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• Exposure of the Prevertebral Fascia:
  • The first step in identifying the superior gland:
    • Is to locate the inferior thyroid artery (ITA)
  • The ITA is a crucial reference point for the location of the superior parathyroid gland:
    • The superior parathyroid gland is usually found in an area 1 cm cranial to the ITA
  • Once the ITA has been identified, blunt dissection cranial to the artery and directly posterior is performed down to the shiny prevertebral fascia
  • The prevertebral fascia defines the posterior extent of the dissection, and the most posterior location possible for a superior parathyroid gland
• Visual:
  • Although it is tempting to dive straight in and attempt to dissect the first piece of tissue that resembles parathyroid tissue, considerable time and effort can be saved by slowly and deliberately confirming the key landmarks and looking for some of the morphological features described in section “Pearls for Identification of Parathyroid Glands” (published in a previous Blog)
  • The identification of a parathyroid gland begins withcareful visual inspection:
    • Start by looking for a gland or fat pad in a 1 to 2-cm area cranial to the ITA on the posterior surface of the thyroid lobe (Figure 1)
• Digital
  • The superior glands can be found in a number of positions in association with structures from the fourth branchial arch, including:
    • Retropharyngeal
    • Retroesophageal
    • Para-esophageal
    • Adjacent the hyoid bone
  • Further, when a superior gland enlarges:
    • It tends to do so in a posterior and caudal direction and can pass behind the ITA to lie below the inferior gland
  • After careful visual inspection in the area 1 cm cranial tothe ITA, these potential positions are digitally palpatedfor using five maneuvers (Fig. 1.4):
    • The index finger is introduced into the space previously created above the ITA and directly down to the prevertebral fascia / retroesophageal space and then swept along the esophagus to feel in the retroesophageal / retropharyngeal positions
    • The finger is then swung caudally until the finger lies vertically with the tip below the ITA
    • The tissue over the tip of the finger is gently balloted, feeling for an enlarged superior gland to contact the tip of the posterior index finger
    • The finger is then swung back to a horizontal position
    • The finger is withdrawn slowly while the tip remain in contact with the esophagus and trachea, deliberately feeling for the trachea-esophageal groove

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👉Normocalcemic hyperparathyroidism (HPT) is characterized by normal calcium, high PTH levels, and may be a distinct entity that behaves differently than classical HPT.

👉Rodrigo Arrangoiz MS, MD, FACS cirujano de tumores de cabeza y cuello / cirugia endocrina es experto en el manejo del hiperparatiroidismo primario.

👉Introdujo a su país (Mexico) la técnica de exploración bilateral de cuello con valoración de la funcionalidad de las glándulas paratiroides con paratiroidectomia radioguiada:

https://m.youtube.com/watch?v=AgvQmtz1gnA&time_continue=127

👉Su entrenamiento fue el siguiente:

• Cirugia general y gastrointestinal:
• Michigan State University:
• 2004 al 2010• Cirugia oncológica / tumores de cabeza y cuello / cirugia endocrina:
• Fox Chase Cancer Center (Filadelfia):
• 2010 al 2012• Maestria en ciencias (Clinical research for healthprofessionals):
• Drexel University (Filadelfia):
• 2010 al 2012• Cirugia de tumores de cabeza y cuello / cirugiaendocrina
• IFHNOS / Memorial Sloan Kettering Cancer Center:
• 2014 al 2016

#Arrangoiz

#CirugiadeTumoresdeCabezayCuello

#CirugiaEndocrina

#CirugiaOncologica

#HeadandNeckSurgery

#EndocrineSurgery

#SurgicalOncology

#Hyperparathyroidism

#Hiperparatiroidism

#MountSinaiMedicalCenter

#MSMC

#Miami

#Mexico

• Primary hyperparathyroidism (PHPT) is seen in 0.1% to 0.5% of the adult population:
  • It is the most common cause of hypercalcemia (high calcium level) in the general population
  • It is about three times to four times more common in women than men
  • Patients are usually older, with an average age at presentation of 65 years:Most cases are over 45 years
• Learn more at:https://collectedmed.com/index.php/article/article/demo_article_display/7545/83/2/1

