PTH (Parathyroid Hormone): Understanding Your Blood Test Series

1. Overview: What this test reveals and why it is important

Parathyroid hormone (PTH) is an 84-amino acid polypeptide hormone secreted by the four parathyroid glands, which are located posterior to the thyroid gland in the neck. PTH is the primary regulator of calcium and phosphate homeostasis, acting directly on bone and kidney and indirectly on the intestine to maintain extracellular calcium concentration within a narrow physiological range.

The secretion of PTH is tightly controlled by the ionized calcium concentration in blood via the calcium-sensing receptor (CaSR) on parathyroid cells. Low ionized calcium stimulates PTH release, while high calcium suppresses it. This feedback loop maintains serum calcium stability essential for neuromuscular function, intracellular signalling, bone mineralization, and blood coagulation.

Measuring PTH is essential for:

· Differential diagnosis of calcium disorders: Distinguishing primary hyperparathyroidism (high calcium with inappropriately normal/elevated PTH) from malignancy-associated hypercalcaemia (high calcium with suppressed PTH) or hypocalcaemia due to hypoparathyroidism (low calcium with low/inappropriately normal PTH)

· Evaluation of bone disease: In osteoporosis, chronic kidney disease-mineral and bone disorder (CKD-MBD), and Paget's disease

· Monitoring chronic kidney disease: As GFR declines, phosphate retention and reduced vitamin D activation stimulate PTH elevation (secondary hyperparathyroidism). PTH targets guide management

· Localization of parathyroid tumours: Preoperative localization studies rely on confirming biochemical diagnosis first

· Post-surgical monitoring: After parathyroidectomy, PTH levels help confirm cure

· Investigation of unexplained hypo- or hypercalcaemia

PTH is measured using immunoassays that detect either the intact hormone (most common) or specific fragments. Interpretation requires simultaneous measurement of serum calcium (preferably ionized or albumin-adjusted), phosphate, vitamin D (25-OH and 1,25-OH), and renal function.

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2. What does it measure

a. Units of measurement

· Intact PTH: Picograms per millilitre (pg/mL) or picomoles per litre (pmol/L)

· Conversion: 1 pg/mL ≈ 0.106 pmol/L (multiply pg/mL by 0.106 to obtain pmol/L)

b. Normal range

Reference intervals vary by laboratory, assay manufacturer, and population. The following are representative for intact PTH assays with simultaneous normal calcium and vitamin D replete status:

· Adults: 10 – 65 pg/mL (1.1 – 6.9 pmol/L)

· Optimal range for bone health (consensus): 20 – 50 pg/mL

· Elderly: May have slightly higher values due to age-related changes

· Chronic kidney disease (CKD) targets: Vary by stage; see Section 5.

Critical interpretive principles:

· PTH must always be interpreted with concurrent serum calcium (albumin-adjusted or ionized), phosphate, 25-hydroxyvitamin D, and renal function (creatinine, eGFR).

· A "normal" PTH in the setting of hypercalcaemia is inappropriately elevated and indicates primary hyperparathyroidism.

· A "normal" PTH in the setting of hypocalcaemia is inappropriately low and indicates hypoparathyroidism or magnesium deficiency.

· PTH secretion is pulsatile and has a circadian rhythm (peaks at night, troughs in late morning). Consistency in sampling time is ideal for serial monitoring.

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3. Other factors connected to this

a. Direct correlation (factors that increase PTH)

Physiological:

· Low ionized calcium (primary stimulus)

· Low 25-hydroxyvitamin D (vitamin D deficiency reduces intestinal calcium absorption, stimulating PTH)

· Pregnancy and lactation (increased calcium demand)

· Nocturnal peak

· Age-related increase (due to declining renal function and vitamin D status)

Pathological:

· Primary hyperparathyroidism: Parathyroid adenoma (80%), hyperplasia (15-20%), carcinoma (less than 1%)

· Secondary hyperparathyroidism: Chronic kidney disease, vitamin D deficiency, calcium malabsorption, chronic phosphate retention, medications (loop diuretics, lithium, anticonvulsants)

· Tertiary hyperparathyroidism: Autonomous hypersecretion after long-standing secondary hyperparathyroidism, typically in end-stage renal disease post-transplantation

