CORRESPONDENCE |
S100B in Guillain–Barré syndrome
* E-mail: orpiazza{at}unina.it
Editor—Guillain–Barré syndrome (GBS), a subacute inflammatory demyelinating polyneuropathy, is the most common cause of acute neuromuscular paralysis. Up to one-third of patients with GBS require mechanical ventilation (MV) in the ICU,1 although outcome is generally good,2 acute mortality remains relatively high and 
20% of hospitalized patients may have a long-term disability.3
Serum protein S100B is a recognized marker of traumatic brain injury. We observed an increase in S100B levels in two GBS patients, pointing to a potential acute influence of peripheral neuropathy on levels not related to CNS injury.
Serum S100B was measured from venous blood samples in two GBS patients requiring MV, on admission to ICU and after 10 days. S100B values >0.2 µg litre–1 are considered abnormal. The patients were examined by a neurologist and the diagnosis was based on the National Institute of Neurological and Communicative Disorders and Stroke diagnostic criteria.4
The first patient was treated with a total of 10 plasma exchanges and steroids and required 13 days of MV. The patient was discharged from hospital at 40 days with severely limited lower limb activity and confined to bed. On admission, the S100 serum level was raised at 0.495 µg litre–1, and at 10 days the level had reduced to 0.093 µg litre–1.
The second patient was treated with plasma exchange and steroids. The patient recovered spontaneous ventilation after 62 days and was discharged, still confined to a chair, 90 days after SGB onset. On ICU admission, the S100B serum level was very high (2.61 µg litre–1), and was still abnormal 10 days later (0.891 µg litre–1).
The serum S100B increases observed in these two GBS patients exceed those attributed to brain tissue damage patients with mild traumatic head injury.5 The physiological role of this neuroprotein is not yet clear, but in GBS it may act as a regeneration stimulus or as marker of neuronal damage. A comparison of CSF and serum levels of S100B would be useful for the understanding of the role played by this protein in GBS. S100B in GBS might be an expression of neurotrophic and neuroprotective activity but no conclusion should be made without extensive and focused clinical and experimental studies.
Naples, Italy
References
1 Sharshar T, Chevret S, Bourdain F, Raphaël J. Early predictors of mechanical ventilation in Guillain-Barré syndrome. Crit Care Med 2003; 31: 278–83[CrossRef][Web of Science][Medline]
2 Henderson RD, Lawn ND, Fletcher DD, McClelland RL, Wijdicks EF. The morbidity of Guillain-Barré syndrome admitted to the intensive care unit. Neurology 2003; 60: 17–20
3 Dornonville de la Cour C, Andersen H, Stalberg E, Fuglsang-Frederiksen A, Jakobsen J. Electrophysiological signs of permanent axonal loss in a follow-up study of patients with Guillain-Barré syndrome. Muscle Nerve 2005; 31:70–7[Medline]
4 National Institute of Neurological and Communicative Disorders and Stroke ad hoc Committee (NINCDS). Criteria for diagnosis of Guillain-Barré syndrome. Ann Neurol 1978; 3: 565–6[CrossRef][Medline]
5 Ingebrigtsen T, Waterloo K, Jacobsen EA, Langbakk B, Romner B. Traumatic brain damage in minor head injury: relation of serum S-100 protein measurements to magnetic resonance imaging and neurobehavioral outcome. Neurosurgery 1999; 45: 468–75[Web of Science][Medline]
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  O. Piazza, E. Russo, S. Cotena, G. Esposito, and R. Tufano Elevated S100B levels do not correlate with the severity of encephalopathy during sepsis Br. J. Anaesth., October 1, 2007; 99(4): 518 - 521. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||