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• Primary Hyperparathyroidism (PHPT):
  • Is a common disorder:
    • Affecting 100,000 individuals annually in the United States
  • PHPT occurs in 0.1% to 0.3% of the general population
  • Is more common in women (1:500) than in men (1:2000)
  • Increased PTH production leads to hypercalcemia via:
    • Increased GI absorption of calcium, increased production of vitamin D3, and reduced renal calcium clearance
  • PHPT is characterized by increased parathyroid cell proliferation and PTH secretion:
    • That is independent of calcium levels

• Atypical presentations of PHPT include a spectrum of disturbances in calcium homeostasis, ranging from:
  • Symptomatic severe hypercalcemia (parathyroid crisis) to normocalcemic PHPT
• Laboratory testing often can distinguish atypical presentations of PHPT from other diseases, such as:
  • Malignancy
  • Familial hypocalciuric hypercalcemia (FHH)
  • Secondary hyperparathyroidism
• In PHPT and FHH:
  • The calcium and PTH levels:
    • Are usually simultaneously elevated
• Nonparathyroid-mediated causes of hypercalcemia, including milk-alkali syndrome, granulomatous disease, and hypervitaminosis D:
  • Are associated with suppressed rather than elevated PTH concentrations
• Malignancy:
  • PHPT and malignancy are the most common causes of hypercalcemia:
    • Accounting for more than 90% of the cases:
      • It is usually not difficult to differentiate between them
  • Malignancy is often evident clinically by the time it causes hypercalcemia:
    • Patients with hypercalcemia of malignancy have higher calcium concentrations and are more symptomatic from hypercalcemia than individuals with PHPT
    • However, it may be difficult to differentiate the two problems clinically when the presentation is less typical:
      • As an example, some patients with occult malignancy may present with mild hypercalcemia
      • Alternatively, patients with hyperparathyroidism can occasionally have acute onset of severe, symptomatic hypercalcemia (parathyroid crisis):
        • In these cases, measurement of intact PTH will usually distinguish the two diseases:
          • Intact PTH concentrations are generally:
            • Undetectable or very low in hypercalcemia of malignancy
            • Elevated or high-normal in PHPT
        • It is uncommon for patients with hypercalcemia of malignancy to have elevated PTH levels:
          • But this finding may occur rarely in individuals with:
            • Hypercalcemia of malignancy and concomitant PHPT or
            • In individuals with PTH-secreting tumors:
              • Which are also rare
    • Patients with parathyroid carcinomas:
      • Have severe hypercalcemia and PTH levels in the hundreds to thousands pg/mL range
• Familial hypocalciuric hypercalcemia (FHH):
  • An autosomal dominant disorder characterized by:
    • Longstanding, mild hypercalcemia:
      • Normal or mildly elevated PTH levels
      • Low urinary calcium excretion:
        • Less than 100 mg/24 hours
  • In most cases, it is due to:
    • An inactivating mutation in the calcium-sensing receptor in the parathyroid glands and the kidneys
  • A family history of hypercalcemia:
    • Especially in young children
    • And the absence of symptoms and signs of hypercalcemia are characteristic of this disorder
  • 15% to 20% of patients with FHH:
    • May have a mildly elevated PTH concentration:
      • In these individuals, it may be difficult to distinguish asymptomatic PHPT from FHH:
        • It is important to make this distinction, however, because FHH is a benign inherited condition:
          • That typically does not require parathyroidectomy and will not be cured by it
  • The major feature that distinguishes FHH from PHPT is:
    • A low urine calcium excretion and calcium/creatinine (Ca/Cr) clearance ratio
