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• Guidelines for the management of asymptomatic primary hyperparathyroidism (PHPT):
  • Were updated in 2013 by the Fourth International Workshop on Asymptomatic Primary Hyperparathyroidism
• Indications for surgery include the following:
  • Serum calcium :
    • 1 mg/dL above the upper limit of the reference range
  • Bone mineral density T-score:
    • At or below -2.5 SD (in perimenopausal or postmenopausal women and in men aged 50 years or older):
      • At the lumbar spine, total hip, femoral neck, or distal 1/3 radius
  • Vertebral fracture:
    • As evidenced via radiography or vertebral fracture assessment (VFA)
  • Creatinine clearance of:
    • Less than 60 ml/min
  • Twenty-four–hour urinary calcium excretion:
    • Greater than 400 mg/day and increased stone risk as assessed through biochemical stone risk analysis
  • Presence of nephrolithiasis or nephrocalcinosis as determined using radiography, ultrasonography, or CT scanning
  • Age younger than 50 years

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• No study has yet identified a reliable predictor:
  • For determining which patients with sporadic hyperparathyroidism:
    • Will have multigland disease:
      • The exception is in familial, secondary, and tertiary hyperparathyroidism:
        • Because of the nearly uniform incidence of four-gland hyperplasia:
          • All these patients are managed with bilateral neck exploration:
            • And either total parathyroidectomy with autotransplantation or three-and-a-half gland parathyroidectomy
• Although some surgeons believe that patients with higher preoperative PTH or calcium levels (or both):
  • Are more likely to have multi-gland disease:
    • This has not been proved to be true in clinical studies

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• Numerous genetic abnormalities have been identified in the development of PHPT, including:
  • Anomalies in tumor suppressor genes
  • Proto-oncogenes
• Specific DNA mutations in a parathyroid cell:
  • May confer a proliferative advantage over normal neighboring cells:
    • Thus allowing for clonal growth:
      • Large populations of these altered cells containing the same mutation within hyperfunctioning parathyroid tissue:
        • Suggest that such glands are a result of clonal expansion
• The majority of PHPT cases are:
  • Sporadic
• Nonetheless, PHPT also occurs within the spectrum of a number of inherited disorders such as:
  • Multiple endocrine neoplasia syndromes (MEN):
    • MEN type 1 (Wermer Syndrome)
    • MEN type 2A (Sipple Syndrome)
    • Isolated familial HPT
    • Familial HPT with jaw-tumor syndrome
      • All of these syndromes are inherited in an:
        • Autosomal dominant fashion
• MEN type 1 (Wermer Syndrome):
  • The earliest and most common presentation of MEN type 1 is:
    • PHPT:
      • Develops in approximately 80% to 100% of patients:
        • By age 40 years
  • These patients also are predisposed to the development of:
    • Pancreatic neuroendocrine tumors
    • Pituitary adenomas
    • Less frequently:
      • Skin angiomas
      • Lipomas
      • Adrenocortical tumors
      • Neuroendocrine tumors of the:
        • Thymus
        • Bronchus
        • Stomach
  • MEN type 1 has been shown to result from:
    • A germline mutation in a tumor suppressor gene:
      • Called MEN1 gene:
        • Located on chromosome 11q12-13:
          • That encodes Menin:
            • A protein that is postulated to interact with the transcription factors JunD and nuclear factor-κB in the nucleus, in addition to replication protein A and other proteins
  • Pre-symptomatic screening for mutation carriers for MEN type 1 is difficult:
    • Because generally MEN1 mutations result in a nonfunctional protein and are scattered throughout the translated nine exons of the gene
  • MEN1 mutations also have been found in kindred’s initially suspected to represent isolated familial HPT
  • Screening for mutation carriers for MEN type 1:
    • Has a very high detection rate:
      • Greater than 94%
    • In Sweden it is used for patients with PHPT with a first-degree relative with a:
      • Major endocrine tumor
      • Age of onset is less than 30 years and/or
      • If multiple pancreatic tumors / parathyroid hyperplasia is detected
• MEN type 2A (Sipple Syndrome):
  • Approximately 20% of patients with MEN type 2A develop PHPT:
    • Which is usually less severe
  • MEN type 2A is caused by a:
    • Germline mutation of the RET proto-oncogene:
      • Located on chromosome 10
    • Genotype and phenotype correlations have been noted in this syndrome:
      • In that individuals with mutations at:
        • Codon 634 are more likely to develop PHPT
• Patients with the familial HPT with jaw-tumor syndrome:
  • Have an increased predisposition to:
    • Parathyroid carcinoma
  • This syndrome maps to a tumor suppressor locus:
    • HRPT2 (parafibromin):
      • On chromosome 1
• Sporadic parathyroid adenomas and some hyperplastic parathyroid glands:
  • Have loss of heterozygosity (LOH) at 11q13:
    • The site of the MEN1 gene:
      • In approximately 25% to 40% of the cases
• Over expression of PRAD1:
  • Which encodes cyclin D1:
    • A cell cycle control protein:
      • Is found approximately 18% of parathyroid adenomas
  • This was proven to result from a rearrangement on chromosome 11:
    • That places the PRAD1 gene under the control of the PTH promoter
• Other chromosomal regions deleted in parathyroid adenomas and possibly reflecting loss of tumor suppressor genes include:
  • 1p, 6q, and 15q
• Amplified regions suggesting oncogenes have been identified at:
  • 16p and 19p
• RET mutations:
  • Are unusual in sporadic parathyroid tumors
• Sporadic parathyroid cancers:
  • Are characterized by uniform loss of the:
    • Tumor suppressor gene RB
      • Which is involved in cell cycle regulation
  • 60% have HRPT2 (CDC73) mutations
  • These alterations are rare in benign parathyroid tumors:
    • May have implications for diagnosis
  • The p53 tumor suppressor gene is also inactivated in a subset (30%) of parathyroid carcinomas

