By Liam Davenport, medwireNews Reporter
A substantial proportion of patients with voltage-gated potassium channel (VGKC)-complex autoimmunity experience chronic idiopathic pain, although the specific antigenic complex associated with pain remains to be determined, conclude US scientists.
"Our findings add VGKC-complex autoimmune pain to the list of potentially treatable autoimmune channelopathies," the team says in Neurology, adding: "Most remarkably, 81% of patients receiving immunotherapy experienced pain symptom improvement not attributable to changes in standard analgesic medication or dosing, and allowing narcotics to be discontinued in some cases."
In an accompanying editorial, David Bennett, from King's College London, UK, and Angela Vincent, from John Radcliffe Hospital, in Oxford, UK, comment: "We may… be entering an exciting phase in which autoantibodies to neural antigens are recognized as having a role in the etiology of a number of hitherto poorly understood chronic pain states, opening new avenues for treatment."
The researchers, led by Christopher Klein, from the Mayo Clinic in Rochester, Minnesota, identified 1992 patients with VGKC-complex-immunoglobulin (Ig)G from 54,853 people who were tested between 2008 and 2010. Of 316 VGKC-complex-IgG-seropositive patients evaluated neurologically, 50% had pain not attributable to an alternative cause, which was isolated in 28% of patients and had accompanying neurologic manifestations in 72% of patients.
Symptoms were subacute in 95%, and became chronic in the majority of patients. Multiple medications were required by 70% of patients, with 30% of patients taking narcotics.
The most commonly affected area was the extremities, in 49% of patients. Total body pain was experienced by 27% of patients, which, prior to VGKC-complex-IgG detection, was diagnosed as psychogenic in 13% and fibromyalgia in 6.2%. Twelve percent of patients reported atypical head and face pain. Overall, pain was descriptively neuropathic or nociceptive, in 58% and 47% of the patients, respectively.
Normal peripheral function, as determined via neuropathy impairment scores and nerve conduction, was detected in 62% of 94 patients tested. Patients with pain were 25 times more likely than those without to have evidence of neuronal hyperexcitability, such as hyperhidrosis, quantitative heat-pain hyperalgesia, or electromyographic excitability.
Pain relief was achieved using immunotherapy in 13 of 16 patients. The presence of IgG antibodies binding the contactin-associated protein-2 antigen was significantly associated with pain, at 16% positivity among patients with pain versus 7% among patients without pain. By contrast, antibodies to the leucine-rich glioma-activated 1 protein were not linked to pain.
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