Guillain-Barre SyndromeNCT04927598
Predictors and Prognostic Factors of Gullian Barrie Syndrome Outcome
An observational study of Guillain-Barre Syndrome, run by Assiut University at 1 site in Egypt.
Trial summary
This study aims to identify clinical and biological determinants and factors that predict outcome including primary outcome (percentage of changes in clinical scales pre- and after 3 months ) and secondary outcome depending on neurophysiologiacal studies and prognostic factors in individual patients with… Read more about this study
- Who is it for?
- Ages 10 years and older
- Conditions the study is for
- Guillain-Barre Syndrome
- What is being tested?
- plasmapheresis
- Type of treatment
- Medical device
- How many people
- 62 participants
- Where
- 1 siteEgypt
- Study dates
- 20 Oct 2020to 1 Apr 2022
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 10 years and older
- All sexes
- No healthy volunteers
- Child, Adult, Older adult
Study population: Guillian Barre syndrome ( GBS ) is a rare disease , its incidence nearly , 0.8 - 1.8 case / 100000 population ( 16,17) . Total coverage of patients with ( GBS ) fitting inclusion criteria and seeking care at Neuro-psychiatric clinics or admitted at Neuro-psychiatry hospital through one year duration about 3 -4 cases per month (36 -38 case per year ) .
Who may be able to join
- Any Age, recent onset of GBS through the first 2 weeks . Gender: Male or Female Inclusion Criteria.
Who cannot join
- patients with metabolic disorders, others
Trial locations and contacts
1 site in 1 country.
About this study
This study aims to identify clinical and biological determinants and factors that predict outcome including primary outcome (percentage of changes in clinical scales pre- and after 3 months ) and secondary outcome depending on neurophysiologiacal studies and prognostic factors in individual patients with Guillain-Barre syndrome i individuals managed by plasmapheresis and IVIG immunoglobulin .
This information will be used to understand the diversity in clinical presentation and response to treatment of GBS.
Read the detailed description
Guillain-Barré syndrome (GBS) is an acute onset, monophasic, immune-mediated peripheral nerve and root disorder (termed polyradiculoneuropathy), GBS has become the most common cause of acute flaccid paralysis worldwide and is a neurological emergency .Guillain-Barré syndrome (GBS) encompasses group of acute immune-mediated disordes restricted to peripheral nerves and roots. Good circumstantial evidence exists for a pathogenic role for molecular mimicry in GBS pathogenesis,especially with its axonal forms, providing insights that could guide future immunotherapy :Intravenous immunoglobulin (IVIg) and plasma exchange (PE) .
Clinical presentation is a sudden onset of rapidly progressive and symmetrical weakness of the limbs, with or without peripheral sensory disturbance, reduction in or loss of tendon reflexes , and cerebrospinal fluid (CSF) analysis showing elevated protein concentrations with a normal white cell count, termed albuminocytologic dissociation, to distinguish it from infections that typically demonstrate elevated protein and white cell counts. The symptoms typically reach maximal severity within four weeks from symptom onset. Most patients generally require hospitalization for treatment, with close cardiopulmonary monitoring performed. Many patients also develop symptoms or signs of autonomic nervous system dysfunction, termed dysautonomia. These commonly consist of sinus tachycardia, arrhythmias,, orthostatic hypotension, increased sweating and bladder and gastrointestinal dysfunction.
Antecedent infections, typically within 4 weeks of neurological symptom onset, commonly occur in GBS patients, resulting in the commonly cited molecular mimicry hypothesis, in which the immune system becomes activated in response to infectious antigen with structural similarity to peripheral nerve myelin or axonal components, with resultant tissue-specific peripheral nerve and nerve root injury in susceptible individuals.
Epidemiological data implies that about two-thirds of GBS adult patients had a prior respiratory or gastrointestinal infection.Pathophysiology and immunopathology of the preceding infections are pathogenically associated with GBS, and may play an essential role in triggering the initial peripheral nerve/ nerve root-specific systemic immune system activation that causes cross-reactive humoral and cellular immune responses with resultant demyelination, axonal injury or both involving peripheral nerves and roots.