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• Hyperparathyroidism can be diagnosed during pregnancy and should be closely monitored to prevent complications associated with hypercalcemia.
• Mild hypercalcemia in gestational PHPT is generally not associated with an increased risk of obstetrical complications.
• https://academic.oup.com/jcem/article/100/5/2115/2829737

#Arrangoiz #ParathyroidSurgeon #ParathyroidExpert #HeadandNeckSurgeon #CancerSurgeon #EndocrineSurgery #MountSinaiMedicalCenter #MSMC #Miami #Mexico

• During the fifth to sixth week of intrauterine development:
  • The embryonic pharynx is marked:
    • Externally by:
      • Four branchial clefts of ectoderm origin
    • Internally by:
      • Five branchial pouches of endoderm origin
• The branchial apparatus:
  • Is made up by the branchial clefts and branchial pouches:
    • Together with the branchial arches of mesoderm origin:
      • Found in between them
  • This apparatus undergoes normal involution:
    • Leaving behind some derivatives which include the thyroid gland, parathyroid glands, thymus, ultimobranchial body, Eustachian tube, middle ear, and external auditory canal
• The parathyroid glands:
  • Develop as epithelial thickenings of the dorsal endoderm of the third and fourth branchial pouches
• The superior parathyroid glands:
  • Are derived from the fourth branchial pouch:
    • Which also gives rise to the thyroid gland
• The inferior parathyroid glands:
  • Are derived from the third branchial pouch:
    • Which also gives rise to the thymus
• The parathyroid glands:
  • Remain intimately connected with their respective branchial pouch derivatives
• The normal anatomic location of the superior parathyroid glands:
  • Is more constant than the inferior parathyroid glands:
    • With 80% of the superior glands being found near the posterior aspect of the thyroid gland at the junction of the upper and middle portion of the thyroid lobes:
      • At the level of the cricoid cartilage:
        • Each gland with its own capsule of connective tissue
  • Roughly one percent of the superior parathyroid glands;
    • May be found in the paraesophageal or retroesophageal space
  • Enlarged superior glands may descend in the tracheoesophageal groove and come to lie below the inferior parathyroid glands
  • Truly ectopic superior parathyroid glands:
    • Are extremely rare:
      • But may be localized to the middle or posterior mediastinum or in the aortopulmonary window 
• During intrauterine development, the thymus and the inferior parathyroid glands migrate caudally in the neck:
  • The most common location for the inferior parathyroid glands:
    • Is within a distance of 1 cm from a point centered where the inferior thyroid artery and the recurrent laryngeal nerve (RLN) cross
  • Approximately 15% to 50% of the inferior glands:
    • Are found in the thymus
  • The position of the inferior parathyroid glands:
    • However, tends to be more variable:
      • Due to their longer migratory route
  • Undescended inferior glands:
    • May be found near the skull base, angle of the mandible, or above the superior parathyroid glands along with an undescended thymus
• The frequency of intrathyroidal glands:
  • Is approximately 2% 
• 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
    • Weighs 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 superior glands usually are dorsal to the RLN at the level of the cricoid cartilage:
  • Whereas the inferior parathyroid glands are located ventral to the nerve