· Lithium therapy: Alters calcium set point, causing hyperparathyroidism in susceptible individuals

· Thiazide diuretics: Reduce urinary calcium excretion, may unmask mild hyperparathyroidism

· Familial hypocalciuric hypercalcaemia (FHH): Inactivating CaSR mutation causes PTH elevation despite hypercalcaemia

b. Indirect correlation (factors that decrease PTH)

Physiological:

· High ionized calcium (suppression)

· Correction of vitamin D deficiency (once 25-OHD exceeds 30 ng/mL, PTH declines)

Pathological:

· Hypoparathyroidism: Surgical (most common, after thyroid/parathyroid surgery), autoimmune, genetic (DiGeorge, APECED, familial isolated), infiltrative (haemochromatosis, Wilson's, metastases)

· Magnesium deficiency or excess: Severe hypomagnesaemia (below 1.0 mg/dL) impairs PTH secretion and action; hypermagnesaemia suppresses PTH

· Hypercalcaemia of malignancy: PTHrP (parathyroid hormone-related protein) mediated; PTH suppressed

· Sarcoidosis/granulomatous diseases: Excess 1,25-dihydroxyvitamin D production causes hypercalcaemia, suppressing PTH

· Thyrotoxicosis: Increases bone resorption, may cause mild hypercalcaemia with suppressed PTH

· Milk-alkali syndrome: Hypercalcaemia from excessive calcium and absorbable antacids

· Drugs: Glucocorticoids, beta-blockers, cimetidine, oral contraceptives (mild effects)

c. Methodological considerations

· Sample handling: PTH degrades rapidly at room temperature; samples should be centrifuged within 2 hours, separated, and frozen if not assayed immediately

· Assay type: "Intact" PTH assays (detecting full-length 1-84) are standard. Some assays also detect large fragments that accumulate in renal failure; newer "bio-intact" or "whole" PTH assays measure only 1-84

· Circadian variation: Samples drawn at different times may vary by 20-30%; for consistency, sample at same time of day (early morning fasting preferred)

· Vitamin D status: Always measure 25-hydroxyvitamin D concurrently to interpret PTH appropriately

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4. Disorders related to abnormal values

a. When elevated (with corresponding calcium context)

1. Hypercalcaemia with elevated PTH:

· Primary hyperparathyroidism: Most common cause of hypercalcaemia in outpatients. Usually mild, asymptomatic, discovered incidentally. Can present with nephrolithiasis, osteoporosis, fractures, neuropsychiatric symptoms.

· Tertiary hyperparathyroidism: After long-standing secondary hyperparathyroidism (e.g., dialysis patients post-renal transplant). Autonomous secretion; often severe hypercalcaemia.

· Lithium-associated hyperparathyroidism: Usually mild; resolves with lithium cessation in some cases.

· Familial hypocalciuric hypercalcaemia (FHH): Mild hypercalcaemia, relative hypocalciuria (low calcium:creatinine clearance ratio), usually benign. Differentiating from mild primary hyperparathyroidism is crucial to avoid unnecessary surgery.

2. Normocalcaemia with elevated PTH:

· Normocalcaemic primary hyperparathyroidism: Increasingly recognized; PTH elevated, calcium consistently normal, no secondary cause (vitamin D deficiency, renal disease). May progress to hypercalcaemia.

· Secondary hyperparathyroidism:

· Vitamin D deficiency (most common cause worldwide)

· Chronic kidney disease (CKD stages 3-5)

· Calcium malabsorption (coeliac disease, bariatric surgery, pancreatic insufficiency)

· Medications (loop diuretics, anticonvulsants)

· Idiopathic hypercalciuria

· Pseudo-hypoparathyroidism: Resistance to PTH action; hypocalcaemia with elevated PTH (see below).

3. Hypocalcaemia with elevated PTH:

· Vitamin D deficiency: Most common. Low calcium stimulates PTH, but vitamin D insufficient to maintain normal calcium.

· Chronic kidney disease: Impaired phosphate excretion and reduced 1-alpha-hydroxylase activity.

· Magnesium deficiency: Severe hypomagnesaemia impairs PTH secretion (paradoxical); after magnesium repletion, PTH rises.

