A final investigation based on biochemical screening, Wermers RA, Kearns AE, Jenkins GD, Melton LJ., 3rd, Incidence and clinical spectrum of thiazide-associated hypercalcemia, Rocca WA, Yawn BP, St Sauver JL, Grossardt BR, Melton LJ., 3rd, History of the Rochester Epidemiology Project: half a century of medical records linkage in a US population. The causes of hypercalcemia can be divided into seven categories: hyperparathyroidism, vitamin D-related causes, malignancy, medications, other endocrine disorders, genetic disorders, and miscellaneous causes (Table 3). IMS Institute for Healthcare Informatics. Thirty seven subjects (51%) continued the thiazide and did not have parathyroid surgery (2 subjects had parathyroid surgery without stopping the thiazide). Federal government websites often end in .gov or .mil. Overall, 221 Olmsted County residents were identified with thiazide-associated hypercalcemia an average of 5.2 years after initiation of treatment. Bordier P, Ryckewart A, Gueris J, Rasmussen H. On the pathogenesis of so-called idiopathic hypercalciuria. Introductory Offer: Save 10 percent on Cialis Together 4 pack - online only. It is notable that all five patients who had parathyroidectomy without thiazide discontinuation in this cohort had successful surgical outcomes. Fifty-nine patients (71%) continued to have hypercalcemia despite stopping the thiazide. It is also possible that thiazides may be beneficial in PHPT patients with renal hypercalciuria, which has been associated with persistent hyperparathyroidism after parathyroidectomy and parathyroid adenomas in the context of preceding chronic secondary hyperparathyroidism (30,32). When compared to those in whom the thiazide was discontinued, the mean serum calcium and parathyroid hormone levels were lower in patients remaining on thiazides (Table 4). In a population-based descriptive study, Olmsted County, Minnesota, residents with thiazide-associated hypercalcemia were identified through the Rochester Epidemiology Project and the Mayo Clinic Laboratory Information System from 20022010 and were added to the historical cohort beginning in 1992. Poisson regression was used to compare male and female incidence rates adjusted for age. Clinical features of thiazide-associated hypercalcemia were similar to those seen in primary hyperparathyroidism. Hydrochlorothiazide is the most commonly prescribed antihypertensive medication worldwide, with over 50 million dispensed prescriptions for monotherapy in the United States alone in 2013 (2). Serum calcium prior to thiazide use, mg/dL, Maximum serum calcium on thiazides, mg/dL, Years from thiazide start to hypercalcemia. Turnbull BW. Jorgensen FS, Transbol I. Brickman AS, Massry SG, Colburn JW. Parathyroidectomy is not beneficial in patients with FHH. Thus, in vitamin D-mediated hypercalcemia, serum phosphate levels tend to be high. Mayo Clinic records contain details of every inpatient hospitalization, outpatient clinic visit, emergency department and nursing home care, as well as all radiographic and pathology reports, including autopsies (12). In patients without an easily identifiable cause of hypercalcemia on thiazides and an unsuppressed parathyroid hormone level, a reasonable strategy may be to follow guidelines for asymptomatic primary hyperparathyroidism.28 Although exacerbation of hypercalcemia is a concern if thiazides are continued, it appears that thiazides do not worsen hypercalcemia in patients who develop mild primary hyperparathyroidism.29 However, there are case reports of severe hypercalcemia in patients with primary hyperparathyroidism who are started on a thiazide diuretic.30 This study did not address the issue of starting thiazides in patients with known primary hyperparathyroidism. Hence, in general, use of typical vitamin D and calcium supplements in patients who are also on thiazides does not appear to be associated with significant problems related to hypercalcemia. Most subjects with hypercalcemia on thiazides were older hypertensive women (90%) on treatment for 115 years. Patients with calcium levels greater than 14 mg per dL or symptomatic patients with calcium levels greater than 12 mg per dL (Table 5) should be immediately and aggressively treated.17 The safest and most effective treatment of hypercalcemic