PTH blood test: what high and low parathyroid hormone means for your calcium
Parathyroid hormone (PTH) · Calcium and bone metabolism (PTH with calcium, vitamin D, phosphorus and creatinine) · reported in pg/mL (identical numerically to ng/L; SI pmol/L = pg/mL × 0.106)
Parathyroid hormone (PTH) is made by four pea-sized parathyroid glands behind the thyroid, and its only job is to keep the calcium in your blood within a narrow band. When calcium dips, PTH rises and pulls calcium from bone, tells the kidneys to keep it rather than lose it in urine, and switches on active vitamin D so the gut absorbs more. The usual test is 'intact PTH', reported in picograms per millilitre, with a normal range of about 10 to 65 pg/mL in most US laboratories, although ranges vary from 12–88 down to 15–65 depending on the assay.
A PTH level is almost never useful on its own. It is read against a calcium drawn at the same time (ideally corrected for albumin, or an ionized calcium), plus vitamin D, phosphorus, magnesium and kidney function. A high PTH with a high calcium almost always means an overactive parathyroid gland (primary hyperparathyroidism, usually a single benign adenoma). A high PTH with a low or normal calcium means the glands are working hard for a reason, most often vitamin D deficiency or chronic kidney disease. A high calcium with a low PTH means the calcium is coming from somewhere else, and cancer, excess vitamin D and certain medicines move to the top of the list.
Primary hyperparathyroidism is common and quietly underdiagnosed. It affects roughly 1 in 100 adults and 1 to 3 in 100 postmenopausal women, and most people are picked up by a mildly high calcium on a routine panel rather than by symptoms. Over years it thins bone and raises the risk of kidney stones, which is why a high PTH with a calcium even slightly above the normal range is worth a proper work-up rather than a shrug.
PTH at a glance
- What it is: the hormone that raises blood calcium by acting on bone, kidney and (through vitamin D) the gut; the 'intact PTH' assay is standard.
- Normal: about 10–65 pg/mL in most US labs (some quote 15–65 or 12–88). Labs differ; use your report's range.
- High PTH + high calcium: primary hyperparathyroidism until proven otherwise (a single benign adenoma in about 85 percent of cases).
- High PTH + low or normal calcium: secondary hyperparathyroidism, most often from vitamin D deficiency, chronic kidney disease or poor calcium absorption.
- Low PTH + high calcium: the parathyroids are correctly switched off and the calcium has another source (cancer, vitamin D excess, sarcoidosis, thiazides). Low PTH + low calcium: hypoparathyroidism, usually after neck surgery or from very low magnesium.
- Next step: repeat calcium with albumin or ionized calcium, 25-hydroxyvitamin D, phosphorus, magnesium, creatinine/eGFR and a 24-hour urine calcium; bone density if hyperparathyroidism is confirmed.
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What PTH measures
PTH is an 84-amino-acid peptide. The second-generation 'intact PTH' immunoassay used by most labs sandwiches the hormone between two antibodies and reports the whole molecule, although it also picks up a large inactive fragment (PTH 7–84) that accumulates when the kidneys fail; third-generation 'whole' or 'bio-intact' assays detect only the full 1–84 hormone and read about half as high in dialysis patients. Results from different assays are therefore not interchangeable, and a person being followed over time should stick with one lab.
The glands respond to calcium within seconds through a calcium-sensing receptor on their surface: a fall of a few tenths of a milligram per decilitre doubles PTH release, and a rise shuts it down. PTH then acts on bone to release calcium and phosphate, on the kidney to reclaim calcium and dump phosphate, and on the kidney enzyme that converts vitamin D into its active form. The net effect is higher calcium and lower phosphate, which is why a high PTH with a low phosphorus is a classic parathyroid pattern.
PTH has a daily rhythm, highest in the early hours and lowest in the late morning, and it rises with a low-calcium meal and falls after a calcium-rich one, so a morning fasting sample is preferred and compared like with like. It is stable in an EDTA (lavender-top) tube for about a day at room temperature. Biotin supplements interfere with some assays, and lithium and loop diuretics raise PTH, while thiazides and calcium-rich antacids lower it.
