{ "schemaVersion": 2, "eyebrow": "Endocrinology", "title": "Hypoparathyroidism", "summary": "Confirm true hypocalcemia with an inappropriately low PTH, correct reversible magnesium or vitamin D abnormalities, stabilize symptomatic patients promptly, and manage chronic disease to control symptoms without creating hypercalciuria, renal injury, or calcium-phosphate complications.", "seoDescription": "Physician guide to diagnosing and managing hypoparathyroidism, including acute hypocalcemia, etiologic testing, chronic targets, renal monitoring, and PTH replacement.", "clinicalQuestion": "How should physicians confirm, stabilize, treat, and monitor acute and chronic hypoparathyroidism?", "specialty": "Endocrinology", "audience": "U.S. physicians and medical trainees", "tags": [ "hypoparathyroidism", "hypocalcemia", "postsurgical hypoparathyroidism", "calcitriol", "PTH replacement", "hypercalciuria", "pseudohypoparathyroidism" ], "keyTakeaways": [ "Diagnose hypoparathyroidism only when low ionized or albumin-corrected calcium occurs with a low or inappropriately normal intact PTH; measure magnesium and 25-hydroxyvitamin D concurrently to identify reversible functional suppression or competing causes. [2][13][16]", "Treat symptomatic hypocalcemia or profound asymptomatic hypocalcemia with corrected calcium below 1.9 mmol/L using prompt intravenous calcium, then transition to oral calcium plus an activated vitamin D metabolite. [16]", "For chronic disease, titrate calcium and active vitamin D to a low-normal or just-below-normal serum calcium target rather than high-normal calcium, which increases hypercalciuria and renal risk. [18][19][20]", "An elevated PTH with hypocalcemia and hyperphosphatemia is PTH resistance, not gland failure; exclude renal insufficiency and hypomagnesemia and pursue molecular or epigenetic evaluation when pseudohypoparathyroidism is suspected. [13][14]", "Monitor serum calcium, phosphate, magnesium, renal function, and urinary calcium; add sodium restriction and a thiazide-type diuretic when hypercalciuria persists during conventional treatment. [17][18][20]", "Reserve PTH replacement for chronic patients not adequately controlled with calcium and active vitamin D; historical rhPTH(1-84) labeling restricted use to patients inadequately controlled on conventional therapy and cautioned against osteosarcoma-risk settings. [1][11]" ], "sections": [ { "id": "confirm-and-triage", "eyebrow": "Initial decision", "heading": "Confirm the biochemical diagnosis and identify patients needing urgent calcium", "intro": "Separate true PTH deficiency from functional suppression, PTH resistance, and non-PTH-mediated hypocalcemia before labeling chronic disease.", "paragraphs": [ "Obtain ionized calcium or albumin-corrected total calcium and intact PTH together. Hypoparathyroidism requires hypocalcemia with a low or inappropriately normal PTH; hyperphosphatemia supports the diagnosis but is not sufficient alone. Order serum phosphate, magnesium, creatinine or estimated GFR, and 25-hydroxyvitamin D at the same evaluation. [2][13][16]", "Treat neuromuscular irritability, seizures, or other symptomatic hypocalcemia promptly with calcium replacement under careful monitoring; use intravenous calcium for symptomatic disease or profound asymptomatic hypocalcemia with corrected calcium below 1.9 mmol/L, then establish oral calcium and activated vitamin D therapy. Replace magnesium when low because normal magnesium is required for normal PTH secretion. [2][16][17]", "Obtain an ECG when clinically significant hypocalcemia is suspected or symptoms are severe; hypocalcemia can prolong the QT interval. Do not delay calcium replacement for completion of etiologic testing in a symptomatic patient. [8]" ], "bullets": [ "Low calcium plus low or inappropriately normal PTH: proceed as hypoparathyroidism after assessing magnesium, vitamin D status, renal function, and cause. [2][13][16]", "Low calcium plus elevated PTH: evaluate for PTH resistance, vitamin D deficiency, chronic kidney disease, or other secondary hyperparathyroid states rather than primary hypoparathyroidism. [13][14][15][16]", "Low magnesium: correct magnesium and reassess calcium and PTH before diagnosing irreversible parathyroid failure. [2][16][17]" ], "subsections": [], "table": { "caption": "Biochemical patterns that redirect the hypocalcemia workup. [2][13][14][15][16]", "columns": [ "Calcium/PTH pattern", "Key accompanying findings", "Interpretation and next action" ], "rows": [ [ "Low calcium; low or inappropriately normal PTH", "Often high phosphate; assess magnesium, 25-hydroxyvitamin D, and renal function. [2][13][16]", "Hypoparathyroidism or functional PTH suppression; correct hypomagnesemia and define surgical versus nonsurgical etiology. [2][16][17]" ], [ "Low calcium; elevated PTH", "Hyperphosphatemia with normal renal function and normal 25-hydroxyvitamin D supports PTH resistance. [13][14]", "Suspect pseudohypoparathyroidism; exclude renal insufficiency and hypomagnesemia, assess phenotype and family history, and obtain targeted molecular or epigenetic testing. [13][14]" ], [ "Low 25-hydroxyvitamin D with low calcium", "Vitamin D deficiency classically produces an elevated PTH and subsequently low phosphorus from PTH-mediated phosphaturia. [15]", "Treat vitamin D inadequacy and avoid misclassifying secondary hyperparathyroidism as PTH resistance or gland failure. [15]" ] ] } }, { "id": "define-etiology", "eyebrow": "Etiologic branch", "heading": "Distinguish postsurgical disease from nonsurgical hypoparathyroidism", "intro": "The operative history usually determines the first etiologic branch; absent that history, prioritize autoimmune, genetic, infiltrative, and magnesium-related causes.", "paragraphs": [ "Prior anterior neck surgery is the dominant clinical clue: approximately 75% of hypoparathyroidism is postsurgical, whereas about 25% is nonsurgical. Document the procedure, timing, prior calcium and PTH results, and ongoing requirement for calcium or activated vitamin D. [18]", "Persistent low intact PTH with hypocalcemia requiring treatment for at least 6 months after surgery is commonly considered permanent postsurgical hypoparathyroidism, although some guidelines use 12 months. Continue reassessment during this interval rather than assuming permanent loss immediately after surgery. [2][3]", "In patients without anterior neck surgery, elicit personal and family history of autoimmune disease, congenital syndromic features, childhood onset, or affected relatives. Autoimmune disease and genetic mutations are prominent nonsurgical causes; genetic testing is advised for an unknown cause, especially in patients younger than 40 years with syndromic features. [7][11][16]" ], "bullets": [ "Review medications and clinical circumstances associated with hypomagnesemia or hypermagnesemia because either can impair PTH secretion. [16]", "Consider autoimmune hypoparathyroidism when no surgical explanation exists; AIRE-related failure of central tolerance is implicated in autoimmune disease. [13]", "For suspected infiltrative or destructive disease, direct further evaluation to the clinical context rather than using routine imaging as a diagnostic substitute for the calcium-PTH pattern. [16]" ], "subsections": [ { "heading": "When elevated PTH changes the diagnosis", "paragraphs": [ "Pseudohypoparathyroidism is characterized by end-organ PTH resistance: hypocalcemia, hyperphosphatemia, and elevated PTH despite normal renal function. The phenotype of Albright hereditary osteodystrophy—short stature, brachydactyly, subcutaneous calcifications, growth impairment, and obesity—supports a GNAS-related disorder, but phenotype may be variable. [13][14]" ], "bullets": [ "Check calcium, phosphate, PTH, and 25-hydroxyvitamin D together; rule out renal insufficiency and hypomagnesemia before assigning a diagnosis of PTH resistance. [14]", "A synthetic PTH challenge (Ellsworth-Howard test) can be performed but is not required for diagnosis; molecular and epigenetic testing provides diagnostic refinement. [8][14]", "In PHP1, monitor PTH, calcium, phosphate, TSH, and urine calcium-to-creatinine ratio annually. [14]" ] } ], "table": { "caption": "Etiologic clues that determine the next diagnostic action. [2][7][11][13][14][16][18]", "columns": [ "Clinical setting", "Most informative discriminator", "Next action" ], "rows": [ [ "After thyroid, parathyroid, or other anterior neck surgery", "Low or inappropriately normal PTH with hypocalcemia; establish duration of treatment dependence. [2][18]", "Manage as postsurgical disease; reassess recovery before designating permanence, recognizing 6- and 12-month definitions are both used. [2][3]" ], [ "No surgical history; early onset, family history, or syndromic findings", "Unknown etiology, especially age younger than 40 years with syndromic features. [11]", "Obtain genetic testing and assess for associated genetic disease. [7][11]" ], [ "Hypocalcemia with high PTH