👉The first report for using intraoperative parathyroid hormone (IOPTH) level as an adjunct to guide removal of hyperfunctioning parathyroids was published by Dr. G. Irvin the 3rd et al. in 1993.

👉There are many criteria, however, all require judgement to balance risk of removing multiple glands with risk of recurrent / persistent disease, as outlined in this review.

https://www.sciencedirect.com/science/article/abs/pii/S1521690X19300612?via%3Dihub

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

• Shorter life span
• Increase risk of developing cardiovascular disease
• Increase risk of developing cerebrovascular disease
• Increase risk of developing a malignancy
• Increase risk of developing bone disease
• Increase risk of developing renal disease
• Decrease quality of life

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• The most frequent gastrointestinal manifestations of PHPT are:
  • Constipation:
    • That occurs in 33% of the cases
  • Heartburn:
    • That occurs in 30% of the cases
  • Nausea:
    • That occurs in 24% of the cases
  • Anorexia:
    • That occur in 15% of the cases
• A significant reduction in patient symptoms:
  • Is seen after parathyroidectomy
• The precise pathophysiology is not fully known:
  • Variations in gene expression secondary to sustained stimulation of PTH result:
    • In gut dysmotility:
      • That often leads to constipation and dyspepsia
• PHPT has been associated with increased incidence of malignancies:
  • Especially of the colon and rectum
• PHPT has been associated with peptic ulcer disease:
  • The incidence varies between:
    • 5% to 30 % of the cases
  • In animal models:
    • Elevated gastric levels have been shown to result from PTH infusion into blood vessels supplying the stomach:
      • Independent of its effects on serum calcium
• An increased incidence of pancreatitis has been reported in patients with PHPT:
  • PHPT as a cause of acute pancreatitis was first described by Cope et al, in 1957
  • In retrospective series:
    • The incidence of acute pancreatitis in patients with PHPT:
      • Has varied from 1% to 12%
  • In a study by Jacob et al:
    • They showed a 28-fold increase in the risk of developing pancreatitis in patients with PHPT compared to the general population
    • After removing all other causes:
      • The average serum calcium level seems to be the only predictive factor for pancreatitis development
    • In the diagnostic work-up of acute pancreatitis:
      • PHPT should be included in the differential diagnosis:
        • Although PHPT is found in less than 1% of individuals who present with acute pancreatitis
    • The mechanism of origin that leads to pancreatitis:
      • Seems to be related more to the hypercalcemia than to the PHPT
    • Experimental studies have validated that calcium ions cause calculus deposition within the pancreatic ducts:
      • With subsequent obstruction and inflammation
    • Calcium can also trigger the pancreatitis cascade:
      • By promoting conversion of trypsinogen to trypsin
• Patients with PHPT also have an increased incidence of cholelithiasis:
  • Presumably due to PTH inhibition of:
    • Gallbladder wall emptying, hepatic bile secretion and sphincter Oddi dysmotility, as well as modification of bile composition (increase in biliary calcium):
      • Which leads to the formation of calcium bilirubinate stones

#Arrangoiz #ParathyroidSurgeon #ParathyroidExpert #HeadandNeckSurgeon #EndocrineSurgery #MountSinaiMedicalCenter #Miami #Mexico #Teacher #Surgeon #Parathyroidectomy #Hypercalcemia #ElevatedCalcium #MSMC

