• 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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• Despite what most of the literature reports:
  • PHPT is symptomatic in more than 95% of the cases if proper attention is payed to the subtle symptoms and signs that this disease can produce due to the fluctuating calcium levels
• The “classic” pentad of:
  • Kidney stones
  • Painful bones
  • Abdominal groans
  • Psychic moans. and
  • Fatigue overtones
    • Are rarely seen today since the advent and general use of automated blood analyzers in the early 1970s
• At this point in time most patients present with:
  • Fatigue (# 1 symptom)
  • General malaise
  • Decrease levels of energy
  • Anxiety
  • Irritability leading to decrease social interaction
  • Depression (10% of cases)
  • Memory loss
  • Decrease concentration
  • Decrease ability to learn new things
  • Decrease ability to complete daily tasks at home
  • Decrease ability to complete daily tasks at work
  • Decrease social interaction
  • Insomnia
  • Arthralgia’s (32% of the cases)
  • Myalgia’s (14% to 41% of the cases)
  • Bone pain
  • Muscle weakness (specially proximal muscle groups)
  • Intermittent headaches
  • Polydipsia
  • Polyuria
  • Nocturia
  • Nausea (24% of the cases)
  • Anorexia (15% of the cases)
  • Non-specific abdominal pain
  • Heartburn (30% of the cases)
  • Constipation (33% of the cases)
  • Palpitations, arrhythmias (usually atrial fibrillation)
  • Elevated blood pressure
  • Thinning of the hair (specially in women in the frontal region)
  • Pruritus
• Patients with PHPT also tend to score lower than healthy controls when evaluated by general multidimensional health assessment tools:
  • Such as the Medical Outcomes Study Short-Form Health Survey (SF-36) and other specific questionnaires
• PHPT that is truly “asymptomatic” is a rare occurrence:
  • Seen in less than 5% of patients:
    • This is important when talking about management based on current guidelines
• Patients with PHPT have some degree of renal dysfunction or symptoms in approximately 80% of the cases. The renal manifestations implicated with PHPT are decreased glomerular filtration rate, hypercalciuria, nephrolithiasis, nephrocalcinosis, impaired urinary concentrating ability sometimes leading to polyuria, polydipsia, and nocturia, reduced fractional phosphate reabsorption leading to hypophosphatemia, and increased urinary exertion of magnesium [66]. Nephrolithiasis was previously reported in approximately40% to 80% of patients [77], but now occur only in about 20% to 25% of the cases [78]. The pathophysiology is thought to be related to the filtered load of calcium in the glomerulus that increases proportionately with the degree of hypocalcaemia [79]. Most renal stones in patients with PHPT are composed of calcium oxalate, although slightly alkaline urine may favor the precipitation of calcium phosphate stones [79,80]. Stone formers are more likely to be hypercalciuric, but less than one-third of the hypercalciuric patients with PHPT actually develop renal stones [80]. Hypercalciuria is not a predictor of nephrolithiasis in patients with PHPT and is no longer considered as an indication for surgery [81]. At the present
• Skeletal manifestations includingosteopenia, osteoporosis, and osteitis fibrosacystica, are found in approximately 15% of patients with PHPT [88,89]. PHPT is linked with a reduction in bone mineral density (BMD), particularly in the cortical bone, such as in the distal third of the radius [88,89]. In the lumbar region, composed all most exclusively by trabecular bone, and in the femoral region, composed by cortical and trabecular bone, the decrease in BMD is less severe . Osteitis fibrosacystica, a skeletal manifestation that is rarely seen today (seen in less than five percent of patients with PHPT), is caused by an increase in bone turnover and can be determined by finding an elevated serum alkaline phosphatase level [91]. The radiologic findings seen in patients with PHPT with bone disease are characterized by subperiosteal resorption (most obvious on the radial aspect of the middle phalanx of the second and third fingers), bone cysts, and tufting of the distal phalanges [92], which are best evaluated on plain x-rays of the hands. Brown or osteoclastic tumors (accumulations of osteoclasts and fibrous tissue) and bone cysts also may be present [93]. Brown tumors have a slightly greater incidence in PHPT than in secondary HPT (3% versus 2%) [94]. In patients with chronic kidney disease, persistent and excessive urinary calcium elimination can lower serum calcium level and lead to an increase in PTH secretion. This results in mobilization of calcium from the bones through rapid osteoclastic turnover of bone to maintain normal serum calcium levels . In regions where bone loss is exceptionally fast, hemorrhage, and reparative granulation tissue, with active, vascular, proliferating fibrous tissue may replace the normal marrow contents, resulting in a brown tumor. Hemosiderin imparts the brown color(hence the name of the lesions). The skull also may be affected and appears mottled with a loss of definition of the inner and outer cortices . Patients with normal serum alkaline phosphatase levels almost never have clinically apparent osteitis fibrosacystica. Bone disease correlates with serum PTH and vitamin D levels. The most frequent gastrointestinal manifestations of PHPT are constipation, heartburn, nausea and anorexia that occur in 33%, 30%, 24% and 15% of cases, respectively [69]. 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
• 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 [82]. 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 and, in contrast to other symptoms, is least likely to improve after parathyroidectomy [84]. 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.

• The primary treatment for secondary hyperparathyroidism:
  • Is medical using:
    • Calcium supplementation
    • Phosphate binders
    • Vitamin D
    • Calcitriol
    • Calcimimetics:
      • Such as cinacalcet
• Therapy is targeted to:
  • Reduce serum calcium and phosphate:
    • With improvement in medical management through the advent of:
      • Vitamin D analogs and cinacalcet:
        • Rates of parathyroidectomy for secondary hyperparathyroidism have declined
• Indications for parathyroidectomy include:
  • Failure of medical management, including:
    • Persistent hypercalcemia
    • Persistent hyperphosphatemia
    • PTH less than 800 pg/mL
    • Additionally, uncontrollable symptoms including:
      • Intractable pruritus
      • Skeletal pain or fractures
      • Progressive extraskeletal calcifications
• Removal of the parathyroid glands in secondary hyperparathyroidism:
  • Has been shown to quickly lower calcium, phosphorus, and PTH:
    • It is associated with greater survival in patients on hemodialysis
• It is estimated that 0.5% to 2% of patients with end-stage renal disease:
  • Require parathyroidectomy for secondary hyperparathyroidism
• Additional indications for surgery include:
  • Patient preference and inability to establish routine medical follow-up
• 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 and is associated with a high rate of mortality (87% to 93%) Figure

• Less than 30% of patients with Primary Hyperparathyroidism (PHPT) are referred for surgery:
  • Surgery is the BEST treatment and only cure for this disease:
    • https://www.ncbi.nlm.nih.gov/pubmed/28678063

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.

He is currently an Assistant Professor at the Columbia University Division of Surgical Oncology at Mount Sinai Medical Center

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.

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• What if my calcium level is normal but PTH level is elevated?
  • And other causes of secondary hyperparathyroidism (renal calcium loss and GI malabsorption) have been ruled out:
    • In some patients the total serum calcium (albumin corrected) these patients may be determined to have normocalcemic hyperparathyroidism:
      • Many consider it to be an early form of traditional primary Hyperparathyroidism (PHPT)
• More info:
  • https://collectedmed.com/index.php/directory/Coach_directory/articlelist/13076

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• Most parathyroid glands are the size of a grain of rice.
• Enlarged parathyroid glands can be 5 times that size!

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