and high phosphate", "Normal renal function and normal 25-hydroxyvitamin D increase suspicion for PTH resistance. [13][14]", "Evaluate for pseudohypoparathyroidism and obtain targeted molecular or epigenetic testing. [14]" ], [ "Hypocalcemia with low magnesium", "Magnesium deficiency can impair PTH secretion. [16][17]", "Replete magnesium, then reassess calcium-PTH physiology before assigning chronic gland failure. [2][17]" ] ] } }, { "id": "chronic-conventional-treatment", "eyebrow": "Chronic management", "heading": "Use calcium and active vitamin D to control symptoms without overshooting calcium", "intro": "Conventional therapy remains first-line; dose to clinical and renal safety targets rather than to a high-normal serum calcium value.", "paragraphs": [ "Use oral calcium supplementation plus an activated vitamin D analogue as first-line chronic therapy. The treatment target is serum calcium in the low-normal range or just below the laboratory reference range, with normalization of serum phosphate, magnesium, and urine calcium when achievable. [11][18][20]", "Select calcium formulation according to absorption conditions: calcium carbonate should be taken with food and requires an acidic gastric environment, whereas calcium citrate is absorbed without gastric acid and is preferred when gastric acid secretion is low. Correct low magnesium concurrently. [17]", "Avoid pursuing upper-normal calcium solely to normalize the laboratory value. Serum calcium in the upper normal range increases hypercalciuria in the absence of PTH-mediated renal calcium reabsorption and can promote nephrolithiasis, nephrocalcinosis, and renal damage. [19][20]" ], "bullets": [ "Assess symptoms together with calcium values: some patients remain symptomatic at low-normal calcium, whereas others experience hypercalcemia symptoms at high-normal calcium; individualize the target while avoiding unnecessary elevation. [20]", "Follow serum phosphate and urinary calcium during conventional therapy; reducing calcium or calcitriol may be necessary when these remain elevated. [18]", "Aim to avoid a calcium-phosphorus product near or above 55 mg2/dL2 because chronically elevated phosphate with this degree of product elevation is associated with ectopic soft-tissue calcification. [19]" ], "subsections": [ { "heading": "Address hypercalciuria before accepting renal injury", "paragraphs": [ "Loss of PTH-mediated tubular calcium reabsorption predisposes treated patients to hypercalciuria. If urinary calcium remains elevated while calcium and calcitriol are required, add dietary sodium restriction and consider a thiazide-type diuretic such as hydrochlorothiazide, chlorthalidone, or indapamide. [17]" ], "bullets": [ "Obtain 24-hour urine calcium and creatinine every 6 to 12 months during chronic conventional treatment. [17]", "Monitor kidney function because impaired renal function is a common long-term complication and has been associated with disease duration and hypercalcemia during treatment. [17]" ] } ], "table": { "caption": "Chronic conventional-management targets and surveillance. [17][18][19][20]", "columns": [ "Parameter", "Practical target or interval", "Management consequence" ], "rows": [ [ "Serum calcium", "Low-normal or just below the reference range; approximately 8.0-9.0 mg/dL is a chronic hypocalcemia target described in Endotext. [18][19][20]", "Avoid high-normal calcium because it increases hypercalciuria and renal complications. [19][20]" ], [ "Serum phosphate and magnesium", "Normalize when possible; measure during conventional treatment. [18]", "Adjust calcium and active vitamin D exposure as needed and correct magnesium abnormalities. [17][18]" ], [ "Serum calcium and phosphate after a stable regimen", "Every 3-6 months. [20]", "Detect hypo- or hypercalcemia and persistent hyperphosphatemia before complications develop. [20]" ], [ "Urinary calcium excretion", "At least yearly; 24-hour urine calcium and creatinine every 6-12 months is also described. [17][20]", "If elevated, review calcium/calcitriol exposure, restrict sodium, and consider a thiazide-type diuretic. [17]" ] ] } }, { "id": "pth-replacement", "eyebrow": "Escalation", "heading": "Select PTH replacement for inadequately controlled chronic disease", "intro": "Consider replacement when conventional therapy cannot achieve biochemical control and acceptable symptom burden without excessive treatment burden or renal risk.", "paragraphs": [ "Conventional therapy is first-line, but PTH