This protocol is aimed at investigating three research questions related to innate immunity in GBS:1. Do patients with viral GBS have a different innate response to microbial triggers compared to healthy controls?2. Do patients with recurrent GBS…
ID
Source
Brief title
Condition
- Peripheral neuropathies
Synonym
Research involving
Sponsors and support
Intervention
Outcome measures
Primary outcome
The primary study parameter is the innate response of leukocytes to microbial
triggers as determined by the type I interferon production in response to
stimulation of Toll-like receptor 3, 7 or 9.
Secondary outcome
The production of other cytokines and the expression of maturation/activation
markers will be determined at the cell surface of leukocytes. Additionally,
genetic variants that influence the innate response of leukocytes to microbial
triggers will be determined.
Background summary
The Guillain-Barré syndrome (GBS) is a life-threatening acute polyneuropathy
typically preceded by a gastro-intestinal or a respiratory infection.
Campylobacter jejuni is the most frequent cause of GBS, but also viruses can
precede the development of GBS. The factors that determine the development of
this severe post-infectious complication are unclear. Activation of the innate
immune system is critical for the development of an antibody response that
damages the nerves. Our recent data show that a strong innate immune response
was present in former C. jejuni-associated GBS patients. Importantly, this
response was correlated with long-term residual disability. We hypothesize that
the innate response to microbial triggers is key to the development of
post-infectious GBS.
Study objective
This protocol is aimed at investigating three research questions related to
innate immunity in GBS:
1. Do patients with viral GBS have a different innate response to microbial
triggers compared to healthy controls?
2. Do patients with recurrent GBS have a different innate response to microbial
triggers compared to non-recurrent GBS patients?
3. Which genetic variants determine the response to microbial triggers leading
to (recurrent) GBS?
Study design
case-control study
Study burden and risks
Subjects will be asked to visit the Outpatient clinic neurology. Blood will be
drawn to isolate white blood cells and DNA. Clinical characteristics will be
assessed using questionnaires. The visit will take less than 45 minutes and
will carry negligible risks.
The identification of host factors that cause GBS will mainly benefit future
patients since persons could be identified with a high risk of developing GBS
after an infection. For the participants themselves, the study is of less
benefit, although possibly, we may be able to identify persons with a high risk
of recurrent disease or determine whether family members of patients have an
increased risk for GBS.
Wytemaweg 80
Rotterdam 3015 CN
NL
Wytemaweg 80
Rotterdam 3015 CN
NL
Listed location countries
Age
Inclusion criteria
Healthy controls:
- Age 18 years or older
- Written informed consent given by the subject
Former GBS patients:
- Fulfilling the diagnostic criteria for GBS (Asbury, 1990), or its variant Miller Fisher syndrome (MFS).
- Current age 18 years or older
- Written informed consent given by the patient;Recurrent GBS patients:
- Occurrence of at least two episodes of GBS, as determined by the diagnostic criteria for GBS (Asbury, 1990), or its variant Miller Fisher syndrome (MFS).
- Age 18 years
- Written informed consent given by the patient
Exclusion criteria
Healthy controls:
- No serological evidence for exposure to a virus, as determined by IgG serology for EBV, CMV, HEV or influenza antigens.;All groups:
Additional diseases or disorders at time of blood sampling that may influence the endpoints:
- autoimmune diseases (like multiple sclerosis, psoriasis, Crohn*s disease, ulcerative colitis, rheumatoid arthritis, SLE and other systemic diseases)
- acute and chronic infectious diseases (like infectious mononucleosis, HIV/AIDS)
- malignancies (not in remission)
Medicines at time of blood sampling that may affect endpoints (i.e. inflammatory processes):
- NSAIDs, oral corticosteroids, cyclosporine
- Cytostatic compounds
- Cytokines (analogues) and biologicals
- Intravenous immunoglobulins.
Design
Recruitment
Followed up by the following (possibly more current) registration
No registrations found.
Other (possibly less up-to-date) registrations in this register
No registrations found.
In other registers
| Register | ID |
|---|---|
| CCMO | NL59611.078.17 |