Author: Rodrigo Arrangoiz MS, MD, FACS, FSSO

• 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

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• 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.

👉Patients with PHPT have higher coronary calcium scores than population-based controls.

👉Read more at : https://www.surgjournal.com/article/S0039-6060(19)30612-9/fulltext

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• Recent cure rates of hyperparathyroidism following parathyroidectomy:
  • Are reported between 92% and 97%
• When cure is not obtained, it is due to either:
  • Recurrent or persistent disease (Figure)
• Persistent hyperparathyroidism:
  • Is defined as hypercalcemia and elevated parathyroid hormone (PTH) levels:
    • During the 6-month period after parathyroidectomy:
      • It occurs in 0.4% to 7.8% of patients
• Recurrent hyperparathyroidism:
  • Is defined as hypercalcemia and elevated PTH levels that occur after normal values have been obtained for 6 months after parathyroidectomy and may be slightly less common than persistent disease:
    • Occurring in 0.4% to 4.8% of patients
• It is most common in:
  • Familial hyperparathyroidism
• Advances in imaging modalities and surgical techniques have decreased the rate of persistent disease significantly over the past two decades
• Persistent disease is considered a technical error:
  • Most commonly due to a missed single parathyroid adenoma
• A rare but notable cause of persistent or recurrent hyperparathyroidism is parathyromatosis:
  • A condition in which multiple benign hyperfunctioning parathyroid tissues are
    scattered throughout the neck and superior mediastinum and that occurs due to surgical implants from the fragmentation of abnormal parathyroid tissue in the previous operation
• Other causes are detailed in Table 1 (Table 1)
• Additional studies have shown that specific clinical factors are associated with an increased or decreased risk of having persistent hyperparathyroidism:
  • Negative, equivocal, or discordant imaging including ultrasonography and sestamibi is associated with a higher likelihood of persistent disease
  • Whereas intraoperative PTH (IOPTH) monitoring, with 50% decrease in serum PTH after removal of parathyroid tissue, increased weight of the affected gland, and surgery performed at high-volume centers is associated with successful initial parathyroidectomy

