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      Hypercalcemia of Malignancy and Colorectal Cancer

      case-report

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          Abstract

          Our aim is to describe the association between colorectal cancer (CRC) and humoral hypercalcemia of malignancy (HHM). Causes of hypercalcemia of malignancy include parathyroid hormone-related peptide (PTHrP) secretion, local osteolysis, calcitriol production and ectopic parathyroid hormone (PTH) secretion. Hypercalcemia of malignancy in patients with CRCs is a rare scenario. A patient with anal squamous cell carcinoma was admitted with hypercalcemia, suppressed PTH and hypophosphatemia. He was found to have metastatic anal squamous cell carcinoma to the liver. Further evaluation revealed elevated PTHrP and 1,25-dihydroxyvitamin D and low 25-hydroxyvitamin D. Over a 5-month course, the hypercalcemia responded poorly to bisphosphonates, transiently to prednisone, but showed marked improvement with chemotherapy. A review of English language publications in Pubmed and a reference search of retrieved articles revealed 29 cases of CRC causing PTHrP-mediated hypercalcemia. Most patients were middle-aged men (mean ± SD: 56.7 ± 13.4 years), with advanced metastatic cancer (85% with hepatic metastasis) and severe hypercalcemia (mean ± SD: 15.6 ± 1.9 mg/dL, 62% with Ca > 14). This condition is associated with high mortality (79%) and short survival (median 54.5 days, CI: 21 - 168). Despite being uncommon, HHM (PTHrP-mediated) should be considered in patients with metastatic CRC presenting with hypercalcemia. Clinicians should be aware that combined etiologies may be present, particularly in cases of resistant hypercalcemia. Treatment of the underlying malignancy is essential for calcium control.

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          Clinical practice. Hypercalcemia associated with cancer.

          Andrew F Stewart (2005)
          Article 0 comments Cited 192 times – based on 0 reviews     Review now
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            Extrarenal expression of the 25-hydroxyvitamin D-1-hydroxylase.

            J.S. Adams, M Hewison (2012)
            Like the vitamin D receptor (VDR), the CYP27B1-hydroxylase is expressed widely in human tissues. This expression profile establishes the potential for interaction of the VDR with the product of the CYP27B1, 1,25-dihydroxyvitamin D (1,25-(OH)(2)D), in either an intracrine or paracrine mode. This expansive expression profile also suggests that the local production and action of 1,25-(OH)(2)D to regulate VDR-directed gene expression may be similarly wide-ranging and distinct from what occurs in the kidney; the proximal renal tubular epithelial cell is the richest source of the CYP27B1 and the site for production of 1,25-(OH)(2)D destined to function as a hormone. Existence of the CYP27B1 at extrarenal sites has been widely documented, although the functional impact of the enzyme in these tissues has yet to be fully demonstrated. Two notable exceptions are the disease-activated macrophage (e.g., in sarcoidosis or tuberculosis) and the placenta. These two tissues are capable of generating enough 1,25-(OH)(2)D so as to be detectable in the general circulation. As such, this review will focus on CYP27B1 expression only at these two sites, theorizing that 1,25-(OH)(2)D production at these sites is for the purpose of local immunoregulatory function, not for controlling calcium balance in the host or the fetus. Copyright © 2012 Elsevier Inc. All rights reserved.
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              Role of FGF23 in vitamin D and phosphate metabolism: implications in chronic kidney disease.