crisis is saline rehydration followed by furosemide (Lasix) diuresis, calcitonin, and bisphosphonates. Persistence of hypercalcemia in patients discontinuing thiazides, and similarities in the clinical spectrum, suggest that underlying primary hyperparathyroidism is common in patients who develop hypercalcemia while on thiazide diuretics. Normal serum calcium levels are 8 to 10 mg per dL (2.0 to 2.5 mmol per L, Figure 1), although the exact range can vary among laboratories. National Library of Medicine the contents by NLM or the National Institutes of Health. The site is secure. Rare cases of thiazide-associated severe hypercalcemia have been reported, but they were generally associated with other factors contributing to hypercalcemia (27). Hypercalcemia can occur in up to 30% of persons with a malignancy. However, randomized trials of continuation vs discontinuation of thiazides would be required to elucidate the best management recommendations for patients with thiazide-associated hypercalcemia. Before The most commonly available vitamin D supplements consist of 25-hydroxyvitamin D2. Thiazide therapy was discontinued in 83 patients (38%) an average of 85 months (range, 1.6 to 397 months) after thiazide initiation (Figure 2). If untreated, prolonged high phosphate and low vitamin D levels can lead to increased PTH secretion and subsequent hypercalcemia. Specific treatments for osteoporosis first became available in the mid- 1990s. The mean maximum serum calcium in this subset was 10.85 0.40 mg/dL [2.71 0.10 mmol/L]. A person viewing it online may make one printout of the material and may use that printout only for his or her personal, non-commercial reference. Hypercalcemia means you have higher-than-normal calcium in your blood. In contrast to primary hyperparathyroidism, the humoral hypercalcemia of malignancy is associated with suppressed PTH levels and normal calcitriol levels. Patients with hypercalcemia before thiazide initiation were excluded. See permissionsforcopyrightquestions and/or permission requests. Patients diagnosed with PHPT also had PTH levels 50% of normal in 90% of those in whom it was measured, compared to 77% in the overall cohort. Approved as a pharmacy medicine, Sanofi will launch Cialis Together in the second half of the year. The authors thank Mrs. Mary Roberts for assistance in preparing the manuscript. However, PTH and calcium measurement were more common in women and at older agesthe same groups at risk for osteoporosis. Low albumin levels can affect the total serum calcium level. Decreased hydrogen reabsorption. However, Christensson and colleagues reported that hypercalcemia resolved in only 5 of 20 subjects 1-3 months after thiazide discontinuation and 14 of the 15 subjects with persistent hypercalcemia had pathologically confirmed primary hyperparathyroidism.11 This is consistent with our finding that 64% of community patients identified with thiazide-associated hypercalcemia remained hypercalcemic after treatment was discontinued, suggesting another underlying cause, e.g., primary hyperparathyroidism. The serum parathyroid hormone was 2.1 pmol/L in 7 subjects (13.2 %), 2.2-5.2 pmol/L in 29 subjects (54.7%), and > 5.2 pmol/L in 17 subjects (32.1%). The relationship between thiazides and PHPT may also reflect a chance association with hypertension because both are more prevalent with older age. PTH levels can be normal or only mildly elevated despite the hypercalcemia. Although the association between thiazide use and PHPT is not entirely clear, thiazides have been implicated as a cause of parathyroid gland enlargement (18). Sensitivity of the parathyroid hormone-1,25-dihydroxyvitamin D axis to variations in calcium intake in patients with primary hyperparathyroidism. Hypercalcemia was identified a mean of 6 7 years after thiazide initiation, and the average highest serum calcium was 10.7 0.3 mg/dL with serum parathyroid hormone (obtained in 53 patients) of 4.8 2.7 pmol/L. We did not have prospective measurements of serum calcium in all patients on thiazides, and serum calcium was not measured at specific time points prior to or after thiazide initiation. We were unable to confidently assess thiazide prescriptions at our institution due to changes in the prescription ordering system during the period