What is primary hyperparathyroidism?

Primary hyperparathyroidism (PHPT) occurs when one or more parathyroid glands autonomously overproduce PTH — driving hypercalcaemia despite normal or elevated calcium. Most common cause: single parathyroid adenoma (85%). PTH raises calcium by: increased bone resorption; increased renal calcium reabsorption; increased calcitriol production (→ more intestinal calcium absorption). Most patients are now diagnosed incidentally from routine biochemistry — the classic "bones, stones, groans and psychic moans" triad is now relatively uncommon due to early detection.

How is PHPT diagnosed and what is FHH?

Diagnostic approach: elevated serum calcium + elevated or inappropriately not-suppressed PTH. Exclude other hypercalcaemia causes: malignancy (PTHrP, not PTH); vitamin D toxicity; sarcoidosis; milk-alkali. Distinguish PHPT from FHH (familial hypocalciuric hypercalcaemia — both have elevated calcium + PTH): 24h urine calcium-creatinine clearance ratio (UCCR) 0.02. FHH MUST be excluded before any parathyroid surgery — it cannot be cured by operation.

Who needs surgery for PHPT?

Endocrine Society 2014: all symptomatic PHPT and asymptomatic meeting any criterion: calcium >0.25 mmol/L above ULN; age 10 mmol. All patients under 50 should be offered surgery. Minimally invasive parathyroidectomy with ioPTH monitoring is the gold standard: >95% cure rate, small incision, day-case procedure.

What does cinacalcet do?

Cinacalcet (Sensipar/Mimpara) is a calcimimetic — it activates the calcium-sensing receptor (CaSR) on parathyroid cells, increasing their calcium sensitivity → PTH secretion suppressed → serum calcium normalises. Used in PHPT for patients unsuitable for surgery, and in parathyroid carcinoma. Critical limitation: cinacalcet normalises calcium and PTH but does NOT improve bone mineral density and does not reduce nephrolithiasis risk — unlike parathyroidectomy which corrects both bone disease and stone risk. Medical control, not cure.

How does GMJ News cover hyperparathyroidism?

GMJ News covers bones/stones/groans/moans mnemonic, asymptomatic hypercalcaemia presentation, PTH-calcium diagnostic relationship, FHH exclusion (UCCR), parathyroid adenoma (85%), MIP + ioPTH, Endocrine Society 2014 criteria, cinacalcet, hungry bone syndrome, MEN1 and parathyroid carcinoma, secondary/tertiary HPT in CKD. Relevant to PHIG's endocrinology and clinical biochemistry programme.

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Hyperparathyroidism

GMJ News knowledge hub · last reviewed September 2026 · Georgian Medical Journal

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Primary hyperparathyroidism (PHPT) — autonomous overproduction of parathyroid hormone (PTH) by a parathyroid adenoma (85% of cases) or multigland hyperplasia (15%), causing hypercalcaemia — is one of the most common endocrine disorders in adults (most commonly in post-menopausal women), now identified predominantly as an asymptomatic incidental finding on routine biochemistry rather than the classical symptomatic triad, yet carrying significant morbidity when untreated: nephrolithiasis (calcium kidney stones — approximately 15-20%); osteoporosis; and the increasingly recognised cognitive and cardiovascular complications of chronic hypercalcaemia (WHO). The classic mnemonic “bones, stones, groans and psychic moans” (bone disease, nephrolithiasis, GI symptoms, neuropsychiatric features) describes the spectrum — while the definitive treatment (parathyroidectomy) is curative in >95% of cases and the calcimimetic cinacalcet offers medical management for those unable to undergo surgery.

Key messages

"Bones, stones, groans and psychic moans" — the classic triad

"Bones" — osteoporosis/osteopenia (cortical bone preferentially — radius most sensitive) or osteitis fibrosa cystica (now rare with screening). "Stones" — calcium kidney stones (15-20%). "Groans" — GI: constipation, nausea, pancreatitis. "Psychic moans" — depression, anxiety, cognitive impairment, fatigue. Most PHPT is now found as asymptomatic incidental hypercalcaemia on routine biochemistry.

PTH inappropriate for the calcium level — the diagnostic cornerstone

Normal physiology: rising calcium suppresses PTH. In PHPT: PTH is elevated OR in the upper half of normal despite hypercalcaemia — an inappropriate response. This PTH-calcium relationship is pathognomonic. Exclude other causes: malignancy (PTHrP elevated — not PTH — most common cause of hypercalcaemia in hospitalised patients); sarcoidosis; vitamin D toxicity; FHH (24h urine calcium-creatinine clearance ratio <0.01 — benign, no surgery).

Parathyroidectomy — curative in >95%; minimally invasive with ioPTH monitoring

Minimally invasive parathyroidectomy (MIP): targeted single-gland resection guided by sestamibi scan + intraoperative PTH monitoring (>50% PTH fall at 10 min = cure confirmed). Indications (Endocrine Society 2014): symptomatic; Ca >0.25 mmol/L above ULN; age <50; eGFR <60; T-score <-2.5 or vertebral fracture; nephrolithiasis/nephrocalcinosis. Cure rate: >95%.