  • In contrast, in the absence of hypovitaminosis D, most patients with PHPT have either normal or elevated urinary calcium excretion. Because the calcium-sensing receptor is a cation receptor, urinary magnesium excretion parallels calcium excretion and is therefore low in FHH, in contrast with PHPT. Measurement of urinary magnesium is not, however, recommended in the evaluation of PHPT or FHH.
• Drugs — Two drugs deserve special consideration when evaluating a patient for hyperparathyroidism: thiazide diuretics and lithium.
• Thiazide diuretics, including chlorthalidone, reduce urinary calcium excretion and therefore can cause mild hypercalcemia (up to 11.5 mg/dL [2.9 mmol/L). In addition, some patients with hyperparathyroidism may be prescribed thiazides, which may elevate the serum calcium further and thereby unmask the hyperparathyroidism. Following discontinuation of the drug, these individuals remain hypercalcemic, although perhaps less so, and are found to have surgically proven hyperparathyroidism. Thus, if a patient taking a thiazide is found to be hypercalcemic, the drug should be withdrawn, if possible, and calcium and PTH assessed three months later. Persistent hypercalcemia (with elevated or high-normal PTH) after drug withdrawal suggests that the thiazide has unmasked PHPT.
• Lithium decreases parathyroid gland sensitivity to calcium, shifting the calcium-PTH curve to the right. Lithium may also reduce urinary calcium excretion. Lithium is thought to affect calcium-PTH dynamics through an action downstream of the calcium-sensing receptor, but the exact locus is still unknown. Some patients taking lithium develop hypercalcemia and hypocalciuria, and a subset of these individuals have high serum PTH concentrations. If the lithium can be stopped without exacerbating the psychiatric condition, the hypercalcemia may resolve. Following discontinuation, the serum calcium concentration is more likely to normalize if the duration of lithium use had been relatively short (eg, less than a few years), but less likely if it had been longer (eg, more than 10 years).
• Secondary hyperparathyroidism — Occasionally, patients with PHPT have consistently normal total and ionized calcium concentrations (normocalcemic PHPT). These patients typically come to medical attention in the setting of an evaluation for low bone mineral density (BMD). In these cases, it may be difficult to distinguish secondary hyperparathyroidism from early PHPT because the biochemical findings may be similar.
• Secondary hyperparathyroidism occurs when the parathyroid gland appropriately responds to a reduced level of extracellular calcium. PTH concentrations rise, and calcium is mobilized by increasing intestinal absorption (via increase in calcitriol) and by increasing bone resorption. Thus, it is characterized biochemically by elevated PTH and normal or low serum calcium concentrations.
• Secondary hyperparathyroidism may occur in patients with renal insufficiency or failure and impaired calcitriol (1,25 dihydroxyvitamin D) production, as well as in individuals with inadequate calcium intake or absorption, as can occur with vitamin D deficiency or with gastrointestinal diseases causing malabsorption. Assessment of renal function (serum creatinine), vitamin D status (25-hydroxyvitamin D [25(OH)D]), and calcium sufficiency (urinary calcium excretion) may help differentiate normocalcemic primary and secondary hyperparathyroidism. Further assessment and work-up for specific gastrointestinal disorders is generally undertaken only when the clinical suspicion is high.
• Some patients may have more than one condition leading to increased PTH secretion. Co-existing PHPT and vitamin D deficiency is not uncommon. When this occurs, the serum calcium level in the primary hyperparathyroid patient may be reduced (into the normal range in some cases) due to vitamin D deficiency.