Normal range for PTH
Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.
| Group | Typical range (pg/mL (identical numerically to ng/L; SI pmol/L = pg/mL × 0.106)) | Notes |
|---|---|---|
| Adults, intact PTH | About 10–65 pg/mL | Most US labs; some quote 15–65, 14–72 or 12–88 pg/mL. Always interpret with a simultaneous calcium. Labs differ; use the interval on your report. |
| Primary hyperparathyroidism | Above the upper limit, or 'inappropriately normal' (typically above 20–25 pg/mL) with a high calcium | About one in five people with a parathyroid adenoma have a PTH inside the normal range; it is abnormal because a high calcium should push PTH below about 20. |
| Secondary hyperparathyroidism (vitamin D deficiency) | Mildly to moderately high, often 65–150 pg/mL | PTH starts climbing once 25-hydroxyvitamin D falls below about 20–30 ng/mL, particularly when calcium intake is under 800 mg a day. Calcium is normal or low-normal. |
| Chronic kidney disease, stages 3–5 (not on dialysis) | Progressively higher as eGFR falls | No fixed target; a steadily rising PTH prompts a look at phosphorus, calcium and vitamin D. The intact assay over-reads in kidney failure because inactive fragments pile up. |
| Dialysis patients | Target about 2–9 times the upper limit (roughly 130–600 pg/mL on an assay with a 65 pg/mL upper limit) | KDIGO 2017 guidance; values far above this suggest tertiary hyperparathyroidism and risk of bone disease and calcification. |
| Hypercalcemia from a non-parathyroid cause | Suppressed, usually below 20 pg/mL | Cancer (PTH-related peptide), vitamin D excess, granulomatous disease, hyperthyroidism, immobilisation, thiazides, milk-alkali syndrome. |
| Hypoparathyroidism | Low or undetectable, or 'inappropriately normal' with a low calcium | A calcium under 8.5 mg/dL should drive PTH well above the normal range; a normal PTH in that setting is a failing gland. |
| Familial hypocalciuric hypercalcemia (FHH) | Normal or mildly high, with a high calcium and very low urine calcium | An inherited, harmless mimic of hyperparathyroidism; a 24-hour urine calcium-to-creatinine clearance ratio under 0.01 and family history point to it, and surgery is not helpful. |
| Children and pregnancy | Similar to adults; falls modestly in pregnancy | Pregnancy and breastfeeding use PTH-related peptide from the placenta and breast rather than PTH, so PTH is often low-normal. |
High PTH
A high PTH means the parathyroid glands are releasing more hormone than usual, and the calcium level says why. If calcium is high (above the lab's upper limit, usually 10.2 to 10.5 mg/dL) or even high-normal, the glands are overactive in their own right: primary hyperparathyroidism. About 85 percent of cases are a single benign adenoma, 10 to 15 percent are enlargement of all four glands, and under 1 percent are parathyroid cancer, which is suspected when calcium is very high (often above 14 mg/dL) and PTH is several times normal. The extra calcium comes largely from bone, so bone density falls, particularly at the wrist and hip, and the kidneys filter more calcium, so stones become more likely. Many people have no symptoms; others have fatigue, low mood, poor concentration, constipation, thirst, bone or joint aches and, over years, fractures.
If calcium is low or normal, the glands are responding appropriately to something that is pulling calcium down, which is called secondary hyperparathyroidism. In outpatients the usual reason is vitamin D deficiency: without enough 25-hydroxyvitamin D the gut absorbs less calcium, and PTH rises to hold the blood level steady, often to 65 to 150 pg/mL. The other large group is chronic kidney disease, where the failing kidney retains phosphate, makes less active vitamin D and lets calcium slip, and PTH climbs steadily from about stage 3 onward. Low calcium intake, malabsorption from celiac disease or bariatric surgery, loop diuretics, lithium and bone-building drugs such as denosumab or bisphosphonates (which briefly lower calcium) all do the same.
