The Adrenal, Gonadal, and Parathyroid-Vitamin D Axes

Timing, posture, tube, and temperature

These reference intervals assume specific collection conditions. When collection differs, the result may no longer be comparable with the interval. Two requirements in the table below are opposites, and confusing them is the most common preanalytic error in adrenal testing. ACTH must be chilled immediately. Renin must not be chilled before its plasma is separated.

Zones and their products

The cortex makes three classes of steroid from cholesterol under separate control. The zona glomerulosa makes aldosterone, driven principally by angiotensin II and potassium, with ACTH contributing only transiently, which is why aldosterone is not an ACTH-dependent test. The zona fasciculata makes cortisol under the hypothalamic-pituitary-adrenal (HPA) axis, and cortisol closes the loop by suppressing corticotropin-releasing hormone (CRH) and ACTH. The zona reticularis makes the adrenal androgens dehydroepiandrosterone (DHEA), DHEA-S, and androstenedione, which follow ACTH without a dedicated tropic hormone. ACTH acutely drives cholesterol transfer mediated by steroidogenic acute regulatory protein (StAR) into the mitochondrion, the rate-limiting step, after which CYP11A1 converts cholesterol to pregnenolone and zone-enriched enzymes distributed between mitochondria and endoplasmic reticulum complete each pathway.^{11 Rifai N, et al. Tietz Textbook of Laboratory Medicine. 2023.}

CRH from the hypothalamus stimulates pituitary ACTH, and ACTH stimulates adrenal cortisol. Low cortisol with high ACTH supports primary adrenal failure. Low cortisol with ACTH that is low or inappropriately normal supports central insufficiency. Routine localization uses the paired ACTH and cortisol results because pituitary and hypothalamic causes do not share one CRH pattern.^{13,1413 Fleseriu M, et al. Hormonal replacement in hypopituitarism in adults. 2016.14 Bornstein SR, et al. Diagnosis and treatment of primary adrenal insufficiency. 2016.}

Cortisol and ACTH

Corticosteroid-binding globulin carries about 80 to 90% of serum cortisol and albumin about 10 to 15%, leaving roughly 3 to 5% unbound and biologically active. Estrogen therapy, oral contraceptives, and pregnancy raise the binding globulin and therefore total cortisol. Critical illness, hypoalbuminemia, nephrotic syndrome, and liver disease lower total cortisol without an equivalent change in the free fraction. A total cortisol result cannot be interpreted in those states without knowing the binding status, which is why a measure of the unbound fraction, serum free cortisol or salivary cortisol, is preferred there.^{1515 Choi MH. Clinical and technical aspects in free cortisol measurement. 2022.}

Cortisol reference intervals are method-specific, so quote them from the performing method. Standardized monoclonal immunoassays and LC-MS/MS read lower than the older polyclonal assays from which many published cutoffs were derived. A legacy threshold applied to a modern assay therefore overcalls insufficiency.

ACTH has the strictest handling requirements of these endocrine specimens. Collect it in EDTA, place it on ice at once, centrifuge it in a refrigerated centrifuge, and freeze a plastic aliquot. The peptide adsorbs to untreated glass and is degraded by proteases at room temperature, and both cause a falsely low result, as does hemolysis. Secretion is episodic with a morning peak, so record the collection time with the result. Draw the specimen before any glucocorticoid is given.

Screening for hypercortisolism

Once exogenous glucocorticoid exposure is excluded, screening uses one of three specimen-defined tests, each repeated because within-subject variation is high: 24-hour urine free cortisol on at least two collections, late-night salivary cortisol on at least two samples, or the 1 mg overnight dexamethasone suppression test. An abnormal result is followed by a second recommended test, and two concordantly abnormal different tests support the diagnosis.^{1616 Nieman LK, et al. The diagnosis of Cushing's syndrome. 2008.} The laboratory is responsible for the collection conditions that each test requires.

For 24-hour urine free cortisol, the patient discards the first morning void, collects every void for 24 hours including the next morning's first void, and refrigerates during collection. Creatinine on the same collection assesses completeness, because an incomplete collection reads falsely low and an over-collection falsely high. Forced high fluid intake raises measured excretion, and the test is unreliable once creatinine clearance falls below about 60 mL/min.^{99 Casals G, et al. Cortisol measurements in Cushing's syndrome. 2020.}

Late-night salivary cortisol is collected between about 11 PM and midnight, or at a habitual bedtime validated locally for shift workers, with no food, drink, or toothbrushing for at least 30 minutes beforehand. Blood contamination from gingival bleeding invalidates the sample, and topical or oral hydrocortisone contaminates it directly. Saliva requires a method validated for that matrix, and a serum cortisol assay cannot be used on saliva without that validation.