replacement is an option for adults with chronic hypoparathyroidism who remain inadequately controlled. Conventional-treatment limitations include serum calcium fluctuation, high pill burden, poor quality of life, hypercalciuria, and renal complications. [11][18]", "Historical FDA labeling for rhPTH(1-84) (NATPARA) limited use to an adjunct to calcium and vitamin D in patients who cannot be well controlled on conventional therapy. The label warned of potential osteosarcoma risk and advised avoiding use in patients with Paget disease, unexplained alkaline phosphatase elevation, open epiphyses, hereditary osteosarcoma-predisposition syndromes, or prior skeletal external-beam or implant radiation. [1]", "Palopegteriparatide is available for adults with hypoparathyroidism and has been reported to normalize serum calcium, phosphorus, and urine calcium and improve quality of life. Initiation and titration require monitoring of calcium, phosphate, urinary calcium, renal function, and concurrent calcium and active vitamin D requirements; do not use historical rhPTH(1-84) dosing data to dose another product. [11][20][21]" ], "bullets": [ "Review baseline serum calcium, phosphate, magnesium, renal function, 25-hydroxyvitamin D, and urine calcium before changing chronic therapy. [17][18][20]", "After a stable PTH-replacement regimen is reached, monitor serum calcium and phosphate every 3-6 months and urinary calcium at least yearly. [20]", "Expect both directions of calcium excursion during PTH therapy: rhPTH(1-84) trials reported hypercalcemia and hypocalcemia, supporting active titration rather than fixed-dose assumptions. [18]" ], "subsections": [], "table": { "caption": "When to remain on conventional treatment versus escalate to PTH replacement. [1][11][18][20]", "columns": [ "Clinical state", "Preferred approach", "Key safety issue" ], "rows": [ [ "Symptoms and biochemical targets controlled with tolerable oral calcium plus active vitamin D", "Continue conventional therapy with calcium, phosphate, renal, and urinary calcium surveillance. [11][18][20]", "Avoid high-normal serum calcium and detect hypercalciuria before nephrolithiasis or nephrocalcinosis occurs. [17][19]" ], [ "Persistent fluctuations, excessive pill burden, poor quality of life, hypercalciuria, or renal complications despite conventional therapy", "Consider PTH replacement in an adult with chronic hypoparathyroidism; monitor and titrate concurrent supplementation. [11][18][20]", "Monitor for hypo- and hypercalcemia during titration. [18]" ], [ "Considering historical rhPTH(1-84) in a patient with osteosarcoma-risk factors", "Avoid NATPARA in specified high-risk settings. [1]", "Risk factors include Paget disease, unexplained alkaline phosphatase elevation, open epiphyses, hereditary predisposition, and prior skeletal radiation. [1]" ] ] } }, { "id": "complication-surveillance", "eyebrow": "Long-term follow-up", "heading": "Monitor renal and calcium-phosphate complications throughout chronic disease", "intro": "Long-term follow-up should detect treatment-related renal injury and biochemical exposure before irreversible complications occur.", "paragraphs": [ "Renal complications are central to chronic management because absent PTH reduces tubular calcium reabsorption and conventional calcium-calcitriol therapy can further increase urinary calcium. Nephrolithiasis and nephrocalcinosis may occur with overtreatment; chronic kidney disease stage 3 or higher has been reported at rates 2- to 17-fold higher than in normal controls in one review. [17]", "At each maintenance review, integrate symptoms with serum calcium, phosphate, magnesium, renal function, and urinary calcium rather than adjusting therapy from serum calcium alone. High calcium-phosphorus exposure increases concern for ectopic calcification, while low calcium targets that leave ongoing symptoms justify individualized adjustment or consideration of PTH replacement. [18][19][20]", "In chronic postsurgical disease, the diagnosis itself warrants surveillance for multisystem complications. For nonsurgical and genetic disease, pair biochemical follow-up with cause-specific assessment, including thyroid testing in PHP1 because multihormone resistance can occur. [11][14]" ], "bullets": [ "Recheck serum calcium and phosphate every 3-6 months once stable; shorten the interval after a regimen change or clinically meaningful calcium excursion. [20]", "Obtain urinary calcium at least annually and more often within the 6- to 