· Pseudo-hypoparathyroidism: End-organ resistance to PTH (genetic); presents with hypocalcaemia, hyperphosphataemia, elevated PTH, and characteristic features (Albright's hereditary osteodystrophy).

b. When low (with corresponding calcium context)

1. Hypercalcaemia with suppressed PTH:

· Malignancy-associated hypercalcaemia: PTHrP mediated (squamous cell, breast, renal, ovarian) or osteolytic (multiple myeloma, lymphoma, metastases)

· Granulomatous diseases: Sarcoidosis, tuberculosis, histoplasmosis – excess 1,25-dihydroxyvitamin D from activated macrophages

· Thyrotoxicosis

· Milk-alkali syndrome

· Vitamin D intoxication

· Immobilization (prolonged bed rest, spinal cord injury)

· Adrenal insufficiency

2. Hypocalcaemia with low or inappropriately normal PTH:

· Hypoparathyroidism:

· Post-surgical (neck surgery)

· Autoimmune (isolated or APECED syndrome)

· Genetic (DiGeorge, familial isolated, CaSR activating mutations – autosomal dominant hypocalcaemia)

· Infiltrative (haemochromatosis, Wilson's, metastases)

· Radiation-induced

· Magnesium deficiency: Severe hypomagnesaemia impairs PTH secretion; after magnesium repletion, PTH rises and calcium normalizes

· Severe burns or critical illness (multifactorial)

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5. Best way to address aberrant levels

Critical principle: PTH is a marker of parathyroid function and calcium homeostasis, not a therapeutic target itself. Treatment is directed at the underlying disorder: correcting calcium, vitamin D, phosphate, or magnesium abnormalities; managing renal disease; or surgically removing overactive parathyroid tissue. All interventions must be guided by a physician, usually an endocrinologist or nephrologist.

a. Medical Management (by condition)

Primary Hyperparathyroidism:

· Surgical parathyroidectomy: Definitive treatment. Indications for surgery (consensus guidelines):

· Age below 50 years

· Serum calcium more than 1 mg/dL (0.25 mmol/L) above upper normal limit

· Creatinine clearance below 60 mL/min

· Nephrolithiasis or nephrocalcinosis

· Osteoporosis (T-score below -2.5 at any site or previous fragility fracture)

· Patient preference or unable/unwilling to undergo long-term monitoring

· Medical management (if surgery not indicated, declined, or not possible):

· Adequate hydration (avoid dehydration)

· Avoid thiazide diuretics and lithium

· Moderate calcium intake (dietary, not supplements) – 800-1000 mg daily; avoid high-dose calcium supplements

· Vitamin D repletion if deficient (25-OHD below 30 ng/mL) – cautiously, with monitoring, as vitamin D can increase calcium absorption and potentially worsen hypercalcaemia; start low (400-800 IU) and titrate

· Bisphosphonates (alendronate, risedronate) to reduce fracture risk in osteoporosis

· Cinacalcet (calcimimetic): Lowers PTH and calcium by increasing CaSR sensitivity. Used in those unable to undergo surgery, with severe symptoms, or in parathyroid carcinoma. Not a cure; does not improve bone density.

Secondary Hyperparathyroidism (CKD):

Goals per KDIGO guidelines:

· CKD stage 3-5 (not on dialysis): Maintain PTH in range appropriate for stage; optimal range uncertain but generally 35-70 pg/mL for stage 3, 70-110 for stage 4, 150-300 for stage 5.

· Correct hyperphosphataemia: Dietary phosphate restriction, phosphate binders (calcium acetate, sevelamer, lanthanum)

· Optimize vitamin D: 25-hydroxyvitamin D repletion, then active vitamin D analogues (calcitriol, paricalcitol, doxercalciferol) as needed

· Calcimimetics (cinacalcet) for refractory cases, especially in dialysis patients

Secondary Hyperparathyroidism (Vitamin D Deficiency):

· Replete vitamin D: 50,000 IU weekly for 8 weeks, then maintenance 1000-2000 IU daily; or 3000-6000 IU daily for 8 weeks, then maintenance

· Ensure adequate calcium intake (dietary or supplements) during repletion to avoid "hungry bone" syndrome

· Monitor PTH and calcium after 2-3 months

Hypoparathyroidism:

· Acute hypocalcaemia (symptomatic, with tetany, seizures, prolonged QT): Intravenous calcium gluconate (10-20 mL of 10% calcium gluconate diluted in D5W, infused over 10-20 minutes, followed by continuous infusion). Monitor ECG, cardiac status.

