Parathyroid cancer

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ammu Susheela, M.D. [2]

Synonyms and keywords: Parathyroid carcinoma; Parathyroid neoplasm; Cancer of parathyroid; Parathyroid tumor

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ammu Susheela, M.D. [2]

Overview

Parathyroid cancer was first described by Sainton and Millot, in 1933. In 1928, the first parathyroidectomy operation was conducted by Isaac Y. Olch to treat parathyroid lesions. On gross pathology, stony-hard consistency, lobulation, and dense, fibrous, grayish-white capsule are characteristic findings of parathyroid cancer. On microscopic histopathological analysis, dense fibrous trabeculae, mitoses, and capsular invasions are characteristic findings of parathyroid cancer. The etiology of parathyroid cancer is unknown. Parathyroid cancer must be differentiated from renal disease, immobility, and thiazides adverse effect. The incidence of parathyroid cancer is approximately 0.015 per 100,000 individuals in United States. Parathyroid cancer affects men and women equally. Common risk factors in the development of parathyroid cancer are multiple endocrine neoplasia type 1, hyperparathyroidism, and familial isolated hyperparathyroidism. The hallmark of parathyroid cancer is neck mass. A positive history of multiple endocrine neoplasiab type I, hyperparathyroidism, and previous radiation therapy to the head or neck is suggestive of parathyroid cancer. The most common symptoms of parathyroid cancer include weight loss, muscle weakness, fractures, constipation, fatigue, and bone pain. Patients with parathyroid cancer usually appear well. Physical examination of patients with parathyroid cancer is usually remarkable for lymphadenopathy and a palpable lump in the neck. Neck CT scan may be diagnostic of parathyroid cancer. Laboratory findings consistent with the diagnosis of parathyroid cancer include elevated serum calcium and serum parathyroid hormone. Findings on CT suggestive of parathyroid cancer include metastasis and invasion of surrounding tissues. The predominant therapy for parathyroid cancer is surgical resection. Adjunctive supportive therapy, chemotherapy, and radiation may be required. Supportive therapy for parathyroid cancer includes IV fluids, diuretics, and calcimimetic agents. Surgery is the mainstay of treatment for parathyroid cancer. There are no primary preventive measures available for parathyroid cancer. Secondary prevention strategy recommended following parathyroid cancer is germline DNA analysis for HRPT2/CDC73.

Historical Perspective

Parathyroid cancer was first described by Sainton and Millot, in 1933. In 1928, the first parathyroidectomy operation was conducted by Isaac Y. Olch to treat parathyroid lesions.

Pathophysiology

On gross pathology, stony-hard consistency, lobulation, and dense, fibrous, grayish-white capsule are characteristic findings of parathyroid cancer. On microscopic histopathological analysis, dense fibrous trabeculae, mitoses, and capsular invasions are characteristic findings of parathyroid cancer.

Causes

The etiology of parathyroid carcinoma is unknown.

Differential Diagnosis

Parathyroid cancer must be differentiated from renal disease, immobility, and thiazide adverse effect.

Epidemiology and Demographics

The incidence of parathyroid cancer is approximately 0.015 per 100,000 individuals in United States. Parathyroid cancer affects males and females equally.

Risk Factors

Common risk factors in the development of parathyroid cancer are multiple endocrine neoplasia type 1, hyperparathyroidism, and familial isolated hyperparathyroidism.

Natural history, Complications and Prognosis

Depending on the extent of the tumor at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as good. Common complications of parathyroid cancer include hypercalcemia, metastasis, and death.

Diagnostic Criteria

The diagnosis of parathyroid cancer is made when if any of the following 5 diagnostic criteria are met: Hypercalcemia greater than 14 milligrams per deciliter, serum parathyroid hormone levels greater than twice that of normal, a palpable cervical mass in a hypercalcemic patient, unilateral vocal cord paralysis with hypercalcemia, and concomitant renal and skeletal disease observed in a patient with a markedly elevated serum parathyroid hormone.

Staging

The staging of parathyroid cancer is based on whether there is localized or metastatic disease.

History and Symptoms

The hallmark of parathyroid cancer is a neck mass. A positive history of multiple endocrine neoplasia type I, hyperparathyroidism, and previous radiation therapy to the head or neck is suggestive of parathyroid cancer. The most common symptoms of parathyroid cancer include weight loss, muscle weakness, fractures, constipation, fatigue, and bone pain.

Physical Examination

Patients with parathyroid cancer usually appear well. Physical examination of patients with parathyroid cancer is usually remarkable for lymphadenopathy and palpable lump in the neck.

