis, multi-organ dysfunction and death. Phosphine can lead to severe cardiac suppression and cardiogenic shock. One of the proposed mechanisms of toxicity is the reduction of the true cholinesterase and serum cholinesterase (butyrylcholinesterase) enzyme, but usually do not show obvious clinical manifestations .

Interventions

None listed

Study design

Observational model

CASE_CONTROL

Time perspective

PROSPECTIVE

Eligibility

Sex/Gender

ALL

Healthy volunteers

Inclusion criteria

cases of aluminum phosphide poisoning -

Exclusion criteria

concomitant ingestion \-

Design outcomes

Primary

Measure	Time frame	Description
persistent cholineastrase inhibition is one of the pathological pathway of the ALP poisoning	3 months	definite assessment of the pathogenesis of ALP helps in applying adaquqte treatment regmin

Countries

Egypt

Outcome results