Tucked behind the thyroid sit four tiny glands—often no larger than grains of rice—that guard the most tightly regulated mineral in the human body: calcium. They do so by secreting parathyroid hormone, or PTH. When ionized calcium dips, PTH rises within minutes and signals bones to release calcium, kidneys to reclaim it while discarding phosphate, and the kidneys again to activate vitamin D into calcitriol so the intestine absorbs more dietary calcium. When calcium is plentiful, PTH quiets down. Because calcium powers nerve impulses, muscle contraction, and heart rhythm, even small disturbances in this loop create dramatic symptoms. The image you provided captures the big picture: too much PTH produces hypercalcemia with low phosphate and the classic stones, bones, abdominal moans, and psychic groans; too little PTH produces hypocalcemia with high phosphate and neuromuscular irritability marked by Trousseau’s and Chvostek’s signs. This article turns that snapshot into a complete, exam-ready and clinic-practical guide.
How to Read Calcium and PTH Together
A sensible workflow starts with confirming true hypocalcemia or hypercalcemia, ideally using ionized calcium or albumin-corrected calcium. PTH then tells you which direction the parathyroids are pushing. Inappropriately high PTH in the face of high calcium points to hyperparathyroidism. Suppressed or low-normal PTH during hypercalcemia suggests non-parathyroid causes such as malignancy or vitamin D excess. Low calcium with low or inappropriately normal PTH defines hypoparathyroidism, while low calcium with very high PTH points to secondary hyperparathyroidism from vitamin D deficiency or chronic kidney disease.
| Pattern | Calcium | Phosphate | PTH | Typical interpretation |
|---|---|---|---|---|
| Primary hyperparathyroidism | High | Low to low-normal | High or inappropriately normal | Parathyroid adenoma or hyperplasia driving excess PTH |
| Secondary hyperparathyroidism (CKD or vit D deficiency) | Low or low-normal | High in CKD, low in vitamin D deficiency | High | Compensatory rise in PTH due to hypocalcemia or phosphate retention |
| Tertiary hyperparathyroidism | High | High-normal | Very high | Autonomous glands after long-standing secondary HPT, often post-transplant |
| Hypoparathyroidism | Low | High | Low or inappropriately normal | Surgical removal, autoimmune damage, genetic causes, or severe hypomagnesemia |
| PTH-independent hypercalcemia | High | Variable | Low | Malignancy (PTHrP), vitamin D intoxication, granulomatous disease, thyrotoxicosis, drugs |
Hyperparathyroidism Explained
Primary hyperparathyroidism usually arises from a single benign parathyroid adenoma; less often multiple glands are hyperplastic, and rarely a carcinoma is responsible. The biochemical signature is persistent hypercalcemia with low phosphate and an elevated or “inappropriately normal” PTH that refuses to suppress. Many people are discovered incidentally on routine metabolic panels; others present with kidney stones, osteoporosis or fragility fractures, bone pain, gastrointestinal discomfort with constipation, and neurocognitive changes that range from irritability to difficulty concentrating. The mnemonic stones, bones, abdominal moans, and psychic groans accurately summarizes the syndrome. Blood pressure can be elevated and peptic symptoms may be prominent.
Secondary hyperparathyroidism is different. Here the glands are responding to chronic hypocalcemic stimuli—most commonly chronic kidney disease driving phosphate retention and reduced calcitriol, and worldwide, vitamin D deficiency from low sun exposure, darker skin at high latitudes, or limited dietary sources. Tertiary hyperparathyroidism refers to glands that become autonomously overactive after years of secondary stimulation, a pattern often seen after kidney transplantation.
Diagnosing Primary Hyperparathyroidism Confidently
Diagnosis requires more than one elevated calcium value, checked alongside PTH. Vitamin D status should be assessed with 25-hydroxyvitamin D, since repletion can normalize PTH in some borderline cases. A 24-hour urinary calcium helps distinguish familial hypocalciuric hypercalcemia (FHH), a benign genetic condition with low urinary calcium, from true primary hyperparathyroidism; the calcium-to-creatinine clearance ratio is typically under 0.01 in FHH. Bone mineral density by DXA assesses skeletal involvement, and renal ultrasound or CT screens for nephrolithiasis or nephrocalcinosis. Imaging with neck ultrasound and sestamibi or 4D-CT localizes an adenoma when surgery is planned; it is not required to make the diagnosis.