Laboratory Findings

Laboratory findings consistent with the diagnosis of parathyroid cancer include elevated serum calcium and serum parathyroid hormone.

Chest Xray

On chest x-ray, parathyroid cancer is characterized by metastases into lungs and bones.

CT

Neck CT scan may be diagnostic of parathyroid cancer.

MRI

MRI scan may be diagnostic of parathyroid cancer. Findings on MRI suggestive of parathyroid cancer include metastasis and invasion of surrounding tissues.

Echocardiography or Ultrasound

Neck ultrasound may be helpful in the diagnosis of parathyroid cancer. Findings on neck ultrasound suggestive of parathyroid cancer include structural irregularities of parathyroid gland and invasion of the surrounding tissues.

Other Imaging Findings

Other imaging studies for parathyroid cancer include sestamibi scan, venous sampling, or PET scan.

Medical Therapy

The predominant therapy for parathyroid cancer is surgical resection. Adjunctive supportive therapy, chemotherapy, and radiation may be required. Supportive therapy for parathyroid cancer includes IV fluids, diuretics, and calcimimetic agents.

Surgery

Surgery is the mainstay of treatment for parathyroid cancer.

Primary Prevention

There are no primary preventive measures available for parathyroid cancer.

Secondary Prevention

Secondary prevention strategy recommended following parathyroid cancer is germline DNA analysis for HRPT2/CDC73.

Reference

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ammu Susheela, M.D. [2]

Overview

Parathyroid cancer was first described by Sainton and Millot, in 1933. In 1928, the first parathyroidectomy operation was conducted by Isaac Y. Olch to treat parathyroid lesions.

Discovery

In 1904, Dr. Fritz de Quevain first mentioned the term parathyroid cancer when he observed a non-functioning parathyroid lesion in one of his patients.^[1]
Parathyroid cancer was first described in 1933 by Sainton and Millot.^[2]

Landmark Events in the Development of Treatment Strategies

The first successful removal of the parathyroid may have been carried out in 1928 by doctor Isaac Y. Olch, whose intern had noticed elevated calcium levels in an elderly patient who complained of muscle weakness. Prior to this surgery, patients with removed parathyroid gland typically died from muscular tetany.^[3]

References

↑ Quervain, F. (1909). “Parastruma maligna aberrata”. Deutsche Zeitschrift für Chirurgie. 100 (1): 334–353. doi:10.1007/BF02819737. ISSN 0367-0023.
↑ McClenaghan F, Qureshi YA (2015). “Parathyroid cancer”. Gland Surg. 4 (4): 329–38. doi:10.3978/j.issn.2227-684X.2015.05.09. PMC 4523631. PMID 26312219.CS1 maint: PMC format (link)
↑ Parathyroid gland. Wikipedia (2015). https://en.wikipedia.org/wiki/Parathyroid_gland Accessed on December 28, 2015

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Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ammu Susheela, M.D. [2]

Overview

On gross pathology, stony-hard mass with lobulations and a dense, fibrous, grayish-white capsule are characteristic findings of parathyroid cancer. On microscopic histopathological analysis, dense fibrous trabeculae, mitoses, and capsular invasions are characteristic findings of parathyroid cancer.

Pathogenesis

Parathyroid cancer typically runs an indolent course because the tumor has a rather low malignant potential.^[1]
At initial presentation, very few patients with parathyroid carcinoma have metastases either to regional lymph nodes (<5%) or distant sites (<2%).
A higher proportion of parathyroid cancers may locally invade the thyroid gland, overlying strap muscles, recurrent laryngeal nerve, trachea, or esophagus. Parathyroid carcinoma tends to originate from the inferior parathyroid glands; one series reported that the primary tumor originating in the inferior parathyroid glands was found in 15 of 19 cases involving local invasion.
Approximately 40% to 60% of patients experience a postsurgical recurrence, typically in the range of 2 to 5 years after the initial resection. In most cases, hypercalcemia precedes the evidence of recurrent disease on physical examination.
The location of recurrence is typically regional, either in the tissue of the neck or in the cervical lymph nodes, where these account for approximately two thirds of recurrent cancer cases.
Distant metastases were reported to occur in 25% of patients, which primarily occurs in the lungs, but may also occurs in the bone and liver. Serum parathyroid hormone levels may be 3 to 10 times above the upper limit of normal and hence cause nephrolithiasis or nephrocalcinosis.

Genetics

HRPT2/CDC73 gene mutation is involved in the pathogenesis of parathyroid cancer.