of interest. In suspected overdose of over-the-counter vitamin D, the level of 25-hydroxyvitamin D3 (not 1,25-dihydroxyvitamin D3) should be measured. For each potential case, the complete (inpatient and outpatient) community medical record was reviewed by one of the investigators (M.L.G.). Ninety-five percent confidence intervals (CIs) for the incidence rates were calculated under the Poisson distribution. This is important because PHPT appears to be more common among blacks compared to other races (39). Long-term discontinuation of hydrochlorothiazide may not be necessary in patients with thiazide-associated hypercalcemia. This material may not otherwise be downloaded, copied, printed, stored, transmitted or reproduced in any medium, whether now known or later invented, except as authorized in writing by the AAFP. Hypercalcemia is considered mild if the total serum calcium level is between 10.5 and 12 mg per dL (2.63 and 3 mmol per L).5 Levels higher than 14 mg per dL (3.5 mmol per L) can be life threatening. Cardiovascular effects include hypertension, vascular calcification, and a shortened QT interval on the electrocardiogram. Hypercalcemia. Parathyroid hormone is suppressed in malignancy-associated hypercalcemia and elevated in primary hyperparathyroidism. The mean time to identification of hypercalcemia after initiation of the thiazide in patients diagnosed with primary hyperparathyroidism was 7.3 years. Since there is increasing utilization of thiazides as first-line antihypertensive agents, combined with an aging population at increased risk for parathyroid disease, a further increase in the incidence of thiazide-associated hypercalcemia might be expected. HHS Vulnerability Disclosure, Help To qualify for the study, patients must have been residents of Olmsted County on the date the first elevated serum calcium was discovered. Calcitonin is a weak inhibitor of osteoclast activation and opposes the effects of PTH on the kidneys, thereby promoting calcium and phosphate excretion. We also identified all patients with primary hyperparathyroidism as described elsewhere.16 The following diagnostic rubrics were searched through 2003 (to allow patients in the process of being examined to be included on the diagnostic index): hyperparathyroidism (ICD-9 code, 252.0), parathyroid adenoma (ICD-9 code, 227.1), osteitis fibrosa cystica (ICD 9-code, 588.8), malignant hypercalcemia/ectopic hormone secretion (ICD-9 code, 259.3), and hypercalcemia not otherwise specified (ICD-9 code, 275.4). This product is available in the following dosage forms: Tablet In this study, we excluded patients who had hypercalcemia before thiazide initiation and did not address the use of thiazides in patients with preexisting hypercalcemia. Keywords: Epidemiology, Hypercalcemia, Incidence, Thiazide diuretic, Trends, Hyperparathyroidism Go to: The overall age-adjusted incidence was much higher in women (19.5 per 100 000 person-years; 95% CI, 16.722.3) than in men (3.6 per 100 000 person-years; 95% CI, 2.35.0; P < .001). Conversely, loop diuretics induce natriuresis by inhibiting the Na-K-2Cl transporter in the thick ascending limb of the loop of Henle, causing increased urinary calcium losses and increased PTH (5, 8). Abbreviation: NS, not significant. Aggressive intravenous rehydration is the mainstay of management in severe hypercalcemia, and antiresorptive agents, such as calcitonin and bisphosphonates, frequently can alleviate the clinical manifestations of hypercalcemic disorders. Most patients with thiazide-associated hypercalcemia are older (mean age, 67 years) and female (86%), which compares to 77% females and a mean age of 60 years in Rochester PHPT patients in 19982010. Rejnmark L, Vestergaard P, Heickendorff L, Andreasen F, Mosekilde L. Loop diuretics alter the diurnal rhythm of endogenous parathyroid hormone secretion. In patients diagnosed with primary hyperparathyroidism, 18 (90%) were asymptomatic. In patients who continued thiazides, the mean serum calcium level at last measurement was 10.07 0.48 mg/dL [2.51 0.12 mmol/L] an average of 4.7 3.4 years after detection of hypercalcemia, with continued hypercalcemia on the last measurement in 72 subjects (52.1%). In addition, the renal tubular Na-Cl co-transporter (NCTT) has been suggested as a link between