For the 1 mg overnight test, dexamethasone is taken at 11 PM to midnight and cortisol collected at 8 to 9 AM, with a value above 1.8 µg/dL (50 nmol/L) indicating failure to suppress. Drugs that induce dexamethasone metabolism, including rifampin and enzyme-inducing anticonvulsants, cause false nonsuppression, and raised binding globulin from estrogen can lift total cortisol above the cutoff. Measuring dexamethasone on the same specimen distinguishes poor exposure or nonadherence from true nonsuppression.^{99 Casals G, et al. Cortisol measurements in Cushing's syndrome. 2020.} ACTH is measured after hypercortisolism is confirmed, to separate ACTH-dependent from ACTH-independent disease.

Adrenal insufficiency

Morning cortisol thresholds differ for suspected central and suspected primary insufficiency. For suspected central insufficiency, an 8 to 9 AM cortisol below 3 µg/dL (about 80 nmol/L) is indicative, above 15 µg/dL (about 400 nmol/L) makes it unlikely, and intermediate values call for stimulation testing.^{1313 Fleseriu M, et al. Hormonal replacement in hypopituitarism in adults. 2016.} For suspected primary insufficiency, a morning cortisol below 5 µg/dL (about 140 nmol/L) with an ACTH above twice the assay upper limit is preliminary evidence when stimulation cannot be performed, and the paired ACTH localizes the defect to the adrenal gland.^{1414 Bornstein SR, et al. Diagnosis and treatment of primary adrenal insufficiency. 2016.} A random cortisol neither confirms nor excludes insufficiency.

The standard cosyntropin test gives 250 µg of ACTH 1-24, with cortisol at baseline and at 30 or 60 minutes, measured by the same assay throughout. The traditional peak threshold of 18 µg/dL (500 nmol/L) came from older immunoassays and runs too high for current specific methods, where reported 30-minute cutoffs sit nearer 15 µg/dL and vary by platform and sampling time.^{1717 Javorsky BR, et al. New cutoffs for the biochemical diagnosis of adrenal… 2021.} Separate morning cortisol bands apply when testing for recovery of the axis after chronic glucocorticoid therapy: above 10 µg/dL (300 nmol/L) suggests recovery, 5 to 10 µg/dL (150 to 300 nmol/L) calls for a later repeat, and below 5 µg/dL (150 nmol/L) indicates continued suppression.^{1818 Beuschlein F, et al. European Society of Endocrinology and Endocrine Society joint… 2024.}

Aldosterone and renin

Primary aldosteronism is aldosterone production that is relatively autonomous and not appropriately suppressible by sodium loading. Hypokalemia and metabolic alkalosis accompany the more severe presentations, but normokalemia is common, so a normal potassium does not exclude it. Current guidance suggests screening hypertensive patients with aldosterone, renin, and their ratio, interpreted alongside potassium, and no longer requires confirmatory suppression testing in every positive case.^{22 Adler GK, et al. Primary aldosteronism. 2025.}

Most errors with this pair involve renin, because two different measurands share the name. Plasma renin activity is an enzymatic assay reporting angiotensin I generated per volume per unit time, in ng/mL/h. Direct renin concentration is an immunoassay reporting mass or activity units, commonly mIU/L. They are not interchangeable, conversion between them is unreliable, and the ratio cutoff differs with the measurand and the units, so report the ratio with its units and the renin method. A positive screen generally requires suppressed renin together with an inappropriately high aldosterone, and the guideline's aldosterone threshold is itself method-dependent, set lower for LC-MS/MS than for immunoassay because immunoassays overestimate low aldosterone.^{22 Adler GK, et al. Primary aldosteronism. 2025.}

Two analytical problems are common. Cryoactivation converts prorenin to active renin when EDTA blood or plasma is chilled, refrigerated, or repeatedly frozen and thawed, giving a falsely high renin and a falsely low ratio. For this reason, renin specimens are transported at room temperature. Suppressed renin also has to be measured near the assay's lowest reportable concentration, where imprecision is worst, so a ratio calculated from a renin below that limit is reported as a greater-than value.