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• The renal manifestations implicated with PHPT are:
  • Decreased glomerular filtration rate:
    • Up to 20% of patients with asymptomatic PHPT:
      • Have an estimated glomerular filtration rate (eGFR):
        • Below 60 mL/min/1.73 m²
    • The development of kidney insufficiency in PHPT is related to:
      • The degree and duration of hypercalcemia:
        • Mild hypercalcemia is rarely associated with kidney insufficiency
        • In randomized trials of two to three years duration, there is little evidence that kidney function deteriorates in patients with mild chronic hypercalcemia due to PHPT
  • Hypercalciuria:
    • Hypercalciuria is a contributing factor for stone formation in PHPT
    • Although PTH directly stimulates the distal tubular reabsorption of calcium:
      • This effect is overshadowed by the increase in filtered calcium due to hypercalcemia:
        • Leading to increased urinary calcium excretion in 35% to 40% of patients with PHPT
        • Nephrolithiasis
        • Nephrocalcinosis
        • Impaired urinary concentrating ability sometimes leading to polyuria, polydipsia, nocturia
        • Reduced fractional phosphate reabsorption leading to hypophosphatemia
        • Increased urinary exertion of magnesium
• Nephrolithiasis:
  • Is the universally accepted:
    • Classical kidney manifestation of PHPT
    • It was previously reported in approximately 40% to 80% of patients with PHPT:
      • But now occur only in about 20% to 25% (5% to 55% in some series) of the cases:
        • This wide range likely reflects differences in the methods used for kidney imaging, as well as heterogeneity in PHPT severity
    • Conversely, approximately 5% of patients with nephrolithiasis have hyperparathyroidism
    • Among normocalcemic patients with nephrolithiasis:
      • PHPT should be suspected if the serum calcium concentration is in the high-normal range:
        • Because the hypercalcemia of PHPT may be intermittent and detected only by multiple measurements
    • In one series of 48 patients with nephrolithiasis and PHPT:
      • 30 patients (63%) had serum calcium concentrations between 10.2 and 11 mg/dL
    • The pathophysiology is thought to be related to the filtered load of calcium in the glomerulus:
      • That increases proportionately with the degree of hypercalcemia
    • Most renal stones in patients with PHPT are composed of:
      • Calcium oxalate although slightly alkaline urine may favor the precipitation of calcium phosphate stones
      • Contributing factors for calcium oxalate stone formation in PHPT include:
        • Hypercalciuria
        • Hyperoxaluria
        • Hypocitraturia
        • Hypomagnesuria
        • Dietary risk factors such as a low calcium intake, high oxalate intake, high animal protein intake, high sodium intake, low fluid intake
        • A high serum calcitriol concentration – The high serum calcitriol concentration, caused by PTH stimulation of renal hydroxylation of 25-hydroxyvitamin D (25[OH]D), may contribute to both hypercalciuria and stone formation. Genetic factors such as polymorphisms in calcium-sensing receptor (CaSR) gene have also been described
      • Stone formers are more likely to be hypercalciuric:
        • But less than one-third of the hypercalciuric patients with PHPT actually develop renal stones
      • Hypercalciuria is not a predictor of nephrolithiasis in patients with PHPT and is no longer considered as an indication for surgery:
        • At the present time, it is almost impossible to securely foresee which patients with PHPT will develop nephrolithiasis bases on biochemical analysis of urine
• Nephrocalcinosis:
  • Which refers to renal parenchymal calcification:
    • Is found in less than five percent of patients and is more likely to lead to renal dysfunction
• Subclinical nephrocalcinosis and nephrolithiasis:
  • Are more common in patients with than without hyperparathyroidism
  • In a retrospective review of 271 renal ultrasounds from patients with surgically proven, asymptomatic PHPT:
    • The prevalence of kidney stones on ultrasound performed within six months prior to surgery was significantly higher than in age-matched subjects who had renal ultrasounds for other reasons (7% versus 1.6%)
  • In a cross-sectional analyses of asymptomatic patients with PHPT:
    • Occult urolithiasis or kidney calcifications (nephrolithiasis and / or nephrocalcinosis) were identified in approximately 20% of patients
• Hypertension:
  • The incidence of hypertension is variable:
    • Anywhere between 30% to 50% of patients with PHPT
  • Hypertension appears to be more common in:
    • Older patients and correlates with the magnitude of renal dysfunction
  • In contrast to other symptoms:
    • Is least likely to improve after parathyroidectomy
  • Another plausible explanation of the origin of hypertension in patients with PHPT:
    • Is the synthesis of parathyroid hypertensive factor that triggers an increase in blood pressure
  • The elevated levels of PTH is also linked with the disruption in the renin-angiotensin- aldosterone system

👉Higher rates of hypertension, arrhythmias, left ventricular hypertrophy/dysfunction, and coronary artery disease have been observed in patients with Primary hyperparathyroidism.

