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Research on Fibromyalgia
Mutations in the c-erbA beta 1 gene: do they underlie
euthyroid fibromyalgia?
| AUTHORS:
| Lowe JC; Cullum ME; Graf LH Jr;
Yellin J
| AUTHOR AFFILIATION:
| Fibromyalgia Research Foundation,
Houston, TX 77277, USA. JLowe55555@aol.com
| SOURCE:
| Med Hypotheses 1997
Feb;48(2):125-35
| CITATION IDS:
| PMID: 9076694 UI: 97231299
| ABSTRACT:
| Fibromyalgia, a chronic condition
of widespread pain, stiffness, and fatigue, has proven unresponsive to
drugs, the use of which is based on the 'serotonin-deficiency hypothesis'.
An alternative hypothesis-failed transcription regulation by thyroid
hormone-can explain the serotonin deficiency and other objective findings
and symptoms of euthyroid fibromyalgia. Virtually every feature of
fibromyalgia corresponds to signs or symptoms associated with failed
transcription regulation by thyroid hormone. In hypothyroid fibromyalgia,
failed transcription regulation would result from thyroid-hormone
deficiency. In euthyroid fibromyalgia, failed transcription regulation may
result from low- affinity thyroid hormone receptors coded by a mutated c-erbA
beta 1 gene, yielding partial peripheral resistance to thyroid hormone.
The hypothesis of this paper is that, in euthyroid fibromyalgia, a mutant
c- erbA beta 1 gene (or alternately, the c-erbA alpha 1 gene) results in
low-affinity thyroid-hormone receptors that prevent normal thyroid hormone
regulation of transcription. As in hypothyroidism, this would cause a
shift toward alpha-adrenergic dominance and increases in both cyclic
adenosine 3'-5'-phosphate phosphodiesterase and inhibitory Gi proteins.
The result would be tissue-specific hypothyroid-like symptoms despite
normal circulating thyroid-hormone levels.
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