hypertension and calcium homeostasis.24 Specifically, higher urinary calcium excretion and higher parathyroid hormone levels have been reported in patients with essential hypertension.24 Finally, thiazides might unmask mild or normocalcemic primary hyperparathyroidism.25 Conversely, thiazide use theoretically could reduce parathyroid gland stimulation through renal3-6 and intestinal8,9 mechanisms and delay the development of primary hyperparathyroidism.26. Farias ML, Delgado AG, Rosenthal D, et al. In patients with continued hypercalcemia after stopping the thiazide, 5 patients had initial normalization of their serum calcium level, followed by recurrent hypercalcemia an average of 3.1 1.2 years later. Thiazide diuretic therapy can unmask many cases of primary hyperparathyroidism. Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. The remainder is bound to albumin, globulin, and other inorganic molecules. In patients with mild hypercalcemia, adequate hydration should be encouraged and immobilization discouraged. The diagnosis often is made incidentally in asymptomatic patients. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. The mean time to identification of hypercalcemia after initiation of the thiazide in patients diagnosed with PHPT was 5.8 7.2 years. Patients with PHPT had serum calcium levels above 11 mg/dL [2.74 mmol/L] in 26% compared to 10% of all patients on thiazides without formally diagnosed PHPT (P < .001). The most common causes of hypercalcemia are primary hyper-parathyroidism and malignancy. Of the patients with primary hyperparathyroidism, 10 (50%) had pathologic confirmation, 7 (35%) had an inappropriate parathyroid hormone in the setting of hypercalcemia, and 3 (15%) had persistent hypercalcemia for a year or more after stopping the thiazide. Coe FL, Canterbury J, Reiss E. Hyperparathyroidism in idiopathic hypercalciuria: primary or secondary? government site. Data are expressed as mean SD or number (percentage). If diuretics aren't enough to lower your blood pressure, your doctor might add other blood pressure medications to your treatment plan. Objective: To update the incidence of thiazide-associated hypercalcemia and clarify its clinical features. The incidence of thiazide-associated hypercalcemia increased after 1997, with an incidence of 19.3 and 19.7 per 100 000 person-years in 1998 and 1999, respectively, and a subsequent peak incidence in 2006 of 20.4 per 100 000 person-years (Figure 1). Only 10% of the patients had maximal serum calcium levels >11 mg/dL [2.74 mmol/L], and no hypercalcemia emergencies were seen. 19.79. The principal challenges in the management of hypercalcemia are distinguishing primary hyperparathyroidism from conditions that will not respond to parathyroidectomy and knowing when it is appropriate to refer the patient for surgery. The incidence of thiazide-associated hypercalcemia increased after 1996, with a peak incidence of 16.3 (95% CI, 8.3-24.3) per 100,000 in 1998 (Table 2). A potential concern is vitamin D and calcium supplementation in thiazide-treated patients, which could be associated with increased hypercalcemia via increased intestinal absorption of calcium. 8600 Rockville Pike Guidelines for the management of asymptomatic primary hyperparathyroidism: summary statement from the Fourth International Workshop, Familial primary hyperparathyroidism (including MEN, FHH, and HPT-JT), Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism. As a service to our customers we are providing this early version of the manuscript. The only available data are from the early 1970s in Sweden where, in a health screen, 1034 of 15,903 persons between 20 and 63 years of age (66% women) were on thiazides; among the thiazide-treated subjects, 20 (1.9%) were found to have hypercalcemia.11 The prevalence of hypercalcemia in this group was greater than that in the entire population (0.6%). ); and Divisions of Biomedical Statistics and Informatics (E.R., P.T., M.A.H.) How these effects occur is related to the mechanisms of sodium, chloride, and calcium transport in the different diuretic-sensitive segments. Mayo Clinic records contain the details of every inpatient hospitalization at its two hospitals, every outpatient office or clinic visit, all emergency room and nursing home care, as well