👉There is also an increased all-cause and cardiovascular mortality when compared to the general population.

👉Currently, the impact of parathyroidectomy on cardiovascular events and mortality is not well-defined, but some research has suggested a benefit may exist.

👉The Appropriate Diagnosis of Primary Hyperparathyroidism

http://mdpub.net/fulltext/172-1564440673.pdf?1583602321

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• Calcium:
  • Is the most abundant cation in human beings and has several crucial functions
  • Approximetely 900 mg
• Extracellular calcium levels:
  • Are 10,000-fold higher than intracellular levels:
    • Both are tightly controlled
• Extracellular calcium:
  • Is important for excitation-contraction coupling in muscle tissues, synaptic transmission in the nervous system, coagulation cascade , and secretion of other hormones
• Intracellular calcium:
  • Is an important second messenger regulating cell division, motility, membrane trafficking, and secretion
• Calcium:
  • Is absorbed from the small intestine:
    • In its inorganic form
• Calcium fluxes in the steady state are depicted in Figure

• Extracellular calcium (900 mg):
  • Accounts for only 1% of the body’s calcium stores:
    • The majority of which is sequestered in the skeletal system
  • Approximately 50% of the serum calcium is in the ionized form:
    • Which is the active component
  • The remainder is bound to albumin (40%) and organic anions such as phosphate and citrate (10%)
  • The total serum calcium levels range from:
    • 8.5 to 10.5 mg/dL (2.1 to 2.6 mmol/L)
  • Ionized calcium levels range from:
    • 4.4 to 5.2 mg/dL (1.1 to 1.3 mmol/L)
  • Both concentrations are tightly regulated
• The total serum calcium level:
  • Must always be considered in its relationship to plasma protein levels:
    • Especially serum albumin:
      • For each gram per deciliter of alteration of serum albumin above or below 4.0 mg/dL:
        • There is a 0.8 mg/dL increase or decrease in protein-bound calcium and, thus, in total serum calcium levels
• Total and, particularly, ionized calcium levels:
  • Are influenced by various hormone systems
• Parathyroid Hormone
  • The parathyroid cells rely on a G-protein–coupled membrane receptor:
    • Designated the calcium-sensing receptor (CASR):
      • To regulate PTH secretion By sensing extracellular calcium levels (Figure)

