Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2025
Low Vasopressin in Myalgic Encephalomyelitise/Chronic Fatigue Syndrome.
СтатьяНаблюдательное исследованиеНазвание и аннотация: Перевод в очереди
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Huhmar Helena M, Soinne Lauri S, Bertilson Bo Christer, Ghatan Per Hamid, Bragée Björn A, Polo Olli J
Аннотация
OBJECTIVE: The complex clinical picture of myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS) includes orthostatic intolerance with symptoms and signs suggesting abnormal water homeostasis and hypovolemia. Since many ME/CFS patients report polyuria-polydipsia, we conducted an observational study based on series of plasma and urine osmolality (P-Osm and U-Osm) as well as plasma levels of vasopressin (P-VP) or copeptin in consecutive patients diagnosed with ME/CFS according to the International Consensus Criteria.
METHODS: P-VP as well as P-Osm and U-Osm were measured in 111 patients after 10 h overnight fasting and fluid deprivation. Additional 13 patients were assessed for copeptin, when P-VP measurements were no longer available. The clinical routine also included brain MRI and blood chemistry.
RESULTS: P-Osm was abnormally high (>292 mOsm/kg) in 71 of 124 (57.3%) and U-Osm below the reference interval (<750 mOsm/kg) in 82 of 124 (66.1%) patients. P-VP was below the level of detection (<1.6 pg/mL) in 91 of 111 (82.0%) patients. A normal P-VP level compared with their P-Osm was found in 11 of 111 (9.9%) patients. Copeptin levels were all within the given reference range, albeit in the lower end in most patients. No indication of relevant pathology in either hypothalamus or hypophysis was present.
CONCLUSIONS: Our findings suggest that chronic down-regulation of VP mimicking central diabetes insipidus is an important measurable part of the disease mechanism that potentially contributes to criterial symptoms of ME/CFS.
METHODS: P-VP as well as P-Osm and U-Osm were measured in 111 patients after 10 h overnight fasting and fluid deprivation. Additional 13 patients were assessed for copeptin, when P-VP measurements were no longer available. The clinical routine also included brain MRI and blood chemistry.
RESULTS: P-Osm was abnormally high (>292 mOsm/kg) in 71 of 124 (57.3%) and U-Osm below the reference interval (<750 mOsm/kg) in 82 of 124 (66.1%) patients. P-VP was below the level of detection (<1.6 pg/mL) in 91 of 111 (82.0%) patients. A normal P-VP level compared with their P-Osm was found in 11 of 111 (9.9%) patients. Copeptin levels were all within the given reference range, albeit in the lower end in most patients. No indication of relevant pathology in either hypothalamus or hypophysis was present.
CONCLUSIONS: Our findings suggest that chronic down-regulation of VP mimicking central diabetes insipidus is an important measurable part of the disease mechanism that potentially contributes to criterial symptoms of ME/CFS.