Clinical Trial Details
— Status: Not yet recruiting
Administrative data
| NCT number |
NCT04702906 |
| Other study ID # |
Aluminum Phosphide Poisoning |
| Secondary ID |
|
| Status |
Not yet recruiting |
| Phase |
N/A
|
| First received |
|
| Last updated |
|
| Start date |
February 2021 |
| Est. completion date |
July 2021 |
Study information
| Verified date |
January 2021 |
| Source |
Tanta University |
| Contact |
nadia helal, MD |
| Phone |
00201099752866 |
| Email |
dr_nadia_helal86[@]yahoo.com |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Interventional
|
Clinical Trial Summary
The aim of the present study is to evaluate the potential adjuvant therapeutic effect of
trimetazidine in treatment of acute AlP poisoning-induced cardiotoxicity.
Description:
Aluminium phosphide (AlP) is an inorganic phosphide. It is used as a fumigant to protect
stored grains from insects, rodents and other pests.It is a solid fumigant widely used in
Egypt as a grain preservative. Its tablets are commonly used due to their low cost, high
efficacy, and availability .
Toxic effects of AlP are related to phosphine gas release when AlP comes in contact with
moisture or gastric acidity. Phosphine gas is rapidly absorbed from the gastrointestinal
tract and lungs inhibiting cytochrome-c oxidase and oxidative phosphorylation which results
in adenosine triphosphate depletion and resulting cellualr death.
The direct toxic effects of phosphine on cardiac myocytes, fluid loss and adrenal gland can
induce profound circulatory collapse. Phosphides and phosphine can exert a direct corrosive
effect on body tissues.
Toxic manifestations usually appear rapidly upon phosphide exposure. Impaired myocardial
contractility, fluid loss, pulmonary edema, metabolic acidosis and acute renal failure are
the most frequent manifestations. Disseminated intravascular coagulation and hepatic necrosis
may also occur. Patients generally die due to multi-organ failure .However, myocardial
damage- induced cardiovascular collapse is reported to be the primary cause of death.
Severity of manifestations depends on different factors such as dose, exposure route, and
time delay before treatment initiation. Diagnosis is based on history of exposure, garlic
odor of the breath, suggestive clinical manifestations and detection of phosphine gas in
gastric aspirate or breath.
Treatment of acute AlP toxicity is mainly supportive as there is no specific antidote since
the exact mechanism of toxicity is still unknown. The most important factor is resuscitation
of shock. Many researches are directed towards finding a specific treatment for this fatal
poison.
Trimetadizine is described as the first cytoprotective anti-ischemic agent developed. It has
a protective of the myocardium due to its preservation of oxidative metabolism. It improves
myocardial glucose utilization through inhibition of long-chain 3-ketoacyl CoA thiolase
activity, which results in a reduction in fatty acid oxidation and a stimulation of glucose
oxidation .
Trimetadizine reduces the tissue accumulation of malonyldialdehyde, the lipid peroxidation
index, and the sodium influx related to activation of the Na+ -K + pump. Moreover, it lack of
haemodynamic effects. These effects result in a decrease in the cellular accumulation of
calcium and improved intracellular ATP levels).
Oral administration of the anti-ischaemic drug trimetazidine, was tried in a case report of
occupational inhalation exposure to phosphine gas from AlP. It was temporally associated with
clinical improvement.