12-month interval used for 24-hour urine calcium and creatinine monitoring when hypercalciuria is a concern. [17][20]", "Escalate chronic management when serum calcium control depends on high exposure to calcium or active vitamin D, urinary calcium remains elevated, kidney function declines, or the patient remains symptomatic despite low-normal calcium. [11][17][18][20]" ], "subsections": [], "table": { "caption": "Triggers for chronic-treatment reassessment. [11][17][18][19][20]", "columns": [ "Trigger", "Likely concern", "Immediate reassessment" ], "rows": [ [ "High-normal or recurrently elevated serum calcium", "Hypercalciuria, nephrolithiasis, nephrocalcinosis, or renal injury risk. [17][19][20]", "Review calcium and active vitamin D exposure; measure urinary calcium and renal function. [17][18]" ], [ "Persistent hyperphosphatemia or calcium-phosphorus product near 55 mg2/dL2", "Risk of ectopic soft-tissue calcification. [19]", "Review calcium and active vitamin D dosing and repeat calcium-phosphate assessment. [18][19]" ], [ "Persistent symptoms at a low-normal calcium concentration", "Individual calcium sensitivity or inadequately controlled disease. [20]", "Confirm magnesium, phosphate, vitamin D status, adherence and urinary calcium; individualize target or consider escalation. [17][18][20]" ], [ "Declining renal function or recurrent stone disease", "Long-term renal complication of disease and treatment. [17]", "Quantify urinary calcium, avoid unnecessary hypercalcemia, and consider sodium restriction, thiazide therapy, or PTH-replacement evaluation. [17][18]" ] ] } } ], "faq": [], "references": [ { "number": 1, "title": "This label may not be the latest approved by FDA. For current ...", "detail": "www.accessdata.fda.gov", "url": "https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/125511s020lbl.pdf", "authors": "www.accessdata.fda.gov", "host": "www.accessdata.fda.gov" }, { "number": 2, "title": "Hypoparathyroidism - Symptoms, diagnosis and treatment | BMJ Best Practice", "detail": "bestpractice.bmj.com", "url": "https://bestpractice.bmj.com/topics/en-gb/132", "authors": "bestpractice.bmj.com", "host": "bestpractice.bmj.com" }, { "number": 3, "title": "Hypoparathyroidism - Symptoms, diagnosis and treatment | BMJ Best Practice US", "detail": "bestpractice.bmj.com", "url": "https://bestpractice.bmj.com/topics/en-gb/132?locale=ko", "authors": "bestpractice.bmj.com", "host": "bestpractice.bmj.com" }, { "number": 4, "title": "Efficacy and Safety of Parathyroid Hormone Replacement With ...", "detail": "onlinelibrary.wiley.com", "url": "https://onlinelibrary.wiley.com/doi/full/10.1002/jbmr.4726", "authors": "onlinelibrary.wiley.com", "host": "onlinelibrary.wiley.com" }, { "number": 5, "title": "Evaluation and Management of Hypoparathyroidism Summary ...", "detail": "onlinelibrary.wiley.com", "url": "https://onlinelibrary.wiley.com/doi/10.1002/jbmr.4691", "authors": "onlinelibrary.wiley.com", "host": "onlinelibrary.wiley.com" }, { "number": 6, "title": "UK national chronic hypoparathyroidism audit - 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Endocrine Society", "detail": "www.endocrine.org", "url": "https://www.endocrine.org/-/media/endocrine/files/endo-2025/agenda_parathyroid-summit_15may2025_posting.pdf", "authors": "www.endocrine.org", "host": "www.endocrine.org" }, { "number": 23, "title": "Detailed Schedule", "detail": "endo2026.endocrine.org", "url": "https://endo2026.endocrine.org/agenda.asp?startdate=6%2F14%2F2026&enddate=6%2F14%2F2026&BCFO=&pfp=FullSchedule&fa=&fb=&fc=&fd=", "authors": "endo2026.endocrine.org", "host": "endo2026.endocrine.org" }, { "number": 24, "title": "Management of Hypoparathyroidism - Khan - 2022", "detail": "onlinelibrary.wiley.com", "url": "https://onlinelibrary.wiley.com/doi/10.1002/jbmr.4716", "authors": "onlinelibrary.wiley.com", "host": "onlinelibrary.wiley.com" } ], "editorialNote": "Prepared from cited clinical literature using Astra's research workflow. Verify recommendations against current guidance and patient-specific factors.", "citations": [ { "number": 1, "title": "This label may not be the latest approved by FDA. For current ...", "detail": "www.accessdata.fda.gov", "url": "https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/125511s020lbl.pdf", "authors": "www.accessdata.fda.gov", "host": "www.accessdata.fda.gov", "snippet": "A risk to humans could not be excluded (5.1, 13.1) • Because of the potential risk of osteosarcoma, prescribe NATPARA only to patients