ACTA ENDOCRINOLOGICA (BUC)

Background. Skull metastasis has not been reported from mixed medullary follicular thyroid carcinoma (MMFTC). Objective. To present a patient with expansile lytic skull metastasis. Case report. A 61 year lady is presented with goiter for 7 years and 8 cm diameter painful swelling over frontal bone for 18 months, aspiration from which revealed sheets and clusters of polygonal cells, similar to aspiration from hypoechoic nodule in right thyroid lobe. Serum calcitonin (569pg/mL) and carcinoembryonic antigen (11.2ng/mL) were elevated. Histopathology of 3.8×3.1cm nodule in thyroidectomy specimen revealed irregular islands of small polygonal tumor cells with extracellular amyloid deposits (suggesting medullary thyroid carcinoma (MTC)), intermingled with thyroid follicular cells showing capsular and vascular invasion (follicular thyroid carcinoma (FTC)). Immunohistochemistry of the thyroid tumor was negative for calcitonin and for thyroglobulin. Post-operative serum calcitonin and stimulated thyroglobulin were respectively 97 pg/mL and 11.5 ng/mL. I131 whole body scan revealed intense uptake in region of the skull metastasis with small uptake in thyroid bed. She received 150 mCi of I131with resolution of pain, heaviness, throbbing, reduction in swelling size, and lack of disease progression. Conclusions. Skull metastasis was the presenting feature of MMFTC which improved with I131 therapy. Patients with lytic skull metastasis should be evaluated for occult thyroid malignancy.

Context and objective. Somatostatin analogues and cinacalcet have been suggested to have some role in managing hypophosphatemia. This report highlights challenges in managing surgically incurable tumor induced osteomalacia (TIO) with somatostatin analogues and cinacalcet. Patient and methods. A twenty-two year old patient with severe osteomalacia was diagnosed to have TIO due to left hemipelvis tumor (June 2013). Partial surgical removal of tumor (due to its proximity to neurovascular bundles), led to transient remission for 6 weeks. Clinical worsening in spite of maximum tolerable phosphate and calcitriol dose led to trial of octreotide. Acute improvement in phosphate following subcutaneous octreotide 100 mcg was the basis for use of long acting depot octreotide, which was associated with maximal improvement for 4 months, followed by reduced efficacy. Repeated MRI revealed an increase in residual tumor size. Reevaluation revealed very a high parathyroid hormone. Cinacalcet titrated to 90 mg/day induced hypoparathyroidism, improved hypophosphatemia but caused symptomatic hypocalcemia. Cinacalcet at lower doses (30mg/day), though well tolerated, was less effective in improving hypophosphatemia. There was a near 10-fold reduction (2406 to 246RU/ml) in C-terminal FGF-23 levels with cinacalcet. Reduction in phosphate and calcitriol requirements with cinacalcet may contribute to decreased FGF-23. There was no decrease in tumor size. Conclusion. Octreotide and cinacalcet are effective in controlling hypophosphatemia over short periods. Progressive nature of TIO leading to an increased disease severity, tachyphylaxis may explain decreased efficacy of octreotide, higher cinacalcet requirement, poor tolerability, thus limiting their role in long-term management of TIO.