Beta-trace protein in chronic inflammatory demyelinating polyradiculoneuropathy and Guillain-Barré syndrome - clinical utilization and a new insight into pathophysiological mechanisms.

INTRODUCTION: Beta-trace protein (BTP) is primarily used as a marker for traumatic CSF leakage. Spinal leptomeningeal cells adjacent to the spinal nerve roots are a major producer of this protein, which has prompted interest in its relevance to inflammatory polyradiculoneuropathies. BTP has not previously been investigated in patients with Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculopathy (CIDP).

MATERIAL AND METHODS: BTP was measured in the cerebrospinal fluid (CSF) and plasma in patients with GBS, CIDP, disease-free controls, non-inflammatory polyneuropathies, and multiple sclerosis.

RESULTS: Pre-treatment levels of BTP in plasma were increased in patients with CIDP, but not GBS compared to all controls. Pre-treatment levels of BTP in CSF were increased in patients with CIDP compared to all controls but in patients with GBS compared only to disease-free controls. In patients with GBS and CIDP, levels of BTP in CSF were increased compared to disease-free controls irrespective of Q.alb, and the levels correlated with axonal damage markers in CSF and plasma. Elevated pre-treatment levels of BTP in CSF predicted therapy failure 3 months after initiation of immunotherapy in CIDP.

CONCLUSIONS: BTP in CSF and plasma may be a potential biomarker to aid in the diagnosis of CIDP. BTP in CSF could be a potentially more informative biomarker than albumin in a subgroup of patients with GBS and CIDP who have a normal or mildly elevated Q.alb. BTP in CSF may be predictive for therapy response in patient with CIDP, but needs to be validated in larger studies.