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Evaluation of the Safety and Efficacy of Parecoxib in Patients With Subarachnoid Hemorrhage

Phase 2
Not yet recruiting
Conditions
Neurological Complication
Interventions
Drug: Placebo
Registration Number
NCT06579274
Lead Sponsor
St. Anne's University Hospital Brno, Czech Republic
Brief Summary

Because of the important role of inflammation in the pathophysiology of SAH, it was hypothesized that its pharmacological manipulation might improve the prognosis of patients. In recent years, the effects of several groups of anti-inflammatory drugs on the development of complications after SAH have been described. Initially promising, glucocorticoids, thought to reduce cerebrovascular inflammation, brain swelling, and headache, failed in clinical trials. Studies have not provided clear evidence of the beneficial effects of these drugs in patients after SAH. Therefore, the administration of glucocorticoids is not currently part of the recommended practice. In addition, glucocorticoid treatment is associated with adverse effects that worsen outcomes, including hyperglycemia, infection, and the risk of gastrointestinal bleeding.

Detailed Description

Spontaneous subarachnoid hemorrhage (SAH) is a specific type of hemorrhagic stroke with a worldwide incidence ranging from 0.5 to 28 per 100,000 population, with large regional variations. Despite improvements in diagnosis, treatment and care, SAH remains a disease with high mortality and morbidity. According to the literature, one third of patients die within the first few days after SAH, and most survivors have cognitive impairment or long-term disability. The overall clinical outcome depends on the severity of early brain injury (EBI), cerebral edema, hydrocephalus, development of delayed ischemic neurological deficit (DIND), epileptic seizures, and other complications. The pathophysiological cascades responsible for the development of these complications remain poorly understood. However, numerous studies support the important role of aseptic cerebrovascular inflammation induced by blood and blood breakdown products in the subarachnoid space after SAH. The increased interest in the development of cerebrovascular inflammation after SAH is confirmed by the increasing number of clinical and experimental studies devoted to this topic. Cerebrovascular aseptic inflammation as a potential treatment target is also mentioned in current guidelines for the management of patients after SAH.

The results of experimental studies formed the basis for the clinical evaluation of the effects of NSAIDs after SAH. The effects of several commonly used NSAIDs, particularly dexketoprofen, ibuprofen, diclofenac, indomethacin, or dipyrone, have been evaluated in prospective and retrospective clinical trials over the past decade. In addition to reducing pro-inflammatory markers such as IL6, lowering body temperature and platelet aggregation, the administration of NSAIDs has been associated with reduced mortality and improved clinical outcomes. Despite the beneficial effects of some NSAIDs, more robust studies are still lacking, except for one study that evaluated the effect of meloxicam in patients after SAH. This study was a randomized, double-blind, placebo-controlled trial. It showed a trend towards a better outcome with a lower incidence of vasospasm or mortality in patients after SAH.

Despite encouraging experimental results, no clinical trials have yet evaluated the anti-inflammatory and other potentially beneficial effects of cyclooxygenase-2 (COX-2) inhibitors. COX-2 inhibitors, or coxibs, belong to the group of NSAIDs that selectively inhibit the COX-2 enzyme, which is responsible for developing inflammation and pain. A planned clinical study will evaluate the effects of parecoxib, a specific COX-2 inhibitor in the NSAIDs group, on overall clinical outcome and development of complications in patients following spontaneous SAH.