Optimal treatment of individual patients may depend on the pathogenesis and clinical severity. Patients with severe forms of GBS may possibly need more intensive treatment to recover. Patients with a milder course that fully recover after standard therapy could suffer from possibly more side effects of more aggressive forms of treatment. This could only be possible if there are prognostic models that accurately predict the clinical course in individual patients. Ideally such models should be based on clinical and biological predictors that are strongly associated with disease course and known as early as possible in the acute phase of illness, when treatment with immunomodulatory therapy is most effective. Prognostic models could help to guide selective trials in specific GBS subtypes. Because of this it will be possible to treat GBS with more effective and more individual therapy
- Conditions
- Guillain-Barre Syndrome
- Being tested
- plasmapheresis
- Keywords
- predictors and prognostic factors of outcome
- Medical subject headings
- Guillain-Barre Syndrome
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
plasmapheresisDevice
patients of Gullian Barrie syndrome undergo plasmapharesis
What is being measured
The primary outcome is the main question the study is designed to answer.
clinical scales :The GBS Disability Scale
the percentage of changes in clinical scales pre- and 3 months after treatment depending on clinical assessment scales : The GBS Disability Scale has six levels: 0 points (healthy), 1 point (minor symptoms and capable of running), 2 points (able to walk 10 m without assistance but unable to run), 3 points (able to walk 10 m across an open space with help), 4 points(bedridden or wheelchair-bound), 5points (requiring assisted ventilation for at least part of the day), and 6 points (dead).
Measured: change from baseline scale at 3 months
Clinical grading scale MRC ( medial research council sum score )
Clinical grading scale MRC ( medial research council sum score ) from zero ( no power ) up to 60 full power : sum score of muscle power in both upper limbs and lower limbs in points .
Measured: change from baseline scale at 3 months
ERASMUS GBS respiratory insufficiency score EGRIS :
ERASMUS GBS respiratory insufficiency score EGRIS :
Predict the probability of respiratory insufficiency within the first week of admission, in individual patients with Guillain-Barre . syndrome from zero to 7 points score : 0 point ( no affection ) , 7 point ( severe affection )
Measured: change from baseline scale at 3 months
Erasmus GBS Outcome Score (EGOS)
Erasmus GBS Outcome Score (EGOS) is a prognostic model based on age, diarrhea, and GBS disability score at 2 weeks after hospital admission that accurately predicts the chance of being able to walk independently at 3 months
Measured: change from baseline scale at 3 months
overall neuropathy limitations scale ONLS .
it is modified disability sum score : sum of arm grade and leg grade limitation score ; arm grade from zero point ( less limitation ) to 5 points ( most limitation ) and leg grade from zero point ( less limitation) to 7 points (more limitation)
Measured: change from baseline scale at 3 months
Secondary outcomes (1)
comparison between pre and post neurophysiological studies
neurophysiological study pre- and after 3 months change of degree of affection and improvement in latency in nerve conduction m/ sec. amplitude m/v , velocity of nerve /s conduction and F-wave of both upper limbs and lower limbs
Measured: change from baseline scale at 3 months
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted16 Jun 2021
- Study start20 Oct 2020
- Primary completion15 Oct 2021
- Study completion1 Apr 2022
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (11)Papers the sponsor has linked to this study.
- Other trials for Guillain-Barre SyndromeStudies of the same condition, open and under way.
- More trials run by Assiut UniversityThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 62 participants (actual)
Sponsor and investigators
- Lead sponsor
- Assiut University
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Mohamed Zayed Saber, Assiut University
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT04927598
- Sponsor's protocol ID
- Gullian Barrie syndrome
- Status last verified
- Dec 2022
- First submitted
- 15 Apr 2021
- Last updated
- 8 Dec 2022
- Results posted
- No
- Data monitoring committee
- Yes
- FDA-regulated drug
- No
- FDA-regulated device
- No
Publications
van Doorn PA, Ruts L, Jacobs BC. Clinical features, pathogenesis, and treatment of Guillain-Barre syndrome. Lancet Neurol. 2008 Oct;7(10):939-50. doi: 10.1016/S1474-4422(08)70215-1.
PubMed 18848313Raphael JC, Chevret S, Hughes RA, Annane D. Plasma exchange for Guillain-Barre syndrome. Cochrane Database Syst Rev. 2012 Jul 11;(7):CD001798. doi: 10.1002/14651858.CD001798.pub2.
PubMed 22786475Fokke C, van den Berg B, Drenthen J, Walgaard C, van Doorn PA, Jacobs BC. Diagnosis of Guillain-Barre syndrome and validation of Brighton criteria. Brain. 2014 Jan;137(Pt 1):33-43. doi: 10.1093/brain/awt285. Epub 2013 Oct 26.
