{"id":4422021,"date":"2024-12-31T11:36:42","date_gmt":"2024-12-31T17:36:42","guid":{"rendered":"https:\/\/myendoconsult.com\/learn\/?p=4422021"},"modified":"2024-12-31T11:38:46","modified_gmt":"2024-12-31T17:38:46","slug":"normal-pth-levels-by-age","status":"publish","type":"post","link":"https:\/\/myendoconsult.com\/learn\/normal-pth-levels-by-age\/","title":{"rendered":"Normal PTH levels by Age"},"content":{"rendered":"\n<h2 class=\"wp-block-heading\"><strong>Parathyroid Hormone (PTH) Blood Test<\/strong><\/h2>\n\n\n\n<p>Parathyroid hormone (PTH) is an <strong>84\u2013amino-acid peptide<\/strong> secreted predominantly by <strong>two pairs of parathyroid glands<\/strong>, located behind or adjacent to the thyroid gland in the neck. Occasionally, ectopic <a href=\"https:\/\/myendoconsult.com\/learn\/anatomy-of-the-parathyroid-gland\/\"  data-wpil-monitor-id=\"25\">parathyroid glands<\/a> may be found along their developmental route from the mediastinum to the neck. The 84-amino-acid PTH is packaged into <strong>dense secretory granules<\/strong> for regulated secretion.<\/p>\n\n\n\n<figure class=\"wp-block-image size-full\"><img loading=\"lazy\" decoding=\"async\" width=\"960\" height=\"672\" src=\"https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/PTH-Molecule.png\" alt=\"\" class=\"wp-image-4422027\" srcset=\"https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/PTH-Molecule.png 960w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/PTH-Molecule-300x210.png 300w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/PTH-Molecule-768x538.png 768w\" sizes=\"auto, (max-width: 960px) 100vw, 960px\" \/><\/figure>\n\n\n\n<p><strong>Figure 1. Structure of <a href=\"https:\/\/myendoconsult.com\/learn\/parathyroid-hormone-action-a-comprehensive-review\/\"  data-wpil-monitor-id=\"26\">Parathyroid hormone<\/a> (1-84)<\/strong><\/p>\n\n\n\n<p>Clinically, <strong>measurement of PTH in serum or plasma<\/strong> is vital for the <strong>evaluation and management<\/strong> of:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Thyroid disorders<\/strong> (e.g., in the context of thyroid surgery),<\/li>\n\n\n\n<li><strong>Kidney disorders<\/strong> (particularly chronic renal failure [CRF] and secondary Hyperparathyroidism),<\/li>\n\n\n\n<li><strong>Various causes of hyper- or hypocalcemia<\/strong> (to differentiate parathyroid vs. nonparathyroid etiologies).<\/li>\n<\/ul>\n\n\n\n<p>Since <strong>PTH<\/strong> directly influences <strong>calcium and phosphate<\/strong> homeostasis, this assay is <strong>routinely monitored<\/strong> in patients with <strong>chronic renal failure<\/strong> and in suspected or established <strong>primary Hyperparathyroidism<\/strong>.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\"><strong>Reference Ranges<\/strong> of PTH by Age<\/h2>\n\n\n\n<p>Because PTH assays measure <strong>different fragments<\/strong> of the hormone (or the intact molecule), reference ranges may <strong>vary<\/strong> based on the methodology. Standard reported ranges include:<\/p>\n\n\n\n<ol class=\"wp-block-list\">\n<li><strong>Adults (Serum)<\/strong>\n<ul class=\"wp-block-list\">\n<li><strong>C-terminal <\/strong>: 50\u2013330 pg\/mL (50\u2013330 ng\/L)<\/li>\n\n\n\n<li><strong>N-terminal<\/strong>: 8\u201324 pg\/mL (8\u201324 ng\/L)<\/li>\n\n\n\n<li><strong>Intact PTH<\/strong>: 10\u201365 pg\/mL (10\u201365 ng\/L)<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Adults (Plasma)<\/strong>\n<ul class=\"wp-block-list\">\n<li><strong>C-terminal <\/strong>: &lt;50 microLEq\/mL (&lt;50 mLEq\/L)<\/li>\n\n\n\n<li><strong>N-terminal<\/strong>: &lt;6.1 pmol\/L<\/li>\n\n\n\n<li><strong>Intact PTH<\/strong>: 1\u20135 pmol\/L<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Pediatrics<\/strong>\n<ul class=\"wp-block-list\">\n<li><strong>C-terminal <\/strong>(ages 1\u201316): 51\u2013217 pg\/mL (51\u2013217 ng\/L)<\/li>\n\n\n\n<li><strong>N-terminal<\/strong> (ages 2\u201313): 14\u201321 pg\/mL (14\u201321 ng\/L)<\/li>\n\n\n\n<li><strong>Intact PTH<\/strong> (ages 2\u201320): 9\u201352 pg\/mL (9\u201352 ng\/L)<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n\n\n\n<p>Table 1. Laboratory ranges for fractions of the PTH molecule<\/p>\n\n\n\n<table id=\"tablepress-137\" class=\"tablepress tablepress-id-137\">\n<thead>\n<tr class=\"row-1\">\n\t<th class=\"column-1\"><strong><\/strong><\/th><td class=\"column-2\"><\/td><td class=\"column-3\"><\/td><td class=\"column-4\"><\/td>\n<\/tr>\n<\/thead>\n<tbody class=\"row-striping row-hover\">\n<tr class=\"row-2\">\n\t<td class=\"column-1\"><\/td><td class=\"column-2\"><\/td><td class=\"column-3\"><\/td><td class=\"column-4\"><\/td>\n<\/tr>\n<tr class=\"row-3\">\n\t<td class=\"column-1\"><strong>Assay<\/strong><\/td><td class=\"column-2\"><strong>Assay Includes<\/strong><\/td><td class=\"column-3\"><strong>Conventional Normal Values (pg\/mL)<\/strong><\/td><td class=\"column-4\"><strong>SI Units (ng\/L)<\/strong><\/td>\n<\/tr>\n<tr class=\"row-4\">\n\t<td class=\"column-1\">PTH Intact (whole)<\/td><td class=\"column-2\">Intact PTH<\/td><td class=\"column-3\">10\u201365<\/td><td class=\"column-4\">10\u201365<\/td>\n<\/tr>\n<tr class=\"row-5\">\n\t<td class=\"column-1\">PTH N-terminal<\/td><td class=\"column-2\">N-terminal<\/td><td class=\"column-3\">8\u201324<\/td><td class=\"column-4\">8\u201324<\/td>\n<\/tr>\n<tr class=\"row-6\">\n\t<td class=\"column-1\">PTH C-terminal<\/td><td class=\"column-2\">C-terminal<\/td><td class=\"column-3\">50\u2013330<\/td><td class=\"column-4\">50\u2013330<\/td>\n<\/tr>\n<tr class=\"row-7\">\n\t<td class=\"column-1\">Midmolecule<\/td><td class=\"column-2\">Midregion<\/td><td class=\"column-3\">Not routinely measured<\/td><td class=\"column-4\">Not routinely measured<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<!-- #tablepress-137 from cache -->\n\n\n\n<h2 class=\"wp-block-heading\"><strong>Physiology and Secretory Regulation of PTH<\/strong><\/h2>\n\n\n\n<h3 class=\"wp-block-heading\"><strong>Parathyroid Glands and PTH Synthesis<\/strong><\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li>PTH is synthesized as a <strong>115-amino-acid pre-pro-peptide<\/strong> but <strong>84\u2013amino-acid PTH<\/strong> is the primary secreted form.<\/li>\n\n\n\n<li>The <strong>major regulatory signal<\/strong> for PTH secretion is <strong>serum calcium<\/strong>. When <strong>ionized calcium<\/strong> rises, PTH secretion <strong>falls<\/strong>. When calcium levels drop, PTH levels <strong>increase<\/strong>.<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\"><strong>Calcium-Sensing Receptor (CaSR)<\/strong><\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li>The <strong>parathyroid glands<\/strong> express a <strong>cell-surface calcium-sensing receptor (CaSR)<\/strong>, which detects extracellular calcium.<\/li>\n\n\n\n<li><strong>Gain-of-function mutations<\/strong> of the CaSR can lead to <strong>autosomal dominant hypocalcemia (ADH)<\/strong>, while <strong>loss-of-function<\/strong> mutations cause <strong>familial hypocalciuric hypercalcemia (FHH)<\/strong>.