It’s a recurring theme, but the diagnosis of ME/CFS is severely hampered by the lack of a test that can distinguish people with the illness from those without. This is a challenge in many diseases, but particularly in ME/CFS which affects so many different systems of the body.
ME/CFS is currently identified by the presence of specific signs and symptoms, but there are several different criteria in use, and much debate over which are the most precise or appropriate. The quest for a biomarker is therefore a top priority since an accurate diagnosis is essential for patients to receive the medical care they need.
Generally speaking, biomarkers are measurable substances or processes in the body that can indicate the risk, presence or severity of a disease, or how well it will respond to a specific treatment.
For example, a high white blood cell count may indicate the presence of an infection, while raised levels of prostate-specific antigen in the blood are associated with an increased risk of prostate cancer.
Researchers have looked at a number of different measures as potential biomarkers for ME/CFS, including brain imaging findings, ECG abnormalities, and immunosignatures based on antibodies in the blood.
In fact, ME Research UK has recently funded work to look for an immunosignature that can predict patients’ responses to rituximab therapy.
New research from a team in Australia, led by Prof. Brett Lidbury at the Australian National University in Canberra, has added another potential biomarker to this list.
Prof. Lidbury has a longstanding interest in the search for biomarkers for ME/CFS, and ME Research UK recently awarded his group funding to analyse genetic data which might provide clues about the mechanisms of the disease.
But in this recent study, published in the Journal of Translational Medicine, the team focused on a different potential biomarker: activin.
The two types of activin (A and B) are produced in several organs in the body, and have a number of different roles, including regulation of the menstrual cycle, and involvement in metabolism and wound repair.
Prof. Lidbury is interested in two of its functions which have particular relevance to ME/CFS, namely the control of inflammation and muscle mass. Inflammation is important because the immune system is thought to be involved in the illness, while muscle mass will have an obvious influence on muscle weakness and pain.
The researchers took blood samples from 45 patients with ME/CFS (as defined by the Canadian Diagnostic Criteria) and from 17 healthy controls. Concentrations of both activin A and activin B were measured (as they have some different functions), as well as follistatin (a binding protein that regulates levels of activin).
Levels of activin B in the blood were markedly higher in the ME/CFS patients than in the healthy individuals (and also higher than in a previously studied normal group), whereas activin A and follistatin levels were no different.
This exciting finding suggests that the combination of elevated activin B and normal activin A may represent a useful biomarker for the presence of ME/CFS, although this would need to be validated in larger groups of patients.
Another intriguing prospect is whether follistatin might have some value as a treatment for ME/CFS since it can inhibit the actions of activin B. In fact, follistatin could have a two-pronged attack because it also blocks myostatin, a protein that inhibits muscle cell growth.
Prof. Lidbury’s study has certainly borne fruit, giving us a potential diagnostic biomarker for ME/CFS, as well as some hope for a new treatment. It’s early days on both fronts, however, so we will be keeping a close eye on further developments from this group.