Medications shift both components, and the ratio can be falsely positive or negative depending on which drug is on board. Mineralocorticoid receptor antagonists, amiloride, and potassium-wasting diuretics have the largest effect, followed by ACE inhibitors, angiotensin receptor blockers, beta blockers, and central alpha-2 agonists. Estrogen-containing contraceptives affect renin activity and direct renin concentration differently, so the choice of renin measurement can determine whether a false positive occurs. Drugs are withdrawn only with the prescriber's agreement, so in practice the result is interpreted against the medications actually taken.

Adrenal androgens and 21-hydroxylase deficiency

DHEA-S is the most abundant adrenal steroid and the preferred adrenal androgen marker. Its long half-life gives a stable pool without the circadian variation that DHEA and androstenedione share with cortisol, and because the ovary lacks the relevant sulfotransferase, circulating DHEA-S is overwhelmingly adrenal. DHEA itself has adrenal, ovarian, and peripheral sources. Interpretation depends entirely on age- and sex-specific intervals: concentrations rise after adrenarche (the childhood onset of adrenal androgen production), peak in the third decade, then fall by a few percent per year to a small fraction of peak in old age. Results are not transferable between methods, and immunoassay bias is greatest in neonatal and pediatric specimens.

Congenital adrenal hyperplasia is an enzyme defect in this pathway, and the laboratory identifies the steroid that accumulates before the defective step.^{44 Speiser PW, et al. Congenital adrenal hyperplasia due to steroid 21-hydroxylase… 2018.}

Newborn screening measures 17-hydroxyprogesterone in a dried blood spot by immunoassay. False positives are common because prematurity, low birth weight, and illness raise 17-hydroxyprogesterone and because fetal steroid sulfates cross-react, so cutoffs are stratified by gestational age and collection age, and preterm or sick infants are rescreened. Collection before 24 hours of life is unreliable, so programs sample at 24 to 48 hours. Second-tier LC-MS/MS steroid profiling reduces false positives, and each laboratory validates the ratios used in it locally. Confirmatory serum 17-hydroxyprogesterone is drawn early in the morning, and in the follicular phase for menstruating patients.^{44 Speiser PW, et al. Congenital adrenal hyperplasia due to steroid 21-hydroxylase… 2018.}

Catecholamine synthesis runs from tyrosine through DOPA to dopamine in the cytosol and to norepinephrine in storage vesicles, and cortisol-dependent phenylethanolamine N-methyltransferase (PNMT) converts norepinephrine to epinephrine. Most circulating norepinephrine comes from sympathetic nerves, and most circulating epinephrine comes from the adrenal medulla.^{11 Rifai N, et al. Tietz Textbook of Laboratory Medicine. 2023.}

The preferred test follows from catecholamine metabolism. Catechol-O-methyltransferase (COMT) methylates norepinephrine to normetanephrine, epinephrine to metanephrine, and dopamine to 3-methoxytyramine. Vanillylmandelic acid is a downstream hepatic end product. Membrane-bound COMT inside chromaffin cells performs that conversion continuously on catecholamines leaking from storage vesicles, independently of hormone release, so the O-methylated metabolites provide more useful measurements than the catecholamines.^{33 Eisenhofer G, et al. Biochemical assessment of pheochromocytoma and paraganglioma. 2023.}

First-line testing is plasma free metanephrines or 24-hour urine fractionated metanephrines by LC-MS/MS, with plasma performing better in patients screened because of an incidentaloma or genetic predisposition. Plasma 3-methoxytyramine identifies dopamine-producing tumors, head and neck paragangliomas, and metastatic disease. Published sensitivity and specificity vary with assay, posture, and population, so no single figure applies to every laboratory.^{33 Eisenhofer G, et al. Biochemical assessment of pheochromocytoma and paraganglioma. 2023.}

Preanalytical control determines specificity, and seated collection is the leading cause of false positives. Draw blood fully supine after at least 20 to 30 minutes of rest, and read the result against supine intervals. Refrigerate urine collections and document the volume and interval; creatinine assesses completeness. Acidify only when the method calls for it, because low pH degrades some current methods. Reduced kidney function raises upper reference limits substantially, and acute illness and obstructive sleep apnea raise normetanephrine.