<\/li>\n\n\n\n<li><strong>Calcimimetics<\/strong> (e.g., cinacalcet, etelcalcetide) activate the CaSR to reduce PTH secretion, useful in secondary Hyperparathyroidism (CKD) and certain severe <a href=\"https:\/\/myendoconsult.com\/learn\/primary-hyperparathyroidism-a-comprehensive-guide-for-patients\/\"  data-wpil-monitor-id=\"27\">primary hyperparathyroid<\/a> cases.<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\"><strong>Magnesium and Vitamin D Impact<\/strong><\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Magnesium<\/strong> also plays a role: severe or prolonged hypomagnesemia can <strong>blunt<\/strong> PTH secretion.<\/li>\n\n\n\n<li><strong>1,25-Dihydroxyvitamin D (1,25-D)<\/strong> also <strong>inhibits<\/strong> PTH gene transcription.<\/li>\n\n\n\n<li>Serum phosphate may <strong>directly<\/strong> or <strong>indirectly<\/strong> modulate PTH, although data are somewhat mixed.<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\"><strong>Metabolism and Clearance of PTH<\/strong><\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>PTH<\/strong> has a <strong>circulating half-life<\/strong> of about <strong>&lt;5 minutes<\/strong>.<\/li>\n\n\n\n<li>Hormone fragments (N-terminal, midregion, C-terminal) are produced mainly in the <strong>liver<\/strong> and <strong>kidney<\/strong>.<\/li>\n\n\n\n<li><strong>C-terminal<\/strong> fragments are cleared by <strong>glomerular filtration<\/strong>, so they <strong>accumulate in renal failure<\/strong>.<\/li>\n\n\n\n<li>Only the <strong>amino terminus<\/strong> (PTH 1\u201334) has <strong>full biological<\/strong> activity.<\/li>\n\n\n\n<li><strong>Intact PTH<\/strong> assays measure PTH 1\u201384 plus certain fragments (e.g., 7\u201384). \u201cWhole\u201d or \u201cbio-intact\u201d assays aim to detect only <strong>PTH 1\u201384<\/strong>, but many labs still use the <strong>intact PTH<\/strong> test.<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\"><strong>Biologic Effects of PTH<\/strong><\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Bone<\/strong>: In high levels (as in Hyperparathyroidism), PTH <strong>increases osteoclastic bone resorption<\/strong>. Intermittent low-dose PTH can <strong>increase osteoblastic bone formation<\/strong> (used therapeutically for osteoporosis, e.g., teriparatide).<\/li>\n\n\n\n<li><strong>Kidney<\/strong>: PTH <strong>increases calcium reabsorption<\/strong> in the distal tubule and <strong>decreases phosphate reabsorption<\/strong> in the proximal tubule, contributing to <strong>hypercalcemia<\/strong> and <strong>hypophosphatemia<\/strong>.<\/li>\n\n\n\n<li><strong>Intestine<\/strong>: PTH indirectly <strong>enhances calcium<\/strong> and <strong>phosphate<\/strong> absorption <strong>via<\/strong> increased renal synthesis of <strong>1,25-dihydroxyvitamin D<\/strong>.<\/li>\n\n\n\n<li><strong>Major Receptor<\/strong>: PTH\/PTHrP receptor, activating cAMP and phospholipase C pathways.<\/li>\n<\/ul>\n\n\n\n<h2 class=\"wp-block-heading\"><strong>Indications &amp; Uses<\/strong><\/h2>\n\n\n\n<ol class=\"wp-block-list\">\n<li><strong>Parathyroidectomy for Primary Hyperparathyroidism<\/strong>\n<ul class=\"wp-block-list\">\n<li><strong>Intraoperative PTH monitoring<\/strong>: a drop of >50% post-resection suggests surgical success.<\/li>\n\n\n\n<li><strong>Long-term cure<\/strong> is also linked to normal serum calcium (&lt;10.2 mg\/dL) within six months after surgery.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Hypocalcemia Secondary to Thyroidectomy<\/strong>\n<ul class=\"wp-block-list\">\n<li>A <strong>single intraoperative or postoperative<\/strong> intact PTH measurement can predict development of symptomatic hypocalcemia and guide <strong>vitamin D supplementation<\/strong>.