Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) Antibodies
CIDP is an acquired inflammatory disorder that occurs when the immune system attacks the myelin sheath of neurons in the peripheral nervous system (PNS). Over time, the myelin in the spinal cord is destroyed, leading to loss of strength and sensation throughout the body. Some cases can occur with involvement in the central nervous system (CNS) – these cases are termed Combined Central and Peripheral Demyelination (CCPD).
The onset of CIDP can be insidious and is poorly understood. In some cases, infections, often of the respiratory or the gastrointestinal systems, have been reported to precede developing the disorder. Initial symptoms typically include weakness of the limbs, followed by sensory symptoms such as tingling and numbness occurring later.
In ~10% of patients, autoantibodies for specific axonal targets have been identified as causative. These include neurofascin (NF) 140, NF155, and NF186, as well as contactin-1 (CNTN1) and contactin-associated protein 1 (Caspr1). These are proteins that are involved in formation and proper functioning of the Nodes of Ranvier, gaps in the myelin sheath of neurons that permit faster signaling speed. Autoantibodies can interfere with proper functioning at either the nodal or the paranodal (directly adjacent to the node) regions and disrupt the axonal-glial junctions.
Typical treatments for CIDP include intravenous immunoglobin (IVIg); however, CIDP that presents with these antibodies (seropositive CIDP) does not respond effectively to these interventions. Instead, plasmapheresis and rituximab, an immunosuppressant drug that causes B cell depletion, can be employed effectively.
Our antibody screen for CIDP employs a fixed cell-based assay (CBA) and can detect NF140, NF155, NF186, CNTN1, and Caspr1 antibodies with high specificity. Early diagnosis is crucial to prevent axonal degeneration and permanent damage.
Our CIDP fixed CBA is awaiting accreditation. In may presently be ordered for research purposes only.