who cannot be well-controlled on calcium and active forms of vitamin D and for whom the potential benefits are considered to outweigh the potential risk. (1, 5.1) • ", "score": 0.97089 }, { "number": 2, "title": "Hypoparathyroidism - Symptoms, diagnosis and treatment | BMJ Best Practice", "detail": "bestpractice.bmj.com", "url": "https://bestpractice.bmj.com/topics/en-gb/132", "authors": "bestpractice.bmj.com", "host": "bestpractice.bmj.com", "snippet": "Laboratory testing should confirm low ionised or albumin-corrected total calcium and low or inappropriately normal intact plasma parathyroid hormone, while also verifying normal serum magnesium and 25-hydroxyvitamin D levels.\n\nIf symptoms are present, replacement of calcium and/or magnesium should b", "score": 0.6391287 }, { "number": 3, "title": "Hypoparathyroidism - Symptoms, diagnosis and treatment | BMJ Best Practice US", "detail": "bestpractice.bmj.com", "url": "https://bestpractice.bmj.com/topics/en-gb/132?locale=ko", "authors": "bestpractice.bmj.com", "host": "bestpractice.bmj.com", "snippet": "Laboratory testing should confirm low ionized or albumin-corrected total calcium and low or inappropriately normal intact plasma parathyroid hormone, while also verifying normal serum magnesium and 25-hydroxyvitamin D levels.\n\nIf symptoms are present, replacement of calcium and/or magnesium should b", "score": 0.6326168 }, { "number": 4, "title": "Efficacy and Safety of Parathyroid Hormone Replacement With ...", "detail": "onlinelibrary.wiley.com", "url": "https://onlinelibrary.wiley.com/doi/full/10.1002/jbmr.4726", "authors": "onlinelibrary.wiley.com", "host": "onlinelibrary.wiley.com", "snippet": "Current consensus guidelines for the long-term management of chronic hypoparathyroidism have identified six therapeutic goals: (i) prevent", "score": 0.61168414 }, { "number": 5, "title": "Evaluation and Management of Hypoparathyroidism Summary ...", "detail": "onlinelibrary.wiley.com", "url": "https://onlinelibrary.wiley.com/doi/10.1002/jbmr.4691", "authors": "onlinelibrary.wiley.com", "host": "onlinelibrary.wiley.com", "snippet": "An international task force on hypoparathyroidism ... Impaired immune function in patients with chronic postsurgical hypoparathyroidism", "score": 0.56719416 }, { "number": 6, "title": "UK national chronic hypoparathyroidism audit - Wiley Online Library", "detail": "onlinelibrary.wiley.com", "url": "https://onlinelibrary.wiley.com/doi/full/10.1111/cen.14798", "authors": "onlinelibrary.wiley.com", "host": "onlinelibrary.wiley.com", "snippet": "In 2015 the European Society for Endocrinology published consensus guidelines on the management of chronic hypoparathyroidism. We set out to", "score": 0.51105833 }, { "number": 7, "title": "Management of Hypoparathyroidism - Wiley Online Library", "detail": "onlinelibrary.wiley.com", "url": "https://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjbmr.4716", "authors": "onlinelibrary.wiley.com", "host": "onlinelibrary.wiley.com", "snippet": "Approxi- mately 25% of cases are nonsurgical, most commonly due to autoimmune disease or genetic mutations. ... Two systematic reviews informed the", "score": 0.50930125 }, { "number": 8, "title": "Hypoparathyroidism - an overview | ScienceDirect Topics", "detail": "www.sciencedirect.com", "url": "https://www.sciencedirect.com/topics/medicine-and-dentistry/hypoparathyroidism", "authors": "www.sciencedirect.com", "host": "www.sciencedirect.com", "snippet": "The diagnosis should be substantiated by functional tests. The diagnosis of hypoparathyroidism is very likely if administration of intact parathyroid hormone (400 IU i.v.) yields a 5- to 10-fold increase of urinary phosphate excretion. This test is called the Ellsworth–Howard test (Ziegler, 1976; Ke", "score": 0.65412235 }, { "number": 9, "title": "Disorders of Calcium Metabolism - an overview", "detail": "www.sciencedirect.com", "url": "https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/disorders-of-calcium-metabolism", "authors": "www.sciencedirect.com", "host": "www.sciencedirect.com", "snippet": "Hypoparathyroidism is characterized by hypocalcaemia, with plasma total calcium concentrations as low as 1.25 mmol/L being found. Urine calcium excretion is subnormal and the TmP/GFR (see p. 111) is increased, leading to hyperphosphataemia. Bone turnover is reduced, as are intestinal calcium absorpt", "score": 0.6227582 }, { "number": 10, "title": "Calcium Urine Level - an overview | ScienceDirect