Associated Conditions

Multiple endocrine neoplasia 1
Autosomal dominant familial isolated hyperparathyroidism

Gross Pathology

Parathyroid carcinoma may be distinguished from adenomas by the stony-hard consistency and lobulation of parathyroid carcinoma.
In most series, the median maximal diameter of parathyroid carcinomas is between 3.0 cm and 3.5 cm compared with a diameter of approximately 1.5 cm for benign parathyroid adenomas.
In approximately 50% of the patients, the malignant tumor is surrounded by a dense, fibrous, grayish-white capsule that infiltrates adjacent tissues. The clinical features of parathyroid carcinoma are caused primarily by the effects of excessive secretion of parathormone (PTH) by the tumor rather than by the infiltration of vital organs by tumor cells.

Microscopic Pathology

Histopathologically, as with other endocrine neoplasms, the distinction between benign and malignant parathyroid tumors is a difficult process.
On microscopic histopathological analysis, dense fibrous trabeculae, trabecular growth patterns, and capsular invasions are characteristic findings of parathyroid carcinomas.
Capsular and vascular invasions appear to correlate best with the tumor recurrence.

References

↑ Parathyroid cancer. Cancer.gov (2015). http://www.cancer.gov/types/parathyroid/hp Accessed on December 29, 2015

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Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ammu Susheela, M.D. [2]

Overview

The etiology of parathyroid cancer is unknown.

Causes

The etiology of parathyroid cancer is unknown.^[1]

Reference

↑ Parathyroid cancer. Cancer.gov (2015). http://www.cancer.gov/types/parathyroid/hp Accessed on December 29, 2015

Differentiating Parathyroid cancer from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Overview

Parathyroid cancer must be differentiated from other conditions presenting as a neck swelling.^[1]

Differentiating Parathyroid cancer from other Diseases

Parathyroid cancer must be differentiated from other conditions presenting as neck swelling. The differentials include the following:

Category	Diseases	Benign	Demography	History	Pain	Dysphagia	Mass exam	Others	Lab findings	Histopathology	Imaging	Gold standard diagnosis	Associated findings
Neoplasm	Hypopharyngeal cancer^[2]^[3]^[4]	Malignant	More common in males Age: 55-65 years old Incidence: < 1/100,000 in U.S. More common in Japan, India, Iran	Tobacco use Abuse alcohol consumption HPV infection Lump in the neck Odynophagia Hoarseness	−	+	Non tender cervical node	Lymphadenopathy	−	Spindle cells Nuclear atypia Basaloid cells Abundant chromatin	Neck CT scan: Soft tissue mass Irregular thickening of mucosa Necrotic region MRI: Tumors are hypointense on T1 and hyperintense on T2	Biopsy	−
	Parathyroid cancer^[5]^[6]^[7]	Malignant	Incidence: Rare Mean age : 44-54 years old Gender: Female predilection	Presents with the hyperparathyroidism Bone pains Abdominal pain Nausea and vomiting Fatigue Confusion	+	+	Lower neck mass	Tachycardia Weight loss Sweating Neck swelling	Low TSH Increased T4 and T3 Hypercalcemia	Microscopic findings: Trabecular growth pattern High mitosis Surrounding thick fibrotic bands Capsular involvement Vascular invasion is common	CT and MRI shows more frequent lower lobe involvement, vascular involvement , lymph node metastasis, and perineural involvement Bone scan may show decreasing bone density	Biopsy and histopathological examination	Hereditary syndromes MEN-2B syndrome Neurofibromatosis type 1 VHL disease
	Carotid body tumors^[8]^[9]^[10]^[11]	Benign	Age: 26-55 years Male predominance	A slow growing neck mass	+	−	Mobile Non-tender neck mass (horizontally more than vertically) Pulsatile Bruit may be present	Change in voice Dizziness Tinnitus Headache	Rasised catecholamine levels	Microscopically they are extra-adrenal paragangliomas	Doppler ultrasound, CT, MRI and angiography is used to visualize the tumor Metaiodobenzylguanidine (MIBG) testing	Histopathology analysis and catecholamine levels	−
	Paraganglioma^[12]^[13]^[14]	Benign (Majority) Malignant (rare)	Age 50-70 years More in females	May be an accidental finding depending on their secretory nature or present with following symptoms: Palpitation Tremor Pulse-like vibratory sense Headache Change in voice Vertigo Catecholamine secreting paragangliomas presents with : Hypertension Headache Sweating Tachycardia	−	−	No visible mass Located deep in the the neck along the glossopharyngeal nerve	−	Biochemical testing may show catecholamine metabolites in serum or urine samples	Highly vascular tumors that involves nerves around vessels Gross findings: Fleshy tumor Pink to red-brown to gray in color Associated with hemorrhage or fibrosis Microscopic findings: Round or polygonal cells Nests or trabecular structures inside the capsule	Ultrasound Computed tomography Magnetic resonance imaging Angiography metaiodobenzylguanidine (MIBG) 18F-fluoro-2-deoxyglucose Positron emission tomography (FDG-PET)	Imaging and serum catecholamine analysis	−
Category	Diseases	Benign	Demography	History	Pain	Dysphagia	Mass exam	Others	Lab findings	Histopathology	Imaging	Gold standard diagnosis	Associated findings
Neoplasm	Schwannoma^[15]^[16]^[17]	Benign	Rare tumor Incidence: 1-10%	Slow growing mass Localized neural deficit depending on the site of peripheral nerve involved Vagus nerve or superior cervical sympathetic chain involvement (most common locations)	+	±	Multiple Slow growing nodules on the skin	Vagal involvement: Hoarseness Dysphagia Sympathetic nerve involvement may present as Horner’s syndrome: Dilated pupil Decrease sweating Dropping eyelid Vestibular nerve involvement & Hearing impairment (most common)	May be normal	Encapsulated neural tissue growth	Resembling Carotid body tumor on CT MRI and MRI angiography confirm the diagnosis	Imaging	neurofibromatosis type II
	Lymphoma ^[18]^[19]^[20]^[21]^[22]^[23]	Benign or malignant	Age: Predilection for older age Mean age: 55	Insidious onset slow growing lymph nodes Non-specific systemic B symptoms: Fever Night sweats Weight loss) Rash Waxing and waning lymphadenopathy Abdominal fullness	−	±	Multiple chain lymphadenopathy Hepatosplenomegaly Ascites Crackles heard on chest auscultation	Rash and pruritus	Pancytopenia Hypercalcemia Hyperuricemia (increased cell turnover) Monoclonal immunoglobulin (M-spike) Raised LDH levels	On complete node analysis four patterns are described: Nodular/follicular Diffuse pattern Transition from a nodular to a diffuse pattern in adjacent nodes Transition from a lower to a higher grade of involvement within a single node	Imaging to stage the disease Positron emission tomography with computed tomography is preferred over MRI	Lymph node biopsy coupled with cytometry	Infections due to cytopenias With acquired form of C1 inhibitor deficiency patients may develop angioedema
