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العنوان
THE POTENTIAL ROLE OF GLIAL FIBRILLARY ACIDIC PROTEIN IN EVALUATING OF ORGANOPHOSPHORUS-INDUCED NEUROTOXICITY /
المؤلف
Eltawil, Ali Sameh Ali.
هيئة الاعداد
باحث / علي سامح علي الطويل
مشرف / مجدي محمود حسن
مشرف / محمود بدر عبد الوهاب
مشرف / إيمان عبد الفتاح محمد
تاريخ النشر
2023.
عدد الصفحات
172 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الصحة وعلم السموم والطفرات
تاريخ الإجازة
1/1/2023
مكان الإجازة
جامعة عين شمس - معهد البيئة - العلوم الأساسية البيئية
الفهرس
Only 14 pages are availabe for public view

from 172

from 172

Abstract

Organophosphate poisoning is still a major public health problem especially among developing countries. It is the most common toxicological emergency in Egypt. They are alarmingly increasing method of suicide although it can result from occupational exposure or accidental ingestion. High mortality due to OPC is usually attributed to delay in diagnosis and improper treatment.
Consequently, organophosphorus compounds (OPC) poisoning leads to several neurotoxic disorders in humans as acute OPC poisoning known as cholinergic toxidrome, the intermediate syndrome, and organophosphate induced delayed polyneuropathy (OPIDP) and chronic organophosphate-induced neuropsychiatric disorder (COPIND).
Biomarker levels can predict the degree of neurotoxicity caused by OPC and identify patients who are most likely to develop long term sequelae. These patients may benefit the most by being targeted for rehabilitation therapy. Elevated biomarker levels may also identify patients who are at highest risk for secondary deterioration and who would benefit from repeated imaging, monitoring, and increased surveillance.
This study aimed to:
 Evaluate the association of early levels of GFAP with severity of acute OPC poisoning.
 Assess the usefulness of GFAP as a tool for predicting of OPC related neurotoxic disorders both in acute and chronic poisoning. Thus, helping to limit or prevent secondary neuronal damage at the early stage of OPC poisoning and attenuate the subsequent neuropsychiatric and neurological impairments.
This prospective study was carried out at the Poison Control Center (PCC), Ain Shams University Hospitals during the period from the beginning of January 2019 until the end of January 2020.
Subjects were divided into the following groups:
group I (Control group): 23 normal volunteers not exposed to OPC and didn’t suffer from any diseases will be served as controls.
group (II): Acute moderate organophosphorus poisoned (OPP) patients group: with mild, transient and spontaneously resolving symptoms or signs, this group consisted of 19 patients.
group (III): Acute severe OPC patients group: with severe or life threatening symptoms or signs, this group consisted of 25 patients.
group (IV): chronic OPC exposure group: 41farmers chronically exposed to OPs during their work in the fields with duration not less than 5 years. They were selected from the outpatient laboratory of the PCC.
 Blood samples were collected from all subjects for determination of the different parameters.
In this study, the following parameters will be investigated:
 Serum Glial fibrillary acidic protein (GFAP) by ELISA technique.
 Serum acetylcholine.
 Plasma Pseudo cholinesterase.
 Liver enzymes: Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT).
 Kidney functions:
o Serum urea
o Serum creatinine
o Serum electrolytes: Sodium and potassium.
o Serum Creatine phosphokinase (CPK) and lactate dehydrogenase (LDH)
o S. Lactate
The study revealed that there were high significant differences between GFAP and acetylcholine in all patient groups when compared with the control group. On the other hand, serum pseudo cholinesterase showed highly significant decreases in acute severe and acute moderate groups when compared to both control and chronic groups. While no significant difference was observed between chronic group and control group.
Liver enzymes (AST and ALT) showed statistically significant increase in acute patient groups, while no significant difference was reported in chronic exposure group. Kidney function markers (urea and creatinine) did not show valuable significant difference in all patient groups when compared with control group.
Serum glucose and Potassium levels in studied groups were significantly high in acute severe group as well as acute moderate group compared to controls. While no significant difference was found in chronic group when compared to controls.
The markers of tissue destruction (Serum Lactate, LDH and CPK levels) were also significantly increased in acute patient groups when compared with the control group.
Positive correlations were detected between GFAP and acetylcholine as well as GFAP and the following parameters CPK, LDH, AST and PCO2.
Acetylcholine was positively correlated to CPK. Negative correlations were detected between pseudo cholinesterase and the following parameters: GFAP, glucose, Lactate, LDH and CPK. Positive correlations between lactate and glucose, LDH, CPK On the other hand, high significant negative correlations were detected between lactate with potassium as well as with pH and HCO3.
Therefore, serum GFAP and acetylcholine can be used as early markers in brain cells injury in OPC. Serum GFAP and acetylcholine were significantly elevated in both acute OPC poisoned groups and chronic exposure. However, no significant relation was found between acute GFAP nor acetylcholine and the degree of severity of OPC in acutely poisoned patients.
The chronic exposure to OPCs affected the CNS cells as neuro-degenerative markers (GFAP and acetylcholine) showed significant increase in chronic group.