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Methanol Poisoning clinical trials

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NCT ID: NCT06173817 Recruiting - Methanol Poisoning Clinical Trials

The Use of Isocapnic Hyperventilation (iHV) for Treatment of Methanol Poisoned Patients

iHV-Met
Start date: December 20, 2023
Phase: Phase 2/Phase 3
Study type: Interventional

The projects investigate if treatment with isocapnic hyperventilation can eliminate methanol from the body in a similar manner to dialysis. This is achieved by administering the antidote (fomepizole) and let the patient breathe on a isocapnic hyperventilation device while samples of blood, urine and maybe the breath are collected to measure the contents of methanol and its metabolites.

NCT ID: NCT04877067 Completed - Clinical trials for Magnetic Field Exposure

Therapy of Toxic Optic Neuropathy Via Combination of Stem Cells With Electromagnetic Stimulation

Magnovision
Start date: April 1, 2019
Phase: Phase 3
Study type: Interventional

The axons of the retinal ganglion cells combine to form the optic nerve. The optic nerve transmits electrical signals to the visual cortex by various synapses. Optic nerve axons are more sensitive to toxins than retina because they are outside the blood retinal barrier. Methanol, various solvents and heavy metals, carbon dioxide, antiarrhythmic, antiepileptic, antibiotics and some vasoactive drugs can cause toxic optic neuropathy. There is a different pathophysiology for each toxin. Methanol is easily accessible alcohol in all types of disinfectants. Methanol is converted into formaldehyde and formic acid while metabolized in the liver. Formaldehyde disrupts ATP synthesis by blocking mitochondrial function and oxidative phosphorylation. Formic acid causes demyelination as a result of metabolic acidosis. Neuroinflammation occurs when denatured proteins block axoplasmic flow. All these processes can lead to apoptosis and permanent vision loss. Sildenafil is a vasoactive drug used in erectile dysfunction. Sildenafil decreases optic nerve head blood flow. Neuroinflammation develops secondary to the cessation of axoplasmic flow after hypoxia. If hypoxia and neuroinflammatiom persists, apoptosis and permanent vision loss develop. Amiodarone is an ion channel blocker used in the treatment of cardiac arrhythmias. Long-term use may cause disruption of ion channel balance in the optic nerve. This condition leads to asymmetric neuroinflammation and apoptosis. Wharton's jelly derived mesenchymal stem cells (WJ-MSC) can increase mitochondrial ATP synthesis with paracrine effects and suppress neuroinflammation with immunomodulatory effects. Repetitive electromagnetic stimulation (rEMS) can rearrange ion channel balances and axoplasmic flow. The aim of this prospective phase-3 clinical study is to investigate the effect of WJ-MSC and rEMS combination in the therapy of toxic optic neuropathies. This combination is the first study in the literature for the therapy of toxic optic neuropathies.

NCT ID: NCT04064801 Completed - Methanol Poisoning Clinical Trials

Red Cell Distribution Width as a Predictor of Mortality in Acute Methanol Poisoning

Start date: March 15, 2020
Phase:
Study type: Observational

The study aimed to investigate the association between RDW and in-hospital mortality in methanol poisoning.