| Literature DB >> 30449544 |
Janet Y Lee1, Dolores M Shoback2.
Abstract
Familial hypocalciuric hypercalcemia (FHH) causes hypercalcemia by three genetic mechanisms: inactivating mutations in the calcium-sensing receptor, the G-protein subunit α11, or adaptor-related protein complex 2, sigma 1 subunit. While hypercalcemia in other conditions causes significant morbidity and mortality, FHH generally follows a benign course. Failure to diagnose FHH can result in unwarranted treatment or surgery for the mistaken diagnosis of primary hyperparathyroidism (PHPT), given the significant overlap of biochemical features. Determinations of urinary calcium excretion greatly aid in distinguishing PHPT from FHH, but overlap still exists in certain cases. It is important that 24-h urine calcium and creatinine be included in the initial workup of hypercalcemia. FHH should be considered if low or even low normal urinary calcium levels are found in what is typically an asymptomatic hypercalcemic patient. The calcimimetic cinacalcet has been used to treat hypercalcemia in certain symptomatic causes of FHH.Entities:
Keywords: Ca-sensing receptor; familial hypocalciuric hypercalcemia; hyperparathyroidism
Mesh:
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Year: 2018 PMID: 30449544 PMCID: PMC6767927 DOI: 10.1016/j.beem.2018.05.004
Source DB: PubMed Journal: Best Pract Res Clin Endocrinol Metab ISSN: 1521-690X Impact factor: 4.690