Ignite Creation Date:
2024-05-06 @ 5:51 PM
Last Modification Date:
2024-10-26 @ 2:36 PM
Study NCT ID:
NCT05451537
Status:
NOT_YET_RECRUITING
Last Update Posted:
2022-07-11
First Post:
2022-06-23
Brief Title:
Correlation of Formyl Peptide Receptor 1 With Sepsis-related Encephalopathy
Sponsor:
General Hospital of Ningxia Medical University
Organization:
General Hospital of Ningxia Medical University
Study Overview
Official Title:
Correlation of Formyl Peptide Receptor 1 With Sepsis-related Encephalopathy A Prospective Cohort Study
Status:
NOT_YET_RECRUITING
Status Verified Date:
2022-06
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
The pathogenesis of sepsis-associated encephalopathy SAE is unclear Formylpeptide receptor 1 FPR1 is a cell membrane receptor that recruits leukocytes and mediates inflammatory responses after activation but its role and mechanism in SAE are unknown This project intends to clarify the relationship between FPR1 activation and SAE from the clinical The investigators enrolled 100 patients with sepsis in ICU Patients were divided into two groups according to diagnostic criteria SAE group and none-SAE group Whole blood was collected The serum FPR1 protein level was measured using a commercial enzyme-linked immunosorbent assay After whole blood RNA was extracted the expressions of FPR1 and a reference gene were quantified by an automated one-step Taqman RT-PCR assay Multiple logistical regression analysis was used to identify the independent factors including FPR1 activation for the prediction of SAE outcomes
Detailed Description:
Background The pathogenesis of sepsis-associated encephalopathy SAE is unclear and there are no desired therapeutic methods Formylpeptide receptor 1 FPR1 is a cell membrane receptor that recruits leukocytes and mediates inflammatory responses after activation but its role and mechanism in SAE are unknown Our previous studies have shown that the expression of FPR1 in the hippocampus of septic mice is increased FPR1 knockout reduces mortality and microglial activation Based on this it is hypothesized that during sepsis FPR1 induces the migration and recruitment of neutrophils and monocytes to the brain at the same time FPR1 activation of microglia mediates brain inflammatory response and cell death these factors induces or aggravates cognitive dysfunction This project intends to clarify the relationship between FPR1 activation and SAE from the clinical The study will provide some useful data for the mechanism study of SAE
Methods Inclusion criteria for participants were patients with an age of 18-70 years and an inclusion within 24 hours after the beginning of severe sepsis or septic shock according to the criteria that were established by the international guidelines for management of severe sepsis and septic shock
Patients were excluded from the study if they had a previous diagnosis of a neuropsychiatric disease head trauma cerebral stroke epilepsy and intracranial infection current brain disorders hepatic encephalopathy pulmonary encephalopathy and severe electrolyte imbalance concurrent hematologic diseases malignant tumor postcardiac arrest or melanoma or if they were undergoing cancer chemotherapy
Demographic clinical and laboratory data were retrieved after intensive care unit ICU admission from the medical records made by two physicians Age gender Acute Physiology and Chronic Health Evaluation II score APACHE II score Sequential Organ Failure Assessment SOFA score GCS score and infection sites were collected and determined during the first 24 hours of admission basic laboratory tests including blood lactate B-type natriuretic peptide and inflammatory markers of white blood cell count WBC procalcitonin PCT and C-reactive protein CRP were detected on admission The GCS and mental status of the patients were evaluated twice a day at eight oclock in the morning and six oclock in the afternoon including SAE symptoms of somnolence stupor coma confusion disorientation agitation irritability and decreased level of GCS Sepsis-associated encephalopathy SAE was defined as cerebral dysfunction in the presence of severe sepsis as well as the presentation of two or more of the symptoms listed above after complete withdrawal of sedation
Original cerebral dysfunction derived from hypoxic encephalopathy severe hypoglycemia intracranial hemorrhage epilepsy relapse acute ischemic stroke and hyponatremia were excluded Supportive treatments such as the use of a ventilator length of ICU stay and 28-day mortality were also included for assessment
Blood samples were collected from patients on admission through venipuncture the resultant serum samples were aliquoted and stored at -80C until further analysis The serum FPR1 protein level was measured using a commercial enzyme-linked immunosorbent assay