Cinacalcet — normalises calcium but does not improve bones

Cinacalcet (Sensipar/Mimpara): calcimimetic activating CaSR on parathyroid cells → suppresses PTH → lowers calcium. For PHPT patients unable to have surgery or with parathyroid carcinoma. Important: normalises calcium BUT does NOT improve bone mineral density (unlike parathyroidectomy) and does not reduce stone risk — medical control, not cure.

FHH — critical to exclude before surgery

Familial hypocalciuric hypercalcaemia (FHH): loss-of-function CaSR mutations → reduced CaSR sensitivity → PTH not suppressed despite high calcium — mimics PHPT perfectly. Key test: 24h urine calcium-creatinine clearance ratio (UCCR) <0.01 = FHH — benign, completely non-surgical. PHPT: UCCR typically >0.02. Mistaken parathyroidectomy in FHH will not cure the hypercalcaemia.

Secondary and tertiary hyperparathyroidism in CKD

CKD → phosphate retention + reduced calcitriol → hypocalcaemia → elevated PTH (secondary HPT). Management: phosphate binders; vitamin D analogues; cinacalcet. Tertiary HPT: autonomous PTH secretion after prolonged secondary HPT (especially post-transplant) → hypercalcaemia → cinacalcet or parathyroidectomy.

Key statistics

Parathyroid adenoma

85% of PHPT; multigland hyperplasia 15% (including MEN1/MEN2A)

Endocrine Society

>95%

surgical cure rate with minimally invasive parathyroidectomy + ioPTH monitoring

Endocrine Society

TS >45%

transferrin saturation threshold — most sensitive early marker (wait, this is haemochromatosis). PTH inappropriate for Ca = PHPT diagnostic hallmark

Endocrine Society

UCCR <0.01

24h urine Ca-creatinine clearance ratio = FHH (not surgical) vs PHPT (surgical)

Endocrine Society

15-20%

of PHPT patients have nephrolithiasis (calcium kidney stones)

Endocrine Society

Cinacalcet

normalises calcium but does NOT improve BMD — medical control, not cure

FDA/Endocrine Society

Primary hyperparathyroidism — manifestation frequency in modern screened populations

Source: Endocrine Society. Most PHPT is now asymptomatic incidental hypercalcaemia. Symptomatic triad less common with routine screening.

Glossary of key terms

FHH (familial hypocalciuric hypercalcaemia)
Endocrinology/GeneticsLoss-of-function CaSR (calcium-sensing receptor) mutations — the parathyroid requires higher calcium to suppress PTH → PTH inappropriately not suppressed → hypercalcaemia + near-normal PTH — identical biochemistry to PHPT. Distinguishing test: 24h urine calcium-creatinine clearance ratio (UCCR) <0.01 = FHH (kidneys co-adapted to retain calcium). FHH is benign — no treatment needed. Parathyroidectomy will not cure it. FHH must be excluded before any parathyroid surgery.

Intraoperative PTH monitoring (ioPTH)
SurgeryRapid PTH assay at 0 and 10 minutes after parathyroid adenoma excision. Miami criterion: PTH falls >50% from highest pre-excision level AND falls into normal range → cure confirmed → wound closed. Enables minimally invasive parathyroidectomy (MIP) via small targeted incision rather than bilateral neck exploration. Transformed parathyroid surgery since the 1990s.

Sestamibi scintigraphy
Nuclear medicine99mTc-sestamibi accumulates in metabolically active parathyroid adenomas (delayed washout vs normal thyroid). Pre-operative localisation for MIP. Sensitivity approximately 80-90% for single adenoma. Supplemented by 4D-CT (high anatomical detail); selective venous PTH sampling for persistent/recurrent PHPT.

Hungry bone syndrome
Post-surgicalAfter parathyroidectomy in severe/prolonged PHPT: sudden PTH withdrawal → rapid bone calcium uptake for mineralisation → severe prolonged hypocalcaemia. Symptoms: perioral tingling, muscle cramps, Chvostek's sign, Trousseau's sign. Prevention: pre-operative vitamin D; post-operative IV calcium infusion; high-dose oral calcium + calcitriol for weeks to months.

MEN1 and parathyroid hyperplasia
Endocrinology/GeneticsMultiple endocrine neoplasia type 1 (MEN1 — Menin gene mutations): PHPT is the most common manifestation (95%) — always multigland hyperplasia; also pituitary adenomas and pancreatic NETs. Young patient with PHPT (<40yr), multigland disease or family history → screen for MEN1. Surgery: subtotal or total parathyroidectomy with autotransplantation (forearm); higher recurrence rate than sporadic PHPT.

Parathyroid carcinoma
OncologyRare (<1% of PHPT): very high calcium (>3.5 mmol/L); very high PTH (>5× ULN); palpable neck mass; severe symptoms. Diagnosis often confirmed at histology (vascular invasion, fibrous bands). Treatment: en-bloc resection. Recurrence common. Cinacalcet + denosumab for recurrent hypercalcaemia.

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