Clinical Trial Details
— Status: Completed
Administrative data
| NCT number |
NCT04718155 |
| Other study ID # |
IRB5566000 |
| Secondary ID |
|
| Status |
Completed |
| Phase |
N/A
|
| First received |
|
| Last updated |
|
| Start date |
March 1, 2021 |
| Est. completion date |
June 1, 2022 |
Study information
| Verified date |
June 2022 |
| Source |
Assiut University |
| Contact |
n/a |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Interventional
|
Clinical Trial Summary
3-Hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, known as statins, are widely used
to reduce levels of low-density lipoprotein-cholesterol. As lipid-lowering drugs, statins
exert neuroprotective effects on ischemic stroke. this study will investigate whether the
protective effect of statins is mediated by their ability to impact inflammation and oxygen
free radical levels in cerebral ischemia/reperfusion injury.
Could Statins affect the neuroinflamation which occurs after traumatic brain injury?
Description:
Traumatic brain injury (TBI) is one of the most common and financially devastating health
problems in our society. Once the acute care period has ended, many TBI patients are left
with motor, cognitive, or emotional dysfunction as a result of their injury. The treatment of
TBI remains largely supportive, directed toward management of cerebral edema and intracranial
hypertension via temporizing measures, such as administration of osmotic agents,
hyperventilation, and ventricular drainage. None of these interventions have been
definitively demonstrated to improve long-term functional outcome. The failure of preclinical
therapies to translate into clinical benefit may derive from the heterogeneity of TBI
pathology, which includes diffuse axonal injury, cerebral contusion, intracerebral hemorrhage
(ICH), subarachnoid hemorrhage (SAH), and extra parenchymal hemorrhage. These primary insults
are exacerbated by a secondary neuroinflammatory cascade of cerebral hypoperfusion and
ischemia, oxidative stress, cerebral edema, and intracranial hypertension. There are a series
of reactions following cerebral ischemia/reperfusion, such as inflammation and an increase in
free radicals, which may trigger secondary injury in ischemic tissue. Indeed, the inhibition
of inflammation reduces tissue damage in ischemia. Thus, understanding the roles of
inflammation and free radicals in ischemia/reperfusion injury is therefore of great
importance.
3-Hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, known as statins, are widely used
to reduce levels of low-density lipoprotein-cholesterol. As lipid-lowering drugs, statins
exert neuroprotective effects on ischemic stroke. In this study, teh study will investigate
whether the protective effect of statins is mediated by their ability to impact inflammation
and oxygen free radical levels in cerebral ischemia/reperfusion injury. Statins have been
shown to reduce morbidity in patients who did not have high serum cholesterol or
cardiovascular disease but did have evidence of systemic inflammation. Statins have strong
efficacy on modulation of inflammatory responses. conditions where statins have been found to
have a positive effect on disease progression or mortality are primarily dependent on
leucocyte accumulation. Statins may thus promote the timely resolution of the inflammatory
response, preventing persistence of inflammation and resultant pathology.
Magnetic resonance spectroscopy (MRS) allows for measurement of metabolites that are
undetectable by conventional neuroimaging thereby holding potential to identify traumatic
brain injury patients that could benefit from specific neuropsychiatric and cognitive
rehabilitation . Brain energy metabolism is altered after TBI due to posttraumatic
inflammation and ischemia with mitochondrial dysfunction and loss of neuronal integrity with
increased cell membrane turnover. MRS is an MRI technique that can detect nuclei with spins
such as 1H, an abundant by-product of cellular respiration and brain tissue metabolites. As a
noninvasive and safe technique, MRS is available on clinical MR scanners (1.5 and 3.0 T)
without ionizing radiation [15]. This method holds the potential to identify compromised
brain metabolism, but evidence after traumatic brain injury is rare .
