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Phantom lymphadenopathy. An association with chronic fatigue syndrome
  1. R Baschetti
  1. Retired Medical Inspector of the Italian State Railways, CP 671, 60001–970 Fortaleza (CE), Brazil; baschetti{at}

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    Shee reports an association between chronic fatigue syndrome (CFS) and what he regards as a “phantom lymphadenopathy”.1 However, his failure to observe “true lymphadenopathy” in patients with CFS complaining of swollen lymph glands does not exclude a real, albeit subclinical enlargement of those glands, because he did not compare their dimensions with the ones that were measurable before the appearance of patients’ complaints.

    As someone who suffered from CFS and reported on its dramatic resolution thanks to old and new drugs for Addison’s disease,2 I clearly remember that my lymph nodes, just a few days after the abrupt onset of CFS, became mildly painful and began to swell gradually. This slow process of enlargement lasted approximately one month. However, even when my lymph glands stopped swelling further (but continued to be mildly painful), their dimensions were still clinically within normal limits. This may indirectly explain why Shee found that “careful examination did not confirm lymphadenopathy” in CFS patients with “self diagnosed enlarged lymph glands”.

    Shee proposes some explanations for his patients’ complaints about their lymph glands, but surprisingly fails to mention adrenal insufficiency as a possible cause of those symptoms. Enlargement of lymph nodes is one of the many of clinical features that CFS shares with primary adrenal insufficiency.3 As a consequence of their common adrenal abnormalities,3 CFS4 and Addison’s disease5 also share an additional feature, namely, impaired production of dehydroepiandrosterone sulphate, which is secreted from the adrenal glands.4

    Shee points out that general and neurological examination and other investigations were normal in all patients with CFS. His article, however, does not specify whether those investigations also included an assessment of adrenal function. Hypocortisolism, for example, despite being present in CFS (as well as in Addison’s disease),3 is not mentioned in Shee’s article as a possible explanation for the symptoms of his patients with CFS and, therefore, he probably omitted to measure their cortisol levels.

    In view of the 42 clinical features that CFS shares with Addison’s disease,2–5 I believe that a careful evaluation of the adrenal function of patients with CFS would have enlightened Shee more than did all other investigations combined.