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Suspected Hypercalcemia due to Hyperparathyroidism<\/strong>\n<ul class=\"wp-block-list\">\n<li><strong>Mild hypercalcemia<\/strong> + <strong>high-normal or elevated PTH<\/strong> suggests primary Hyperparathyroidism.<\/li>\n\n\n\n<li><strong>Decreased PTH<\/strong> is typical in <strong>nonparathyroid hypercalcemic disorders<\/strong> (e.g., malignancy).<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Chronic Kidney Disease (CKD)<\/strong>\n<ul class=\"wp-block-list\">\n<li><strong>Elevated PTH<\/strong> and <strong>secondary Hyperparathyroidism<\/strong> are common, especially in stage 3 or worse (GFR &lt;60 mL\/min\/1.73 m^2).<\/li>\n\n\n\n<li><strong>Target ranges<\/strong> of intact PTH vary by CKD stage. For example:\n<ul class=\"wp-block-list\">\n<li>Stage 3: 35\u201370 pg\/mL<\/li>\n\n\n\n<li>Stage 4: 70\u2013110 pg\/mL<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li>Patients with repeated iPTH >800 pg\/mL who fail standard interventions may be candidates for <strong>parathyroidectomy<\/strong>.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Hypocalcemia<\/strong>\n<ul class=\"wp-block-list\">\n<li>Elevated PTH in the face of low serum calcium can be seen with <strong>intestinal malabsorption, vitamin D deficiency, renal failure, or hereditary vitamin D resistance<\/strong>.<\/li>\n\n\n\n<li>If PTH is <strong>not<\/strong> elevated in hypocalcemia, consider <strong>primary parathyroid failure<\/strong>.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Suspected or Known Bone Disease<\/strong>\n<ul class=\"wp-block-list\">\n<li><strong>Elevated PTH<\/strong> is associated with <strong>hyperparathyroid bone disease<\/strong>.<\/li>\n\n\n\n<li>CKD patients often require <strong>2\u20133 times<\/strong> normal PTH for normal <a href=\"https:\/\/myendoconsult.com\/learn\/bone-turnover-markers-in-osteoporosis\/\"  data-wpil-monitor-id=\"28\">bone turnover<\/a>.<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n\n\n\n<p><\/p>\n\n\n\n<h2 class=\"wp-block-heading\"><strong>Chronic Kidney Disease and PTH Monitoring<\/strong><\/h2>\n\n\n\n<ul class=\"wp-block-list\">\n<li>In CKD, the test helps distinguish <strong>secondary Hyperparathyroidism<\/strong>, especially in:\n<ul class=\"wp-block-list\">\n<li>Stage 3: GFR 30\u201359 mL\/min\/1.73 m^2 \u2192 measure PTH every 12 months<\/li>\n\n\n\n<li>Stage 4: GFR 15\u201329 mL\/min\/1.73 m^2 \u2192 measure PTH every 3 months<\/li>\n\n\n\n<li>Stage 5: GFR &lt;15 or on dialysis \u2192 measure PTH every 3 months<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Dietary phosphorus<\/strong> restriction (800\u20131,000 mg\/day) is recommended if iPTH levels exceed target.<\/li>\n\n\n\n<li><strong>Elevated iPTH<\/strong> (>500\u2013600 pg\/mL) can indicate moderate\/severe secondary Hyperparathyroidism.<\/li>\n<\/ul>\n\n\n\n<h2 class=\"wp-block-heading\"><strong>Clinical Application<\/strong> Of pTH monitoring<\/h2>\n\n\n\n<ul class=\"wp-block-list\">\n<li>PTH is secreted in <strong>response to hypocalcemia<\/strong>, returning serum calcium to normal. When serum calcium normalizes, PTH secretion <strong>diminishes<\/strong>.<\/li>\n\n\n\n<li>This test is <strong>critical<\/strong> for diagnosing <strong>Hyperparathyroidism<\/strong> and differentiating <strong>parathyroid vs. nonparathyroid<\/strong> causes of <strong>hypercalcemia<\/strong>.<\/li>\n\n\n\n<li><strong>Simultaneous measurement<\/strong> of <strong>serum calcium<\/strong> is essential for interpretation. Many labs provide <strong>PTH\/calcium nomograms<\/strong>.