When and How to Treat Hyperparathyroidism
Parathyroidectomy is curative in most people with primary hyperparathyroidism and is clearly indicated in symptomatic disease. In asymptomatic cases, consensus guidelines favor surgery when serum calcium is more than 1.0 mg/dL (0.25 mmol/L) above the upper limit of normal, when DXA shows osteoporosis or there is a history of fragility fracture, when estimated GFR is under 60 mL/min or there is nephrolithiasis or nephrocalcinosis, or when the patient is younger than fifty years since lifelong exposure increases risk. Experienced endocrine surgeons use focused or bilateral exploration with intraoperative PTH monitoring to confirm removal of hypersecreting tissue.
Medical management is reasonable for selected patients who decline or are poor surgical candidates. Hydration, avoidance of thiazides and lithium, moderation—not restriction—of dietary calcium, and careful vitamin D repletion reduce exacerbations. Bisphosphonates or denosumab improve bone density without lowering calcium substantially. Cinacalcet, a calcimimetic, lowers calcium by sensitizing the calcium-sensing receptor and is particularly useful in tertiary hyperparathyroidism and in primary disease when surgery is not feasible. Secondary hyperparathyroidism from chronic kidney disease is managed with phosphate control, active vitamin D analogs, and calcimimetics, with parathyroidectomy reserved for refractory cases. After surgery, hungry bone syndrome can occur as newly suppressed PTH allows rapid skeletal uptake of calcium and phosphate; proactive calcium and calcitriol replacement and magnesium support are the antidote.
Hypoparathyroidism Explained
Hypoparathyroidism means insufficient PTH action and the predictable combination of hypocalcemia and hyperphosphatemia. The most common cause is inadvertent removal or devascularization of parathyroid tissue during thyroidectomy, parathyroidectomy for multigland disease, or extensive neck dissections. Autoimmune hypoparathyroidism, DiGeorge syndrome and other genetic defects of parathyroid development, prior radiation, and severe magnesium deficiency also appear in practice. Because calcium stabilizes neuronal membranes, deficiency produces tingling around the mouth and in the fingertips, painful muscle cramps, carpopedal spasm, and sometimes laryngospasm or seizures. Blood pressure can be low and mood symptoms such as anxiety or depression are common during a flare.
Two bedside signs help when a meter is not immediately at hand. Trousseau’s sign is a carpal spasm induced by inflating a blood pressure cuff and holding it for several minutes above systolic pressure. Chvostek’s sign is a twitch of facial muscles when the facial nerve is lightly tapped. Neither sign is perfectly sensitive or specific, but in context both point toward hypocalcemia.
Diagnosing and Managing Hypoparathyroidism
Laboratory confirmation shows low total and ionized calcium with elevated phosphate and a low or inappropriately normal PTH. Magnesium should always be checked, since deficiency suppresses PTH release and causes PTH resistance; without correcting magnesium, calcium will not normalize. Acute symptomatic hypocalcemia is treated with intravenous calcium gluconate given cautiously while monitoring cardiac rhythm and serum magnesium and phosphate. Once stabilized, oral calcium carbonate or citrate and active vitamin D in the form of calcitriol maintain levels. Thiazide diuretics may be used to reduce urinary calcium loss when hypercalciuria threatens kidneys. Dietary guidance emphasizes adequate calcium intake with controlled phosphate; dark colas and phosphate-additive snack foods are minimized. Selected adults with chronic postsurgical hypoparathyroidism who cannot reach stable control on conventional therapy may benefit from recombinant human PTH, prescribed under specialist care with careful renal monitoring to avoid hypercalciuria and nephrocalcinosis.