Recruitment & Eligibility

Status
NOT_YET_RECRUITING
Sex
All
Target Recruitment
112
Inclusion Criteria
  • Signed informed consent
  • Age: 18-85 years
  • Weight> 50 kg
  • Spontaneous SAH diagnosed on a native CT brain max. 48 hours after the first symptoms
  • Spontaneous SAH caused by rupture of the cerebral aneurysm confirmed on DSA or CT angiography (Fisher grade 1 to 4) OR Spontaneous SAH without a source on CT AG, DSA or MRI with Fisher grade 3 and 4
  • For women capable of becoming pregnant (see definitions from the CTFG guideline for contraception): use of the following highly reliable contraceptive method within 3 months after the end of the study: adherence to sexual abstinence or contraception containing progesterone with inhibition of ovulation (oral administration, injection) or non-hormonal intrauterine device or hormonal or bilateral tubal occlusion or partner vasectomy. Males: adherence to sexual abstinence or use of an adequate contraceptive method (i.e. condom) in case of sexual intercourse within 3 months after the end of the study.
Exclusion Criteria
  • Symptoms of SAH without the finding of blood on the initial native CT scan of the brain
  • SAH from a cause other than a ruptured aneurysm, e.g. A-V malformation, traumatic SAH
  • Pregnancy and breastfeeding (pregnancy test)
  • Known hypersensitivity to the components of the product
  • Allergic reaction to the active substance or sulfonamides in the anamnesis
  • Concomitant treatment with other non-steroidal anti-inflammatory drugs, aspirin or corticosteroids (at least five half-lives before administration of the medicinal product under investigation)
  • Severe hepatic insufficiency (serum albumin level <25 g/l or Child-Pugh score less than 10).
  • Active peptic ulcer or bleeding from the gastrointestinal tract in the anamnesis
  • Inflammatory bowel disease in the anamnesis
  • Congestive heart failure (NYHA II-IV) in history.
  • Proven ischemic heart disease, peripheral arterial insufficiency.
  • Participation in another clinical study (a gap of at least five half-lives before administration of the medicinal product under investigation).

Study & Design

Study Type
INTERVENTIONAL
Study Design
PARALLEL
Arm && Interventions
GroupInterventionDescription
Control - PlaceboPlaceboA placebo is a substance administered to a participant as a comparison without any pharmacological effect. However, unlike conventional medicines, it does not contain any active ingredients. In this clinical trial, the placebo is an isotonic sodium chloride solution. The placebo is injected into a peripheral or central venous catheter within 12 hours of the patient's enrollment in the study (from when informed consent is signed). Placebo 100 mL per dose will continue to be administered every 12 hours for five days. Participants will be followed for six months for any adverse events and changes in subjective status. In the event of adverse effects, patients will be followed until resolution. After that, their participation in this clinical trial will be terminated. The total duration of the patient's participation in the clinical trial will be six months.
Active - ParecoxibParecoxibParecoxib 40 mg/100 ml will be injected into a peripheral or central venous catheter within 12 hours of the patient's inclusion in the study (from when informed consent is signed). Parecoxib 40 mg/100 ml is administered every 12 hours for 5 days. The maximum daily dose is 80 mg. In patients with moderate hepatic impairment (Child-Pugh score 7-9), parecoxib is started at 20 mg/50 mL and continued at this dose every 12 hours. The maximum daily dose is 40 mg. Participants will be monitored for six months for adverse events and changes in subjective status. In the event of adverse events, patients will be followed until resolution. After that, their participation in this clinical trial will be terminated. The total duration of the patient's participation in the clinical trial will be six months.
Primary Outcome Measures
NameTimeMethod
Influence of parecoxib on outcome of patients with SAH180 days ± 14 days after first dose of parecoxib/placebo

The primary outcome measure is the percentage of patients in the active and control groups whose outcome is categorized as favorable (mRS 0-3) or unfavorable (mRS 4-6) according to the modified Rankin Scale (mRS).

Secondary Outcome Measures
NameTimeMethod
Influence of parecoxib on outcome of patients with SAHDischarge from hospital and 90 days ± 7 days after first dose of parecoxib/placebo

The secondary monitored parameter is the percentage of patients in the active and control groups whose outcome, according to the modified Rankin scale (mRS), is divided into favourable (mRS 0-3) or unfavourable (mRS 4-6).

Occurrence of symptomatic vasospasms (vasospasms confirmed on TCD / CT AG / MR AG / DSASix, eight and ten days after the application of the first dose of the evaluated medicinal product /placebo.

Number of patients with vasospasms confirmed on TCD / CT AG / MR AG / DSA

Incidence of delayed ischemic neurological deficit (DIND)Six, eight and ten days, three and six months after the application of the first dose of the evaluated medicinal product /placebo.