<\/li>\n<\/ul>\n\n\n\n<table id=\"tablepress-138\" class=\"tablepress tablepress-id-138\">\n<thead>\n<tr class=\"row-1\">\n\t<th class=\"column-1\"><strong>Condition<\/strong><\/th><th class=\"column-2\"><strong>PTH Levels<\/strong><\/th><th class=\"column-3\"><strong>Calcium Levels<\/strong><\/th><th class=\"column-4\"><strong>Underlying Mechanism<\/strong><\/th>\n<\/tr>\n<\/thead>\n<tbody class=\"row-striping row-hover\">\n<tr class=\"row-2\">\n\t<td class=\"column-1\">Primary Hyperparathyroidism<\/td><td class=\"column-2\">Elevated<\/td><td class=\"column-3\">Elevated<\/td><td class=\"column-4\">Adenoma or carcinoma autonomously producing PTH<\/td>\n<\/tr>\n<tr class=\"row-3\">\n\t<td class=\"column-1\">Secondary Hyperparathyroidism<\/td><td class=\"column-2\">Elevated<\/td><td class=\"column-3\">Normal\/Low<\/td><td class=\"column-4\">CRF or malabsorption causing compensatory PTH increase<\/td>\n<\/tr>\n<tr class=\"row-4\">\n\t<td class=\"column-1\">Tertiary Hyperparathyroidism<\/td><td class=\"column-2\">Elevated<\/td><td class=\"column-3\">Elevated<\/td><td class=\"column-4\">Autonomous PTH production in prolonged secondary hyperparathyroidism<\/td>\n<\/tr>\n<tr class=\"row-5\">\n\t<td class=\"column-1\">Hypoparathyroidism<\/td><td class=\"column-2\">Decreased<\/td><td class=\"column-3\">Low<\/td><td class=\"column-4\">Surgical\/autoimmune ablation or compensatory response to hypercalcemia<\/td>\n<\/tr>\n<tr class=\"row-6\">\n\t<td class=\"column-1\">Pseudohyperparathyroidism<\/td><td class=\"column-2\">Elevated<\/td><td class=\"column-3\">Low<\/td><td class=\"column-4\">Congenital renal resistance to PTH<\/td>\n<\/tr>\n<tr class=\"row-7\">\n\t<td class=\"column-1\">Malignancy-related Hypercalcemia<\/td><td class=\"column-2\">Decreased\/Normal<\/td><td class=\"column-3\">Elevated<\/td><td class=\"column-4\">Ectopic PTH-related protein or bone metastasis<\/td>\n<\/tr>\n<tr class=\"row-8\">\n\t<td class=\"column-1\">Vitamin D Deficiency<\/td><td class=\"column-2\">Elevated<\/td><td class=\"column-3\">Low<\/td><td class=\"column-4\">Impaired intestinal calcium absorption<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<!-- #tablepress-138 from cache -->\n\n\n\n<p>In patients with <strong>secondary<\/strong> or <strong>tertiary hyperparathyroidism (HPT)<\/strong>, especially those with <strong>chronic renal failure (CRF)<\/strong> or post\u2013renal transplant, <strong>intraoperative parathyroid hormone (IOPTH) monitoring<\/strong> offers a valuable tool for guiding surgical management. By measuring the <strong>drop in PTH levels<\/strong> immediately after resecting hyperfunctioning parathyroid tissue, clinicians can confirm <strong>adequate gland removal<\/strong> and reduce the likelihood of missed or supernumerary glands.<\/p>\n\n\n\n<p><strong>Clinical Pearls<\/strong>:<\/p>\n\n\n\n<ol class=\"wp-block-list\">\n<li><strong>Indicator of Surgical Success<\/strong>\n<ul class=\"wp-block-list\">\n<li>A <strong>significant decline<\/strong> in IOPTH (for example, <strong>>50\u201380%<\/strong> at 10 to 20 minutes) strongly predicts <strong>operative cure<\/strong> in both secondary (CRF-related) and tertiary (post-transplant) HPT.<\/li>\n\n\n\n<li>In some studies, a <strong>\u226590% drop<\/strong> has been associated with nearly <strong>100% specificity<\/strong>, indicating near-certain success if that threshold is met.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Practical Advantages<\/strong>\n<ul class=\"wp-block-list\">\n<li><strong>Prevents Reoperation<\/strong>: Rapid IOPTH feedback helps detect any remaining hyperfunctioning parathyroid tissue, reducing the risk of persistent or recurrent disease.