· Chronic management:

· Oral calcium supplements: 1000-2000 mg elemental calcium daily in divided doses

· Active vitamin D (calcitriol): 0.25-2 mcg daily; or alfacalcidol

· Thiazide diuretics: Reduce urinary calcium excretion in some patients

· Recombinant human PTH (teriparatide, rhPTH 1-84): Approved for hypoparathyroidism not controlled on conventional therapy. Costly, requires subcutaneous injection, long-term safety data evolving.

· Magnesium repletion: If hypomagnesaemia is present, correct with oral or IV magnesium before calcium will normalize.

PTH management in special populations:

· Pregnancy: Primary hyperparathyroidism in pregnancy is high-risk for mother and fetus; surgery in second trimester if indicated. Hypoparathyroidism requires careful calcium and calcitriol titration to avoid fetal hypocalcaemia.

· Post-parathyroidectomy: "Hungry bone syndrome" – prolonged hypocalcaemia due to rapid bone uptake of calcium; requires high-dose calcium and calcitriol, often IV initially, then oral.

Do not self-prescribe calcium, vitamin D, or calcimimetics. All require physician supervision and monitoring.

b. Using Supplements or Holistic medicine

No supplement directly targets PTH. The following support calcium homeostasis and bone health and may indirectly affect PTH by correcting underlying deficiencies. Always inform your physician before initiating any supplement, especially if you have hypercalcaemia, kidney stones, or CKD.

· Vitamin D3 (cholecalciferol):

· Rationale: Vitamin D deficiency is the most common cause of secondary hyperparathyroidism worldwide. Repletion lowers PTH to normal in most cases.

· Source: Lichen-derived cholecalciferol (D3) – plant-based, sustainable, and more effective than D2 (ergocalciferol) at raising and maintaining 25-OHD levels.

· Dose: Depends on baseline 25-OHD:

· Deficiency (below 20 ng/mL): 3000-6000 IU daily or 50,000 IU weekly for 8 weeks

· Insufficiency (20-30 ng/mL): 2000-4000 IU daily

· Maintenance (after repletion): 1000-2000 IU daily

· Monitoring: Recheck 25-OHD, PTH, calcium after 3 months.

· Caution: In primary hyperparathyroidism, vitamin D repletion must be done cautiously with close monitoring, as it may increase calcium absorption and worsen hypercalcaemia.

· Calcium:

· Rationale: Adequate calcium intake is essential for bone health and preventing secondary hyperparathyroidism. However, excess calcium supplements can suppress PTH and cause hypercalcaemia, nephrolithiasis, and vascular calcification.

· Source (ecological hierarchy):

· Plant-based: Calcium-set tofu, fortified plant milks (soy, almond, oat), leafy greens (collards, kale, bok choy – but note oxalate content), broccoli, bok choy, okra, almonds, tahini, blackstrap molasses.

· Fungi/algae: Some algae (lithothamnion) are rich in calcium and marketed as supplements; sustainable harvest.

· Supplements: Calcium citrate (better absorbed, can be taken with or without food, preferred for those with achlorhydria or on acid blockers) or calcium carbonate (cheaper, requires stomach acid, best with food). Avoid unrefined calcium sources (dolomite, bone meal, oyster shell) due to heavy metal contamination risk.

· Dose: Total daily intake (diet + supplements) should generally not exceed:

· 1000-1200 mg for most adults

· 1200-1500 mg for postmenopausal women, elderly, or those on corticosteroids

· In primary hyperparathyroidism: 800-1000 mg from diet, avoid high-dose supplements unless osteoporotic and bone-protective therapy indicated

· In hypoparathyroidism: 1000-2000 mg elemental calcium daily in divided doses, as prescribed

· Caution: Do not exceed 2000-2500 mg total daily intake (upper limit). Excess linked to kidney stones, vascular calcification, and possible cardiovascular events.

