Assessment of Nerve Damage Biomarkers in Acute and Chronic Organophosphate Toxicity

Neurotoxicity Clinical Trial

Official title:

Assessment of the Prognostic Value of Nerve Damage Biomarkers in Acute and Chronic Organophosphate Toxicity

Clinical Trial Details — Status: Recruiting

Administrative data

• NCT number: NCT06021262
• Other study ID #: 0107603
• Status: Recruiting
• Start date: August 2023
• Est. completion date: January 2024

Study information

• Verified date: August 2023
• Source: Alexandria University
• Contact: Ahmed F. El Yazbi, professor
• Phone: 01155881772
• Email: Ayazbi[@]aiu.edu.eg
• Is FDA regulated: No
• Study type: Observational

Clinical Trial Summary

The aim of this observational study is to answer the following questions in individuals with acute and chronic exposure to organophosphates. The main questions to be addressed are

1. What are the prognostic values of neuroinflammatory markers?

2. What are the genotoxic effects of organophosphates?

3. what are the changes occurring in the levels of traditional oxidative stress and inflammatory markers?

Description:

This is a cross-sectional study that aims to assess the possible prognostic value of markers of neuroinflammation and nerve damage in patients with acute and chronic exposure to organophosphate pesticides by conducting a full proteomic and metabolomic profile. The possible genotoxic effect of common organophosphate pesticides will be studied as well. This will be conducted in parallel to the assessment of traditional markers of inflammation and oxidative stress. The target populations are patients with acute and chronic exposure to organophosphates with a total estimated number of 90 including individuals assigned to the control group with matched age and gender.

Recruitment information / eligibility

• Status: Recruiting
• Enrollment: 90
• Est. completion date: January 2024
• Est. primary completion date: December 2023
• Accepts healthy volunteers: Accepts Healthy Volunteers
• Gender: All
• Age group: 18 Years and older

Eligibility

Inclusion Criteria:

• For the control group: healthy individuals without previous exposure to organophosphates, with the specified age limits.

• For the acute exposure group: patients with acute exposure to organophosphates, with the specified age limits

• For the chronic exposure group: patients with chronic exposure to organophosphates, with the specified age limits

No restrictions on comorbidities in the three groups except those mentioned under Exclusion Criteria

Exclusion Criteria:

• Pediatric patients.

• Patients with neurological diseases (Parkinsonism, epilepsy, Alzheimer's disease, etc.)

• Patients who does not meet the inclusion criteria.

Related Conditions & MeSH terms

• Genotoxicity
• Nerve Degeneration
• Nerve Injury
• Neuroinflammatory Response
• Neurotoxicity
• Organophosphate Poisoning

Intervention

Other:
• exposure to organophosphates
organophosphates are esters of phosphoric acids or Thio phosphoric acids that exist in pesticides, where patients can be chronically or acutely exposed to such compounds.

Locations

Country	Name	City	State
Egypt	Alexandria Main University Hospital	Alexandria

Sponsors (1)

Lead Sponsor	Collaborator
Alexandria University

Country where clinical trial is conducted

Egypt, 

References & Publications (9)

Caba IC, Streanga V, Dobrin ME, Jitareanu C, Jitareanu A, Profire BS, Apotrosoaei M, Focsa AV, Caba B, Agoroaei L. Clinical Assessment of Acute Organophosphorus Pesticide Poisoning in Pediatric Patients Admitted to the Toxicology Emergency Department. Toxics. 2022 Oct 2;10(10):582. doi: 10.3390/toxics10100582. — View Citation

Kobeissy F, Kobaisi A, Peng W, Barsa C, Goli M, Sibahi A, El Hayek S, Abdelhady S, Ali Haidar M, Sabra M, Oresic M, Logroscino G, Mondello S, Eid AH, Mechref Y. Glycomic and Glycoproteomic Techniques in Neurodegenerative Disorders and Neurotrauma: Towards Personalized Markers. Cells. 2022 Feb 8;11(3):581. doi: 10.3390/cells11030581. — View Citation

Lionetto MG, Caricato R, Calisi A, Giordano ME, Schettino T. Acetylcholinesterase as a biomarker in environmental and occupational medicine: new insights and future perspectives. Biomed Res Int. 2013;2013:321213. doi: 10.1155/2013/321213. Epub 2013 Jul 11. — View Citation

Naughton SX, Terry AV Jr. Neurotoxicity in acute and repeated organophosphate exposure. Toxicology. 2018 Sep 1;408:101-112. doi: 10.1016/j.tox.2018.08.011. Epub 2018 Aug 23. — View Citation

Rahimi R, Nikfar S, Abdollahi M. Increased morbidity and mortality in acute human organophosphate-poisoned patients treated by oximes: a meta-analysis of clinical trials. Hum Exp Toxicol. 2006 Mar;25(3):157-62. doi: 10.1191/0960327106ht602oa. — View Citation

Salvi RM, Lara DR, Ghisolfi ES, Portela LV, Dias RD, Souza DO. Neuropsychiatric evaluation in subjects chronically exposed to organophosphate pesticides. Toxicol Sci. 2003 Apr;72(2):267-71. doi: 10.1093/toxsci/kfg034. — View Citation

Syed S, Gurcoo SA, Farooqui AK, Nisa W, Sofi K, Wani TM. Is the World Health Organization-recommended dose of pralidoxime effective in the treatment of organophosphorus poisoning? A randomized, double-blinded and placebo-controlled trial. Saudi J Anaesth. 2015 Jan;9(1):49-54. doi: 10.4103/1658-354X.146306. — View Citation

Tallat S, Hussien R, Mohamed RH, Abd El Wahab MB, Mahmoud M. Caspases as prognostic markers and mortality predictors in acute organophosphorus poisoning. J Genet Eng Biotechnol. 2020 Apr 13;18(1):10. doi: 10.1186/s43141-020-00024-y. — View Citation

Therkorn J, Drewry DG, Tiburzi O, Astatke M, Young C, Rainwater-Lovett K. Review of Biomarkers and Analytical Methods for Organophosphate Pesticides and Applicability to Nerve Agents. Mil Med. 2020 Mar 2;185(3-4):e414-e421. doi: 10.1093/milmed/usz441. — View Citation

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Identification of neuroinflammatory biomarker	The biomarker should correlate with nerve injury	1.5 years
Primary	Identification of the mechanism of neuroinflammation	To detect the possible pathways involved in initiation of systemic inflammation rather than inhibition of choline esterase enzyme. As well as, studying the possible relation of these identified mechanisms with neuronal inflammation and damage.	1.5 years