<\/li>\n\n\n\n<li><strong>Flexible Cutoffs<\/strong>: Different thresholds (e.g., <strong>70%\u201380%<\/strong> at 20 minutes versus <strong>>90%<\/strong> at 40 minutes) can be tailored to the clinical setting, surgical timing, and renal clearance considerations.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Role in Renal HPT<\/strong>\n<ul class=\"wp-block-list\">\n<li>Patients with <strong>CKD<\/strong> often accumulate inactive PTH fragments, affecting standard assays. Despite this, IOPTH still improves the overall cure rate when thresholds are adjusted for delayed PTH clearance.<\/li>\n\n\n\n<li><strong>Total parathyroidectomy with autotransplantation<\/strong>, guided by IOPTH, remains a mainstay for refractory secondary\/tertiary HPT.<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n\n\n\n<p>Overall, <strong>IOPTH monitoring<\/strong> allows surgeons to <strong>confirm complete parathyroid resection intraoperatively<\/strong>, thus minimizing failure rates and improving outcomes for renal HPT patients whose disease is resistant to medical therapy.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\"><strong>Test Procedure &amp; Specimen Requirements<\/strong><\/h2>\n\n\n\n<p>For the <strong>12 hours preceding specimen collection<\/strong>, the patient should <strong>avoid taking<\/strong> any <strong>multivitamins or dietary supplements<\/strong> (including <strong>hair, skin, and nail supplements<\/strong>) that contain <strong>biotin (vitamin B7)<\/strong>. The patient should also <strong>remain fasting<\/strong> for <strong>12 hours<\/strong> before providing the specimen.<\/p>\n\n\n\n<p>The recommended <strong>supply<\/strong> is the <strong>Sarstedt Aliquot Tube (5 mL; T914)<\/strong>. The <strong>preferred collection container<\/strong> is a <strong>serum gel tube<\/strong>, although a <strong>red-top tube<\/strong> is also acceptable. For submission, a <strong>plastic vial<\/strong> is required with a <strong>specimen volume<\/strong> of <strong>1 mL<\/strong>. After collection, <strong>centrifuge<\/strong> the sample and <strong>transfer<\/strong> the serum to the plastic vial for final submission.<\/p>\n\n\n\n<ol class=\"wp-block-list\">\n<li><strong>Sample Tube<\/strong>\n<ul class=\"wp-block-list\">\n<li><strong>Red top<\/strong> or <strong>serum separator tube<\/strong> for serum PTH.<\/li>\n\n\n\n<li><strong>Plasma<\/strong> samples often drawn in <strong>EDTA tubes<\/strong> (check lab protocol).<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Drawing the Sample<\/strong>\n<ul class=\"wp-block-list\">\n<li>Typically, an <strong>8 AM fasting<\/strong> sample is drawn.<\/li>\n\n\n\n<li><strong>PTH<\/strong> has a <strong>diurnal variation<\/strong>: highest ~2 AM, lowest ~2 PM. Adjust if the patient works nights.<\/li>\n\n\n\n<li>Obtain a <strong>serum calcium<\/strong> level simultaneously, if ordered.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Patient Instructions<\/strong>\n<ul class=\"wp-block-list\">\n<li><strong>Explain<\/strong> the procedure.<\/li>\n\n\n\n<li>Generally, the patient is <strong>NPO<\/strong> (nothing by mouth except water) after midnight.<\/li>\n\n\n\n<li>Apply <strong>pressure\/pressure dressing<\/strong> to the site post-venipuncture.<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n\n\n\n<h2 class=\"wp-block-heading\"><strong>Additional Insights from Research<\/strong><\/h2>\n\n\n\n<ol class=\"wp-block-list\">\n<li><strong>Regulation of PTH Secretion<\/strong>\n<ul class=\"wp-block-list\">\n<li><strong>CaSR<\/strong> (calcium-sensing receptor) is pivotal in <strong>familial hypocalciuric hypercalcemia<\/strong> and other genetic variants.