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Published on: August 9, 2013
Serum creatine kinase B concentrations in acute cerebrovascular diseases
Insights
Serum creatine kinase B (CKB) levels fluctuate significantly after ischemic stroke, correlating with tissue damage. These CKB changes help differentiate stroke types and severity in patients.
Area of Science:
- Neurology
- Biochemistry
Background:
- Serum creatine kinase B (CKB) is an enzyme relevant to cellular energy metabolism.
- Understanding CKB dynamics in cerebrovascular diseases can aid in diagnosis and prognosis.
Purpose of the Study:
- To investigate the diagnostic and prognostic value of serum CKB concentrations in acute cerebrovascular diseases.
- To analyze CKB fluctuations in relation to stroke type, severity, and clinical events.
Main Methods:
- Serum CKB levels were measured every 12 hours for five days in 38 patients with acute cerebrovascular diseases and 9 controls.
- CKB concentrations were correlated with stroke volume, type (ischemic infarction, transient vascular events, subarachnoid hemorrhage), and clinical outcomes.
Main Results:
- Elevated and fluctuating CKB concentrations were observed in patients with acute cerebral infarction, correlating with tissue damage volume.
- Normal CKB profiles were noted in patients with transient vascular events.
- Patients with subarachnoid hemorrhage showed wide CKB fluctuations and high concentrations, sometimes linked to angiography or clinical worsening.
Conclusions:
- Serum CKB monitoring can help differentiate between ischemic stroke, transient vascular events, and subarachnoid hemorrhage.
- CKB fluctuation patterns, particularly in ischemic stroke, may serve as a biomarker for infarct size.
- CKB changes in ischemic stroke were not associated with neurological worsening or recurrent events.
Abstract:
Serum creatine kinase B (CKB) concentrations were measured every 12 hours for five days in 38 patients during acute cerebrovascular diseases and in nine controls. Mean CKB concentration was 6.2 +/- 0.8 ng/mL. The fluctuation of the CKB concentration following ischemic stroke was as notable as the elevation immediately after the ischemic event. The two abnormalities were observed in 13 of 17 patients with acute cerebral infarction, and the extent of abnormalities roughly correlated with the volume of tissue damage. The profiles were normal for patients with transient vascular events. Patients with subarachnoid hemorrhage demonstrated wide fluctuation along with high CKB concentration. Although transient elevation of the CKB concentration in some patients with subarachnoid hemorrhage was observed after angiography or clinical worsening, the fluctuation in patients with ischemic stroke was not associated with worsening of neurologic conditions or recurrence of ischemic events.
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