• PTH secretion:
  • Also is stimulated by:
    • Low levels of 1,25-dihydroxy vitamin D
    • Catecholamines
    • Hypomagnesemia
• The PTH gene is located on chromosome 11
• PTH:
  • Is synthesized in the parathyroid gland as a precursor hormone preproPTH:
    • Which is cleaved first to pro-PTH and then to the final 84-amino-acid PTH
  • Secreted PTH:
    • Has a half-life of 2 to 4 minutes
  • In the liver:
    • PTH is metabolized into the active N-terminal component and the relatively inactive C-terminal fraction:
      • The C-terminal component is excreted by the kidneys and accumulates in chronic renal failure
• PTH functions to regulate calcium levels:
  • Via its actions on three target organs:
    • The bone, kidney, and gut
• PTH:
  • Increases the resorption of bone:
    • By stimulating osteoclasts and promotes the release of calcium and phosphate into the circulation
  • At the kidney, calcium is primarily absorbed in concert with sodium in the proximal convoluted tubule:
    • But fine adjustments occur more distally:
      • PTH acts to limit calcium excretion at the distal convoluted tubule:
        • Via an active transport mechanism
    • PTH also inhibits phosphate reabsorption (at the proximal convoluted tubule) and bicarbonate reabsorption
    • It also inhibits the Na+ / H+ antiporter:
      • Which results in a mild metabolic acidosis in hyperparathyroid states
    • PTH and hypophosphatemia:
      • Also enhance 1-hydroxylation of 25-hydroxyvitamin D:
        • Which is responsible for its indirect effect of increasing intestinal calcium absorption
• Calcitonin:
  • Calcitonin is produced by thyroid C cells (parafollicular cells)
  • Functions as an antihypercalcemic hormone:
    • By inhibiting osteoclast-mediated bone resorption
  • Calcitonin production is stimulated b:
    • Calcium and pentagastrin and also by catecholamines, cholecystokinin, and glucagon
  • When administered intravenously to experimental animals, it produces hypocalcemia
  • At the kidney, calcitonin increases phosphate excretion by inhibiting its reabsorption
  • Calcitonin plays a minimal, if any, role in the regulation of calcium levels in humans:
    • However, it is very useful as a marker of MTC and in treating acute hypercalcemic crisis
• Vitamin D
  • Vitamin D refers to vitamin D2 and vitamin D3:
    • Both of which are produced by photolysis of naturally occurring sterol precursors
  • Vitamin D2 is available commercially in pharmaeutical preparations
  • Vitamin D3 is the most important physiologic compound:
    • It is produced from 7-dehydrocholesterol:
      • Which is found in the skin
  • Vitamin D is metabolized in the liver to its primary circulating form:
    • 25-hydroxyvitamin D
  • Further hydroxylation in the kidney results in:
    • 1,25-dihydroxy vitamin D:
      • Which is the most metabolically active form of vitamin D
  • Vitamin D stimulates the absorption of calcium and phosphate from the gut and the resorption of calcium from the bone

• Common labs ordered in the workup of patients with primary hyperparathyroidism include:
  • A serum calcium (+/- ionized calcium)
  • Albumin (for correction of total serum calcium level)
  • Intact PTH
  • Phosphate
  • Creatinine
  • 25-hydroxy vitamin D
  • 24-hour urine calcium and creatinine.
• Hypercalcemia (elevated serum total calcium levels) with with an elevated intact PTH with normal kidney function and without hypocalciuria:
  • Indicates primary hyperparathyroidism (PHPT)
• However, some patients with this disease will have:
  • Hypercalcemia with an “inappropriately normal” PTH:
    • This can be a common cause of delayed diagnosis

Dr. Rodrigo Arrangoiz is a board-certified surgical oncologist who subspecializes in breast cancer and head and neck cancer. Dr. Arrangoiz earned his medical degree at the Anahuac University Medical School in Mexico City, Mexico and graduated Suma Cum Laude. He completed his internship and residency in general surgery at Michigan State University, where he was named chief resident during his fifth year of residency. Dr. Arrangoiz also completed a complex surgical oncology, head and neck fellowship at the Fox Chase Cancer Center in Philadelphia and at the same time he undertook a master’s in science (Clinical Research for Health Care Professionals) at Drexel University in Philadelphia. Dr. Arrangoiz also participated in a two-year global online fellowship in head and neck surgery and oncology through the International Federation of Head and Neck Societies / Memorial Sloan Kettering Cancer Center.

Dr. Arrangoiz has participated in multiple courses and academic congresses as a lecturer and guest professor and has also participated in several publications on topics related to his specialty that include oral cavity cancer, hyperparathyroidism, thyroid cancer, breast cancer, endocrine tumors, squamous cell carcinoma of the head and neck, and more. He is board certified by the American Board of Surgery, the Mexican Board of General Surgery and the Mexican Board of Oncology.

He is a member of various medical associations such as the American College of Surgeons, American Thyroid Association, American Head and Neck Society, American Medical Association, American Society of Clinical Oncology, Association of Academic Surgeons, Society of Surgical Oncology, The Society of Surgery of the Alimentary Tract, Society of American Gastrointestinal Endoscopic Surgeons, and the American Society of Breast Surgeons, among others.