• Work-up and Diagnosis:
  • When a patient presents with recurrent or persistent hyperparathyroidism, all other causes of hyperparathyroidism including:
    • Vitamin D deficiency, renal insufficiency, medications such as lithium resulting in hypercalcemia, and renal calcium leak need to be ruled out and treated if identified
  • Additional work-up should also be done to evaluate for familial causes of hyperparathyroidism
  • The operative reports, imaging studies, and pathology reports associated with prior operation(s) should be obtained and meticulously reviewed
  • Confirmation of the location(s) of abnormal parathyroid glands:
    • Using at least two imaging modalities preoperatively is recommended in all cases of recurrent or persistent disease
  • Imaging modalities include ultrasonography, sestamibi with or without single-photon emission CT, and four-dimensional CT and should include evaluation of the mediastinum
  • When multiple imaging techniques are used:
    • 95% of abnormal glands can be identified
  • Evaluation of the vocal cords:
    • To assess for any previous recurrent laryngeal nerve injury resulting in paralysis is recommended for all neck reoperations
  • Fine-needle aspiration (FNA):
    • May be used preoperatively to confirm presence of abnormal parathyroid tissue when noninvasive imaging studies are unclear but should be used with caution and
      only in select patients:
      • As FNA carries the risk of hematoma, parathyromatosis, and cancer seeding
    • Selective PTH venous sampling (SVS) has also been described to regionalize recurrent or persistent disease when other imaging modalities fail and has been reported as successful in up to 94% of cases:
      • SVS is performed by obtaining serial samples of PTH from the superior vena cava, brachiocephalic, internal jugular, vertebral, thymic, and thyroid veins, after which levels are compared to identify the approximate location of the hyperfunctioning gland
• Indications for Surgery:
  • Reoperation is associated with significantly increased risk of:
    • Hypoparathyroidism (5% to 20%)
    • Recurrent laryngeal nerve injury (10% to 15%)
  • Therefore, it is recommended to have a higher
    threshold before recommending reoperation for recurrent or persistent disease
  • Indications for reoperation:
    • Significant life-limiting symptoms
    • Nephrolithiasis
    • Osteoporosis
    • Hypercalcemia
    • Decrease in renal function
  • If surgery is indicated, early reexcision in the case of persistent disease:
    • Is not recommended, rather revision should be delayed by 4 to 6 months to avoid a surgical bed affected by inflammation and scarring
• Operative Approach:
  • The goal of resection:
    • Is to remove the remaining hyperfunctioning parathyroid tissue while preserving enough to avoid hypoparathyroidism
  • Due to increased scar tissue in a reoperative neck, care is taken to avoid injury to surrounding structures, including the recurrent laryngeal nerve
  • For most patients, resecting the residual hyperfunctioning parathyroid tissue:
    • Is possible through a standard, anterior cervical incision
  • A lateral approach for targeted glands in the
    tracheoesophageal groove or sternocleidomastoid:
    • Is an excellent approach to avoid scar tissue
  • Glands within the mediastinum:
    • Most often lie within the thyrothymic ligament
    • They can be gently pulled up through a cervical incision successfully, even in the reoperative neck
  • A thoracic approach:
    • Is recommended for those with abnormal parathyroid tissue of 6 cm or greater identified below the superior aspect of the clavicle
  • IOPTH is recommended:
    • As it significantly improves the ability to confirm adequate resection of recurrent disease intraoperatively:
      • With sensitivity of up to 100%
  • Additional strategies have been reported to localize parathyroid tissue and minimize injury to surrounding structures in a reoperative neck, including:
    • The use of the gamma probe after injection of 99m technetium-methoxy isobutyl isonitrile preoperatively, ultrasonography-guided methylene blue injection, near-infrared autofluorescence imaging, indocyanine green fluorescence angiography, and recurrent laryngeal nerve monitoring:
    • Previously, IV infusion of methylene blue was
      used by some to identify parathyroid tissue; however, this is no longer recommended due to associated toxicities
  • Parathyroid autotransplantation and cryopreservation are often recommended following resection of the affected parathyroid tissue in reoperative parathyroidectomies:
    • Especially if the abnormal gland is the last viable parathyroid tissue, multiple glands have been previously removed, or there is concern for possible devascularization of the
      remaining glands
    • A case where cryopreservation may not be necessary is that of a missed adenoma
      where other parathyroid glands have not been disturbed in either the initial operation or re-exploration
• Follow-up postoperatively includes monitoring of serum PTH and calcium with the treatment of hypocalcemia if present