· Magnesium:

· Rationale: Magnesium deficiency impairs PTH secretion and action; correction restores parathyroid function. Also essential for vitamin D activation.

· Form: Magnesium glycinate, citrate, or malate. Avoid magnesium oxide (poor absorption).

· Dose: 300-400 mg elemental magnesium daily.

· Caution: Reduce dose if diarrhoea develops; caution in CKD (risk of hypermagnesaemia).

· Vitamin K2 (menaquinone):

· Rationale: Directs calcium into bone (activates osteocalcin) and may reduce vascular calcification. Some studies suggest benefit in osteoporosis, but evidence for PTH modulation is weak.

· Source: Plant-based: Natto (fermented soybeans) is richest; also sauerkraut, kimchi. Supplements: MK-7 (from natto) is preferred form.

· Dose: 90-180 mcg daily (MK-7).

· Caution: Warfarin interaction (vitamin K antagonizes warfarin); stable on warfarin? Do not take without physician approval.

· Boron:

· Rationale: Trace mineral involved in calcium and magnesium metabolism; may reduce urinary calcium loss and support bone health. Evidence limited.

· Source: Fruits (apples, pears, grapes), nuts, legumes.

· Dose: 3-6 mg daily (as supplement). Do not exceed 20 mg daily.

· Strontium ranelate: Not a supplement; prescription medication for osteoporosis (not available in all countries). Increases bone formation and decreases resorption. Concern for cardiovascular risk; restricted use.

· Herbs and Phytochemicals from Indian subcontinent:

Note: These herbs do NOT directly lower or raise PTH. They may support bone health, reduce inflammation, or modulate calcium metabolism indirectly. They are not substitutes for medical treatment of parathyroid disorders.

· Guduchi / Giloy (Tinospora cordifolia):

· Rationale: Immunomodulatory; traditionally used for bone health and inflammatory conditions. May support overall health in autoimmune hypoparathyroidism.

· Form: Standardised aqueous extract.

· Caution: Theoretical immune stimulation; use only under guidance.

· Ashwagandha (Withania somnifera):

· Rationale: Adaptogen; reduces cortisol, which may benefit bone density (chronic hypercortisolism causes bone loss).

· Form: Standardised root extract (withanolides 2.5-5%).

· Caution: Avoid in hyperthyroidism; may stimulate thyroid.

· Amla (Emblica officinalis):

· Rationale: Rich in vitamin C and tannins; antioxidant, supports collagen synthesis and bone health.

· Form: Fresh fruit, juice, or standardised extract.

· Arjuna (Terminalia arjuna):

· Rationale: Traditionally used for bone health and fracture healing. Contains calcium and other minerals.

· Form: Bark extract.

· Hadjod (Cissus quadrangularis):

· Rationale: Ayurvedic herb for bone healing and fracture repair. Contains calcium and promotes osteoblast activity in animal studies.

· Form: Standardised extract.

· Shallaki (Boswellia serrata):

· Rationale: Anti-inflammatory; may benefit bone health in inflammatory conditions.

· Form: Standardised to boswellic acids.

· Important cautions:

· Avoid high-dose calcium supplements in primary hyperparathyroidism and in those with kidney stones unless specifically advised.

· Avoid calcium supplements with vitamin D in sarcoidosis/granulomatous disease (risk of hypercalcaemia).

· Avoid herbal "bone health" blends with unknown ingredients, especially if they contain synthetic folic acid, cyanocobalamin, or undeclared pharmaceuticals.

· Always inform your endocrinologist about all supplements.

c. Using Diet and Foods (Following a plant-forward, ecologically sustainable, bone-healthy approach)

Core dietary principles for calcium homeostasis and bone health:

The dietary pattern that most effectively supports bone health, maintains calcium balance, and minimizes kidney stone risk is a whole-food, plant-forward, low-sodium, adequate-protein, and high-fruit-and-vegetable diet. This aligns perfectly with ecological sustainability.

Fundamental pattern:

· Mediterranean-style, plant-dominant diet: Abundant vegetables, fruits, legumes, whole grains, nuts, seeds, extra virgin olive oil.

· Adequate but not excessive protein: Plant proteins (lentils, chickpeas, beans, tofu, tempeh) support bone health without the acid load of high animal protein.