as all laboratory, radiographic and pathology reports, including autopsies. Copyright 2023 American Academy of Family Physicians. Wermers RA, Khosla S, Atkinson EJ, et al. 1 Mean 24-hour plasma calcium concentrations are increased with thiazide use, but mean 24-hour plasma parathyroid hormone levels remain unchanged in subjects with normal baseline parathyroid hormone levels and no evidence of hypercalciuria. Consultation with an endocrinologist is recommended. Patients with thiazide-associated hypercalcemia who were subsequently diagnosed with PHPT had higher maximum serum calcium levels (10.9 mg/dL [2.72 mmol/L]) compared to the overall cohort (10.7 mg/dL [2.67 mmol/L]). Tohme JF, Bilezikian JP, Clemens TL, Silverberg SJ, Shane E, Lindsay R. Suppression of parathyroid hormone secretion with oral calcium in normal subjects and patients with primary hyperparathyroidism, Incidence and prevalence of primary hyperparathyroidism in a racially mixed population, The Journal of Clinical Endocrinology and Metabolism, http://www.imshealth.com/deployedfiles/imshealth/Global/Content/Corporate/IMS%20Health%20Institute/Reports/Secure/IIHI_US_Use_of_Meds_for_2013.pdf, Serum calcium before thiazide use, mmol/L, Maximum serum calcium on thiazides, mg/dL, Maximum serum calcium on thiazide, mmol/L, Years from thiazide start to hypercalcemia, Maximum serum calcium on thiazides, mmol/L. Increased bone resorption, increased gastrointestinal absorption of calcium, and decreased renal excretion of calcium cause hypercalcemia. Serum parathyroid hormone levels were elevated in 34% of patients and were in the upper half of the normal range in 43%. A reduction in urine calcium excretion is the most likely explanation,3-6 but a metabolic alkalosis associated with diuretic use could also cause an elevation in total serum calcium through a pH-dependent increase in protein-bound calcium. Federal government websites often end in .gov or .mil. A comparable prospective study to identify thiazide-associated hypercalcemia would require an estimated 3600 study subjects followed for at least 6 years. Thiazides are first-line treatment in essential hypertension and reduce mortality and cardiovascular events (1, 3). This constellation of symptoms has led to the mnemonic Stones, bones, abdominal moans, and psychic groans, which is used to recall the signs and symptoms of hypercalcemia, particularly as a result of primary hyperparathyroidism. Six patients receiving thiazide diuretics were referred for evaluation of mild to moderate hypercalcaemia (serum calcium 2.65-2.98 mmol/l). In many patients, primary hyperparathyroidism progresses very slowly. Bilezikian JP, Brandi ML, Eastell R, et al. Thiazide-sensitive NaCl-cotransporter in the intestine: possible role of hydrochlorothiazide in the intestinal Ca2+ uptake. Familial hypocalciuric hypercalcemia16 (FHH) is an autosomal-dominant condition with virtually 100 percent penetrance. The date of diagnosis of thiazide-induced hypercalcemia was the date of the first elevated calcium level while on thiazides, consistent with prior criteria (11). Vitamin D is a steroid hormone that is obtained through. Also, we did not have routine measurements of serum albumin or a formal assessment of dietary calcium and vitamin D intake, all of which may influence serum calcium measurements. This information was supplemented by that available from other providers for local residents, most notably the Olmsted Medical Center (13). None of the patients with a suppressed parathyroid hormone level had an identifiable secondary cause of their hypercalcemia and the onset of hypercalcemia in all of these patients was more than 1 year after thiazide initiation. The subsequent incidence of thiazide-associated hypercalcemia remained above 19921997 rates despite a decline after 2006. Objective: To update the incidence of thiazide-associated hypercalcemia and clarify its clinical features. The UK is the first country to allow OTC access to Sanofi's tadalafil-based erectile dysfunction drug Cialis following a successful switch. Arnold A, Brown MF, Urena P, Gaz RD, Sarfati E, Drueke TB. Patients without a serum parathyroid hormone measurement had less severe hypercalcemia (10.46 0.19), but were otherwise similar to the overall cohort. An official website of the