• Primary Hyperparathyroidism (PHPT):
  • Occurs when one (or more) of the four parathyroid glands grows into a tumor and behaves inappropriately by constantly making excess parathyroid hormone (PTH)
  • The parathyroid glands grow into a tumor and produce too much parathyroid hormone (PTH):
    • Which removes calcium from the bones
• In Primary Hyperparathyroidism (PHPT) the tumor (Adenoma):
  • Has lost its control mechanism and makes large amounts of parathyroid hormone (PTH):
    • Thus, even when the serum calcium level is high:
      • When the normal response of the parathyroid glands should be to stop making any PTH at all:
        • One of the parathyroid glands keeps making the parathyroid hormone
• One important thing to remember as you read about PHPT:
  • Is that the abnormal PTH production is caused by a benign parathyroid tumor, called ADENOMA:
    • It is not a cancer:
      • However this disease (PHPT) can increase the occurrence of other cancers:
        • Breast Cancer
        • Prostate Cancer
        • Renal Cancer
        • Skin Cancer
        • Colon and rectal cancer
• The most common cause of excess hormone production (primary hyperparathyroidism):
  • Is the development of a benign tumor in one of the parathyroid glands:
    • This enlargement of one parathyroid glands is called a:
      • Parathyroid adenoma:
        • Which accounts for roughly 85% to 90% of all patients with primary hyperparathyroidism:
          • The other 10% to 15% will have more than one bad gland (mulitiglandular disease):
            • Doble Adenomas:
              • 6% to 9% of the cases
            • Triple Adenomas:
              • Less than 0.3% of the cases
            • Parathyroid Gland Hyperplasia:
              • 3% of the cases
• This out of control (autonomously functioning) parathyroid gland:
  • Is essentially never cancerous (virtually 99% of them are benign tumors):
    • However, PHPT slowly causes damage to the body:
      • Because it induces an abnormally high level of calcium in the blood:
        • Which can slowly destroy a number of tissues
• Parathyroid adenomas:
  • Typically are much bigger than the normal “grain-of-rice” parathyroid and will frequently be about the size of an olive or grape:
    • Thus, the typical patient with primary hyperparathyroidism will be cured of the disease when this “grape” size tumor is removed
  • Up to 30% will have more than one tumor
  • This tumor / adenoma will almost always continue to grow until it is removed:
    • As it grows, it makes more PTH and will make you feel worse (symptomatic)
  • This tumor is constantly making parathyroid hormone (PTH):
    • Which is what takes the calcium out of your bones and makes the calcium in your blood too high

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• Bone disease, including:
  • Osteopenia, osteoporosis, and osteitis fibrosa cystica:
    • Is found in approximately 15% of patients with primary hyperparathyroidism at the time of diagnosis
  • Increased bone turnover:
    • As found in patients with osteitis fibrosa cystica:
      • Can be determined by documenting:
        • Elevated alkaline phosphatase concentration
  • Advanced PHPT with osteitis fibrosa cystica:
    • Now occurs in less than 5% of patients
  • The classic manifestation of PHPT bone disease is:
    • Osteitis fibrosa cystica:
      • Which is characterized clinically by bone pain and radiographically by subperiosteal bone resorption
    • It has pathognomonic radiological findings:
      • Which are best seen on radiographs of the hands:
        • And are characterized by subperiosteal resorption:
          • Most evident in the radial aspect of the middle phalanx of the second and third fingers
        • Bone cysts
        • Tuft formation of the upper part of the distal phalanges
      • Brown or osteoclastic tumors of the long bones:
        • Result from excess osteoclast activity:
          • And consist of collections of osteoclasts intermixed with fibrous tissue and poorly mineralized woven bone
        • The brown coloration is due to:
          • Hemosiderin deposition
      • Tapering of the distal clavicle
    • Patients with normal serum alkaline phosphatase levels:
      • Rarely have clinically apparent osteitis fibrosa cystica
• PHPT typically results in a loss of bone volume:
  • At the cortical bone sites such as:
    • The radius
  • Relative preservation of cancellous bone:
    • As found in vertebral bodies
    • Patients with primary hyperparathyroidism, however:
      • May also have osteoporosis in the lumbar spine that dramatically improves after parathyroidectomy
• Fractures are also more common in patients with primary hyperparathyroidism, and the incidence of fractures:
  • Also decreases after parathyroidectomy:
    • Bone disease is correlated with serum PTH and vitamin D levels

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• Sestamibi characteristics:
  • Radioactive uptake by the adenoma:
    • Should be different from the thyroid gland
  • Rest of the study should not have any abnormality
• Patients greater than 25 years of age
• No family history of:
  • PHPT or
  • Multiple endocrine neoplasia (MEN)
• Absence of goiter
• No history of lithium intake
• No history of radiation to the neck
• No history of diseases of the:
  • Pancreas, adrenal gland and pituitary gland