Drugs and physiologic factors raise specific metabolites. Tricyclic antidepressants, serotonin-norepinephrine reuptake inhibitors, and phenoxybenzamine raise normetanephrine; monoamine oxidase inhibitors raise both metanephrines; levodopa raises 3-methoxytyramine; and sympathomimetics, nicotine, and caffeine raise catecholamines and their metabolites. Essential medications are not stopped without the prescriber, so a borderline result is repeated after the preanalytic conditions are corrected. Values above twice the upper reference limit, or elevations of two or more metabolites, strongly suggest a tumor. An isolated borderline normetanephrine is the usual indication for a clonidine suppression test.

Two elements of the older testing algorithm are now superseded. Vanillylmandelic acid and urinary total or deconjugated catecholamines and metanephrines are no longer first-line tests, and colorimetric and fluorometric methods have been replaced for this purpose. LC-MS/MS is the preferred method, and a validated liquid chromatography method with electrochemical detection remains acceptable.^{3,263 Eisenhofer G, et al. Biochemical assessment of pheochromocytoma and paraganglioma. 2023.26 Lenders JWM, et al. Pheochromocytoma and paraganglioma. 2014.} The benign and malignant categories have also been retired. The 2022 WHO classification treats all pheochromocytomas and paragangliomas as having metastatic potential and uses the term metastatic only where spread is documented.^{1919 Mete O, et al. Overview of the 2022 WHO classification of paragangliomas and… 2022.} Roughly 80 to 85% of these tumors are adrenal pheochromocytomas and 15 to 20% are sympathetic paragangliomas, with metastatic behavior varying widely by site and genotype. Chromogranin A is not a first-line test, and proton pump inhibitors and reduced kidney function raise it.

Testosterone, SHBG, and free testosterone

Total testosterone is measured on a fasting morning specimen and confirmed on a second morning specimen, because a single value misclassifies frequently. Direct automated immunoassays are inaccurate and imprecise at the concentrations found in women, children, and hypogonadal men, so measure those specimens by LC-MS/MS.^{5,105 Bhasin S, et al. Testosterone therapy in men with hypogonadism. 2018.10 Centers for Disease Control and Prevention. Hormone standardization program.}

Changes in sex hormone-binding globulin (SHBG) can make total testosterone misleading. Testosterone circulates bound tightly to SHBG and loosely to albumin, leaving a small free fraction. SHBG rises with aging, hyperthyroidism, estrogen therapy and oral contraceptives, cirrhosis, anticonvulsants, and HIV infection, and falls with obesity, insulin resistance and type 2 diabetes, hypothyroidism, nephrotic syndrome, glucocorticoids, androgens, and growth hormone excess. When SHBG is abnormal, or total testosterone sits near the lower reference limit, free testosterone is the appropriate measurement.

Free testosterone methods differ in reliability. Equilibrium dialysis or ultrafiltration with mass spectrometry is the reference method. Calculation from total testosterone, SHBG, and albumin is acceptable when the equation is accurate. The direct analog free testosterone immunoassay is unreliable and is not recommended.^{55 Bhasin S, et al. Testosterone therapy in men with hypogonadism. 2018.} Dihydrotestosterone likewise requires mass spectrometry, because immunoassays cross-react with testosterone present at far higher concentrations.

Estradiol, progesterone, and cycle timing

Cycle timing matters for selected reproductive tests. Record the cycle day when it is relevant and available, along with menstrual and medication history. Basal FSH, LH, and estradiol for ovarian-reserve assessment are commonly drawn early in the follicular phase, progesterone in the mid-luteal phase about 7 days before expected menses to document ovulation, and 17-hydroxyprogesterone in the early follicular phase. Anti-Müllerian hormone is comparatively cycle-independent but is not fully harmonized across assay generations.

Estradiol immunoassays have the same problem at low concentrations. Automated immunoassays are unreliable in men, postmenopausal women, children, and patients on aromatase inhibitors, and they cross-react with estrone, estriol, conjugated estrogens, and exogenous preparations, so measure low concentrations by LC-MS/MS.^{1010 Centers for Disease Control and Prevention. Hormone standardization program.} At the other extreme, ovarian stimulation produces concentrations above the measuring range and requires validated dilution. Progesterone immunoassays cross-react with 17-hydroxyprogesterone and progestin medications, and secretion is pulsatile, so a single mid-luteal value is supporting evidence only.

