Case report of Borrelia burgdorferi infection as a possible trigger of Riedels thyroiditis
Gábor László Kovács, István Szabolcs, Zoltán Görömbey, László Kovács, Erika Hubina, Judit Dénes & Miklós Góth
Background: The detectable levels of thyroid antibodies in patients suffering from Riedels chronic fibrosing thyroiditis (RT) suggest a link between RT and Hashimotos thyroiditis, but the pathogenesis of RT is not really known. Lyme disease is the most frequent tick-borne infection with variable manifestations in different organs caused by Borrelia burgdorferi (Bb).
Case report: A 59-year-old woman presented in our outpatient clinic with a painful swelling and cervical discomfort in the anterior area of the neck. 30 years ago she was treated with thiamazol for Graves disease. The symptoms started following two tick bites on the neck. She presented with elevated inflammatory markers (westergren 91 mm/h, CRP 88.6 mg/l), anaemia, and thrombocytosis (haemoglobin 112 g/l, PLT 513 G/l) with normal level of procalcitonin and white blood cells. Primary hypothyroidism was detected (TSH 37.8 μIU/ml, fT4 6.22 pmol/l). Ultrasonography showed bilateral enlargement, hypovascularisation of the thyroid with multiple hypoechogenic nodular formation and bilateral large lymph nodes. Tc scintigraphy showed a low Tc uptake (0.69%). Transitional methylprednisolone treatment with thyroxin substitution was started. The planned near total thyroidectomy was unsuccessful. The histological investigation suggested the diagnosis of RT. The microbiological tests confirmed a Bb acute infection with elevated IgM/IgG levels. Amoxicillin treatment (3×500 mg/21 days) was advised, then pulsatile steroid therapy administered (250 mg methylprednisolone/7 day cycles up to 1500 mg). After treatment the symptoms and inflammatory laboratory results improved; the former trachea compression did not worsen. According to the literature data some parts of the human TSH receptor match outer surface protein A, flagellar rotation protein A, DNA recombinase/ATP dependent helicase of Bb.
Conclusion: Our case strengthens the former hypothesis: Bb might be an environmental trigger of autoimmune thyroid disease through a molecular mimicry mechanism. To our knowledge this is the first case of Bb infection and Riedels thyroiditis co-morbidity.