A metabolic basis for fibromyalgia and its related disorders: the possible role of resistance to thyroid hormone.
It has long been recognized that the symptom complex of fibromyalgia can be seen with hypothyroidism. Hypothyroidism may been categorized, like diabetes, into type I (hormone deficient) and type II (hormone resistant). Most cases of fibromyalgia fall into the latter category. The syndrome is reversible with treatment, and is usually of late onset. It is likely more often acquired than due to mutated receptors. Now that there is evidence to support the hypothesis that fibromyalgia may be due to thyroid hormone resistance, four major questions appear addressable. First, can a simple biomarker be found to help diagnose it? Second, what other syndromes similar to Fibromyalgia may share a thyroid-resistant nature? Third, in non-genetic cases, how is resistance acquired? Fourth, what other methods of treatment become available through this new understanding? Preliminary evidence suggests that serum hyaluronic acid is a simple, inexpensive, sensitive, and specific test that identifies fibromyalgia. Overlapping symptom complexes suggest that chronic fatigue syndrome, Gulf war syndrome, premenstrual syndrome, post traumatic stress disorder, breast implant silicone sensitivity syndrome, bipolar affective disorder, systemic candidiasis, myofascial pain syndrome, and idiopathic environmental intolerance are similar enough to fibromyalgia to merit investigation for possible thyroid resistance. Acquired resistance may be due most often to a recently recognized chronic consumptive coagulopathy, which itself may be most often associated with chronic infections with mycoplasmids and related microbes or parasites. Other precipitants of thyroid resistance may use this or other paths as well. In addition to experimentally proven treatment with supraphysiologic doses of thyroid hormone, the thyroid-resistant disorders might be treatable with anti-hypercoagulant, anti-infective, insulin-sensitizing, and hyaluronolytic strategies.
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D000890:Anti-Infective Agents / Q000627:therapeutic use; D004211:Disseminated Intravascular Coagulation / Q000209:etiology; D004351:Drug Resistance; D005356:Fibromyalgia / Q000209:etiology / Q000235:genetics / Q000378:metabolism* / Q000628:therapy; D006801:Humans; D006820:Hyaluronic Acid / Q000378:metabolism; D008954:Models, Biological; D009175:Mycoplasma Infections / Q000209:etiology; D018923:Persian Gulf Syndrome / Q000209:etiology; D012282:Rickettsia Infections / Q000209:etiology; D013577:Syndrome; D013963:Thyroid Hormones / Q000378:metabolism* / Q000627:therapeutic use; D014158:Transcription, Genetic
D000890:Anti-Infective Agents; D013963:Thyroid Hormones; D006820:Hyaluronic Acid