Topics", "detail": "www.sciencedirect.com", "url": "https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/calcium-urine-level", "authors": "www.sciencedirect.com", "host": "www.sciencedirect.com", "snippet": "# Calcium Urine Level. Urine calcium levels refer to the concentration of calcium in urine, which is assessed to evaluate conditions such as kidney stones and hypercalcemia, with specific screening tests indicating hypercalciuria when certain ratios or concentrations are exceeded. ### 21Explain the ", "score": 0.61668247 }, { "number": 11, "title": "Best practice recommendations for the diagnosis and management of hypoparathyroidism - ScienceDirect", "detail": "www.sciencedirect.com", "url": "https://www.sciencedirect.com/science/article/abs/pii/S0026049525002045", "authors": "www.sciencedirect.com", "host": "www.sciencedirect.com", "snippet": "Title: Best practice recommendations for the diagnosis and management of hypoparathyroidism - ScienceDirect\n## Metabolism. # Best practice recommendations for the diagnosis and management of hypoparathyroidism. https://doi.org/10.1016/j.metabol.2025.156335Get rights and content. **HypoPT Diagnosis**", "score": 0.5852203 }, { "number": 12, "title": "Pseudohypoparathyroidism with normocalcemia: a rare case... : Annals of Medicine and Surgery", "detail": "journals.lww.com", "url": "https://journals.lww.com/annals-of-medicine-and-surgery/fulltext/2025/07000/pseudohypoparathyroidism_with_normocalcemia__a.73.aspx", "authors": "journals.lww.com", "host": "journals.lww.com", "snippet": "Title: Pseudohypoparathyroidism with normocalcemia: a rare case... : Annals of Medicine and Surgery\nPseudohypoparathyroidism (PHP), a rare genetic disorder is characterized by features of hypoparathyroidism due to tissue resistance to effect of parathyroid hormone (PTH). Lab results revealed high se", "score": 0.5021246 }, { "number": 13, "title": "Hypocalcemia: Diagnosis and Treatment - Endotext - NCBI Bookshelf", "detail": "www.ncbi.nlm.nih.gov", "url": "http://www.ncbi.nlm.nih.gov/books/NBK279022", "authors": "www.ncbi.nlm.nih.gov", "host": "www.ncbi.nlm.nih.gov", "snippet": "or affected family members. Critical initial laboratory testing involves measuring serum phosphate, magnesium, intact parathyroid hormone (PTH), 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D levels. Further evaluation is directed by the clinical and laboratory profiles that emerge. Significant fu", "score": 0.6964752 }, { "number": 14, "title": "Pseudohypoparathyroidism and Related Disorders - StatPearls - NCBI Bookshelf", "detail": "www.ncbi.nlm.nih.gov", "url": "https://www.ncbi.nlm.nih.gov/books/NBK547709", "authors": "www.ncbi.nlm.nih.gov", "host": "www.ncbi.nlm.nih.gov", "snippet": "PHP is a rare group of inactivating PTH/PTHrP signaling disorders (iPPSD) caused by genetic or epigenetic alterations of the GNAS locus, leading to end-organ resistance to parathyroid hormone with hypocalcemia, hyperphosphatemia, and elevated PTH levels. Patients may present with Albright hereditary", "score": 0.6551821 }, { "number": 15, "title": "Index of Suspicion In the Nursery | NeoReviews | American Academy of Pediatrics", "detail": "publications.aap.org", "url": "https://publications.aap.org/neoreviews/article/5/8/e356/87025/Index-of-Suspicion-In-the-Nursery", "authors": "publications.aap.org", "host": "publications.aap.org", "snippet": "Title: Index of Suspicion In the Nursery | NeoReviews | American Academy of Pediatrics\n**Neoreviews** August 2004; 5 (8): e356–e359. We agree with you that this patient definitely has vitamin D deficiency, as confirmed by the low 25OH vitamin D concentration. Classic vitamin D deficiency is characte", "score": 0.57035583 }, { "number": 16, "title": "Hypoparathyroidism - PubMed", "detail": "www.ncbi.nlm.nih.gov", "url": "http://www.ncbi.nlm.nih.gov/pubmed/22863393", "authors": "www.ncbi.nlm.nih.gov", "host": "www.ncbi.nlm.nih.gov", "snippet": "Title: Hypoparathyroidism - PubMed\nAn official website of the United States government. **The .gov means it’s official.