	Liposarcoma ^[24]^[25]^[26]^[27]	Malignant	Rare tumor Age: Relatively in older age Gender: No gender predilection	Mobile mass Few symptoms until they grow enough to compress the surrounding structures Symptoms of neural deficit, pain, tingling, or skin changes	±	−	Mobile soft mass Intact overlying skin Blue discoloration due to intra-lesion hemorrhage	Intact skin and normal color	Normal	Gross examination: Bulk of yellow colored fat tissue Microscopic features: Adipose tissue containing lipoblasts Atypical nucleus pushed to side by intracytoplasmic vacuoles Tissue biopsy may show histological sub-groups: Well-differentiated Myxoid/round cell Pleomorphic liposarcomas	Imaging not usually required for diagnosis May show deeper invasion Ultrasound shows homogeneous hyperechoic mass	Biopsy and histopathology analysis	−
Category	Diseases	Benign	Demography	History	Pain	Dysphagia	Mass exam	Others	Lab findings	Histopathology	Imaging	Gold standard diagnosis	Associated findings
Neoplasm	Lipoma ^[28]^[29]^[30]	Benign	Genetic predisposition Unspecific gender or age association	One or multiple soft, painless skin nodules May causes pain or compressive symptoms	±	−	Mobile soft nodule Intact overlying skin	Normal	Normal	Diagnoses is usually clinical Tissue biopsy may show: Bundle of well-demarcated lipocytes Single nuclei aligned to the side Intra-cytoplasimic fat granules	Diagnosis is usually clinical ultrasound is used to differentiate lipoma from other benign lesions such as: Epidermoid cyst A ganglion	Clinical evaluation	Multiple lipomas Associated with familial multiple lipomatosis
	Glomus vagale, glomus jugulare tumors^[31]^[32]^[33]^[34]^[35]^[36]	Benign	Rare tumor	Painless slowly enlarging mass in the neck	−	±	Non-compressible Firm Non-tender swelling No thrill or bruit Normal overlying skin	Secretory tumors May have compressive signs such as: Dysphagia Hoarseness Cranial nerves deficits Horner’s syndrome	Normal	Glomus tumors arise from Non Chromaffin cells histopathology reveals “salt and pepper” chromatin On immunohistochemistry tumor cells show chromogranin and S-100 positivity	MRI (Imaging of choice): Typical appearance of the tumor along vagus nerve Ultrasonography (early stage of diagnosis): Isoechoic to hypoechoic well defined tumor CT: Vascularity of the tumor Biochemical testing: Shows secretary nature of the tumor	Imaging and Metaiodobenzylguanidine (MIBG) testing	−
	Metastatic head and neck cancer^[37]^[38]	Malignant	Depends on the nature of metastatic tumor	Asymptomatic Painless lymphadenopathy Supra clavicular fullness in case of stomach cancer metastasis	−	±	Non-tender mass in the neck Non-tender lymphadenopathy	Majority of metastatic head and neck cancer Metastatise from GIT and lungs	Vary depending on the underlying cancer	Histology of primary cancer	CT and MRI to see extent of tumor	Biopsy and histopathology of the primary site of tumor	−
Category	Diseases	Benign	Demography	History	Pain	Dysphagia	Mass exam	Others	Lab findings	Histopathology	Imaging	Gold standard diagnosis	Associated findings
Other	Laryngeal cancer^[39]^[40]	Benign/Malignant	Older males Younger patients with HPV infection or smoking history	Neck mass Hoarseness Throat pain Snoring Obstructive sleep apnea	±	±	Examination of neck and oral cavity may show : mass lymphadenopathy Examination of laryngeal cancer is done using flexible laryngoscopy under anesthesia.	Smoking is the most common risk factor Smoking with alcohol increases the risk Oropharyngeal cancers presenting with neck masses are associated with human papillomavirus (HPV) infection	HPV testing may show HPV infection	FNA of neck mass Followed by biopsy of laryngeal cancer Show type cancer cells	CT, MRI and PET are used to see local infiltration by cancer Also to see distant metastases. Panendoscopy is done to see extent of the tumor.	Laryngoscopy and biopsy	−
	Arteriovenous fistula ^[41]^[42]	Benign/Malignant	Depends on the risk factors	Expanding neck mass Headaches Dizziness Neurological sequels	−	−	Pulsating neck mass Bruit	May be associated with vasculopathies metastatic invasion of vessels and neck surgery		Varies depending on the etiology	MR angiography	MR angiography	−
	Thyroid nodule/ Goiter ^[43]^[44]^[45]^[46]	Benign/ Malignant	Female predominance Young age (benign causes) Old age (malignant etiology)	Growing painless neck mass in front of neck Weight loss Palpitation Hoarseness Irritability	±	±	Painless Non-tender Asymmetrical neck mass in front of neck With smooth overlying skin Nodular surface Depending on the type: May be mobile Adherent to the underlying structure Lymphadenopathy in case of malignant features	Goiter is most commonly associated with iodine deficiency	Normal to low TSH levels in case of malignancy High TSH levels in case of goiter	FNA is done in case of goiter Core biopsy is performed if malignancy is suspected	USG: Shows nodular or non- nodular lesions in Thyroid US is better than CT. Thyroid radionuclide imaging: Shows radioiodine uptake Cold in case of malignancy Cold or hot in case of goiter.	Biopsy and histopathology of nodules	−
Category	Diseases	Benign	Demography	History	Pain	Dysphagia	Mass exam	Others	Lab findings	Histopathology	Imaging	Gold standard diagnosis	Associated findings

