Endocrine Abstracts

Most common causes of primary hypothyreosis are destruction of thyroidal parenchyma by the autoimmune antibodies, interventions on the gland (surgery, radioiodine treatment) and external actinotherapy (hematologic and ENT malignancies). Drug induced thyroidal impairment is well-known too (amiodarone, lithium, interferon). Our case demostrates the primary hypothyreosis caused by cobalt. The source was Co-Cr hip prostehis after its rupture (PHACT). A 55 old man was reffered to endocrinologist in 2011 with enlargement of thyroid gland (volume 84 ml) and signs of primary hypothyreoidism (TSH 76 mU/l). No elevation of antibodies levels was present, family history of thyroid disease negativ. Thyroxin substitution treatment resulted in both normalisation of thyroid function and thyroid gland volume (TSH 1.3 mU/l, 18 ml).

Personal history: Hyperlipoproteinema, smoking. The man also underwent implantation of right hip prosthesis after an injury in 2002. The course was complicated by deep venous thrombosis of the right leg and massive pulmonary embolism requiring thrombolysis treatment. The prosthesis was damaged in 2010 because of necrosis and replaced with the Co–Cr type. Since 2010 the patient was examined by multidisciplinary specialists because of polymorhpic atypical complaints (arrhytmias – considered cardiomyopathy, atypical neuropathy, hypacusis). In 2014 patient was admitted to hospital with atypical back and pelvis pains. Following RDG imaging of the right trochanter and acetabulum a diagnosis was finally obtaned showing pathology - local osteal reaction. The puncture of the affected spot revealed dark fluid with high levels of cobalt and chromium. The defficient prosthesis was then removed. PHACT id.e prosthetic hip-associates cobalt toxicity. The symptoms are atypical – arrhytmias, different neurological symptoms, changes of thyroid gland functions, deafnes, eye disorders.