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18 year old African American female saw her GYN in 9/2008 for abdominal pain. CT: bilateral adnexal masses (10×8 cm left; 6.3×3.1 cm right). Surgical pathology reported a left benign cystic teratoma and right corpus luteum cyst. Pain recurred in 2010. MRI showed: 9×7.5×4 cm right adnexal mass. Repeat surgery was done. Pathology: benign cystic teratoma with focal thyroid tissue - "Struma Ovarii". Abdominal pain recurred yet again in 2012. Sonography revealed a mixed solid/cystic pelvic mass measuring 10.6×7.9×7.6 cm. Exploratory laparotomy 9/2012 revealed a right adnexal mass and widespread peritoneal nodules. Pathology reported follicular tissue with colloid in the nodules - "Peritoneal Strumatosis" suggesting benignity. Upon further review was reclassified as metastatic well differentiated follicular thyroid cancer of ovarian origin with follicular thyroid tissue identified in peritoneal lymph nodes, spleen, bladder and rectal wall. The patient was then referred to endocrinology at our facility. On exam she was clinically euthyroid without thyromegaly or nodularity. Thyroid hormone levels were normal. Antithyroid antibodies were absent. Serum Thyroglobulin (Tg): elevated (229; normal 2-35 ng/ml) as was CA125 (64; normal <21 U/ml). Immunohistochemistry: positive for Tg and Thyroid transcription factor-1. Molecular markers: no mutations in BRAF, RAS, or TP53. In preparation for radioactive iodine (RAI) therapy, total thyroidectomy was performed 4/13/2013 and reported as normal thyroid tissue. Dosimetry findings: very iodine avid tissue with prolonged retention (33% at 6 days). Maximum tolerated dose: 200 mCi. A 62.8 mCi RAI was administered 7/13/2013. Post RAI whole body scan (WBS): numerous focal areas of increased uptake in abdomen and pelvis consistent with metastatic disease. Treatment with L-thyroxine was given to suppress TSH. Follow up WBS 12/26/2013 showed persistent increased uptake in abdomen and pelvis. Serum Tg was high (198. 0). A second RAI dose of 104.8 mCi was given. Post RAI WBS confirmed multiple areas of metastatic disease in abdomen and pelvis. Subsequent serum Tg levels down trended. WBS 11/12/2014: only two residual abnormal foci in the lower neck and one inferior to the liver without abdominal or pelvic foci. Given the dosimetry issue and the reassuring serum Tg levels, surveillance was continued. WBS 9/25/2015: unchanged. Now age 27, WBS 1/26/2022: only residual faint lower neck uptake, resolution of the focus inferior to the liver and no distant foci. Stimulated Tg was normal at 2.2 ng/ml with stimulated TSH >110. 0 uIU/ml. Presentation: No date and time listed

Introduction: Although rare, one of the most common inherited disorders is multiple endocrine neoplasia. It is an autosomal dominant disorder that predisposes individuals to certain endocrine abnormalities depending on which type. The type 2A is a combination of medullary thyroid cancer, hyperparathyroidism, and pheochromocytoma which have been explained to be due to a mutation in the RET proto-oncogene. This abstract present a case of a patient with hyperparathyroidism whom family members also have pheochromocytoma and papillary thyroid cancer. Case description: A 45 year-old Hispanic male came to the endocrinology clinic complaining of constipation and headache. He has a personal history of non-toxic multinodular goiter and underwent right sided thyroidectomy in 2015 with pathology report showing follicular adenoma. He is currently on thyroid replacement therapy. He is clinically and biochemically euthyroid with TSH of 2.29 IU/ml. Physical examination was unremarkable. His labs were pertinent for calcium 11.5mg/dl, parathyroid 245.7pg/ml, creatinine of 1.5mg/dl. Two years ago, parathyroid was 189.5pg/ml and calcium was 11mg/dl, 1.5 year ago parathyroid level was 235.5pg/ml, calcium was 11.4mg/dl, urine calcium 9.3mg/dl, 24hr urine calcium 286.4mg, calcitonin <2pg/ml, vitamin D 23ng/ml, 1,25 vitamin D 53ng/ml. In 2017, Sestambi scan showed equivocal focus of faint parathyroid activity in the region of the mid to lower left thyroid lobe versus faint residual thyroid activity and in 2019, scan showed no definite parathyroid adenoma. Surgical intervention was recently recommended due to patient’s DEXA scan showing osteoporosis of the femoral neck. The family history of this patient is pertinent for two sisters; one with pheochromocytoma and the other with papillary thyroid cancer. One of the sisters is a 60 years old diagnosed with pheochromocytoma at 51. Her free normetanephrine level was 682pg/ml and total metanephrine was 727pg/ml at time of diagnosis. Her MRI report showed right adrenal mass measuring 3.5x2.8cm. Laparoscopic right adrenalectomy was done and pathology confirmed pheochromocytoma which was RET negative. She still follows up with endocrinology and calcitonin, chromogranin A and plasma metanephrines have been normal. The second sister is now 53 years old diagnosed with papillary thyroid cancer at age 27 and had total thyroidectomy with pathology confirming papillary thyroid cancer. Discussion: Based on the clinical presentation of these family members, the most likely explanation is familial inheritance. This pattern of inheritance cannot be explained by MEN 2A or 2B due to the absence of medullary thyroid cancer. It has also been reported that this unusual presentation could be a variant of MEN 2A.[i] Due to the family history, close follow up is required to monitor for the possible development of other endocrinopathies in the future.

Sporadic reports of factitious elevations of thyroid hormones related to laboratory interference from autoantibodies and multiple myeloma paraproteins have appeared in the literature. Such clinically confusing laboratory results can lead to erroneous diagnoses and inappropriate treatments. We report an additional case of a patient with multiple myeloma and an IgG paraproteinemia who had such a spurious elevation of total T3 complicating her levothyroxine management of hypothyroidism. In addition, we alert clinicians that differences in performance characteristics between various manufacturers’ test platforms may also cause spurious reports.