**. Federal government websites often end in .gov or .mil. sharing sensitive information, make sure you’re on a federal. official website and that any information you provide is enc", "score": 0.53881395 }, { "number": 17, "title": "Review of Hypoparathyroidism", "detail": "pmc.ncbi.nlm.nih.gov", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC5237638", "authors": "pmc.ncbi.nlm.nih.gov", "host": "pmc.ncbi.nlm.nih.gov", "snippet": "elderly patients with low gastric acid secretion, calcium citrate is the preferred preparation for the management of hypocalcemia because calcium carbonate requires an acidic gastric environment for digestion and absorption, whereas calcium citrate is easily absorbed without stomach acid. Calcium ca", "score": 0.80771893 }, { "number": 18, "title": "Management of Hypoparathyroidism - PMC", "detail": "pmc.ncbi.nlm.nih.gov", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC13202617", "authors": "pmc.ncbi.nlm.nih.gov", "host": "pmc.ncbi.nlm.nih.gov", "snippet": "Hypoparathyroidism (HypoPT) is a rare disorder characterized by hypocalcemia in the presence of a low or inappropriately normal parathyroid hormone level. HypoPT is most commonly seen after neck surgery, which accounts for approximately 75% of cases, whereas approximately 25% have HypoPT due to nons", "score": 0.7474137 }, { "number": 19, "title": "Hypocalcemia - Endotext - NCBI Bookshelf", "detail": "www.ncbi.nlm.nih.gov", "url": "https://www.ncbi.nlm.nih.gov/books/NBK344077", "authors": "www.ncbi.nlm.nih.gov", "host": "www.ncbi.nlm.nih.gov", "snippet": "used are calcium carbonate and calcium citrate (Table 5). Recombinant human PTH (1-84) has been recently approved for the treatment of chronic hypoparathyroidism in adults and can reduce the amount of calcium and activated vitamin D supplements that a patient is required to take to control serum cal", "score": 0.7318455 }, { "number": 20, "title": "Management of Hypoparathyroidism: Present and Future - PMC", "detail": "pmc.ncbi.nlm.nih.gov", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC5393596", "authors": "pmc.ncbi.nlm.nih.gov", "host": "pmc.ncbi.nlm.nih.gov", "snippet": "calcium supplement use is high, should also be possible. The final dosage requirement of rhPTH (1–84) required for each patient to achieve optimized management cannot be predicted by parameters such as weight or previous amounts of calcium and active vitamin D via conventional treatment. After the i", "score": 0.7180613 }, { "number": 21, "title": "Multicenter retro-prospective observational study on chronic hypoparathyroidism and rhPTH (1–84) treatment", "detail": "pmc.ncbi.nlm.nih.gov", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC9360119", "authors": "pmc.ncbi.nlm.nih.gov", "host": "pmc.ncbi.nlm.nih.gov", "snippet": "Serum creatinine (µmol/L; n.v.: 49–90)707.953–86.6 25 oh vitamin D (ng/ml; n.v.: 30–100)29.437.6016–42 Serum magnesium (mmol/l; n.v.: 0.6–1)0.70.10.7–0.94Prescribed calcium:Frequency (%)0–2000 mg/day7/14 (50)> 2000 mg/day7/14 (50)Prescribed calcitriol:Frequency (%)≤ 0.25 μg/day0/14 (0)0.25–0.5 μg/da", "score": 0.71088976 }, { "number": 22, "title": "[PDF] Hypoparathyroidism 2025 Summit - Endocrine Society", "detail": "www.endocrine.org", "url": "https://www.endocrine.org/-/media/endocrine/files/endo-2025/agenda_parathyroid-summit_15may2025_posting.pdf", "authors": "www.endocrine.org", "host": "www.endocrine.org", "snippet": "how modification of various prodrug components support different therapeutic objectives) • Understand how Patient Centric Drug Design has been applied in the design of palopegteriparatide • Update: latest evidence of efficacy (what is the post-marketing Hypoparathyroidism 2025 Summit: Translating Sc", "score": 0.96863 }, { "number": 23, "title": "Detailed Schedule", "detail": "endo2026.endocrine.org", "url": "https://endo2026.endocrine.org/agenda.asp?startdate=6%2F14%2F2026&enddate=6%2F14%2F2026&BCFO=&pfp=FullSchedule&fa=&fb=&fc=&fd=", "authors": "endo2026.endocrine.org", "host": "endo2026.endocrine.org", "snippet": "Charting A New Course in Severe Hypertriglyceridemia Care: Optimizing Diagnosis, Therapeutic Strategies, and Pancreatitis Prevention in sHTG and FCS. Uncovering a Hidden Driver of Hypoparathyroidism: Improving ADH1 Detection and Cracking the Case With CaSR-Targeted Therapies. PL03-02 - Mechanism-Bas", "score": 0.96515 }, { "number": 24, "title": "Management of Hypoparathyroidism - Khan - 2022", "detail": "onlinelibrary.wiley.com", "url": "https://onlinelibrary.wiley.com/doi/10.1002/jbmr.4716", "authors": "onlinelibrary.wiley.com", "host": "onlinelibrary.wiley.com", "snippet": "Two systematic reviews informed the recommendations provided in this document: a survey of panel practice() and a review of randomized trials of", "score": 0.48865002 } ], "publishedAt": "2026-09-16T00:24:10.932302+00:00", "updatedAt": "2026-09-16T00:24:10.932302+00:00", "readingMinutes": 6, "slug": "hypoparathyroidism" }