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Clinical Trial Summary

Asthma, a disease characterized by chronic airway inflammation and hyper -responsiveness, is a common disease that affects all age groups. Asthma may be manifested as irreversible airflow obstruction in some patients. Although the pathogenesis of asthma is not well understood, increased oxidative stress due to an imbalance of oxidants and antioxidants has been found to be associated with asthma. In asthma, inflammation-related oxidative stress is driven by exposure to a variety of triggers, including allergens and viruses, which activate components of both the innate and acquired immune responses. Protection by escaping from triggering factors or standardization of asthma medication is difficult and usually is not enough for effective treatment. On the other hand, correction of antioxidative systems may be more efficacious in the control of asthmatic inflammation and asthma symptoms.

Little is known about the role of asymmetric dimethylarginine in the pathogenesis of asthmatic airway inflammation. The lung is a major source of asymmetric dimethylarginine that can promote oxidative stress by a reduction in nitric oxide synthesis which would result in higher levels of peroxynitrite, that causes oxidative cell damage, and exacerbate airway inflammation. asymmetric dimethylarginine can modify lung function, increase airway hyper-reactivity even in non-inflamed airways, and promote lung collagen production and deposition. Increased asymmetric dimethylarginine in serum has been found to be associated with the severity of symptoms of asthma in obese adults.

Malondialdehyde is an oxidant marker of pulmonary oxidative stress, and lipid peroxidation. Paraoxonase, an antioxidant enzyme may play a protective role in asthma. It hydrolyzes lipid peroxides and prevents low-density lipoprotein oxidation.


Clinical Trial Description

n/a


Study Design


Related Conditions & MeSH terms


NCT number NCT04175093
Study type Observational
Source Assiut University
Contact
Status Not yet recruiting
Phase
Start date November 29, 2019
Completion date November 21, 2021

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