Recalcitrant Hypocalcemia: Postsurgical Hypoparathyroidism Exacerbated by a Chyle Leak Treated With Octreotide.

Background/Objective: To report a case of recalcitrant post-surgical hypocalcemia caused by hypoparathyroidism complicated by a chyle leak and octreotide use. Case Report: A man in his 60s with a 4-month history of voice changes, 10-pound weight loss, and a right-sided neck mass presented with difficulty breathing for 1 week. He had a right laryngeal/hypopharyngeal mass, which was biopsied. Pathology results were positive for invasive squamous cell carcinoma. He underwent an extensive neck surgery, including total thyroidectomy. Postsurgical laboratory results revealed serum corrected calcium of 7.6 mg/dL (ref 8.0-10.2 mg/dL) and parathyroid hormone <6.3 pg/mL (ref. 10-65). Despite treatment with calcium carbonate 12 g (elemental) daily, calcitriol and hydrochlorothiazide, his corrected serum calcium levels remained low. Patient also had a chyle leak that was treated with octreotide. Resolution of his hypocalcemia occurred after substitution of calcium carbonate with calcium citrate, cessation of octreotide, and management of the chyle leak. Discussion: Our patient likely developed recalcitrant hypocalcemia from: 1) postsurgical hypoparathyroidism, 2) a chyle leak, and 3) the use of octreotide. Administration of octreotide to seal the chyle leak most likely decreased gastric acid production and contributed to decrease in absorption of calcium carbonate. Oral calcium citrate may be better absorbed in this case. Conclusion: Postsurgical hypoparathyroidism can lead to hypocalcemia. This case is unique in that the patient's chyle leak and the use of octreotide contributed to recalcitrant hypocalcemia.

Cytokine secretion in breast cancer cells - MILLIPLEX assay data.

Metastatic breast cancer is the most advanced stage of breast cancer and the leading cause of breast cancer mortality. Although understanding of the cancer progression and metastasis process has improved, the bi-directional communication between the tumor cell and the tumor microenvironment is still not well understood. Breast cancer cells are highly secretory, and their secretory activity is modulated by a variety of inflammatory stimuli present in the tumor microenvironment. Here, we characterized the cytokine expression in human breast cancer cells (MDA-MB-231, MCF-7, T-47D, and BT-474) in vitro using 41 cytokine MILLIPLEX assay. Further, we compared cytokine expression in breast cancer cells to those in non-tumorigenic human breast epithelial MCF-10A cells.