· High in fruits and vegetables: Provide alkaline precursors, potassium, magnesium, vitamin K, and antioxidants that support bone.

· Low in sodium: High sodium increases urinary calcium excretion; limit processed foods, use herbs/spices for flavouring.

· Avoid excessive caffeine and alcohol: Both increase calcium loss.

Key dietary components for calcium intake (plant-based sources, ecological hierarchy):

· Calcium-set tofu (100 g): Approximately 350 mg. Made with calcium sulphate; check label. Sustainable soy if non-GMO, responsibly sourced.

· Fortified plant milk (250 mL): 300-450 mg. Choose unsweetened, fortified with calcium and vitamin D (lichen D3 if available).

· Fortified orange juice (250 mL): 300-350 mg. Choose brands with no added sugar.

· Tahini (sesame paste) (2 tbsp): Approximately 130 mg. Rich in copper; use in dressings, hummus.

· Almonds (30 g): Approximately 75 mg. Also provide magnesium, vitamin E.

· Collard greens (1 cup cooked): Approximately 350 mg. Low oxalate; calcium well absorbed.

· Bok choy (1 cup cooked): Approximately 160 mg. Low oxalate; good absorption.

· Kale (1 cup cooked): Approximately 100 mg. Low oxalate; good absorption.

· Broccoli (1 cup cooked): Approximately 60 mg. Also rich in vitamin K.

· Okra (1 cup cooked): Approximately 120 mg. Good source.

· Butternut squash (1 cup cooked): Approximately 85 mg.

· Chickpeas (1 cup cooked): Approximately 80 mg.

· Black beans (1 cup cooked): Approximately 45 mg.

· Figs, dried (5 figs): Approximately 135 mg. Also provide potassium, fibre.

· Oranges (1 medium): Approximately 65 mg.

· Amla (Indian gooseberry) (100 g): Approximately 50 mg. Vitamin C powerhouse; supports collagen.

Fungi and algae:

· Mushrooms: Not significant calcium sources but provide vitamin D2 if exposed to UV light during growth. Some commercially grown mushrooms are UV-treated; check labels.

· Seaweed (wakame, kombu, nori): Contain calcium but also sodium and iodine; variable. Use in moderation. Kombu very high iodine; limit in thyroid disorders.

Fermented plant foods:

· Tempeh: Made from fermented soybeans; provides calcium (especially if calcium-set), protein, and probiotics.

· Natto: Fermented soybeans; richest food source of vitamin K2 (MK-7). Excellent for bone health. Acquired taste.

· Kimchi, sauerkraut: Contain small amounts of calcium; support gut microbiome.

Dairy and eggs (permitted, not emphasised):

· Yoghurt, milk, cheese: Excellent calcium sources but ecological footprint higher than plant sources. If consumed, choose organic, pasture-raised where possible.

· Eggs: Contain calcium in shell only; flesh provides minimal.

Meat, fish, poultry (lowest priority):

· Sardines and canned salmon (with bones): Excellent calcium sources but ecological cost (overfishing) and mercury risk (sardines lower trophic level, safer).

· Not required; plant sources adequate when diet properly planned.

Practical dietary approach for bone health and calcium balance (with ecological hierarchy):

1. Base meals around calcium-set tofu, fortified plant milks, and leafy greens. Aim for at least 3-4 servings of calcium-rich plant foods daily.

2. Include daily sources of magnesium and potassium: Nuts, seeds, legumes, bananas, potatoes with skin, leafy greens.

3. Ensure adequate vitamin D: Sunlight (sensible exposure) and/or lichen-derived D3 supplement.

4. Incorporate fermented foods (tempeh, natto, kimchi, sauerkraut) for vitamin K2 and microbiome support.

5. Limit sodium: Cook from scratch, use herbs and spices, avoid ultra-processed foods.

6. Moderate caffeine (maximum 2-3 cups coffee/tea daily).

7. Limit or avoid alcohol.

8. If you consume dairy, use it as a complement, not the primary calcium source.

9. If you consume fish, choose low-trophic, sustainably sourced options (sardines, mackerel, farmed shellfish with responsible practices) occasionally.