PubMed 24163275van Doorn PA. Diagnosis, treatment and prognosis of Guillain-Barre syndrome (GBS). Presse Med. 2013 Jun;42(6 Pt 2):e193-201. doi: 10.1016/j.lpm.2013.02.328. Epub 2013 Apr 28.
PubMed 23628447van Nes SI, Vanhoutte EK, van Doorn PA, Hermans M, Bakkers M, Kuitwaard K, Faber CG, Merkies IS. Rasch-built Overall Disability Scale (R-ODS) for immune-mediated peripheral neuropathies. Neurology. 2011 Jan 25;76(4):337-45. doi: 10.1212/WNL.0b013e318208824b.
PubMed 21263135Mori M, Kuwabara S, Fukutake T, Hattori T. Intravenous immunoglobulin therapy for Miller Fisher syndrome. Neurology. 2007 Apr 3;68(14):1144-6. doi: 10.1212/01.wnl.0000258673.31824.61.
PubMed 17404197Kalita J, Misra UK, Goyal G, Das M. Guillain-Barre syndrome: subtypes and predictors of outcome from India. J Peripher Nerv Syst. 2014 Mar;19(1):36-43. doi: 10.1111/jns5.12050.
PubMed 24456386Dornonville de la Cour C, Jakobsen J. Residual neuropathy in long-term population-based follow-up of Guillain-Barre syndrome. Neurology. 2005 Jan 25;64(2):246-53. doi: 10.1212/01.WNL.0000149521.65474.83.
PubMed 15668421van Koningsveld R, Steyerberg EW, Hughes RA, Swan AV, van Doorn PA, Jacobs BC. A clinical prognostic scoring system for Guillain-Barre syndrome. Lancet Neurol. 2007 Jul;6(7):589-94. doi: 10.1016/S1474-4422(07)70130-8.
PubMed 17537676Walgaard C, Lingsma HF, Ruts L, van Doorn PA, Steyerberg EW, Jacobs BC. Early recognition of poor prognosis in Guillain-Barre syndrome. Neurology. 2011 Mar 15;76(11):968-75. doi: 10.1212/WNL.0b013e3182104407.
PubMed 21403108Khedr EM, Shehab MM, Mohamed MZ, Mohamed KO. Early electrophysiological study variants and their relationship with clinical presentation and outcomes of patients with Guillain-Barre syndrome. Sci Rep. 2023 Aug 26;13(1):14000. doi: 10.1038/s41598-023-41072-x.
PubMed 37634022
Study at a glance
From the registry record, last updated by the sponsor on 8 Dec 2022. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Predictors and Prognostic Factors of Gullian Barrie Syndrome Outcome
- ClinicalTrials.gov ID
- NCT04927598
- Acronym / sponsor ID
- Gullian Barrie syndrome
- Conditions
- Guillain-Barre Syndrome
- Keywords
- predictors and prognostic factors of outcome
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 62 participants (actual)
- Lead sponsor
- Assiut UniversityUniversity, hospital or other
- Study start
- 20 Oct 2020 (actual)
- Primary completion
- 15 Oct 2021 (actual)
- Study completion
- 1 Apr 2022 (actual)
- First posted
- 16 Jun 2021 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
This study aims to identify clinical and biological determinants and factors that predict outcome including primary outcome (percentage of changes in clinical scales pre- and after 3 months ) and secondary outcome depending on neurophysiologiacal studies and prognostic factors in individual patients with Guillain-Barre syndrome i individuals managed by plasmapheresis and IVIG immunoglobulin .
This information will be used to understand the diversity in clinical presentation and response to treatment of GBS.
Detailed description
Guillain-Barré syndrome (GBS) is an acute onset, monophasic, immune-mediated peripheral nerve and root disorder (termed polyradiculoneuropathy), GBS has become the most common cause of acute flaccid paralysis worldwide and is a neurological emergency .Guillain-Barré syndrome (GBS) encompasses group of acute immune-mediated disordes restricted to peripheral nerves and roots. Good circumstantial evidence exists for a pathogenic role for molecular mimicry in GBS pathogenesis,especially with its axonal forms, providing insights that could guide future immunotherapy :Intravenous immunoglobulin (IVIg) and plasma exchange (PE) .