Number of patients with delayed ischemic neurological deficit

MortalityDuring the treatment and post treatment period of hospitalization, 90 days ± 7 days and 180 days ± 14 days

Number of deaths

Length of hospitalization in ICU3 months

Length of hospitalization in ICU

Total length of hospitalization3 months

Total length of hospitalization

Occurrence of acute hydrocephalusDuring the treatment and post treatment period of hospitalization

Number of patients with acute hydrocephalus

Occurrence of chronic hydrocephalusDuring the treatment and post treatment period of hospitalization, 90 days ± 7 days, 180 days ± 14 days

Number of patients with chronic hydrocephalus with V-P shunt implantation

Occurrence of feversDuring the treatment and post treatment period of hospitalization

Number of patients with fever above 38 degrees Celsius

Occurrence of inflammationDuring the treatment and post treatment period of hospitalization

Evaluation of the systemic inflammatory response (assessed daily during hospitalization) meeting at least 2 parameters:

* heart rate \> 90/min.

* leukocytosis \> 12x109/l) or leukopenia \< 9x109

* respiratory rate \> 20/min. or PaCO2 \< 32 mm Hg (4.3 kPa)

* body temperature \< 36.0 °C or \> 38.0 °C

Evaluation of pain according to Visual Analogue ScaleDuring the treatment and post treatment period of hospitalization, discharge from hospital, 90 days ± 7 days and 180 days ± 14 days after first dose of parecoxib/placebo

The comparison of the patients in the treatment and placebo arm with pain according to the Visual Analogue Scale, a numerical scale from 0 to 10 points, where increasing pain is indicated by a higher score.

Evaluation of prostaglandins and pro-inflammatory cytokines in the cerebrospinal fluid in the case of the below-mentioned external ventricular drainage after 2 days and in the serum0, 2, 4, 6, 8 and 10 days after implantation of drainage

Evaluation of prostaglandins (COX-2, PGH2, PGI2, PGE2, PGD2, PF2a, TXA2) and pro-inflammatory cytokines (TNF, IL-1, IL-4, IL-6, IL-8, IL-12) in the cerebrospinal fluid in the case of the below-mentioned external ventricular drainage after 2 days and in the serum regardless of the established cerebrospinal fluid drainage after two days to day 10 from initial symptoms

Evaluatioon of laboratory markers of inflammatory response in peripheral bloodTwo, four, six, eight and ten days after the application of the first dose parecoxib/placebo

C-reactive protein (CRP), procalcitonin (PCT) and white blood cell count

Evaluation of the functionality of the blood-cerebrospinal fluid barrier every 2 days if cerebrospinal fluid drainage is necessary.0, 2, 4, 6, 8 and 10 days after implantation of drainage

This evaluation will compare the number of patients in the treatment and placebo arms who undergo cerebrospinal fluid drainage.

Quality of life measured through questionnairesDischarge from hospital, 90 days ± 7 days and 180 days ± 14 days after the application of the first dose parecoxib/placebo

Evaluation of quality of life (SF-36 score)

Evaluation of the difference in efficacy parameters between subgroups according to the source of bleedingAfter discharge from hospital, six days after administration of the 1st dose of parecoxib/placebo

Number of patients with inflamation based on source of bleeding

Serious adverse eventsDuring hospitalization, at discharge, 90 days ± 7 days, 180 days ± 14 days after the first dose of parecoxib/placebo

Percentage of patients in the experimental and placebo groups with the occurrence of serious adverse events (SAE) (assessed during hospitalization, at discharge, 3 and 6 months after the first dose) supplemented by evaluation in individual subgroups according to the source of bleeding.

HepatotoxicityBefore the 1st dose of parecoxib/placebo, 1., 3. and 5. day of treatment and 10. day of hospitalization

Percentage of patients in the experimental and placebo groups with an increase in blood creatine phosphokinase (CPK), an increase in blood lactate dehydrogenase (LDH), an increase in alanine transaminase (ALT), an increase in aspartate transaminase (AST), and an increase in blood urea level \> 5x ULN; separate analysis for subgroups by source of bleeding.

Trial Locations

Locations (1)

St. Anne's University Hospital Brno

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Brno, Czech Republic, Czechia

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