• Primary hyperparathyroidism
• Malignancy:
  • Hematologic (multiple myeloma)
  • Solid tumors (PTHrP)
• Endocrine diseases:
  • Hyperthyroidism:
    • Mild hypercalcemia occurs in up to 15% to 20% of thyrotoxic patients:
      • Due to a thyroid hormone mediated:
        • Increase in bone resorption:
          • It typically resolves following correction of hyperthyroidism
  • Addisonian crisis:
    • Hypercalcemia occurs in occasional patients with Addisonian crisis:
      • Multiple factors appear to contribute to the hypercalcemia including:
        • Increased bone resorption
        • Volume contraction and increased proximal tubular calcium reabsorption
        • Hemoconcentration
        • Perhaps increased binding of calcium to serum proteins
    • Cortisol administration reverses the hypercalcemia within several days
    • Hypercalcemia has also been reported in patients with secondary adrenal insufficiency due to lymphocytic hypophysitis:
      • The increased release of calcium from bone occurs:
        • Despite appropriate suppression of PTH and calcitriol release:
          • And appears to be mediated, at least in part, by:
            • Thyroid hormone via a process normally inhibited by glucocorticoids
  • Acromegaly
  • Pheochromocytoma:
    • Hypercalcemia is a rare complication of pheochromocytoma
    • It can be due to:
      • Concurrent hyperparathyroidism (in MEN type IIa) or
      • To the pheochromocytoma itself:
        • Appears to be due to:
          • Tumoral production of PTH-related protein
        • Serum PTH-related protein concentrations in these patients can be reduced by alpha-adrenergic blockers:
          • Suggesting a mediating role for alpha-stimulation

• Vipoma
• Milk alkali syndrome:
  • In the absence of renal failure:
    • Hypercalcemia can be induced by a:
      • High intake of milk or more commonly, calcium carbonate:
        • Leading to the Milk-Alkali-Syndrome:
          • Hypercalcemia
          • Metabolic alkalosis
          • Renal insufficiency
    • The metabolic alkalosis augments the hypercalcemia:
      • By directly stimulating calcium reabsorption in the distal tubule:
        • Thereby diminishing calcium excretion
    • A calcium-induced decline in renal function:
      • Due to renal vasoconstriction and, with chronic hypercalcemia:
        • Leads to structural injury:
          • This can also contribute to the inability to excrete the excess calcium
    • Renal function usually returns to baseline after cessation of milk or calcium carbonate intake:
      • But irreversible injury can occur in patients who have prolonged hypercalcemia
    • Milk-alkali syndrome accounted for:
      • 8.8% of hypercalcemia cases between 1998 and 2003
• Granulomatous diseases:
  • Sarcoidosis
  • Tuberculosis
  • Berylliosis
  • Histoplasmosis
  • Wegeners Granulomatosis
    • Mechanism:
      • Increased calcitriol:
        • Activation of extra-renal 1-alpha-hydroxylase
• Medications:
  • Thiazide diuretics:
    • Thiazide diuretics reduce urinary calcium excretion:
      • And therefore can cause mild hypercalcemia (up to 11.5 mg/dL [2.9mmol/L]):
    • In addition, some patients with PHPT 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 diuretic 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 is withdrawal suggests that the thiazide has unmasked primary hyperparathyroidism

• Lithium:
  • Patients receiving chronic lithium therapy often develop mild hypercalcemia:
    • Most likely due to increased secretion of PTH:
      • Due to an increase in the set point at which calcium suppresses PTH release
      • The hypercalcemia usually, but not always:
        • Subsides when the lithium is stopped
          • Lithium can also unmask previously unrecognized mild primary hyperparathyroidism (PHPT)
  • Conversely, lithium can also raise serum PTH concentrations without raising serum calcium concentrations
• Teriparatide
• Abaloparatide
• Theophylline toxicity
• Vitamin A poisoning:
  • Hypervitaminosis A:
    • In which there is prolonged ingestion of more than 50,000 International Units per day or the administration of retinoic acid to patients with certain tumors (as either cis-retinoic acid or all-trans retinoic acid):
      • Retinoic acid causes a dose-dependent increase in bone resorption:
        • Resulting in an overall incidence of hypercalcemia of approximately:
          • 30%
      • All-trans retinoic acid:
        • Inhibits cell growth in part by downregulation of interleukin-6 receptors:
          • The subsequent rise in serum interleukin-6 concentrations:
            • May be responsible for increased bone resorption and hypercalcemia
• Vitamin D poisoning

