Faculty Bibliography

The risk of papillary thyroid carcinoma (PTC) in Graves' disease is increased, with an overall incidence ranging from 7% to 33.7%. Thyroid nodules are found in up to 25% of patients with Graves' disease. The risk of malignancy in hyperfunctioning thyroid nodules is low with an estimated prevalence of 3.1%. We present a rare case of PTC within a hyperfunctioning thyroid nodule in a patient with Graves' disease. A 65 year-old female presented with weight loss, tremors, palpitations and shortness of breath. An asymmetric goiter was discovered on physical exam. Her labs were consistent with hyperthyroidism: TSH <0.005 uIU/mL (0.45-4.5), FT4 3.98 ng/dL (0.82-1.77), Total T3 385 ng/dL (71-180), TPO antibody 272I U/mL (0-34), TSI 309% (0-139) and thyroglobulin antibody <1I U/mL (0-0.9). A thyroid uptake and scan showed an increased uptake (66% at 24 hours) with possibility of a large hyperfunctioning nodule in the right hemithyroid and relative suppression of the left hemithyroid. The patient was diagnosed with Graves' disease. Treatment with Methimazole was initiated with significant improvement in symptoms. She underwent a thyroid ultrasound, which revealed multiple punctate calcifications within the hyperfunctioning right thyroid nodule. An FNA was performed and pathology was diagnostic for PTC (Bethesda class VI). The patient subsequently underwent a total thyroidectomy. Surgical pathology demonstrated a 1.3 cm classic PTC and diffuse follicular hyperplasia with lymphocytic thyroiditis consistent with Graves' disease. The risk of PTC in patients with Graves' disease is increased, however the risk of malignancy in hyperfunctioning thyroid nodules is low. Our case raises the question of whether occult thyroid carcinomas have been missed in patients with Graves' disease due to the assumption that hot nodules are usually benign. Thyroid ultrasounds should be performed in Graves' patients with suspected thyroid nodules, patients with cervical lymphadenopathy and patients with cold areas on thyroid uptake and scan. Thyroid FNA of cold nodules and hot nodules with suspicious characteristics on ultrasound, such as microcalcifications, irregular borders and vascularity should be performed to rule out thyroid carcinoma

OBJECTIVE: To report a case of metastatic insulinoma presenting 11 yr after enucleation of an isolated insulinoma, and 5 yr after distal pancreatectomy for nesidioblastosis. METHODS: We present the clinical, laboratory, radiological and pathological findings in a 34 yr-old-man with recurrent hypoglycemia. The pertinent literature is reviewed. RESULTS: A 34- yr-old man presented in 1992 with symptoms of recurrent hypoglycemia. Laboratory and imaging findings were consistent with insulinoma. After enucleation of the tumor, his symptoms resolved. In 1998 hypoglycemia recurred and biochemical work-up was consistent with endogenous hyperinsulinism. Imaging for recurrent or metastatic insulinoma revealed no mass. He underwent a distal pancreatectomy and pathology revealed islet cell hyperplasia, or nesidioblastosis. However, the patient reported minimal symptomatic improvement. He was started on diazoxide but was poorly compliant and ate frequently to avoid hypoglycemic symptoms. In 2003 he presented with hypoglycemia-induced seizure activity. Imaging showed hepatic and pulmonary lesions, but no pancreatic mass. An octreotide scan revealed increased hepatic uptake and fine needle aspiration of a liver lesion confirmed metastatic insulinoma. Arterial-stimulation venous sampling revealed increased insulin output from the liver and normal insulin output from the pancreas. After failure of medical therapy, radiofrequency ablation of hepatic lesions was performed with subsequent improvement in clinical symptoms. The patient was discharged on a low dose of dexamethasone. CONCLUSION: Although this patient had nesidioblastosis, his recurrent hyperinsulinism was most likely secondary to metastatic insulinoma. Radiofrequency ablation was successfully used for palliative purposes in managing metastatic insulinoma refractory to medical therapy.

Both obesity and the polycystic ovary syndrome (PCOS) are commonly seen in women of reproductive age. Fifty percent of all patients with PCOS are obese, and the presence of obesity affects the clinical manifestations of PCOS. The underlying pathogenetic mechanisms appear to involve insulin resistance and hyperinsulinemia, the magnitude of which is greater in obese than in non-obese women with PCOS. Specific effects of obesity on the manifestations of PCOS, underlying mechanisms of the interactions between obesity and PCOS, and therapeutic implications of these interactions are discussed in this article.