Reference

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↑ Sajid MS, Hamilton G, Baker DM (August 2007). “A multicenter review of carotid body tumour management”. Eur J Vasc Endovasc Surg. 34 (2): 127–30. doi:10.1016/j.ejvs.2007.01.015. PMID 17400487.
↑ Boedeker CC, Ridder GJ, Schipper J (2005). “Paragangliomas of the head and neck: diagnosis and treatment”. Fam. Cancer. 4 (1): 55–9. doi:10.1007/s10689-004-2154-z. PMID 15883711.
↑ Gluckman JL, Robbins KT, Fried MP (1990). “Cervical metastatic squamous carcinoma of unknown or occult primary source”. Head Neck. 12 (5): 440–3. PMID 2211107.
↑ Waltonen JD, Ozer E, Hall NC, Schuller DE, Agrawal A (October 2009). “Metastatic carcinoma of the neck of unknown primary origin: evolution and efficacy of the modern workup”. Arch. Otolaryngol. Head Neck Surg. 135 (10): 1024–9. doi:10.1001/archoto.2009.145. PMID 19841343.
↑ Feldman PS, Kaplan MJ, Johns ME, Cantrell RW (November 1983). “Fine-needle aspiration in squamous cell carcinoma of the head and neck”. Arch Otolaryngol. 109 (11): 735–42. PMID 6639441.
↑ Grénman R, Koivunen P, Minn H (2015). “[Laryngeal cancer in Finland]”. Duodecim (in Finnish). 131 (4): 331–7. PMID 26237923.
↑ Guneyli S, Cinar C, Bozkaya H, Korkmaz M, Oran I (September 2016). “Endovascular management of congenital arteriovenous fistulae in the neck”. Diagn Interv Imaging. 97 (9): 871–5. doi:10.1016/j.diii.2015.08.006. PMID 26972281.
↑ Gobin YP, Garcia de la Fuente JA, Herbreteau D, Houdart E, Merland JJ (November 1993). “Endovascular treatment of external carotid-jugular fistulae in the parotid region”. Neurosurgery. 33 (5): 812–6. PMID 8264877.
↑ Madjar S, Weissberg D (July 1995). “Retrosternal goiter”. Chest. 108 (1): 78–82. PMID 7606997.
↑ Hedayati N, McHenry CR (March 2002). “The clinical presentation and operative management of nodular and diffuse substernal thyroid disease”. Am Surg. 68 (3): 245–51, discussion 251–2. PMID 11893102.
↑ Hughes K, Eastman C (August 2012). “Goitre – causes, investigation and management”. Aust Fam Physician. 41 (8): 572–6. PMID 23145396.
↑ Hermus AR, Huysmans DA (August 2000). “[Diagnosis and therapy of patients with euthyroid goiter]”. Ned Tijdschr Geneeskd (in Dutch; Flemish). 144 (34): 1623–7. PMID 10972051.

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ammu Susheela, M.D. [2]

Overview

The incidence of parathyroid cancer is approximately 0.015 per 100,000 individuals in United States. Parathyroid cancer affects men and women equally.

Epidemiology and Demographics

Prevalence

In developed countries, the prevalence of parathyroid cancer in United States is estimated to be 0.005%.

Incidence

In developed countries, the incidence of parathyroid cancer is 0.015 per 100,000 individuals.

Age

The incidence of parathyroid cancer increases with age; the median age at diagnosis is between 45 and 51 years.

Gender

The female to male ratio is 1:1.

Developed Countries

In the United States, Europe, and Japan, parathyroid carcinoma has been estimated to cause hyperparathyroidism (HPT) in 0.017% to 5.2% of the cases; however, many series report this entity to account for less than 1% of patients with primary hyperparathyroidism.^[1]

References

↑ Parathyroid cancer. Cancer.gov (2015). http://www.cancer.gov/types/parathyroid/hp Accessed on December 29, 2015

Template:WikiDoc Sources

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ammu Susheela, M.D. [2]

Overview

Common risk factors in the development of parathyroid cancer are multiple endocrine neoplasia type 1, hyperparathyroidism, and familial isolated hyperparathyroidism.^[1]

Common Risk Factors

Common risk factors in the development of parathyroid cancer are:

Multiple endocrine neoplasia type 1
Hyperparathyroidism–jaw tumor syndrome
Familial isolated hyperparathyroidism

Less Common Risk Factors

Radiation therapy to the head and neck

References

↑ Parathyroid cancer. Canadian Cancer Society (2015). http://www.cancer.ca/en/cancer-information/cancer-type/parathyroid/parathyroid-cancer/?region=bc Accessed on December 29, 2015

Template:WikiDoc Sources

Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ammu Susheela, M.D. [2]

Overview

Germline DNA analysis for HRPT2/CDC73 is recommended among patients with parathyroid cancer, as early detection can benefit relatives and offsprings.

Screening

Germline DNA analysis for HRPT2/CDC73 is recommended among patients with parathyroid cancer, as early detection can benefit relatives and offsprings.

References

Template:WikiDoc Sources

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ammu Susheela, M.D. [2]

Overview

Depending on the extent of the tumor at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as good. Common complications of parathyroid cancer include hypercalcemia, metastasis, and death.

Natural History

Parathyroid cancer typically runs an indolent, albeit tenacious, course because the tumor has a rather low malignant potential.^[1]

Complications

Hypercalcemia
Metastases to lungs and bones
Cancer recurrence
Death

Prognosis

Parathyroid cancer is a slow growing tumor.^[2]
Surgery prolongs life in advanced stages and improves prognosis.

