LETTERS

Further studies on the treatment of fibromyalgia

  To the editor:

I wish to comment upon the POEM “Useful treatments for fibromyalgia syndrome” (J Fam Pract 2005; 54:105, citing JAMA 2004; 292:2388–2395).¹ Drs Goldenberg, Burckhardt, and Crofford did only a partial job of covering the readily accessible literature. Unfortunately, a useful set of randomized controlled trials^2-4 escaped their search strategy. Furthermore, there is a major error in their conclusions that is inconsistent with the body of the discussion.

In 1997 the cause of the symptoms of fibromyalgia was strongly linked to partial peripheral resistance to thyroid hormone in 3 studies published in an off-Medline journal, the Clinical Bulletin of Myofascial Therapy. This choice of journals, a regrettable decision, consigned the studies to obscurity.

Barnes⁵ first suggested, because of observed high rates of hypometabolism, that resistance to thyroid hormone must be fairly common. That same year, the famous Albright⁶ guessed the same thing for the same reason given by Barnes. In 1981 Kaplan⁷ finally reported the biological parameters of a prototypical case. Since then, textbooks in endocrinology and thyroid disease in particular⁸ make routine reference to thyroid hormone resistance. While the emphasis in these texts is upon genetic lesions, acquired lesions are also suggested.

Our research group⁹ has given doses far in excess of those given to the Kaplan patient, ranging up to 1350 μg of liothyronine (T3) (T4 equivalence 5400 μg) on multiple occasions without thyrotoxic effects. This is prima facie evidence that we have learned to accurately recognize partial peripheral resistance to thyroid hormone, for the consequences of this dosing would otherwise be catastrophic. The 3 studies cited above^2-4 exhaustively document our initial experience with subjects in doses up to 150 μg of liothyronine (T3) (T4 equivalence 600 μg). Symptomatic responses of these patients were dramatically clinically significant as well as statistically significant to tiny values of P.

This establishes thyroid hormone resistance as the most evidence-based proposed cause of fibromyalgia. I know of no evidence refuting this. Also, this information is available from Cochrane, so the authors’ search strategy failed. Lastly, our group has had personal communication with the authors, and still they do not acknowledge it.

Since 1997 our group has concentrated upon refinement of the use of supraphysiological doses of thyroid hormone for the ablation of fibromyalgia symptoms. We have also worked out much of the biological bases of the acquired causes of thyroid resistance. This latter work¹⁰ is summarized in a recent review. Thus the state of the art has moved beyond establishing the etiology of fibromyalgia as T3 resistance, to the causes and successful treatments of that resistance.

As for the error in the conclusions of this review, the paper states that there is strong evidence for efficacy of tricyclic antidepressants (TCAs). In the discussion, however, it is correctly noted that there is no evidence for such efficacy except in the first 12 weeks of treatment; even then only a tiny percentage respond. After that, there is no difference between TCA and placebo. I wish the myth of TCA effectiveness would go away, but this paper perpetuates it.

Richard L. Garrison, MD
San Jacinto Methodist Hospital, Family Practice
Residency Training Program; Baylor College of
Medicine, Department of Family and Community
Medicine, Baytown, Texas

REFERENCES

1. Goldenberg DL, Burchhardt C, Crofford L. Management of fibromyalgia syndrome. JAMA 2004;292:2388–2395.
2. Lowe JC, Garrison RL, Reichman AJ, Yellin J, Thompson M, Kaufman D. Effectiveness and safety of T3 (triiodothyronine) therapy for euthyroid fibromyalgia: a double-blind placebo-controlled response-driven crossover study. Clin Bull Myofascial Ther 1997;2:31–58.
3. Lowe JC, Reichman AJ, Yellin J. The process of change during T3 treatment for euthyroid fibromyalgia: a double-blind placebo-controlled crossover study. Clin Bull Myofascial Ther 1997;2:91–124.
4. Lowe JC, Garrison RL, Reichman AJ, Yellin J. Triiodothyronine (T3) treatment of euthyroid fibromyalgia: a small-n replication of a double-blind placebo-controlled crossover study. Clin Bull Myofascial Ther 1997;2:71–88.
5. Barnes BO. Basal temperature versus basal metabolism. JAMA 1942;119:1072–1074.
6. Albright F, Burnett CH, Smith PH, Parson W. Pseudohypoparathyroidism: an example of “Seabright-Bantam syndrome.” Endocrinology 1942;30:922–932.
7. Kaplan MM, Swartz SL, Larsen PR. Partial peripheral resistance to thyroid hormone. Am J Med 1981;70:1115–1121.
8. Usala SJ. Thyroid hormone resistance syndromes. In: SA Falk (ed). Thyroid Disease: Endocrinology, Surgery, Nuclear Medicine, and Radiotherapy. 2nd ed. Philadelphia, Pa: Lippincott-Raven; 1997:223-230.
9. The Fibromyalgia Research Foundation website. Boulder, Colo. Available at: http://drlowe.com/frf.htm.
10. Garrison RL, Breeding PC. A metabolic basis for fibromyalgia and its related disorders: the possible role of resistance to thyroid hormone. Med Hypotheses 2003;61:182–189.

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