In brief he is a 40 year old male who presented in his early 30s with hypothyroid symptoms and a modest goiter of several month’s duration. A family history of transient hypothyroidism, possibly in the setting of pregnancy, was reported. An elevated TSH and low total T4 were found and corrected with Synthroid. His symptoms completely resolved. No other testing was performed at that time. In the intervening years he experienced increasing sinus and rhinitis symptoms and he failed medication therapy. He underwnet endoscopic surgery, which alleviated his sinus symptoms but his rhinitis persisted. Annual TSH testing was normal on a steady dose of Synthroid. In mid-2001 he suffered a severe, persistent URI with intermittent low-grade temperatures for several months (another family member had a similar URI course). After six weeks of URI symptoms and severe rhinitis he began experiencing what in retrospect appear to be hyperthyroid symptoms (sweating and tachycardia). TSH was in the mid-normal range in mid-2001 but fell to just beneath the normal range by fall 2001. Unfortunately free T4 was not measured. Synthroid was held and beta blockade introduced until TSH returned to normal. Steroid was not administered because of ongoing URI symptoms. His low-grade fever from the previous illness had resolved in the interim, but when sharing new household viral illnesses in late 2001, intermittent sweating and hyperdynamic symptoms recurred for brief durations when acutely ill. By spring 2002 his hyperdynamic symptoms slowly abated and his TSH rose (and hypothyroid symptoms recurred). As of mid 2002 he is on his baseline dose of Synthroid with normal TSH, normal free T4, and normal free T3. Immunological testing performed before his TSH was found to have fallen was unremarkable except for a modest IgE spike. His ESR was never elevated. Viral testing was negative. A bone marrow (performed because of the combination of low-grade fevers and sweating) had a gross appearance remininscent of pernicious anemia but testing was unremarkable (felt to be “reactive”, consistent with either an autoimmune state or viral illness). A thyroid ultrasound was consistent with Hashimoto’s thyroiditis of uncertain duration. Thyroid antibodies were moderately elevated, also consistent with thyroiditis of unclear duration. Of note is that a PET scan, done as part of the work-up prior to frank TSH changes, showed intense thyroid uptake. He now returns concerned about the possibility of future recurrence. At present he is euthyroid but has ongoing rhinitis symptoms. Other findings have resolved.
C. L. Etheridge, MD
I believe you describe one of the more unusual, but not unique, presentations of autoimmune thyroid disease. Probably this is best classified as “Hashimoto’sThyrodiitis”. The course, with periods of hyperthyroidism and hypothyroidism, is occasionally seen. Presumably this is related to changes in the types of antibodies being produced (stimulatory vs inhibitory) or the intensity of the T cell response. The relation to sinusitis (or another infection) is probably real, and has been reported by Amino and co-workers, along with the elevation of IgE. One presumes that the release of cytokines into the circulation (IL-1, IL-2, Il-L-6, IFN gamma, TNF alpha) is the actual cause of the changes in the thyroid inflammatory process. Sometimes the process seems to have a mixture with SAT, with thyroid pain and tenderness, but in your case the low sed rate rules out that process as the primary diagnosis. I think there is a strong likelihood of recurrence. While use of steroids might control the process temporarily, the only “solution” I know of, if the problem is severe enough to merit such , would be to remove the thyroid by either RAI or surgery, and I would favor the latter if a good surgeon is available.
Leslie J De Groot
University of Chicago
Chicago, IL 60637