References

↑ Parathyroid cancer. Canadian Cancer Society (2015). http://www.cancer.ca/en/cancer-information/cancer-type/parathyroid/parathyroid-cancer/?region=bc Accessed on December 29, 2015
↑ Parathyroid cancer. Cancer.gov (2015). http://www.cancer.gov/types/parathyroid/hp Accessed on December 29, 2015

Template:WikiDoc Sources

Diagnosis

Treatment

Case Studies

Case #1

Template:WH Template:WS

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[pmid26312219-2] McClenaghan F, Qureshi YA (2015). “Parathyroid cancer”. Gland Surg. 4 (4): 329–38. doi:10.3978/j.issn.2227-684X.2015.05.09. PMC 4523631. PMID 26312219.CS1 maint: PMC format (link)

[3] Parathyroid gland. Wikipedia (2015). https://en.wikipedia.org/wiki/Parathyroid_gland Accessed on December 28, 2015

[1] Parathyroid cancer. Cancer.gov (2015). http://www.cancer.gov/types/parathyroid/hp Accessed on December 29, 2015

[1] Parathyroid cancer. Cancer.gov (2015). http://www.cancer.gov/types/parathyroid/hp Accessed on December 29, 2015

[1] Parathyroid cancer. Canadian Cancer Society (2015). http://www.cancer.ca/en/cancer-information/cancer-type/parathyroid/parathyroid-cancer/?region=bc Accessed on December 29, 2015

[pmid12560383-2] Helliwell TR (February 2003). “acp Best Practice No 169. Evidence based pathology: squamous carcinoma of the hypopharynx”. J. Clin. Pathol. 56 (2): 81–5. PMC 1769882. PMID 12560383.

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[pmid17713315-6] Sahasranam P, Tran MT, Mohamed H, Friedman TC (August 2007). “Multiglandular parathyroid carcinoma: a case report and brief review”. South. Med. J. 100 (8): 841–4. doi:10.1097/SMJ.0b013e318073ca37. PMID 17713315.

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[pmid174004872-8] Sajid MS, Hamilton G, Baker DM (August 2007). “A multicenter review of carotid body tumour management”. Eur J Vasc Endovasc Surg. 34 (2): 127–30. doi:10.1016/j.ejvs.2007.01.015. PMID 17400487.

[pmid158837112-9] Boedeker CC, Ridder GJ, Schipper J (2005). “Paragangliomas of the head and neck: diagnosis and treatment”. Fam. Cancer. 4 (1): 55–9. doi:10.1007/s10689-004-2154-z. PMID 15883711.

[pmid15063383-10] Pellitteri PK, Rinaldo A, Myssiorek D, Gary Jackson C, Bradley PJ, Devaney KO, Shaha AR, Netterville JL, Manni JJ, Ferlito A (July 2004). “Paragangliomas of the head and neck”. Oral Oncol. 40 (6): 563–75. doi:10.1016/j.oraloncology.2003.09.004. PMID 15063383.

[pmid28478173-11] Darouassi Y, Alaoui M, Mliha Touati M, Al Maghraoui O, En-Nouali A, Bouaity B, Ammar H (August 2017). “Carotid Body Tumors: A Case Series and Review of the Literature”. Ann Vasc Surg. 43: 265–271. doi:10.1016/j.avsg.2017.03.167. PMID 28478173.

[pmid15328326-12] Neumann HP, Pawlu C, Peczkowska M, Bausch B, McWhinney SR, Muresan M, Buchta M, Franke G, Klisch J, Bley TA, Hoegerle S, Boedeker CC, Opocher G, Schipper J, Januszewicz A, Eng C (August 2004). “Distinct clinical features of paraganglioma syndromes associated with SDHB and SDHD gene mutations”. JAMA. 292 (8): 943–51. doi:10.1001/jama.292.8.943. PMID 15328326.

[pmid11701678-13] Erickson D, Kudva YC, Ebersold MJ, Thompson GB, Grant CS, van Heerden JA, Young WF (November 2001). “Benign paragangliomas: clinical presentation and treatment outcomes in 236 patients”. J. Clin. Endocrinol. Metab. 86 (11): 5210–6. doi:10.1210/jcem.86.11.8034. PMID 11701678.

[pmid8678971-14] O’Riordain DS, Young WF, Grant CS, Carney JA, van Heerden JA (September 1996). “Clinical spectrum and outcome of functional extraadrenal paraganglioma”. World J Surg. 20 (7): 916–21, discussion 922. PMID 8678971.

[pmid24450866-15] Hilton DA, Hanemann CO (April 2014). “Schwannomas and their pathogenesis”. Brain Pathol. 24 (3): 205–20. doi:10.1111/bpa.12125. PMID 24450866.

[pmid28237565-16] Albert P, Patel J, Badawy K, Weissinger W, Brenner M, Bourhill I, Parnell J (2017). “Peripheral Nerve Schwannoma: A Review of Varying Clinical Presentations and Imaging Findings”. J Foot Ankle Surg. 56 (3): 632–637. doi:10.1053/j.jfas.2016.12.003. PMID 28237565.

