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Timothy C. Birdsall
Thorne Research Inc Seattle, Wash

JAMA. 1990;264(8):969-970.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—

Clauw et al¹ recently described seven patients who developed a syndrome of eosinophilia, connective-tissue disease, and cutaneous abnormalities (elsewhere termed eosinophilia-myalgia syndrome) while ingesting the amino acid tryptophan. They speculate that an abnormal accumulation of tryptophan metabolites, specifically serotonin (5-hydroxytryptamine), in these patients may have contributed to the disease and cite several other conditions with similar symptoms that also are associated with deranged serotonin metabolism.

Tryptophan is primarily metabolized in the body to either nicotinic acid or serotonin. The critical enzyme in the tryptophan-kynurenine-nicotinic acid pathway is tryptophan oxygenase, an enzyme that is inducible by adrenal hormones,² raising the prospect that a decrease in enzyme activity could shunt excess tryptophan toward the serotonin pathway, resulting in elevated serotonin production. Badawy et al^3,4 have shown that inhibition of tryptophan oxygenase due to long-term ethanol or antidepessant intakes results in elevated serotonin levels. It, therefore, seems . . . [Full Text PDF of this Article]

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