Clinical Features at a Glance
| Domain | Hyperparathyroidism (↑PTH → ↑Calcium ↓Phosphate) | Hypoparathyroidism (↓PTH → ↓Calcium ↑Phosphate) |
|---|---|---|
| Typical causes | Single adenoma; multigland hyperplasia; long-term CKD or vitamin D deficiency driving secondary HPT; tertiary autonomy post-transplant | Postsurgical loss; autoimmune disease; genetic syndromes; radiation; severe magnesium depletion |
| Hallmark symptoms | Kidney stones, bone pain and fractures, abdominal discomfort with constipation and anorexia, fatigue and mood change | Paresthesias, muscle cramps, tetany, laryngospasm or seizures in severe cases, hypotension, anxiety and depression |
| Bedside clues | Bone tenderness, reduced cortical bone on DXA, nephrolithiasis on imaging | Positive Trousseau or Chvostek signs, prolonged QT on ECG |
| Core labs | High calcium, low phosphate, high or inappropriately normal PTH, variable vitamin D; high urinary calcium in most | Low calcium, high phosphate, low or inappropriately normal PTH, low magnesium if contributory |
| First-line treatment | Parathyroidectomy when indicated; otherwise hydration, vitamin D repletion, bone-directed therapy, calcimimetic in select cases | IV calcium for acute crises; chronic oral calcium and calcitriol; magnesium replacement; thiazides for hypercalciuria; recombinant PTH for difficult cases |
Evidence, Experience, and Safety
Evidence underpins every recommendation here: confirm true calcium abnormality, pair it with PTH, and assess kidneys and bone before choosing surgery or medicine. Experience matters in the operating room; cure rates and complication rates improve markedly when high-volume endocrine surgeons perform parathyroidectomy. Safety is the through-line: correct magnesium before insisting calcium will not rise, check urinary calcium periodically in chronic hypoparathyroidism to protect kidneys, and anticipate hungry bone syndrome after successful surgery with proactive calcium–calcitriol support.
Special Populations and Situations
Pregnancy alters calcium physiology. In primary hyperparathyroidism, uncontrolled hypercalcemia increases risks of nephrolithiasis and pancreatitis for the mother and neonatal hypocalcemia for the infant; second-trimester surgery may be considered in severe cases. During lactation, maternal calcium demands change again and careful follow-up prevents swings. Children with parathyroid disorders require pediatric endocrinology input to protect growth and neurodevelopment. After parathyroid surgery, persistent or recurrent hyperparathyroidism prompts a review for multigland disease, ectopic glands, or genetic syndromes such as MEN1, while persistent hypocalcemia suggests hungry bone or true hypoparathyroidism.
Step-Wise Diagnostic Pathway You Can Use Tomorrow
A practical pathway starts with a repeat serum calcium with albumin and, when possible, an ionized calcium. PTH is measured at the same blood draw. Vitamin D status, phosphate, magnesium, creatinine with eGFR, and a spot or 24-hour urine calcium complete the biochemical picture. If primary hyperparathyroidism is confirmed and surgery is planned, localization imaging follows; if hypoparathyroidism is established, attention turns to magnesium, ECG monitoring in symptomatic cases, and a long-term plan for calcium, calcitriol, and kidney-sparing strategies.
Medication and Diet Reference Table
| Goal | Medicine or Measure | Practical notes |
|---|---|---|
| Lower serum calcium when surgery is not feasible | Cinacalcet | Reduces PTH secretion via calcium-sensing receptor; useful in tertiary and selected primary cases |
| Improve bone density in PHPT | Alendronate, zoledronic acid, or denosumab | Treats skeletal fragility; does not correct hypercalcemia by itself |
| Control secondary HPT in CKD | Phosphate binders, calcitriol or analogs, cinacalcet | Coordinated with nephrology; phosphate restriction and dialysis adherence essential |
| Treat acute hypocalcemia | IV calcium gluconate with ECG monitoring | Replace magnesium concurrently; address airway if laryngospasm |
| Maintain calcium in chronic hypoparathyroidism | Oral calcium carbonate or citrate plus calcitriol | Target low-normal serum calcium while avoiding hypercalciuria; consider thiazide if urinary calcium is high |
| Diet in PHPT | Normal calcium, liberal fluids, moderate sodium | Avoid dehydration and excess vitamin A; do not severely restrict calcium |
| Diet in hypoparathyroidism | Adequate calcium, reduced phosphate additives | Check labels for phosphate preservatives; use dairy or fortified alternatives as tolerated |
Frequently Asked Questions
Can primary hyperparathyroidism be mild and still harm bones and kidneys?
