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Letters to the Editor |
Retired Medical Inspector of the Italian State Railways Padua, Italy
Hydrocortisone, the glucocorticoid that is routinely prescribed to correct the chronic cortisol deficiency of patients with Addison’s disease, has recently been confirmed (1) to be significantly effective also in the treatment of chronic fatigue syndrome (CFS). This comes as no surprise if we consider that CFS and Addison’s disease share 26 features (2), including hypocortisolism and a host of neuropsychological complaints (2). What is surprising is the fact that, despite the astonishing similarity between CFS and Addison’s disease, no reported attempt has yet been made to treat CFS patients with both hydrocortisone and fludrocortisone (a mineralocorticoid), the classic therapy for Addisonian patients (2). The failure to assess the effects of hydrocortisone plus fludrocortisone in the treatment of CFS becomes more surprising in light of the remarkable benefits experienced by CFS patients thanks to fludrocortisone (3).
To further support my long advocated suggestion (2, 3) that the classic drugs for Addison’s disease should be urgently explored together (at low doses, of course) as a possible therapy for CFS patients, I point out here that CFS and Addison’s disease share not only 26 features, but also 10 others. In fact, the following abnormalities, besides being present in CFS (4), are also found in Addison’s disease (5, 6, 7, 8, 9) and associated glucocorticoid deficiency (10): reduction in both left ventricular dimensions (5) and other cardiac effects (5, 6), increased heart rate (6), leukocytosis (6), lymphocytosis (6), enhanced thyroid-stimulating hormone secretion (7), elevations of transaminase values (8), sore throat (9), dehydration (9), headaches (9), and raised production of cytokines (10). Moreover, the reduced phosphatemia found in CFS patients (4) is likely to mirror their hypocortisolism (11). Furthermore, both the lowered high density lipoprotein cholesterolemia and the raised triglyceridemia observed in CFS patients (4) may be due to increased thyroid-stimulating hormone secretion (12), which characterizes CFS patients (4) and represents an additional effect of hypocortisolism (7). Finally, cortisol deficiency may also account for the elevated apoptotic cell population found in CFS patients (13). One could object that CFS patients may display raised basal cortisol levels (4). However, baseline cortisol values fail to detect the adrenal insufficiency of CFS patients, as has lately been shown by Scott and colleagues (14). These authors, notably, have suggested that in treating CFS patients, "replacement therapy may more appropriately involve not only glucocorticoid, but mineralocorticoid supplements also" (14), thereby indirectly supporting my old suggestion (3).
In view of the 36 features shared by CFS and Addison’s disease, urgent investigations of the effects of hydrocortisone plus fludrocortisone in the treatment of CFS appear to be both worthwhile and promising.
Footnotes
Address correspondence to: Riccardo Baschetti, M.D., Retired Medical Inspector of the Italian State Railways, CP 1011, 35100 Padua, Italy.
References
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