Gonadotropins and hCG

LH, FSH, thyroid-stimulating hormone (TSH), and hCG share an alpha subunit, and the beta subunit confers specificity. A very high hCG can cross-react in an LH assay. LH is secreted in pulses, so a single LH value is of limited use.

hCG circulates as intact hormone, nicked forms, free beta subunit, and beta core fragment, and assays differ in which forms they detect, so results are not interchangeable between methods. Several method and interpretation problems follow. A high beta core fragment concentration in urine can produce a false negative on a qualitative point-of-care device. Persistent low-level serum hCG with a negative urine result can prompt investigation for heterophile antibody interference or pituitary production. First consider the urine assay's detection limit, urine concentration, and serial serum results. A less sensitive urine test may be negative when serum hCG is detectable. Pituitary hCG is a consideration in perimenopausal and postmenopausal women, where an age-appropriate cutoff and concurrent FSH can help. Tumor and Cardiac Markers covers hCG and PTH-related protein as tumor markers.

Gonadal laboratory patterns

Gonadotropins localize the defect, and sex steroids establish its severity.

Parathyroid glands secrete PTH when their calcium-sensing receptors detect falling ionized calcium. PTH raises calcium by increasing bone resorption, increasing distal tubular calcium reabsorption, and inducing renal 1α-hydroxylation of 25-hydroxyvitamin D. It also increases renal phosphate excretion. The resorptive effect is indirect: the PTH1 receptor sits on osteoblast-lineage cells and osteocytes, which then activate osteoclasts.^{2020 Goltzman D. Approach to hypercalcemia. 2000.} Chloride, Bicarbonate, Calcium, Magnesium, and Phosphate covers the measurement of calcium, phosphate, and magnesium, including ionized calcium preanalytics and albumin adjustment.

PTH assays, fragments, and kidney function

PTH assays come in generations, and interpreting a result requires knowing which generation produced it. First-generation competitive assays measured mid-molecule and C-terminal fragments and were abandoned. Second-generation two-site assays, labeled intact PTH, are the routine assays in use today, and they also detect large C-terminal fragments of the PTH 7-84 type. Third-generation assays, labeled whole or bio-intact PTH, use an N-terminal epitope and measure PTH 1-84 alone. They have not proved clearly superior for general use.^{2121 Cavalier E, et al. The path to the standardization of PTH. 2021.}

The distinction matters most as kidney function falls. PTH 7-84 fragments accumulate with declining filtration and antagonize the PTH receptor, so a second-generation assay overestimates biologically active PTH in chronic kidney disease. For that reason, and because between-method differences are large, PTH targets in kidney disease are expressed relative to the upper limit of the method in use, a trend on one platform is more informative than any single value, and the laboratory notifies clinicians when the method changes.^{2222 Kidney Disease: Improving Global Outcomes… KDIGO 2017 clinical practice guideline update for the diagnosis… 2017.} No accepted reference measurement procedure exists for PTH, and results are not transferable between laboratories.^{66 Sturgeon CM, et al. Perspective and priorities for improvement of parathyroid… 2017.}

EDTA plasma is the more stable specimen and is preferred where the method allows it, since serum loses PTH with delayed separation. Intraoperative monitoring uses the circulating half-life of about 2 to 4 minutes: a rapid assay measures a labeled baseline and timed post-excision specimens, and a fall of more than 50% from baseline within about 10 minutes is a widely used criterion. Local protocol sets the sampling schedule and decision rule.

Interpret a PTH result only with its paired results. Confirm calcium as ionized or albumin-adjusted, and know the vitamin D status and kidney function, because vitamin D deficiency and reduced filtration both raise PTH appropriately.

In primary hyperparathyroidism the pattern is hypercalcemia with an inappropriately normal or elevated PTH, often with a low phosphate. A single adenoma accounts for roughly 85% of cases, multigland disease for about 15%, and carcinoma for under 1%. The recommended evaluation is albumin-adjusted or ionized calcium, PTH, phosphate, 25-hydroxyvitamin D, and creatinine with estimated filtration rate.^{2323 Bilezikian JP, et al. Evaluation and management of primary hyperparathyroidism. 2022.} Two limitations apply: 1,25-dihydroxyvitamin D is neither routine nor diagnostic here, and urinary calcium is raised in only about 35 to 40% of cases, so a normal urine calcium does not exclude the diagnosis.