Special considerations:

· Primary hyperparathyroidism: Do NOT restrict dietary calcium unless advised; moderate intake (800-1000 mg daily) from food is generally safe. Avoid high-dose calcium supplements. Stay well hydrated.

· Hypoparathyroidism: High calcium intake (1000-2000 mg daily) as prescribed, often with active vitamin D. Spread intake throughout day. Avoid high-oxalate foods (spinach, rhubarb, beet greens, Swiss chard) if prone to calcium oxalate stones – but calcium in diet actually binds oxalate in gut, reducing absorption; supplements between meals may increase stone risk. Individualize.

· CKD with secondary hyperparathyroidism: Dietary phosphate restriction is key. Avoid high-phosphate foods: processed foods, colas, organ meats, some legumes/nuts (but these also provide benefits; work with renal dietitian). Calcium intake depends on type of phosphate binder used.

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6. How soon can one expect improvement and the ideal time frame to retest

PTH responds at different rates depending on the intervention:

Vitamin D repletion in deficiency:

· 25-hydroxyvitamin D levels rise over weeks; PTH begins to decline within 2-4 weeks and reaches nadir by 3-6 months.

· Retest 25-OHD, PTH, calcium, phosphate 3 months after initiating therapy.

Correction of hypocalcaemia in hypoparathyroidism:

· Intravenous calcium: Immediate effect.

· Oral calcium and calcitriol: Titration over days to weeks. Monitor calcium frequently (initially weekly, then monthly) until stable.

After parathyroidectomy for primary hyperparathyroidism:

· PTH drops within minutes (used intraoperatively to confirm cure).

· Serum calcium normalises over hours to days.

· Post-operative monitoring: Calcium at 24-48 hours, then as outpatient. PTH at 1-3 months to confirm cure.

· Long-term: Annual calcium and PTH to monitor for recurrence.

CKD-MBD management:

· After initiating phosphate binders, vitamin D analogues, or calcimimetics: Recheck calcium, phosphate, PTH at 1-3 months.

· Once stable, monitor every 3-6 months depending on CKD stage.

Monitoring intervals for stable patients:

· Primary hyperparathyroidism (non-surgical): Calcium and PTH every 6-12 months; DEXA every 1-2 years.

· Hypoparathyroidism (stable): Calcium (albumin-adjusted), PTH, creatinine every 6-12 months; 24-hour urine calcium for stone risk.

· CKD (stable): Per KDIGO guidelines; typically PTH every 3-12 months depending on stage and trend.

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Conclusion

Parathyroid hormone is the conductor of the calcium orchestra – responding to the faintest whisper of hypocalcaemia, directing bone to release its stores, kidney to reclaim every filtered ion, and gut to absorb more. Yet PTH itself is never the target; it is the messenger. Treatment aims at the underlying disorder – the adenoma that secretes autonomously, the failing kidney that drives compensatory excess, the vitamin D deficiency that starves the bones, or the absent glands that leave calcium unguarded. The serum PTH level, interpreted alongside calcium, phosphate, vitamin D, and renal function, illuminates which of these scenarios is unfolding. For the patient, understanding PTH means understanding the delicate balance that keeps nerves firing, muscles contracting, and bones strong. For the clinician, it demands precision, context, and vigilance. And for both, it offers a path to restoring harmony – through surgery when needed, through vitamin D and calcium when deficient, through phosphate binders and calcimimetics when kidneys fail, and always through a diet that honours the body and the planet. PTH is a signal, not a sentence. Listen to it, investigate its cause, and treat the person it serves.

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Note on dietary recommendations on this site:

For the sake of our environment we adhere to the following dietary preference hierarchy:

1. Plant‑based

2. Fungi / algae / fermented

3. Biotechnology / lab‑grown / cultures

4. Dairy / eggs

5. Meat / fish / poultry (only if no effective alternative exists)

This approach reflects ecological responsibility, antibiotic stewardship, and the urgent need to reduce the environmental footprint of dietary recommendations. For bone health and calcium homeostasis, a well-planned plant-forward diet with calcium-set tofu, fortified plant milks, leafy greens, nuts, seeds, and legumes provides adequate calcium and other bone-supporting nutrients without the ecological cost of dairy or fish. Individual medical conditions (hypoparathyroidism, CKD) may require specific adjustments, always under medical supervision.

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