Clinical presentation is a sudden onset of rapidly progressive and symmetrical weakness of the limbs, with or without peripheral sensory disturbance, reduction in or loss of tendon reflexes , and cerebrospinal fluid (CSF) analysis showing elevated protein concentrations with a normal white cell count, termed albuminocytologic dissociation, to distinguish it from infections that typically demonstrate elevated protein and white cell counts. The symptoms typically reach maximal severity within four weeks from symptom onset. Most patients generally require hospitalization for treatment, with close cardiopulmonary monitoring performed. Many patients also develop symptoms or signs of autonomic nervous system dysfunction, termed dysautonomia. These commonly consist of sinus tachycardia, arrhythmias,, orthostatic hypotension, increased sweating and bladder and gastrointestinal dysfunction.
Antecedent infections, typically within 4 weeks of neurological symptom onset, commonly occur in GBS patients, resulting in the commonly cited molecular mimicry hypothesis, in which the immune system becomes activated in response to infectious antigen with structural similarity to peripheral nerve myelin or axonal components, with resultant tissue-specific peripheral nerve and nerve root injury in susceptible individuals.
Epidemiological data implies that about two-thirds of GBS adult patients had a prior respiratory or gastrointestinal infection.Pathophysiology and immunopathology of the preceding infections are pathogenically associated with GBS, and may play an essential role in triggering the initial peripheral nerve/ nerve root-specific systemic immune system activation that causes cross-reactive humoral and cellular immune responses with resultant demyelination, axonal injury or both involving peripheral nerves and roots.
Optimal treatment of individual patients may depend on the pathogenesis and clinical severity. Patients with severe forms of GBS may possibly need more intensive treatment to recover. Patients with a milder course that fully recover after standard therapy could suffer from possibly more side effects of more aggressive forms of treatment. This could only be possible if there are prognostic models that accurately predict the clinical course in individual patients. Ideally such models should be based on clinical and biological predictors that are strongly associated with disease course and known as early as possible in the acute phase of illness, when treatment with immunomodulatory therapy is most effective. Prognostic models could help to guide selective trials in specific GBS subtypes. Because of this it will be possible to treat GBS with more effective and more individual therapy
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
Who may qualify
- Ages
- 10 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Child, Adult, Older adult
- Study population
- Guillian Barre syndrome ( GBS ) is a rare disease , its incidence nearly , 0.8 - 1.8 case / 100000 population ( 16,17) . Total coverage of patients with ( GBS ) fitting inclusion criteria and seeking care at Neuro-psychiatric clinics or admitted at Neuro-psychiatry hospital through one year duration about 3 -4 cases per month (36 -38 case per year ) .
Key inclusion criteria (1 listed)
- Any Age, recent onset of GBS through the first 2 weeks . Gender: Male or Female Inclusion Criteria.
Key exclusion criteria (1 listed)
- patients with metabolic disorders, others
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| plasmapheresispatients of Gullian Barrie syndrome undergo plasmapharesis | Device | – |
Primary outcome
clinical scales :The GBS Disability Scale
Time frame: change from baseline scale at 3 months
the percentage of changes in clinical scales pre- and 3 months after treatment depending on clinical assessment scales : The GBS Disability Scale has six levels: 0 points (healthy), 1 point (minor symptoms and capable of running), 2 points (able to walk 10 m without assistance but unable to run), 3 points (able to walk 10 m across an open space with help), 4 points(bedridden or wheelchair-bound), 5points (requiring assisted ventilation for at least part of the day), and 6 points (dead).
Clinical grading scale MRC ( medial research council sum score )
Time frame: change from baseline scale at 3 months
Clinical grading scale MRC ( medial research council sum score ) from zero ( no power ) up to 60 full power : sum score of muscle power in both upper limbs and lower limbs in points .
ERASMUS GBS respiratory insufficiency score EGRIS :
Time frame: change from baseline scale at 3 months
ERASMUS GBS respiratory insufficiency score EGRIS : Predict the probability of respiratory insufficiency within the first week of admission, in individual patients with Guillain-Barre . syndrome from zero to 7 points score : 0 point ( no affection ) , 7 point ( severe affection )
Erasmus GBS Outcome Score (EGOS)
Time frame: change from baseline scale at 3 months
Erasmus GBS Outcome Score (EGOS) is a prognostic model based on age, diarrhea, and GBS disability score at 2 weeks after hospital admission that accurately predicts the chance of being able to walk independently at 3 months
overall neuropathy limitations scale ONLS .
