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      Unmasking of primary hyperparathyroidism by Vitamin D therapy

      case-report

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          Abstract

          A 38-year-old female on Vitamin D therapy presented with hypercalcemia induced acute kidney injury. Evaluation revealed primary hyperparathyroidism (PHPT) and iatrogenic hypervitaminosis D. After medical stabilization, she underwent surgical removal of the parathyroid adenoma, and made a full recovery. This case highlights unmasking of subclinical hyperparathyroidism by vitamin D therapy leading to severe hypercalcemia.

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          Most cited references12

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          Hyperparathyroidism

          The Lancet, 374(9684), 145-158
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            The rise and fall of primary hyperparathyroidism: a population-based study in Rochester, Minnesota, 1965-1992.

            The introduction of routine measurement of serum calcium levels led to a sharp increase in the incidence of primary hyperparathyroidism in the early 1970s. To evaluate the trends in the incidence of primary hyperparathyroidism since the mid-1970s. Rochester and Olmsted County, Minnesota. Population-based descriptive study. All residents of Rochester, Minnesota, who received an initial diagnosis of primary hyperparathyroidism between 1965 and 1992 were identified through the medical records linkage system of the Rochester Epidemiology Project. Included as persons having definite cases (92% of the total) were patients with pathologically confirmed hyperparathyroidism, hypercalcemia with inappropriately elevated parathyroid hormone levels, or hypercalcemia that had lasted for more than a year and had no cause other than primary hyperparathyroidism. Incidence rates were calculated and directly standardized to the population structure of white persons in the United States in 1990. From 1965 to June 1974 (the prescreening era), the age- and sex-adjusted incidence of primary hyperparathyroidism in Rochester was 15 cases per 100,000 person-years. After measurement of calcium levels was added to the automated serum chemistry panel in July 1974, the incidence increased to 112 per 100,000 person-years in 1975 and then decreased somewhat, reflecting a sweeping effect. Despite improved case ascertainment, however, the incidence rate has continued to decrease; in 1992, the incidence was 4 per 100,000 person-years. A few patients had complications that might have been caused by hyperparathyroidism (22% between 1965 and June 1974 and 6% thereafter), and survival was not impaired in either period. The maximum serum calcium levels did not change (P = 0.15). The progressive decrease in the incidence of primary hyperparathyroidism is unexpected and suggests a significant change in the epidemiology of this disease.
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              Bisphosphonates directly inhibit the bone resorption activity of isolated avian osteoclasts in vitro.

              Bisphosphonates are useful in treatment of disorders with increased osteoclastic activity, but the mechanism by which bisphosphonates act is unknown. We used cultures of chicken osteoclasts to address this issue, and found that 1-hydroxyethylidenediphosphonic acid (EHDP), dichloromethylidenediphosphonic acid (Cl2MDP), or 3-amino-1-hydroxypropylidene-1,1-diphosphonic acid (APD) all cause direct dose-dependent suppression of osteoclastic activity. Effects are mediated by bone-bound drugs, with 50% reduction of bone degradation occurring at 500 nM to 5 microM of the different agents. Osteoclastic bone-binding capacity decreased by 30-40% after 72 h of bisphosphonate treatment, despite maintenance of cell viability. Significant inhibition of bone resorption in each case is seen only after 24-72 h of treatment. Osteoclast activity depends on ATP-dependent proton transport. Using acridine orange as an indicator, we found that EHDP reduces proton accumulation by osteoclasts. However, inside-out plasma membrane vesicles from osteoclasts transport H+ normally in response to ATP in high concentrations of EHDP, Cl2MDP, or APD. This suggests that the bisphosphonates act as metabolic inhibitors. Bisphosphonates reduce osteoclastic protein synthesis, supporting this hypothesis. Furthermore, [3H]leucine incorporation by the fibroblast, which does not resorb bone, is also diminished by EHDP, Cl2MDP and APD except when co-cultured with bisphosphonate-binding bone particles. Thus, the resorption-antagonizing capacities of EHDP, Cl2MDP and APD reflect metabolic inhibition, with selectivity for the osteoclast resulting from high affinity binding to bone mineral.

                Author and article information

                Journal
                Indian J Nephrol
                Indian J Nephrol
                IJN
                Indian Journal of Nephrology
                Medknow Publications & Media Pvt Ltd (India )
                0971-4065
                1998-3662
                Nov-Dec 2015
                : 25
                : 6
                : 377-379
                Affiliations
                [1]Department of Nephrology, Global Hospital, Mumbai, Maharashtra, India
                [1 ]Department of Surgery, Global Hospital, Mumbai, Maharashtra, India
                Author notes
                Address for correspondence: Dr. Bharat Shah, Institute of Renal Sciences, Global Hospital, Mumbai, Maharashtra, India. E-mail: dr_bharatvshah@ 123456yahoo.co.in
                Article
                IJN-25-377
                10.4103/0971-4065.157427
                4663778
                26664216
                fa086537-de6c-48b5-84d1-4c04de97d458
                Copyright: © Indian Journal of Nephrology

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

                History
                Categories
                Case Report

                Nephrology
                hypercalcemia,hypervitaminosis d,parathyroid adenoma,primary hyperparathyroidism
                Nephrology
                hypercalcemia, hypervitaminosis d, parathyroid adenoma, primary hyperparathyroidism

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