Specialty:

Head and Neck Surgery
Thyroid and Parathyroid Surgery
Breast Surgery
Complex Surgical Oncology

Areas of Clinical Interest:

Malignant thyroid disease (papillary, follicular, medullary, anaplastic thyroid cancer, thyroid lymphoma, and metastatic disease to the thyroid gland) benign thyroid diseases (goiter, multinodular goiter, substernal goiter, hyperthyroidism), hyperparathyroidism / hypercalcemia, benign and malignant breast diseases, head and neck surgery and head and neck cancer.

#Arrangoiz #ParathyroidSurgeon #ParathyroidExpert #Hyperparathyroidism #PrimaryHyperparathyroidism #CancerSurgeon #EndocrineSurgery #Teacher #Surgeon #HeadandNeckSurgeon #SurgicalOncologist #ParathyroidAdenoma #Hypercalcemia #ElevatedCalciumLevels #Miami #MountSinaiMedicalCenter #MSMC #Mexico #Hialeah

• Most patients have four parathyroid glands
  • The superior glands usually are dorsal to the RLN at the level of the cricoid cartilage
  • The inferior parathyroid glands are located ventral to the nerve
• Normal parathyroid glands are gray and semitransparent in newborns:
  • But appear golden yellow to light brown in adults:
    • Parathyroid color depends on cellularity, fat content, and vascularity
  • Moreover, they often are embedded in and sometimes difficult to discern from surrounding fat
• There are normally two pairs of parathyroid glands (inferior and superior)
  • The parathyroid gland is oval or bean-shaped (Figure)
  • It typically measures 6 mm × 4 mm × 2 mm
  • They weigh 40 mg to 60 mg
• Most people have four parathyroid glands:
  • Akerström et al, in a series of 503 autopsies:
    • Identified four parathyroid glands in 84% of the cases
  • Supernumerary glands were found in 13% of the cases:
    • Most commonly in the thymus
  • In the literature, the incidence of supernumerary glands:
    • Is anywhere between 3% and 13%
• Only in three percent of the cases less than four parathyroid glands are identified
• The blood supply of the parathyroid glands:
  • Is usually derived from branches of the inferior thyroid artery:
    • Although branches of the superior thyroid artery can supply at least 10% to 45% of the superior parathyroid glands
  • In a study of 354 autopsy specimens, Alverd, observed:
    • That both the superior and inferior parathyroid glands derive their blood supply from the inferior thyroid artery:
      • 86% on the right side and 77% from the left side
  • When the inferior thyroid artery was absent:
    • Both the superior and inferior parathyroid glands were supplied by the superior thyroid artery
  • Branches from the thyroidea ima, and vessels to the trachea, esophagus, larynx, and mediastinum:
    • May also contribute to the irrigation of the parathyroid glands
• Wang et al., in a study of 160 autopsy specimens:
  • Showed that a low lying inferior parathyroid gland could be identified by following the vascular pedicle of the inferior thyroid artery
• The parathyroid glands drain ipsilaterally by the:
  • Superior, middle, and inferior thyroid veins
• The innervation of the parathyroid glands:
  • Occurs via the superior or middle cervical ganglia, or through a plexus in the fascia on the posterior aspect of the thyroid lobe 
• Histologically, parathyroid glands are composed of:
  • Chief cells and oxyphil cells arranged in trabeculae, within a stroma composed primarily of adipose cells (Figure)

• The parathyroid glands of infants and children:
  • Are composed mainly of chief cells:
    • Which produce parathyroid hormone (PTH)
• Acidophilic, mitochondria-rich oxyphil cellsL:
  • Are derived from chief cells:
    • Can be seen around puberty:
      • They increase in numbers in adulthood
• A third group of cells, known as water-clear cells:
  • Also are derived from chief cells
  • Are present in small numbers, and are rich in glycogen
• Although most oxyphil and water-clear cells retain the ability to secrete PTH:
  • Their functional significance is not known.