When PTH is high and calcium is normal after vitamin D has been replaced and kidney function, magnesium and medicines have been accounted for, the label is normocalcemic primary hyperparathyroidism, which is increasingly recognized in people being investigated for osteoporosis or stones and is watched or treated on the same principles. Rarely, a high PTH with a low calcium and high phosphate reflects PTH resistance (pseudohypoparathyroidism), where the glands are shouting but the body cannot hear them.
Common causes
Primary hyperparathyroidism (parathyroid adenoma)
A benign tumor in one gland keeps secreting PTH regardless of the calcium level. Calcium is high or high-normal, phosphorus is low-normal, and 24-hour urine calcium is often above 250 to 400 mg. Women over 50 are affected three times as often as men. A sestamibi scan or neck ultrasound locates the gland once the biochemistry is clear.
Vitamin D deficiency
The commonest cause of a high PTH with a normal calcium. PTH rises as 25-hydroxyvitamin D falls below about 20 to 30 ng/mL and comes back down within two to three months of repletion; in one large study, PTH was about 20 to 30 percent higher in adults with low vitamin D and low calcium intake than in those replete in both.
Chronic kidney disease
Phosphate retention, loss of active vitamin D and rising FGF23 all stimulate the glands from about eGFR 60 downward. Over years the glands can enlarge and become autonomous (tertiary hyperparathyroidism), with calcium climbing above normal.
Low calcium intake or poor absorption
Diets under about 600 to 800 mg of calcium a day, celiac disease, Crohn's disease, gastric bypass, chronic pancreatitis and long-term proton-pump inhibitors reduce absorbed calcium and nudge PTH upward.
Medicines: lithium, loop diuretics, denosumab, bisphosphonates
Lithium resets the glands' calcium set-point and causes hyperparathyroidism in a meaningful minority of long-term users; furosemide wastes calcium in urine; bone-resorption inhibitors lower calcium transiently and PTH responds.
Parathyroid hyperplasia and inherited syndromes
Enlargement of all four glands occurs in multiple endocrine neoplasia types 1 and 2A and in familial isolated hyperparathyroidism; a parathyroid problem under age 40, or with pituitary or pancreatic tumors in the family, prompts genetic assessment.
Familial hypocalciuric hypercalcemia
A mutation in the calcium-sensing receptor makes the glands and kidney 'think' calcium is low. PTH is normal or mildly high, calcium is mildly high from childhood, urine calcium is very low, and no treatment is needed; mistaking it for an adenoma leads to futile surgery.
Pseudohypoparathyroidism
Inherited resistance to PTH: the hormone is high but calcium is low and phosphate high, sometimes with short stature and short fourth fingers. Diagnosed in childhood or early adulthood.
Parathyroid carcinoma
Rare (under 1 percent of primary hyperparathyroidism). Suspected with calcium above 14 mg/dL, PTH more than three to five times normal, a palpable neck mass or hoarseness.
Symptoms that can go with it
- Often none; most primary hyperparathyroidism is found on a routine calcium
- Fatigue, low mood, anxiety, poor memory or 'brain fog'
- Thirst, passing more urine, constipation, nausea or loss of appetite (features of high calcium)
- Bone or joint pain, loss of height, or a fracture from a minor fall; low bone density on a DEXA scan
- Kidney stones, or blood in the urine from a passing stone
- Muscle weakness, particularly climbing stairs
- In chronic kidney disease: bone pain, itching and, with very high levels, calcium deposits in soft tissues and blood vessels
- Tingling, cramps or twitching when the high PTH is a response to low calcium (vitamin D deficiency, malabsorption)
Low PTH
A low PTH with a high calcium is the parathyroid glands doing exactly what they should: calcium is high for another reason and they have shut down, usually to under 20 pg/mL. That other reason needs finding. In hospital the commonest is cancer, either from a bone-dissolving spread of breast, lung, kidney or myeloma, or from a tumor (most often squamous lung, kidney, bladder, head and neck) secreting PTH-related peptide, which behaves like PTH but is not picked up by the PTH assay. In outpatients, more benign explanations are usual: too much vitamin D from high-dose supplements, granulomatous diseases such as sarcoidosis or tuberculosis in which immune cells make active vitamin D, an overactive thyroid, thiazide diuretics, prolonged bed rest, large amounts of calcium carbonate antacids (milk-alkali syndrome), or excess vitamin A.
