Objective: Ectopic paraneoplastic secretion of parathyroid hormone (PTH) is rare, with only 25 cases previously reported in the literature, including only 2 attributed to squamous cell carcinoma. The recent presentation of such a patient and subsequent review of the literature has alerted us to the need for clinicians to consider such an etiology in patients presenting with humeral hypercalcemia of malignancy. Methods: Significant hypercalcemia occurred in a 48-year-old male with metastatic squamous cell carcinoma of the penis. The patient had hypercalcemia, elevated PTH, and normal PTH-related protein (PTHrp), without evidence of tumoral skeletal involvement. Comorbid primary hyperparathyroidism was suspected, but ultrasound and sestamibi scans of the neck were negative, raising the possibility of ectopic PTH production. This was confirmed by computed tomography-guided needle biopsy of a thigh metastatic lesion showing positive histochemical staining for PTH-specific antibodies and markedly elevated PTH levels in the aspirated lesion fluid. Results: Paraneoplastic ectopic PTH production is well documented but rare. This is only the third such case to be reported due to squamous cell carcinoma and the first associated with a penile primary neoplasm. Diagnosis in our patient required exclusion of neoplastic lytic bone lesions, tumoral secretion of PTHrp, or comorbid primary hyperparathyroidism, as well as positive histochemical staining of tumor cells obtained at biopsy for PTH and very high levels of PTH from fluid aspirated from a metastasis. In spite of aggressive chemotherapy and management of hypercalcemia, the patient did not survive. Conclusion: Ectopic paraneoplastic PTH secretion is rare, but clinicians need to be alert to its possibility and aggressively seek out the diagnosis. Unfortunately, management is difficult, and even with aggressive treatment, survival is poor. (AACE Clinical Case Rep. 2018;4:e9-e12) Abbreviations: CT = computed tomography; HHM = humeral hypercalcemia of malignancy; PTH = parathyroid hormone; PTHrp = parathyroid hormone-related protein
Objective: Medullary thyroid cancer (MTC), derived from thyroidal parafollicular C-cells, is a difficult treatment problem when presenting with advanced and metastatic disease. The recent addition of targeted systemic medical therapy with tyrosine kinase inhibitors has shown great promise for disease control and prolonged survival for these patients. We present a case of a young woman with such advanced disease who has had a significant and prolonged response to treatment with the tyrosine kinase inhibitor vandetanib. We wish to alert clinicians to the use of such therapy in appropriate cases. Methods: A 22-year-old woman was referred to our medical center with MTC. Having already undergone total thyroidectomy followed by external beam radiotherapy of involved left neck lymph nodes, she presented to our institution with a significant paratracheal tumor burden and extensive pulmonary metastases. She was given systemic tyrosine kinase inhibitor treatment with vandetanib. Results: The patient, suffering no significant adverse effects of therapy, has responded biochemically showing durable reductions in calcitonin, carcinoembryonic anti-gen, and chromogranin A, and she has had progression-free survival with a documented partial response and disease regression after 39 months of continuous therapy. Conclusion: Advanced and metastatic MTC has classically had a poor prognosis. However, the recent introduction of systemic tyrosine kinase inhibitor therapy has greatly improved the outlook for these patients. Clinicians should be alert to this advance in therapeutics for use in selected appropriate patients.
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