• Increased calcium intake:
  • A high calcium intake alone is rarely a cause of hypercalcemia:
    • Because the initial elevation in serum calcium concentration:
      • Inhibits both the release of parathyroid hormone (PTH) and in turn the synthesis of calcitriol:
        • In patients who also have reduced urinary excretion, however:
          • Increased intake can cause hypercalcemia:
            • This combination of high calcium intake and low urine calcium excretion occurs in two clinical situations:
              • Chronic kidney disease
              • The milk-alkali syndrome
• Chronic kidney disease:
  • Renal failure alone, although associated with decreased calcium excretion:
    • Does not lead to hypercalcemia because of the:
      • Calcium-lowering effects of concurrent hyperphosphatemia and decreased calcitriol synthesis:
        • However, hypercalcemia is not unusual in patients who are given:
          • Calcium carbonate or calcium acetate to bind dietary phosphate:
            • Particularly if they have adynamic bone disease or are also treated with calcitriol (or another form of vitamin D):
              • In an attempt to reverse both hypocalcemia and secondary hyperparathyroidism
• Benign hypocalcuric hypercalcemia
• Paget’s disease of the bone:
  • With immobilization
• Immobilization
• Administration of estrogens or anti-estrogens (Tamoxifen):
  • In patients with breast cancer or bone metastases
• Rhabdomyolysis:
  • With acute renal failure:
    • Hypercalcemia has been described during the diuretic phase of acute renal failure, most often in patients with rhabdomyolysis:
      • Hypercalcemia in this setting is primarily due to:
        • The mobilization of calcium that had been deposited in the injured muscle
      • Correction of hyperphosphatemia (induced by the rise in glomerular filtration rate), mild secondary hyperparathyroidism induced by the renal failure, and an unexplained increase in serum calcitriol concentrations:
        • All appear to contribute to the hypercalcemia

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Primary hyperparathyroidism in pregnancy is of concern primarily for its potential effect on the fetus and neonate. 

Complications of primary hyperparathyroidism in pregnancy include:

• Spontaneous abortion, low birth weight, supravalvular aortic stenosis, and neonatal tetany:

  • The latter condition is a result of fetal parathyroid gland suppression by high levels of maternal calcium, which readily cross the placenta during pregnancy.

  • Infants with this condition, used to hypercalcemia in utero, have functional hypoparathyroidism after birth and can develop hypocalcemia and tetany in the first few days of life.

Calcium levels vary in the pregnant patient due to the physiological changes that occur.

• Carella and Gossain stated that calcium concentrations greater than 10.1 mg/dL during the second or third trimester should prompt an evaluation of PHPT.

In a retrospective patient series in the Norman Parathyroid Clinic in Florida, investigators examined pregnant patients with fetal loss and PHPT:

• They found that patients with calcium levels of 10.7 mg/dL were associated with pregnancy loss, but most pregnancies continued to term.

• Calcium levels  greater than 11.4 mg/dL were associated with higher levels of fetal loss, and 72% of fetal loss occurred at or above this level.

Surgery is the definitive treatment for PHP.T

• However, since surgery for PHPT has inherent potential risks for the pregnant patient, it is often viewed as the last resort.

• However, given the increasing evidence that supports a higher morbidity and mortality associated with calcium levels of  greater than 11.4 mg/dL, surgical intervention is recommended in patients with levels  greater 11.0 mg/dL, particularly in patients with prior pregnancy loss.

Gestational age plays a role in determining surgical candidacy:

• Traditionally, surgery is reserved for patients in the second trimester, given the higher risk in the first and third trimesters.

• First-trimester surgery is avoided due to incomplete organogenesis, and third-trimester surgery has been discouraged because it is associated with a higher risk of preterm labor.

  • In addition, there is a reported 58% fetal mortality associated with third-trimester parathyroidectomy.

  • This mortality rate includes all postoperative complications for the infant, such as premature delivery, intrauterine growth retardation, infant hypocalcemia, neonatal death, and stillbirth.

  • It is impossible to differentiate surgical complications from complications of prolonged hypercalcemia related to the underlying disease process.

Rodrigo Arrangoiz MS, MD, FACS

Cirugía Oncológica