A low or undetectable PTH with a low calcium is hypoparathyroidism, which means the glands themselves have been damaged or switched off. The great majority of cases follow thyroid, parathyroid or other neck surgery, when the glands or their blood supply are injured; a transient dip in the first days after surgery is common and about 1 to 3 percent of thyroidectomies leave permanent hypoparathyroidism. Autoimmune destruction, radiation, infiltration by iron (hemochromatosis) or copper (Wilson's disease), and the genetic absence of the glands in DiGeorge syndrome account for most of the rest.
One cause is reversible within hours and easy to miss: severe magnesium deficiency. Magnesium is needed for PTH release, and a level below about 1.0 to 1.2 mg/dL (seen with long-term proton-pump inhibitors, alcohol use disorder, diuretics, diarrhea and some chemotherapy) produces a low PTH, low calcium and symptoms of tetany that resolve once magnesium is replaced. A normal PTH with a clearly low calcium counts as 'low' in this context too, because the glands should be responding vigorously.
Common causes
Hypercalcemia of malignancy
PTH-related peptide from squamous cancers, bone metastases and multiple myeloma raise calcium, often rapidly to above 12 to 14 mg/dL, while PTH is suppressed. The commonest cause of a high calcium in hospital patients.
Vitamin D excess
Supplement doses well above 4,000 IU a day for months, or a single over-concentrated product, push 25-hydroxyvitamin D above about 150 ng/mL and raise calcium while suppressing PTH; it can take weeks to months to clear because vitamin D is stored in fat.
Sarcoidosis, tuberculosis and other granulomatous diseases
Activated macrophages in granulomas convert vitamin D to its active form outside the kidney, raising calcium and absorbed calcium in urine; summer sun can tip these people into hypercalcemia.
Neck surgery
Thyroidectomy, parathyroidectomy and laryngeal surgery can bruise or remove the glands. Tingling and cramps in the first 24 to 72 hours are watched for; permanent hypoparathyroidism follows about 1 to 3 percent of thyroidectomies.
Severe magnesium deficiency
Below roughly 1.0 to 1.2 mg/dL, magnesium blocks PTH secretion and action. Long-term proton-pump inhibitors, heavy alcohol use, diuretics, chronic diarrhea and cisplatin are the usual reasons; replacing magnesium restores PTH within a day or two.
Autoimmune hypoparathyroidism
Can occur alone or as part of autoimmune polyglandular syndrome type 1, with chronic candida infections and Addison's disease, usually presenting in childhood.
Thiazide diuretics, hyperthyroidism, immobilisation and milk-alkali syndrome
Each raises calcium modestly by a non-parathyroid route (reduced urinary loss, increased bone turnover, or heavy calcium carbonate intake), and PTH falls in response.
Radiation, infiltration and genetic absence
Radioiodine or external-beam neck radiation, hemochromatosis, Wilson's disease, metastases to the glands and DiGeorge (22q11 deletion) syndrome all reduce functioning parathyroid tissue.
Symptoms that can go with it
- With high calcium: thirst, frequent urination, constipation, nausea, confusion, drowsiness, bone pain and, when severe, vomiting and dehydration
- With low calcium: tingling or numbness around the mouth and in the fingers and toes
- Muscle cramps, twitching, or spasm of the hands and feet (carpopedal spasm)
- Seizures, spasm of the voice box with noisy breathing, or fainting from a heart rhythm disturbance when calcium is very low
- Dry skin, brittle nails, coarse hair and early cataracts with long-standing hypoparathyroidism
- Anxiety, irritability or low mood, which improve as calcium is corrected
Read it alongside
- Calcium (with albumin, or ionized calcium) — the pairing that gives PTH its meaning; a calcium corrected for a low albumin can turn a 'normal' value into a high one.
