The study showing that by identifying the biomarkers for guillain barre syndrome; As guillain-barre syndrome is a rare autoimmune condition in which the immune system attacks peripheral nerves and damages the myelin insulation. Symptoms rapidly progress from pain to muscle weakness and even paralysis.
Although Guillain-Barre usually affects the hands, feet, and limbs, it can be life-threatening when nerves controlling breathing are affected. Guillain-Barre syndrome has been clinically sub classifying into several variants; but specific biomarkers for each of the subtypes have not been well defined. Furthermore, there are several other conditions that can cause similar symptoms; such as inflammatory demyelination disorders of the central nervous system.
Consequently, Guillain-Barre syndrome can be difficult to diagnose; especially in younger patients. This can be seriously detrimental to patient outcomes since early effective treatment is critical to preventing rapid progression to a severe clinical course. Metabolomic analysis enables high-throughput molecular profiling, which is a valuable tool in biomarker identification.
Biomarkers for guillain barre
It evaluates all the small molecule intermediates and products of metabolism present in the cell at a given time. This providing a unique chemical fingerprint; that can be compared between different situations to identify the specific cellular processing that are affecting. As all the entities within a cell are measuring there is no need for prior understanding of a process in order to perform a metabolomic investigation.
A metabolomic analysis of CSF has recently been conducting using samples from 86 patients with Guillain-Barre syndrome and 20 healthy controls. Lipidomic profiles were determining in parallel. Metabolites were analyzing by one dimensional 1H-Overhauser effect nuclear magnetic resonance spectroscopy (NOESY NMR); using a Bruker ASCEND III 600 spectrometer equipping with a cryoprobe.
The metabolic phenotypes
The metabolic phenotypes obtained were compared between the three most common clinical subtypes of GBS (acute inflammatory demyelinating polyneuropathy [AIDP]; acute motor axonal neuropathy [AMAN], and Miller Fisher syndrome [MFS]); healthy controls and with data previously obtained for patients with the IDDs, multiple sclerosis, and neuromyelitis optica. Primary metabolite profiles revealed specific metabolic traits that were unique to Guillain-Barre syndrome and inflammatory demyelination disorders.
Biomarker analysis using a panel of 10 primary metabolites enabled reasonably good discrimination between the three Guillain-Barre subtypes; healthy controls, and inflammatory demyelination disorders. The robustness of the biomarker panel was vigorously validating by multi-step statistical evaluation. The primary metabolic profiles were similar for AIDP and AMAN Guillain-Barre syndrome subtypes, which reflects the comparable clinical presentation.