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• Secondary hyperparathyroidism:
  • Is overproduction of parathyroid hormone (PTH):
    • Due to a nonparathyroid cause:
      • Usually a result of renal failure
  • Renal failure decreases the production of 1,25(OH)2 D3:
    • Impairing intestinal absorption of calcium:
      • Leading to hypocalcemia:
        • Which increases PTH secretion by the parathyroid glands:
          • Leading to diffuse or nodular hyperplasia
  • Hyperphosphatemia:
    • From decreased renal excretion also contributes to PTH secretion:
      • The resulting calcium level is low or normal
  • Less common causes of secondary hyperparathyroidism include:
    • Osteomalacia
    • Long-term lithium therapy
    • Vitamin D deficiency
    • Malabsorption syndromes
    • Secondary hyperparathyroidism has beenv increasingly described following bariatric surgery:
      • Most commonly Roux-en-Y gastric bypass and duodenal switch:
        • Due to prolonged vitamin D deficiency:
          • It occurs despite vitamin D replacement
• The pathophysiology of secondary hyperparathyroidism:
  • Is multifactorial and can result from:
    • Phosphorous retention
    • Altered vitamin D metabolism and resistance
    • Altered metabolism of PTH
    • Impaired calcemic response to PTH
    • Possible genetic mutations
• The condition most commonly occurs in patients:
  • With a history of chronic renal failure
• Gastric bypass:
  • Has also been an increasingly recognized cause of altered vitamin D metabolism
• Patients will commonly have:
  • An elevated PTH level and normal or low serum calcium:
    • In such a setting, vitamin D levels should be measured:
      • If low, treated for a minimum of 6 weeks with supplemental vitamin D
• Secondary hyperparathyroidism:
  • Is most commonly managed medically with the use of:
    • Calcimimetic agents:
      • For example cinacalcet
    • Phosphate binders
    • Adequate calcium intake
    • Vitamin D replacement
• Cinacalcet:
  • Works by binding the calcium-sensing receptors on the chief cells of the parathyroid gland:
    • Increasing its sensitivity to extracellular calcium
• Surgical treatment is indicated in patients with:
  • Renal osteodystrophy
  • Calciphylaxis:
    • Calciphylaxis is a rare complication of secondary hyperparathyroidism resulting in acute deposition of calcium in tissues and skin necrosis:
      • That may lead to a systemic inflammatory response:
        • It is associated with a high rate of mortality (87 to 93%)
    • Calcium phosphate product of ≥ 70
    • Soft tissue calcium deposition and tumoral calcinosis
    • Calcium level greater than 11 mg/dL with an inappropriately high level of PTH
• Renal osteodystrophy:
  • Is a major issue in hemodialysis patients:
    • The aluminum present in the dialysate bath:
      • Accumulates in the bone:
        • Contributes to the development of osteomalacia
• Osteitis fibrosa cystica:
  • A type of renal osteodystrophy:
    • Is characterized by marrow fibrosis and increased bone turnover
  • Bone cysts, osteopenia, and decreased bone strength develop
  • To halt the progression of this disease process:
    • These patients with secondary hyperparathyroidism are treated surgically
• Calciphylaxis:
  • Is a rare vascular disorder:
    • In which calcium is deposited in the media of small- to medium-sized arteries
      • As a result, ischemic damage:
        • To the dermal and epidermal structures develops
  • The ulcerated lesions:
    • Are extremely painful and can become infected with subsequent sepsis, and eventually death
  • Patients with early signs of calciphylaxis:
    • Should undergo an urgent parathyroidectomy:
      • Although there is some evidence that aggressive management of serum calcium and parathyroid levels:
        • With cinacalcet may be beneficial
  • Care should be taken in wound care management:
    • Because aggressive debridement can lead to chronic nonhealing wounds:
      • Since wound healing is very poor in these patients
• Uremic pruritus:
  • Is characterized by severe itching:
    • That is thought to result from increased deposition of calcium salt in the dermis:
      • Without the visible lesions of calciphylaxis
  • Parathyroidectomy:
    • Seems to alleviate these symptoms and halts progression to the more serious skin and vascular complications seen with calciphylaxis

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