- 25-hydroxyvitamin D — low vitamin D is the commonest reason for a high PTH with a normal calcium and must be replaced before primary hyperparathyroidism can be called.
- Phosphorus — low with primary hyperparathyroidism, high with kidney disease and hypoparathyroidism.
- Magnesium — very low magnesium shuts PTH off; mildly low magnesium raises it.
- Creatinine and eGFR — chronic kidney disease drives secondary hyperparathyroidism and changes what a given PTH means.
- 24-hour urine calcium — above 400 mg a day is a surgical indication in hyperparathyroidism; very low urine calcium points to familial hypocalciuric hypercalcemia.
- Alkaline phosphatase — rises with high bone turnover in severe hyperparathyroidism and in bone disease of kidney failure.
- Bone density (DEXA) and kidney imaging — not blood tests, but the two that decide whether a confirmed parathyroid adenoma should be removed.
What usually happens next
- A high PTH is repeated as a morning fasting sample with calcium and albumin (or ionized calcium), 25-hydroxyvitamin D, phosphorus, magnesium and creatinine drawn together; many apparent abnormalities resolve into vitamin D deficiency or a lab quirk.
- If vitamin D is low, it is replaced first (typically to a 25-hydroxyvitamin D above 30 ng/mL) and PTH rechecked in about three months, because the diagnosis of primary hyperparathyroidism cannot be made while vitamin D is deficient.
- If calcium is high and PTH is not suppressed, expect a 24-hour urine calcium (to exclude familial hypocalciuric hypercalcemia and to assess stone risk), a bone density scan including the forearm, and a kidney ultrasound or CT for stones.
- Surgery to remove an adenoma is recommended when calcium is more than 1.0 mg/dL above the upper limit, bone density T-score is −2.5 or lower or there has been a fragility fracture, eGFR is under 60, there are kidney stones or a 24-hour urine calcium above 400 mg, or the person is under 50; a success rate above 95 percent is typical with an experienced surgeon.
- If calcium is high and PTH is suppressed, the search moves to PTH-related peptide, vitamin D metabolites, protein electrophoresis, thyroid function and a chest X-ray or CT, and this is done promptly.
- A low PTH with low calcium after neck surgery or with low magnesium is managed by the treating team; ask about magnesium if you take a proton-pump inhibitor long term.
Diet, lifestyle and natural levers with evidence
What can move PTH once the cause is known. Nothing here replaces finding the cause.
Restore vitamin D to above 30 ng/mL
Strong evidenceVitamin D deficiency is the single most common reversible cause of a high PTH, and repletion brings PTH down by roughly 20 to 30 percent in deficient adults within two to three months. Even in confirmed primary hyperparathyroidism, a randomised placebo-controlled trial of 2,800 IU a day for six months lowered PTH by 17 percent without raising blood or urine calcium, and international guidelines now advise keeping 25-hydroxyvitamin D above 30 ng/mL before and after parathyroid surgery. Typical repletion doses are 1,000 to 2,000 IU a day, or a prescribed loading course for severe deficiency.
In sarcoidosis, lymphoma or an already high calcium, vitamin D can push calcium up; it is given with calcium monitoring in those settings. Doses above 4,000 IU a day long term need a reason and a blood level.
PTH rises within days when calcium intake falls below about 600 to 800 mg a day and falls again when intake is adequate. In a study of over 900 Icelandic adults, people eating more than 1,200 mg of calcium a day had PTH levels about 20 percent lower than those eating under 800 mg, and adequate calcium blunted the PTH rise from low vitamin D. Dairy, calcium-set tofu, canned fish with bones, fortified plant milks and leafy greens get most people there; the guidelines for primary hyperparathyroidism specifically say not to restrict calcium, since restriction drives PTH higher still.
Calcium supplements above food needs do not help and may raise kidney stone risk; in chronic kidney disease, calcium and phosphate are balanced with the kidney team rather than self-supplemented.