<\/li>\n\n\n\n<li><strong>Calcimimetics<\/strong> (e.g., cinacalcet, etelcalcetide) are helpful in <strong>CKD<\/strong>-related Hyperparathyroidism or <strong>parathyroid carcinoma<\/strong>.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Metabolism and Clearance<\/strong>\n<ul class=\"wp-block-list\">\n<li>The <strong>liver<\/strong> and <strong>kidney<\/strong> degrade PTH, producing multiple fragments with varying half-lives.<\/li>\n\n\n\n<li>In <strong>renal failure<\/strong>, <strong>C-terminal fragments<\/strong> accumulate, which can affect certain PTH assays.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Biologic Activity<\/strong>\n<ul class=\"wp-block-list\">\n<li>The <strong>N-terminal region<\/strong> (especially residues 1\u201334) has the main <strong>biologic effect<\/strong>.<\/li>\n\n\n\n<li>The <strong>C-terminal<\/strong> portion may have a minor or antagonistic action.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Bone Effects<\/strong>\n<ul class=\"wp-block-list\">\n<li><strong>High PTH<\/strong> => osteoclastic bone resorption (hyperparathyroid bone disease).<\/li>\n\n\n\n<li><strong>Intermittent, low-dose<\/strong> => osteoblastic bone formation (therapeutic usage in <strong>osteoporosis<\/strong>).<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Clinical Relevance<\/strong>\n<ul class=\"wp-block-list\">\n<li><strong>Hyperparathyroidism<\/strong>: elevated PTH with hypercalcemia.<\/li>\n\n\n\n<li><strong>Hypoparathyroidism<\/strong>: low or inappropriately normal PTH with hypocalcemia.<\/li>\n\n\n\n<li><strong>Secondary Hyperparathyroidism<\/strong> in CKD: often very <strong>high PTH<\/strong> with <strong>hypercortical<\/strong> bone changes and electrolyte derangements.<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n\n\n\n<p><strong>Reference<\/strong><\/p>\n\n\n\n<p>Einbinder Y, Benchetrit S, Golan E, Zitman-Gal T. Comparison of Intact PTH and Bio-Intact PTH Assays Among Non-Dialysis Dependent Chronic Kidney Disease Patients. Ann Lab Med. 2017 Sep;37(5):381-387. doi: 10.3343\/alm.2017.37.5.381. PMID: 28643486; PMCID: PMC5500736.<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Parathyroid Hormone (PTH) Blood Test Parathyroid hormone (PTH) is an 84\u2013amino-acid peptide secreted predominantly by two pairs of parathyroid glands, located behind or adjacent to the thyroid gland in the neck. Occasionally, ectopic parathyroid glands may be found along their developmental route from the mediastinum to the neck. The 84-amino-acid PTH is packaged into dense [&hellip;]<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[47],"tags":[],"class_list":["post-4422021","post","type-post","status-publish","format-standard","hentry","category-endocrine-disease-parathyroid-calcium-and-bone-metabolism","post-wrapper","thrv_wrapper"],"_links":{"self":[{"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/posts\/4422021","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/comments?post=4422021"}],"version-history":[{"count":13,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/posts\/4422021\/revisions"}],"predecessor-version":[{"id":4422039,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/posts\/4422021\/revisions\/4422039"}],"wp:attachment":[{"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/media?parent=4422021"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/categories?post=4422021"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/tags?post=4422021"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}