Secondary hyperparathyroidism is an appropriate rise driven by chronic hypocalcemia or low vitamin D, and it matters most in chronic kidney disease, where phosphate retention, raised fibroblast growth factor 23 (FGF23), and impaired calcitriol synthesis sustain parathyroid stimulation. When the response becomes autonomous it is called tertiary.

Familial hypocalciuric hypercalcemia, usually from a heterozygous inactivating CASR variant that raises the calcium set point, mimics primary hyperparathyroidism biochemically. The discriminator is the calcium-to-creatinine clearance ratio, calculated from paired serum and timed urine results:

Calcium-to-creatinine clearance ratio = (urine calcium × serum creatinine) ÷ (serum calcium × urine creatinine) A ratio below 0.01 favors the familial disorder and above 0.02 favors primary hyperparathyroidism, with the interval between them indeterminate. The ranges overlap, and reduced filtration, vitamin D deficiency, low calcium intake, incomplete collection, thiazides, and lithium all lower urine calcium, so genetic testing resolves persistent uncertainty. In PTH-related protein-mediated hypercalcemia of malignancy, PTH is suppressed, and PTH assays do not cross-react with PTH-related protein, so the measured PTH stays low.

Vitamin D metabolites and their laboratory roles

Ultraviolet B radiation photolyzes 7-dehydrocholesterol to previtamin D₃, which isomerizes to cholecalciferol. Hepatic 25-hydroxylation, predominantly by CYP2R1, produces 25-hydroxyvitamin D. Renal CYP27B1 completes activation to 1,25-dihydroxyvitamin D under the combined control of PTH, FGF23, calcitriol feedback, calcium, phosphate, and kidney function, and CYP24A1 provides the catabolic branch that inactivates both metabolites. Macrophages in granulomatous disease express CYP27B1 outside this regulation.^{77 Makris K, et al. Recommendations on the measurement and the clinical use of… 2021.} Intestinal calcium absorption combines a calcitriol-regulated saturable transcellular route, which accounts for roughly 10 to 15% of a dietary load and dominates at low intake, with a nonsaturable paracellular route that carries a larger share as intake rises.

The two metabolites have different uses, and ordering the wrong one is the most common ordering error in this axis. Total 25-hydroxyvitamin D has a half-life measured in weeks and reflects body stores, so it is the marker of vitamin D status. 1,25-dihydroxyvitamin D has a half-life measured in hours, circulates at roughly a thousandth of the concentration, and stays near a set point under the control of PTH, FGF23, calcium, and phosphate, so it is frequently normal or even elevated in frank deficiency because secondary hyperparathyroidism drives its synthesis. It is therefore not a nutritional-status test and should not be ordered as one. It has few indications: hypercalcemia where extrarenal calcitriol production is suspected, calcipenic rickets and osteomalacia, and separating FGF23-mediated from other phosphopenic disorders. It is not a routine monitoring analyte in chronic kidney disease.^{77 Makris K, et al. Recommendations on the measurement and the clinical use of… 2021.} Vitamins and Nutrition covers assay methodology, standardization, and deficiency cutoffs.

In hypercalcemia with a suppressed PTH, these two metabolites separate two different mechanisms. A high 25-hydroxyvitamin D with a normal 1,25-dihydroxyvitamin D fits exogenous vitamin D toxicity. A high or inappropriately normal 1,25-dihydroxyvitamin D with an unremarkable 25-hydroxyvitamin D fits extrarenal calcitriol production in granulomatous disease or lymphoma. Loss of CYP24A1 function raises the ratio of 25-hydroxyvitamin D to 24,25-dihydroxyvitamin D, but proposed ratio cutoffs are method-specific and molecular confirmation is the standard.

FGF23, secreted by osteocytes, suppresses CYP27B1 and promotes phosphaturia, and it contributes to the mineral disturbance of chronic kidney disease. Its assays are not standardized, intact and C-terminal assays measure different things, and established use is confined to hereditary hypophosphatemic rickets and tumor-induced osteomalacia. It is not used for routine kidney disease monitoring.^{2424 Heijboer AC, et al. The measurement and interpretation of fibroblast growth factor… 2023.}

Reading the mineral panel together

Interpret calcium, phosphate, PTH, vitamin D metabolites, and alkaline phosphatase (ALP) together. The combined pattern distinguishes the conditions below.^{7,207 Makris K, et al. Recommendations on the measurement and the clinical use of… 2021.20 Goltzman D. Approach to hypercalcemia. 2000.}