- Last Updated: 02 December 2015 02 December 2015
ME/CFS disease process
Dr. Klimas next turned to an in-depth discussion of the pathophysiology of the ME/CFS illness process. First, she presented a general model of the stages of the disease process.
The model indicates that ME/CFS is triggered, in a genetically susceptible person, by an infection or some other event. Next, in response to the trigger, the immune, endocrine, and neuroendocrine systems are mobilized. However, these systems remain activated or in a state of imbalance.
According to this theory, ME/CFS is not a disease involving an ongoing infection or continuous triggering process. Instead, ME/CFS is the body's prolonged response to the original triggering events. This prolonged neuroimmune and endocrine activation then sets up the cascade of physiological events to follow.
Possible genetic predisposition
As of 1999, there has been only one study (Keller et al.) that assessed genetic factors in ME/CFS. The results showed that ME/CFS has at least one component that runs 4 to 6-fold higher than normal controls for three gene types (HLA DR haploytypes: DR4, DR3, and DQ3)—which happen to be the same three gene types that are associated with juvenile rheumatism, arthritis, juvenile diabetes and Sjogren's Syndrome. These are genes that are connected with immune regulation—thus there might be an autoimmune piece to ME/CFS, since these other illnesses are autoimmune in nature.
Sixty to 80% of ME/CFS patients can date their illness onset to an acute viral-like illness or infection. (However, only 18% of fibromyalgia patients report having an infection just prior to becoming ill.) There is clear documentation that a percentage of patients developed ME/CFS after contracting an Epstein-Barr virus (EBV) or a cytomegalovirus (CMV) infection. However, instead of recovering, the patients remained sick.
In Australia, Dr. Andrew Lloyd has undertaken a large prospective study to identify ME/CFS triggers by looking at patients who get EBV; Q Fever or Ross River viral infections. The latter two illnesses have chronic courses similar to mononucleosis. At onset of their illnesses, Dr. Lloyd is doing a comprehensive battery of immunological tests, and then is following the subjects over time to see what factors could predict patients' failure to recover. Early findings indicate that those subjects with decreased cell-mediated immunity are most likely to have ongoing, persistent symptoms. Cell-mediated immunity is tested by delayed hypersensitivity skin testing. The test consists of an intradermal injection under the skin and is similar to TB, candida, and other allergy testing.
One hypothesis that might explain these findings, according to Dr. Klimas, is that many ME/CFS patients may have an underlying immune abnormality that impedes normal recovery from infections. Dr. Klimas stressed that, as a matter of treatment, it is more important to focus on the "mediators"—the chemicals produced by the neuroimmune and endocrine systems in response to the triggers—because these chemicals can be changed as opposed to invariants such as genetics or triggering events.