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      Hypercalcemia of Malignancy

      review-article
      , MSN, FNP-C, , PharmD, BCPS, BCOP
      Journal of the Advanced Practitioner in Oncology
      Harborside Press

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          Abstract

          CASE STUDY:

          A 60-year-old man initially presented with pain in the right upper quadrant in October 2010. A computed tomography (CT) scan of the abdomen pelvis completed at that time showed a mass at the junction of the body and tail of the pancreas and multiple large liver lesions. A CT-guided liver biopsy revealed low-grade neuroendocrine carcinoma.

          The patient was initially started on systemic treatment with sunitinib (Sutent) and octreotide. He developed intolerable side effects, including nausea and migraine. Therapy was discontinued in October 2011, when a CT scan revealed evidence of disease progression. At this point, he was transitioned to everolimus (Afinitor). He was treated with everolimus, with overall stable disease, until a magnetic resonance image (MRI) of the abdomen and pelvis showed enlarging hepatic metastases in April 2014. Everolimus was discontinued.

          The patient presented to the clinic to start third-line systemic therapy; he described the recent onset of disorientation at home, with difficulty in concentration and mild muscle weakness. He was found to be lethargic on the day of the visit. He was noted to have a 4-kg weight loss. Blood pressure was 82/45 mm Hg, with a heart rate of 115 beats/minute.

          Lab tests revealed a serum calcium level of 12.7 mg/dL (9.5 mg/dL prior). At that time, the serum albumin level was 2.4 mg/dL. The corrected calcium for albumin was 14 mg/dL. The patient was treated with intravenous (IV) hydration, and vital signs normalized post treatment. Labs revealed an improvement in serum calcium to 11.8 mg/dL (corrected = 13.1 mg/dL). Additional laboratory analysis revealed vitamin D, 25-hydroxy level of 40 ng/mL (reference range, 20–50 ng/mL), parathyroid hormone–related protein of 5.2 pmol/L (reference range, < 2.0 pmol/L), thyroid-stimulating hormone of 1.04 mIU/mL (reference range, 0.35–4.00 mIU/mL). An electrocardiogram revealed sinus tachycardia with a QT of 31.6 ms (QTc of 38.4 ms). The patient improved symptomatically and was sent home.

          The patient returned for repeat labs 1 week later, with worsening of previously described weakness and lethargy. The serum calcium level had increased to 13.2 mg/dL, with a serum albumin level of 2.8 mg/dL. Intravenous zoledronic acid (4 mg) was administered, and he was admitted for symptomatic hypercalcemia. He received continuous IV hydration with normal saline at 300 mL/hr and telemetry monitoring. Once hydrated, he was treated with IV furosemide. His serum calcium level rapidly improved to 10 mg/dL by day 2 of admission, and lethargy and weakness symptoms resolved. He was discharged from the hospital at that time.

          After discharge, the patient continued on third-line capecitabine-based systemic therapy, with excellent radiologic and tumor marker response to therapy and monthly zoledronic acid infusion. Serum calcium levels returned to within the normal range and stable, and he remained without relapse of hypercalcemia. After 2 months, zoledronic acid was discontinued, and the serum corrected calcium remained within normal limits.

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          Most cited references12

          • Record: found
          • Abstract: not found
          • Article: not found

          Clinical practice. Hypercalcemia associated with cancer.

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            • Record: found
            • Abstract: not found
            • Article: not found

            Bisphosphonates: mechanisms of action.

              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Hypercalcaemia of malignancy and basic research on mechanisms responsible for osteolytic and osteoblastic metastasis to bone.

              Calcium homeostasis is a tightly regulated process involving the co-ordinated efforts of the skeleton, kidney, parathyroid glands and intestine. Neoplasms can alter this homeostasis indirectly through the production of endocrine factors resulting in humoral hypercalcaemia of malignancy. Relatively common with breast and lung cancer, this paraneoplastic condition is most often due to tumour production of parathyroid hormone-related protein and ensuing increased osteoclastic bone resorption. Although control of hypercalcaemia is generally successful, the development of this complication is associated with a poor prognosis. The metastasis of tumour cells to bone represents another skeletal complication of malignancy. As explained in the 'seed and soil' hypothesis, bone represents a fertile ground for cancer cells to flourish. The molecular mechanisms of this mutually beneficial relationship between bone and cancer cells are beginning to be understood. In the case of osteolytic bone disease, tumour-produced parathyroid hormone-related protein stimulates osteoclasts that in turn secrete tumour-activating transforming growth factor-beta that further stimulates local cancer cells. This 'vicious cycle' of bone metastases represents reciprocal bone/cancer cellular signals that likely modulate osteoblastic bone metastatic lesions as well. The development of targeted therapies to either block initial cancer cell chemotaxis, invasion and adhesion or to break the 'vicious cycle' is dependent on a more complete understanding of bone metastases. Although bisphosphonates delay progression of skeletal metastases, it is clear that more effective therapies are needed. Cancer-associated bone morbidity remains a major public health problem, and to improve therapy and prevention it is important to understand the pathophysiology of the effects of cancer on bone. This review will detail scientific advances regarding this area.
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                Author and article information

                Journal
                J Adv Pract Oncol
                J Adv Pract Oncol
                JADPRO
                Journal of the Advanced Practitioner in Oncology
                Harborside Press
                2150-0878
                2150-0886
                Nov-Dec 2015
                1 November 2015
                : 6
                : 6
                : 586-592
                Affiliations
                University of Arizona Cancer Center, Tucson, Arizona; Greenville Health System, Greenville, South Carolina
                Author notes

                Correspondence to: Steve Malangone, MSN, FNP-C, University of Arizona Cancer Center, North Campus, 3838 North Campbell Avenue, Tucson, AZ 85719. E-mail: steve.malangone@uahealth.com

                Article
                jadpro.v06.i06.pg586
                5017549
                79c22bb8-679d-4a71-893e-723be03e70bb
                Copyright © 2015, Harborside Press

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited and is for non-commercial purposes.

                History
                Categories
                Review Article
                Oncology

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