              L. Quarles (2012)
              FGF23 is a bone-derived hormone that regulates systemic phosphate homeostasis, vitamin D metabolism and α-Klotho expression through a novel bone-kidney axis. FGF23 inhibits renal tubular reabsorption of phosphate through mechanisms independent of PTH as well as reduces circulating 1, 25(OH)(2)D through its dual effects to suppress Cyp27b1 production and to stimulate Cyp24 catabolism of 1,25(OH)(2)D. 1,25(OH)(2)D and other factors regulating bone remodeling/mineralization are the major physiological regulators of FGF23 expression. FGF23 also suppresses the gene transcription of α-klotho by the kidney, which exists as a membrane and soluble protein. Membrane Klotho acts as a coreceptor for and dictates organ specificity of FGF23, whereas soluble Klotho act as an endocrine factor that regulates activity of cell surface glycoproteins and receptors in multiple tissues. Elevated FGF23 levels are responsible for several hereditary and acquired hypophosphatemic rickets disorders. FGF23 and Klotho deficiency have similar phenotypes characterized by hyperphosphatemia, elevated 1,25(OH)(2)D and tumoral calcinosis. FGF23 levels progressively increase during chronic kidney disease (CKD). FGF23 has been proposed to be the initial adaptive response leading to reductions in 1,25(OH)(2)D and secondary hyperparathyroidism (HPT) in CKD. The overall biological effect of this initial step may be to orchestrate a coordinated adaptation to protect the organism from the adverse effects of excess phosphate retention. The second step involves the effects of PTH on bone remodeling that further stimulates FGF23 production through both direct and indirect mechanisms related to alterations in extracellular matrix factors. PTH further amplifies FGF23 expression in later stages of CKD to compensate for the increased phosphate efflux from bone caused by excessive bone turnover. While many aspects of the regulation and functions of FGF23 remain to be established, the idea that FGF23 hormone is the initial adaptive hormonal response in CKD that suppresses 1,25(OH)(2)D, reduces gastrointestinal calcium and phosphate absorption and leads to a secondary HPT represents a paradigm shift in the conceptualization of the pathogenesis of secondary hyperparathyroidism. In addition, the prevalent thought that CKD is a functional "vitamin D deficient state" requiring therapy with 1,25(OH)(2)D analogs is challenged by effects of FGF23 to potentially lower both 25(OH)D and 1,25(OH)D by induction of Cyp24-mediated degradation. Finally, increments in FGF23 are associated with increased cardiovascular mortality in CKD. Whether these effects represent direct effects of FGF23 or represent a marker of other abnormalities in CKD remains to be determined. Copyright © 2012 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-ta): World J Oncol
                Journal ID (iso-abbrev): World J Oncol
                Journal ID (publisher-id): Elmer Press
                Title: World Journal of Oncology
                Publisher: Elmer Press
                ISSN (Print): 1920-4531
                ISSN (Electronic): 1920-454X
                Publication date (Print): February 2016
                Publication date (Electronic): 03 April 2016
                Volume: 7
                Issue: 1
                Pages: 5-12
                Affiliations
                [a ]Icahn School of Medicine at Mount Sinai, Division of Endocrinology, Diabetes and Bone Diseases, Mount Sinai St. Luke’s Hospital, 1111 Amsterdam Ave, Babcock Building 10th Floor, Room 1020, New York, NY 10025, USA
                [b ]Hofstra North-Shore LIJ School of Medicine, Division of Endocrinology Diabetes and Metabolism, 865 Northern Boulevard, Suite 203, Great Neck, NY 11021, USA
                Author notes
                [c ]Corresponding Author: Rodolfo J. Galindo, Icahn School of Medicine at Mount Sinai, Division of Endocrinology, Diabetes and Bone Diseases, Mount Sinai St Luke Hospital, 1111 Amsterdam Ave, Babcock Building 10th Floor, Room 1020, New York, NY 10025, USA. Email: rgalindo@ 123456chpnet.org
                Article
                DOI: 10.14740/wjon953w
                PMC ID: 4797652
                PubMed ID: 26998187
                SO-VID: 160eafe8-191f-4513-8e75-6565dbaeb9d2
                Copyright © Copyright 2016, Galindo et al.
                License:

                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.

                History
                Date accepted : 27 January 2016
                Categories
                Subject: Case Report

                Keywords: hypercalcemia,parathyroid hormone-related peptide,calcitriol,colorectal cancer,combined mechanism of hypercalcemia
                Data availability:
                Keywords: hypercalcemia, parathyroid hormone-related peptide, calcitriol, colorectal cancer, combined mechanism of hypercalcemia

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