Predictors and Prognostic Factors of Gullian Barrie Syndrome Outcome

Guillain-Barre Syndrome Clinical Trial

Official title:

Predictors and Prognostic Factors of Gullian Barrie Syndrome Outcome

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT04927598
• Other study ID #: Gullian Barrie syndrome
• Status: Completed
• Start date: October 20, 2020
• Est. completion date: April 1, 2022

Study information

• Verified date: December 2022
• Source: Assiut University
• Contact: n/a
• Is FDA regulated: No
• Study type: Observational

Clinical 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 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.

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

Recruitment information / eligibility

• Status: Completed
• Enrollment: 62
• Est. completion date: April 1, 2022
• Est. primary completion date: October 15, 2021
• Accepts healthy volunteers: No
• Gender: All
• Age group: 10 Years and older

Eligibility

Inclusion Criteria:

• Any Age, recent onset of GBS through the first 2 weeks . Gender: Male or Female Inclusion Criteria.

Exclusion Criteria:

• patients with metabolic disorders, others

Related Conditions & MeSH terms

• Guillain-Barre Syndrome
• Syndrome

Intervention

Device:
• plasmapheresis
patients of Gullian Barrie syndrome undergo plasmapharesis

Locations

Country	Name	City	State
Egypt	Assiut university	Assuit	Assiut

Sponsors (1)

Lead Sponsor	Collaborator
Assiut University

Country where clinical trial is conducted

Egypt, 

References & Publications (10)

Dornonville 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. — View Citation

Fokke 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. — View Citation

Kalita 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. — View Citation

Mori 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. — View Citation

Raphael 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. — View Citation

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. — View Citation

van 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. — View Citation

van 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. — View Citation

van 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. — View Citation

Walgaard 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. — View Citation

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	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).	change from baseline scale at 3 months
Primary	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 .	change from baseline scale at 3 months
Primary	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 )	change from baseline scale at 3 months
Primary	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	change from baseline scale at 3 months
Primary	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)	change from baseline scale at 3 months
Secondary	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	change from baseline scale at 3 months