mandag den 17. juni 2013

A small peculiarity - ME, "ciguatoxin-look-alike" and TRPA1

I fell upon a small peculiarity regarding my favorite ion channel, TRPA1.

Some years ago a group of researchers pointet out, that the clinical symptoms found in both Chronic Fatigue Syndrome (CFS) and chronic Ciguatera fish poisoning (CCFP) were remarkably similar, including recurrent fatigue, impaired memory and concentration, tender lymph nodes, muscle and joint pain, headaches, and other neurological impairments.

They perfermed a study and found that the serum lipid fraction of patients with CFS has a structural epitope(s) similar to ciguatoxin CTX, a polyether lipid with neurotoxic properties produced by a marine organism (Gambierdiscus toxicus).

Ciguatoxins are sodium channel activator toxins that cause ciguatera, which presents with peripheral sensory disturbances, including the symptom of cold allodynia which is characterized by intense stabbing and burning pain in response to mild cooling.

And now for the peculiarity: Ciguatoxins activate specific cold pain pathways to elicit the burning pain from cooling, and TRPA1 is involved in this pathway.


Acute Phase Phospholipids Related to the Cardiolipin of Mitochondria in the Sera of Patients With Chronic Fatigue Syndrome (CFS), Chronic Ciguatera Fish Poisoning (CCFP), and Other Diseases Attributed to Chemicals, Gulf War, and Marine Toxins

Ciguatoxins activate specific cold pain pathways to elicit burning pain from cooling

If you are up for one more peculiarity..the author, Yoshitsugi Hokama, from the Acute Phase Phospholipid article is also on this paper about CFS, phospholipid cardiolipin (CL) and anticardiolipin antibodies (ACAs)Anticardiolipin Antibodies in the Sera of Patients with Diagnosed Chronic Fatigue Syndrome

..and I quote:
"This study demonstratesthat a large percentage of patients clinically diagnosed with CFS have elevated levels of the IgM isotype to CL (95%), suggesting that CFS may be an autoimmune condition."

"Previous studies have shown that treatment with monoclonal antibodies to B cells reduces ACA levels to normal in patients with autoimmune disease, leading to clinical improvements."

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