Down-regulation of renin-aldosterone and antidiuretic hormone systems in patients with myalgic encephalomyelitis/chronic fatigue syndrome. — CFSMEATLAS
Down-regulation of renin-aldosterone and antidiuretic hormone systems in patients with myalgic encephalomyelitis/chronic fatigue syndrome.
Miwa, Kunihisa · Journal of cardiology · 2017 · DOI
Quick Summary
This study found that ME/CFS patients have smaller hearts and lower levels of certain hormones that control blood volume and fluid balance compared to healthy people. When researchers gave half the ME/CFS patients a synthetic hormone called desmopressin for five days, about half of them felt better, with less dizziness when standing and improved ability to do daily activities.
Why It Matters
This research suggests ME/CFS may involve dysregulation of the body's fluid and blood pressure control systems, offering a potential physiological mechanism for orthostatic intolerance—a common and debilitating symptom. The positive response to desmopressin in some patients points to a possible targeted treatment avenue that warrants further investigation.
Observed Findings
ME patients had significantly lower plasma aldosterone (104 vs 157 pg/ml, p=0.004) and ADH (2.2 vs 3.3 pg/ml, p=0.02) compared to controls.
ME patients demonstrated reduced cardiac structure and function: smaller left ventricular diameter, lower stroke volume index, and lower cardiac index than controls.
Desmopressin administration for 5 days improved orthostatic intolerance symptoms in 50% of treated ME patients (5 of 10) during standing tests.
Desmopressin treatment improved activities of daily living performance scores in 50% of ME patients.
Plasma renin activity was considerably lower in ME patients (1.6 vs 2.5 ng/ml/h, p=0.06, approaching significance).
Inferred Conclusions
Both the renin-aldosterone and ADH systems are abnormally down-regulated in ME/CFS despite evidence of reduced cardiac preload and output.
Desmopressin may be therapeutically beneficial for a subset of ME/CFS patients experiencing orthostatic intolerance.
Central nervous system dysfunction may underlie the observed down-regulation of neurohumoral blood volume regulators in ME.
Remaining Questions
Why do only 50% of ME patients respond to desmopressin, and what distinguishes responders from non-responders?
What This Study Does Not Prove
This study does not prove that low hormone levels cause ME/CFS, only that they are associated with it. The 50% response rate to desmopressin means this treatment does not work for all patients and does not establish it as a standard cure. The small sample size and lack of a placebo control mean results cannot be generalized to all ME/CFS patients.
Tags
Symptom:Orthostatic IntoleranceFatigue
Biomarker:Blood Biomarker
Method Flag:Weak Case DefinitionSmall SampleExploratory Only
Is the down-regulation of these hormone systems a primary cause of ME/CFS or a secondary consequence of the disease?
What is the long-term safety and efficacy of desmopressin treatment in ME/CFS, and would higher doses or longer treatment periods benefit more patients?
Do all ME/CFS patients have reduced cardiac output, or does this represent a subtype of the disease?