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Vitamin D Hypercalcemia

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D About Taking Supplements?

Answer From Katherine Zeratsky, R.D., L.D. Vitamin D toxicity is usually caused by large doses of vitamin D supplements — not by diet or sun exposure. That’s because your body regulates the amount of vitamin D produced by sun exposure, and even fortified foods don’t contain large amounts of vitamin D.

The main consequence of vitamin D toxicity is a buildup of calcium in your blood (hypercalcemia), which can cause nausea and vomiting, weakness, and frequent urination.
Treatment includes stopping vitamin D intake and restricting dietary calcium. Your doctor might also prescribe intravenous fluids and medications, such as corticosteroids or bisphosphonates. Taking 60,000 international units (IU) a day of vitamin D for several months has been shown to cause toxicity.
Recommended Dietary Allowance (RDA) for most adults of 600 IU of vitamin D a day. Doses higher than the RDA are sometimes used to treat medical problems such as vitamin D deficiency, but these are given only under the care of a doctor for a specified time frame. Blood levels should be monitored while someone is taking high doses of vitamin D.

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As always, talk to your doctor before taking vitamin and mineral supplements.
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Of the population in association with malignancy, primary hyperparathyroidism, ingestion of excessive calcium and/or vitamin D, ectopic production of 1,25-dihydroxyvitamin D [1,25(OH) 2 D], and impaired degradation of 1,25(OH) 2 D. The ingestion of excessive amounts of vitamin D 3 (or vitamin D 2 ) results in hypercalcemia and hypercalciuria due to the formation of supraphysiological amounts of 25-hydroxyvitamin D [25(OH)D] that bind to the vitamin D receptor, albeit with lower affinity than the active form of the vitamin, 1,25(OH) 2 D, and the formation of 5,6-trans 25(OH)D, which binds to the vitamin D receptor more tightly than 25(OH)D. In patients with granulomatous disease such as sarcoidosis or tuberculosis and tumors such as lymphomas, hypercalcemia occurs as a result of the activity of ectopic 25(OH)D-1-hydroxylase (CYP27B1) expressed in macrophages or tumor cells and the formation of excessive amounts of 1,25(OH) 2 D. Recent work has identified a novel cause of non-PTH-mediated hypercalcemia that occurs when the degradation of 1,25(OH) 2 D is impaired as a result of mutations of the 1,25(OH) 2 D-24-hydroxylase cytochrome P450 (CYP24A1). Patients with biallelic and, in some instances, monoallelic mutations of the CYP24A1 gene have elevated serum calcium concentrations associated with elevated serum 1,25(OH) 2 D, suppressed PTH concentrations, hypercalciuria, nephrocalcinosis, nephrolithiasis, and on occasion, reduced bone density. Of interest, first-time calcium renal stone formers have elevated 1,25(OH) 2 D and evidence of impaired 24-hydroxylase-mediated 1,25(OH) 2 D degradation.
We will describe the biochemical processes associated with the synthesis and degradation of various vitamin D metabolites, the clinical features of the vitamin D-mediated hypercalcemia, their biochemical diagnosis, and treatmen.

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How Are Hypercalcemia And Hpt Diagnosed And Treated?

● Calcimimetics: Help control an overactive parathyroid gland. Patients who are dealing with one or more overactive parathyroid glands can undergo a minimally invasive parathyroidectomy (MIP), a surgical procedure that can typically be completed in about 20 minutes.
● High Success Rate: The success rate of an MIP generally falls between 93-95%; in contrast, the success rate of a traditional parathyroid surgery is usually between 80-85%. Dr. Larian dedicates time and resources to learn about a patient’s symptoms and find out if one or more defective parathyroid glands are present. Dr. Larian even performs a 4 gland assessment after an MIP to ensure the procedure has delivered the desired results.

Introduction

In patients with MS, low serum levels of vitamin D are associated with a higher relapse rate and an earlier development of persistent disability (6, 7). Based on this association and its assumed harmlessness, physicians frequently recommend high-dose supplementation with cholecalciferol the inactive form of vitamin D, although clear evidence for the efficacy of this interventional regimen is missing.

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