Time frame: change from baseline scale at 3 months
it is modified disability sum score : sum of arm grade and leg grade limitation score ; arm grade from zero point ( less limitation ) to 5 points ( most limitation ) and leg grade from zero point ( less limitation) to 7 points (more limitation)
1 secondary outcome
comparison between pre and post neurophysiological studies
Time frame: change from baseline scale at 3 months
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 8 Dec 2022.
- Background: PubMed 18848313van Doorn PA, Ruts L, Jacobs BC. Clinical features, pathogenesis, and treatment of Guillain-Barre syndrome. Lancet Neurol. 2008 Oct;7(10):939-50. doi: 10.1016/S1474-4422(08)70215-1.
- Background: PubMed 22786475Raphael JC, Chevret S, Hughes RA, Annane D. Plasma exchange for Guillain-Barre syndrome. Cochrane Database Syst Rev. 2012 Jul 11;(7):CD001798. doi: 10.1002/14651858.CD001798.pub2.
- Background: PubMed 24163275Fokke C, van den Berg B, Drenthen J, Walgaard C, van Doorn PA, Jacobs BC. Diagnosis of Guillain-Barre syndrome and validation of Brighton criteria. Brain. 2014 Jan;137(Pt 1):33-43. doi: 10.1093/brain/awt285. Epub 2013 Oct 26.
- Background: PubMed 23628447van Doorn PA. Diagnosis, treatment and prognosis of Guillain-Barre syndrome (GBS). Presse Med. 2013 Jun;42(6 Pt 2):e193-201. doi: 10.1016/j.lpm.2013.02.328. Epub 2013 Apr 28.
- Background: PubMed 21263135van Nes SI, Vanhoutte EK, van Doorn PA, Hermans M, Bakkers M, Kuitwaard K, Faber CG, Merkies IS. Rasch-built Overall Disability Scale (R-ODS) for immune-mediated peripheral neuropathies. Neurology. 2011 Jan 25;76(4):337-45. doi: 10.1212/WNL.0b013e318208824b.
- Background: PubMed 17404197Mori M, Kuwabara S, Fukutake T, Hattori T. Intravenous immunoglobulin therapy for Miller Fisher syndrome. Neurology. 2007 Apr 3;68(14):1144-6. doi: 10.1212/01.wnl.0000258673.31824.61.
- Background: PubMed 24456386Kalita J, Misra UK, Goyal G, Das M. Guillain-Barre syndrome: subtypes and predictors of outcome from India. J Peripher Nerv Syst. 2014 Mar;19(1):36-43. doi: 10.1111/jns5.12050.
- Background: PubMed 15668421Dornonville de la Cour C, Jakobsen J. Residual neuropathy in long-term population-based follow-up of Guillain-Barre syndrome. Neurology. 2005 Jan 25;64(2):246-53. doi: 10.1212/01.WNL.0000149521.65474.83.
- Background: PubMed 17537676van Koningsveld R, Steyerberg EW, Hughes RA, Swan AV, van Doorn PA, Jacobs BC. A clinical prognostic scoring system for Guillain-Barre syndrome. Lancet Neurol. 2007 Jul;6(7):589-94. doi: 10.1016/S1474-4422(07)70130-8.
- Background: PubMed 21403108Walgaard C, Lingsma HF, Ruts L, van Doorn PA, Steyerberg EW, Jacobs BC. Early recognition of poor prognosis in Guillain-Barre syndrome. Neurology. 2011 Mar 15;76(11):968-75. doi: 10.1212/WNL.0b013e3182104407.
- Derived from this study: PubMed 37634022Khedr EM, Shehab MM, Mohamed MZ, Mohamed KO. Early electrophysiological study variants and their relationship with clinical presentation and outcomes of patients with Guillain-Barre syndrome. Sci Rep. 2023 Aug 26;13(1):14000. doi: 10.1038/s41598-023-41072-x.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
The record lists no contact. Use the official record to reach the sponsor.
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Guillain-Barre Syndrome, run by Assiut University at 1 site in Egypt.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 1 inclusion and 1 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 8 Dec 2022. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Egypt. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
clinical scales :The GBS Disability Scale (time frame: change from baseline scale at 3 months). The study lists 5 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT04927598, which also lists 11 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 8 Dec 2022.