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yme Disease Associated Thyroiditis

0 2 years ago

It has been suggested that Borrelia proteins may be capable of triggering autoimmune thyroid disease in persons with certain HLA-DR alleles (1). Clinical case: A 40-year-old male presented to the Emergency Department (ED) with 3 weeks of worsening night sweats, lethargy, and weakness. He previously had 5 oval shaped spots on his body which had appeared after a recent hiking trip but these had disappeared 1.5 weeks prior to his presentation. He had been experiencing positional chest pain for the 3 days prior to coming to the ED.

On admission to the hospital he was found to be febrile and bradycardic with ECG revealing high-grade second-degree type II block. He was started on empiric antibiotics for suspected Lyme disease as he had been hiking in a Lyme endemic area. He also had thyroid indices sent off at the time of presentation which came back consistent with hyperthyroidism. The patient did not endorse neck pain or tenderness, visual symptoms, weight loss, diarrhea, tremors, or palpitations.

Anti-TPO antibodies as well as a nuclear medicine thyroid uptake and scan were ordered. His anti-TPO antibodies were positive at 26 IU/mL (n<=6 IU/mL). His uptake at 5 hours of was 0.75%, which is markedly below the lower limit of normal (5%) and as such a thyroid scan could not be performed as there would have been insufficient counts to generate a diagnostic image. His hyperthyroidism was most in keeping with a thyroiditis. As such no thyroid specific treatment was initiated. His Lyme Western Blot IgG eventually returned positive. When he was seen in follow up in outpatient endocrinology clinic, thyroid indices revealed he was hypothyroid, in keeping with the hypothyroid phase often seen in thyroiditis.

Conclusion: There are a few studies suggesting borrelia proteins may be capable of triggering autoimmune thyroid disease. This case is supportive of this theory and showcases a presentation of Lyme disease associated thyroiditis. References: (1) Benvenga, S., Guarneri, F. Molecular mimicry and autoimmune thyroid disease.

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