United States government. The two patients with symptomatic disease had kidney stones. Age-adjusted (to 2010 U.S. whites) incidence (per 100 000 person-years) of thiazide-associated hypercalcemia among Olmsted County, Minnesota, women (solid line) and men (dashed line), 19922010. Inclusion in an NLM database does not imply endorsement of, or agreement with, We identified 221 Olmsted County residents with thiazide-associated hypercalcemia (191 women, 30 men) during the 19-year study period, 19922010. The typical patients were women with mild, uncomplicated, and non-progressive hypercalcemia that was discovered approximately 6 years after thiazide initiation. Persistence of hypercalcemia in patients discontinuing thiazides, and similarities in the clinical spectrum, suggest that underlying primary hyperparathyroidism is common in patients who develop hypercalcemia while on thiazide diuretics. PTH causes phosphate loss through the kidneys. National Library of Medicine Some examples include diuretics (water pills), lithium, and phenytoin (Dilantan). Thiazide diuretics, the antihypertensive agent prescribed most frequently worldwide, are commonly associated with hypercalcemia. Chronic renal failure generally causes hypocalcemia. A randomized-controlled study on the effects of loop- and thiazide-diuretics on the diurnal rhythms of calcitropic hormones and biochemical bone markers in postmenopausal women, Hypercalcemia and primary hyperparathyroidism. There was an increase in the incidence of thiazide-associated hypercalcemia that began in 1998, peaked in 2006, and subsequently declined thereafter. If you have abnormal calcium levels, there are ways to fix these imbalances. Most subjects were treated with thiazides for hypertension (94%). Twenty one patients (64%) continued to have hypercalcemia despite stopping the thiazide, 18 of whom were formally diagnosed with primary hyperparathyroidism (39.7 % [95% CI, 19.2-55.2%] within 1 year, 48.3% [95% CI, 25.8-68.4%] within 3 years, and 65.5% [95% CI, 32.5-83.7%] within 5 years since discontinuation) (Figure 2). Thus, in patients with PTH-mediated hypercalcemia, serum phosphate levels tend to be low. Prior to initiation of thiazides, the mean serum calcium was 9.7 0.4 mg/dL as measured in 57 subjects. Indirect effects viacalcitriol from 1-hydroxylation, Osteitis fibrosa cystica in hyperparathyroidism (subperiosteal resorption, bone cysts), Shortened QT interval on electrocardiogram, Sporadic, familial, associated with multiple endocrine neoplasia I or II, Associated with chronic renal failure or vitamin D deficiency, Granulomatous disease sarcoidosis, berylliosis, tuberculosis, Humoral hypercalcemia of malignancy* (mediated by PTHrP), Solid tumors, especially lung, head, and neck squamous cancers, renal cell tumors, Local osteolysis* (mediated by cytokines) multiple myeloma, breast cancer, Milk-alkali syndrome (from calcium antacids), Vitamin A intoxication (including analogs used to treat acne), Familial hypocalciuric hypercalcemia: mutated calcium-sensing receptor, Immobilization, with high bone turnover (e.g., Paget's disease, bedridden child), Serum total calcium level > 12 mg per dL (3 mmol per L) at any time, Hyperparathyroid crisis (discrete episode of life-threatening hypercalcemia), Marked hypercalciuria (urinary calcium excretion more than 400 mg per day), Reduced cortical bone density (measure with dual x-ray absorptiometry or similar technique), Bone mass more than two standard deviations below age-matched controls (Z score less than 2), Proximal muscle weakness and atrophy, hyperreflexia, and gait disturbance, Normal saline 2 to 4 L IV daily for 1 to 3 days, May exacerbate heart failure in elderly patients, Furosemide (Lasix) 10 to 20 mg IV as necessary, Inhibits calcium resorption in the distal renal tubule, Inhibits osteoclast action and bone resorption, Calcitonin (Calcimar or Miacalcin) 4 to 8 IU per kg IM or SQ every 6 hours for 24 hours, Initial treatment (after rehydration) in severe/Ca, Inhibits vitamin D conversion to calcitriol, Vitamin D intoxication, hematologic malignancies, granulomatous disease, Plicamycin (Mithracin), 25 mcg per kg per day IV over 6 hours for 3 to 8 doses, Gallium nitrate (Ganite) 100 to 200 mg per m. 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