Correct low magnesium
Strong evidenceMagnesium below about 1.0 to 1.2 mg/dL suppresses PTH release and blocks its action, producing a low PTH and low calcium that do not respond to calcium or vitamin D until magnesium is replaced, after which PTH normalizes within one to two days. Long-term proton-pump inhibitors, loop and thiazide diuretics, heavy alcohol use and chronic diarrhea are the common causes; dietary sources (nuts, seeds, legumes, whole grains, leafy greens) or an oral supplement of 200 to 400 mg a day restore mild deficiency over a few weeks.
Oral magnesium causes diarrhea at higher doses and can accumulate dangerously in advanced kidney disease; a magnesium level is checked before supplementing anyone with an eGFR under 30.
Limit phosphate additives if you have chronic kidney disease
Moderate evidenceRetained phosphate is one of the main drivers of secondary hyperparathyroidism in kidney disease. Inorganic phosphate additives in processed meats, colas, packaged baked goods and fast food are about 90 percent absorbed, compared with 40 to 60 percent from meat and 20 to 40 percent from plant foods. In a randomised trial of dialysis patients, simply teaching people to read labels and avoid phosphate additives lowered serum phosphorus by about 0.6 mg/dL over three months, and KDIGO guidance recommends limiting dietary phosphate as part of PTH control; the effect on PTH itself is modest but real, and it reduces the need for binder tablets.
Do not cut protein to cut phosphate; in kidney disease a dietitian balances the two.
When to see a clinician promptly
- A calcium above 14 mg/dL, or any high calcium with confusion, drowsiness, vomiting, severe weakness or an inability to keep fluids down: hypercalcemic crisis is an emergency that needs intravenous fluids the same day.
- Tingling around the mouth and fingers, muscle spasms, twitching, seizures or noisy breathing after thyroid or neck surgery, or with a low calcium on a recent test: severe hypocalcemia can cause life-threatening spasm of the airway and heart rhythm problems.
- A high calcium with a suppressed PTH, especially with weight loss, bone pain, a cough or a smoking history: cancer is a leading cause and is investigated promptly.
- A confirmed high PTH with high calcium alongside kidney stones, a fracture, osteoporosis or an eGFR under 60: these are indications for surgical referral rather than observation.
- A high PTH under age 40 or with a family history of parathyroid, pituitary, pancreatic or adrenal tumors, which may point to an inherited syndrome.
- Rising PTH on repeat tests in known chronic kidney disease, which calls for a review of phosphate, vitamin D and calcium management with the kidney team.
Frequently asked questions
What is a normal PTH level?
Intact PTH is normal at about 10 to 65 pg/mL in most US laboratories, with some quoting 15 to 65 or 12 to 88 pg/mL depending on the assay. The number only makes sense next to a calcium drawn at the same time: a PTH of 50 is normal if calcium is normal, too high if calcium is above 10.5 mg/dL (it should be suppressed below 20) and too low if calcium is 7.5 mg/dL (it should be well above 65). Always use your lab's printed range.
What does high PTH with high calcium mean?
It almost always means primary hyperparathyroidism: one of the four parathyroid glands has developed a benign adenoma and is making PTH regardless of the calcium level. About 85 percent of cases are a single adenoma, most of the rest are enlargement of all four glands, and parathyroid cancer is rare. The next steps are a vitamin D level, a 24-hour urine calcium, a bone density scan and a kidney scan for stones, and surgery is considered if calcium is more than 1 mg/dL above normal, bone density is low, kidney function is reduced or you are under 50.
Can vitamin D deficiency cause high PTH?
Yes, and it is the commonest reason for a high PTH with a normal calcium. Without enough vitamin D the gut absorbs less calcium, so the glands release more PTH to keep blood calcium steady, often pushing it to 65 to 150 pg/mL. Replacing vitamin D to a 25-hydroxyvitamin D level above 30 ng/mL brings PTH back toward normal in two to three months; if it stays high with calcium normal or raised after that, a primary parathyroid problem is then considered.