Patients were divided into two groups according to diagnostic criteria SAE group and none SAE group Whole blood was collected The serum FPR1 protein level was measured using a commercial enzyme-linked immunosorbent assay After whole blood RNA was extracted the expressions of FPR1 and a reference gene were quantified by an automated one-step Taqman RT-PCR assay
Multiple logistical regression analysis was used to identify the independent factors for the prediction of SAE outcomes using the forward stepwise method with the likelihood ratio test Correlations between variables were tested by the Pearson linear regression test Receiver operating characteristics ROC analysis was used to qualify marker performance and ROC curves were constructed to assess the sensitivity specificity and respective areas under the curves AUCs of the FPR1 protein performance with 95 CI A value of P005 was considered statistically significant
The primary outcome is the comparison of FPR1 levels in patients with and without sepsis related encephalopathy Secondary Outcome Measures the comparison of laboratory data inflammatory cytokines levels in patients with and without sepsis related encephalopathy
Methods Inclusion criteria for participants were patients with an age of 18-70 years and an inclusion within 24 hours after the beginning of severe sepsis or septic shock according to the criteria that were established by the international guidelines for management of severe sepsis and septic shock
Patients were excluded from the study if they had a previous diagnosis of a neuropsychiatric disease head trauma cerebral stroke epilepsy and intracranial infection current brain disorders hepatic encephalopathy pulmonary encephalopathy and severe electrolyte imbalance concurrent hematologic diseases malignant tumor postcardiac arrest or melanoma or if they were undergoing cancer chemotherapy
Demographic clinical and laboratory data were retrieved after intensive care unit ICU admission from the medical records made by two physicians Age gender Acute Physiology and Chronic Health Evaluation II score APACHE II score Sequential Organ Failure Assessment SOFA score GCS score and infection sites were collected and determined during the first 24 hours of admission basic laboratory tests including blood lactate B-type natriuretic peptide and inflammatory markers of white blood cell count WBC procalcitonin PCT and C-reactive protein CRP were detected on admission The GCS and mental status of the patients were evaluated twice a day at eight oclock in the morning and six oclock in the afternoon including SAE symptoms of somnolence stupor coma confusion disorientation agitation irritability and decreased level of GCS Sepsis-associated encephalopathy SAE was defined as cerebral dysfunction in the presence of severe sepsis as well as the presentation of two or more of the symptoms listed above after complete withdrawal of sedation
Original cerebral dysfunction derived from hypoxic encephalopathy severe hypoglycemia intracranial hemorrhage epilepsy relapse acute ischemic stroke and hyponatremia were excluded Supportive treatments such as the use of a ventilator length of ICU stay and 28-day mortality were also included for assessment
Blood samples were collected from patients on admission through venipuncture the resultant serum samples were aliquoted and stored at -80C until further analysis The serum FPR1 protein level was measured using a commercial enzyme-linked immunosorbent assay
Patients were divided into two groups according to diagnostic criteria SAE group and none SAE group Whole blood was collected The serum FPR1 protein level was measured using a commercial enzyme-linked immunosorbent assay After whole blood RNA was extracted the expressions of FPR1 and a reference gene were quantified by an automated one-step Taqman RT-PCR assay
Multiple logistical regression analysis was used to identify the independent factors for the prediction of SAE outcomes using the forward stepwise method with the likelihood ratio test Correlations between variables were tested by the Pearson linear regression test Receiver operating characteristics ROC analysis was used to qualify marker performance and ROC curves were constructed to assess the sensitivity specificity and respective areas under the curves AUCs of the FPR1 protein performance with 95 CI A value of P005 was considered statistically significant
The primary outcome is the comparison of FPR1 levels in patients with and without sepsis related encephalopathy Secondary Outcome Measures the comparison of laboratory data inflammatory cytokines levels in patients with and without sepsis related encephalopathy
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None