Yes. Even modest, chronic elevations in calcium with unsuppressed PTH can promote kidney stones and accelerate cortical bone loss. A baseline DXA and kidney imaging are part of the initial evaluation, and many patients who feel well still meet evidence-based criteria for curative surgery.
How is familial hypocalciuric hypercalcemia different from primary hyperparathyroidism?
FHH is a benign inherited condition caused by variants in the calcium-sensing receptor. Calcium is high from birth, PTH is normal or mildly elevated, and 24-hour urinary calcium is low. Surgery does not help FHH. The calcium-to-creatinine clearance ratio is the key discriminator.
Why do phosphate levels move opposite to calcium in parathyroid disease?
PTH tells kidneys to reclaim calcium and dump phosphate. In hyperparathyroidism this causes hypercalcemia with low phosphate. In hypoparathyroidism the lack of PTH means phosphate is retained while calcium is lost, producing the reverse pattern.
What is hungry bone syndrome after parathyroidectomy?
When excess PTH abruptly falls, previously hyper-resorbed bone captures calcium and phosphate to rebuild. Serum calcium can plummet for days, especially in patients with severe bone disease preoperatively. Scheduled oral or IV calcium, calcitriol, and magnesium prevent complications.
Are cola drinks really a problem in hypoparathyroidism?
Many colas contain phosphoric acid, adding a high phosphate load that worsens hypocalcemia. Patients on long-term calcium–calcitriol therapy also risk kidney calcifications; limiting phosphate additives and monitoring urinary calcium reduces that risk.
Does vitamin D supplementation worsen hyperparathyroidism?
Repleting vitamin D to sufficiency usually helps by lowering PTH secretion and improving bone health. It should be done cautiously with monitoring because severe hypercalcemia can rarely worsen if intake is excessive.
Which diuretics affect calcium most?
Thiazide diuretics reduce urinary calcium excretion and can help treat hypercalciuria in hypoparathyroidism. Loop diuretics increase urinary calcium and are sometimes used short-term to lower calcium in hypercalcemic crises under supervision.
Can stress alone cause parathyroid disease?
Stress does not cause adenomas or hypoparathyroidism, though dehydration during illness or heat can transiently raise calcium in susceptible people. Lasting calcium or PTH abnormalities should always be evaluated with labs.
How quickly should symptoms improve after treating hypocalcemia?
Neuromuscular irritability often eases within hours of IV calcium and magnesium correction. Stable symptom control with oral therapy typically evolves over days as calcitriol reaches steady state and urinary calcium is balanced against serum goals.
When should a generalist refer to an endocrinologist or endocrine surgeon?
Referral is appropriate at the time of confirmed primary hyperparathyroidism, at discovery of recurrent stones or osteoporosis in that setting, in any case of persistent or symptomatic hypocalcemia, and for postoperative management questions such as hungry bone or recurrent disease. High-volume endocrine surgeons are preferred for parathyroidectomy.
Closing Perspective
Parathyroid disorders are small-gland problems with whole-body consequences. On one side lies the calcium-raising power of PTH, capable of provoking stones, fractures, and foggy thinking when left unchecked. On the other side lies the calcium-quiet world of PTH deficiency, where tingling fingers, carpopedal spasm, and seizures threaten unless calcium and magnesium are restored. Mastering the PTH–calcium–phosphate triad, applying a disciplined diagnostic pathway, and pairing surgery or medicines with thoughtful nutrition and monitoring convert that complexity into predictable, safe care. For students, the tables here cement the patterns. For clinicians, they translate the image into everyday decisions. For patients searching online, the goal is clarity and confidence that these conditions are not only understandable, but very often curable or controllable.