What does PTH intact mean on a blood test?
'Intact PTH' means the lab measured the whole 84-amino-acid hormone rather than its fragments, using a two-antibody immunoassay. It is the standard test and is what people mean by 'a PTH level'. Older assays detected inactive fragments and read misleadingly high, particularly in kidney disease; the newest 'whole' or 'bio-intact' assays are stricter still and read about half as high in dialysis patients, which is why results from different labs are not directly comparable.
What are the symptoms of high PTH?
Often none; most people are found through a routine calcium. When symptoms occur they come from the high calcium and bone loss: tiredness, low mood, poor concentration, constipation, thirst and frequent urination, aches in bones and joints, kidney stones and, over years, fractures and loss of height. When the high PTH is a response to low calcium or vitamin D, people may instead notice tingling, cramps and muscle twitching.
Is a PTH of 70, 80 or 100 high?
Any of those is above most labs' upper limit of about 65 pg/mL, but what matters is why. With a normal calcium and a low vitamin D, a PTH of 70 to 100 is a normal response to deficiency and should settle with repletion. With a high calcium, the same value means primary hyperparathyroidism. With an eGFR under 60 it is expected secondary hyperparathyroidism of kidney disease. Values in the several hundreds with a high calcium suggest a large adenoma or, rarely, parathyroid cancer.
What does low PTH mean?
If calcium is high, a low PTH (usually under 20 pg/mL) means the glands have correctly shut down and the calcium has another source, such as cancer, excess vitamin D, sarcoidosis, an overactive thyroid or thiazide diuretics; that source needs finding. If calcium is low, a low PTH means the glands themselves are not working (hypoparathyroidism), most often after thyroid or neck surgery, from autoimmune damage, or because magnesium is severely low, which is quickly reversible.
Do I need to fast for a PTH test?
A morning fasting sample is preferred because PTH has a daily rhythm and changes after meals, falling after a calcium-rich meal and rising after a low-calcium one, and because it is usually drawn with a fasting calcium panel. Take the sample at the same time of day if you are being followed over time, and mention biotin supplements, lithium, diuretics, vitamin D or calcium supplements and any bone medicines, all of which shift the result.
References
- Parathyroid hormone (PTH) test. MedlinePlus, US National Library of Medicine (2023)View source
- Primary hyperparathyroidism. National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) (2019)View source
- Hyperparathyroidism. Mayo Clinic (2022)View source
- Bilezikian JP, Khan AA, Silverberg SJ, et al.. Evaluation and management of primary hyperparathyroidism: summary statement and guidelines from the Fifth International Workshop. Journal of Bone and Mineral Research (2022)
- Wilhelm SM, Wang TS, Ruan DT, et al.. The American Association of Endocrine Surgeons guidelines for definitive management of primary hyperparathyroidism. JAMA Surgery (2016)
- Khan AA, Bilezikian JP, Brandi ML, et al.. Evaluation and management of hypoparathyroidism: summary statement and guidelines from the Second International Workshop. Journal of Bone and Mineral Research (2022)
- Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Update Work Group. KDIGO 2017 clinical practice guideline update for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease–mineral and bone disorder (CKD-MBD). Kidney International Supplements (2017)
- Steingrimsdottir L, Gunnarsson O, Indridason OS, Franzson L, Sigurdsson G. Relationship between serum parathyroid hormone levels, vitamin D sufficiency, and calcium intake. JAMA (2005)
- Rolighed L, Rejnmark L, Sikjaer T, et al.. Vitamin D treatment in primary hyperparathyroidism: a randomized placebo controlled trial. Journal of Clinical Endocrinology and Metabolism (2014)
- Sullivan C, Sayre SS, Leon JB, et al.. Effect of food additives on hyperphosphatemia among patients with end-stage renal disease: a randomized controlled trial. JAMA (2009)
- Holick MF, Binkley NC, Bischoff-Ferrari HA, et al.. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. Journal of Clinical Endocrinology and Metabolism (2011)
- Hyperparathyroidism. Merck Manual Professional Version (2024)
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