[pmid27020268-17] Wong B, Bathala S, Grant D (January 2017). “Laryngeal schwannoma: a systematic review”. Eur Arch Otorhinolaryngol. 274 (1): 25–34. doi:10.1007/s00405-016-4013-6. PMID 27020268. Vancouver style error: initials (help)

[pmid7139563-18] Anderson T, Chabner BA, Young RC, Berard CW, Garvin AJ, Simon RM, DeVita VT (December 1982). “Malignant lymphoma. 1. The histology and staging of 473 patients at the National Cancer Institute”. Cancer. 50 (12): 2699–707. PMID 7139563.

[pmid71395632-19] Anderson T, Chabner BA, Young RC, Berard CW, Garvin AJ, Simon RM, DeVita VT (December 1982). “Malignant lymphoma. 1. The histology and staging of 473 patients at the National Cancer Institute”. Cancer. 50 (12): 2699–707. PMID 7139563.

[pmid15185336-20] Negri E, Little D, Boiocchi M, La Vecchia C, Franceschi S (August 2004). “B-cell non-Hodgkin’s lymphoma and hepatitis C virus infection: a systematic review”. Int. J. Cancer. 111 (1): 1–8. doi:10.1002/ijc.20205. PMID 15185336.

[pmid2406917-21] Moormeier JA, Williams SF, Golomb HM (February 1990). “The staging of non-Hodgkin’s lymphomas”. Semin. Oncol. 17 (1): 43–50. PMID 2406917.

[pmid151853362-22] Negri E, Little D, Boiocchi M, La Vecchia C, Franceschi S (August 2004). “B-cell non-Hodgkin’s lymphoma and hepatitis C virus infection: a systematic review”. Int. J. Cancer. 111 (1): 1–8. doi:10.1002/ijc.20205. PMID 15185336.

[pmid71395633-23] Anderson T, Chabner BA, Young RC, Berard CW, Garvin AJ, Simon RM, DeVita VT (December 1982). “Malignant lymphoma. 1. The histology and staging of 473 patients at the National Cancer Institute”. Cancer. 50 (12): 2699–707. PMID 7139563.

[pmid171979142-24] Evans HL (January 2007). “Atypical lipomatous tumor, its variants, and its combined forms: a study of 61 cases, with a minimum follow-up of 10 years”. Am. J. Surg. Pathol. 31 (1): 1–14. doi:10.1097/01.pas.0000213406.95440.7a. PMID 17197914.

[pmid21253554-25] Conyers R, Young S, Thomas DM (2011). “Liposarcoma: molecular genetics and therapeutics”. Sarcoma. 2011: 483154. doi:10.1155/2011/483154. PMC 3021868. PMID 21253554.

[pmid19194281-26] Alaggio R, Coffin CM, Weiss SW, Bridge JA, Issakov J, Oliveira AM, Folpe AL (May 2009). “Liposarcomas in young patients: a study of 82 cases occurring in patients younger than 22 years of age”. Am. J. Surg. Pathol. 33 (5): 645–58. doi:10.1097/PAS.0b013e3181963c9c. PMID 19194281.

[pmid176106862-27] Serpell JW, Chen RY (July 2007). “Review of large deep lipomatous tumours”. ANZ J Surg. 77 (7): 524–9. doi:10.1111/j.1445-2197.2007.04042.x. PMID 17610686.

[pmid24800932-28] Bree E, Karatzanis A, Hunt JL, Strojan P, Rinaldo A, Takes RP, Ferlito A, de Bree R (May 2015). “Lipomatous tumours of the head and neck: a spectrum of biological behaviour”. Eur Arch Otorhinolaryngol. 272 (5): 1061–77. doi:10.1007/s00405-014-3065-8. PMID 24800932.

[pmid6670522-29] Rydholm A, Berg NO (December 1983). “Size, site and clinical incidence of lipoma. Factors in the differential diagnosis of lipoma and sarcoma”. Acta Orthop Scand. 54 (6): 929–34. PMID 6670522.

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[pmid8164483-31] Urquhart AC, Johnson JT, Myers EN, Schechter GL (April 1994). “Glomus vagale: paraganglioma of the vagus nerve”. Laryngoscope. 104 (4): 440–5. doi:10.1288/00005537-199404000-00008. PMID 8164483.

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[pmid17400487-35] Sajid MS, Hamilton G, Baker DM (August 2007). “A multicenter review of carotid body tumour management”. Eur J Vasc Endovasc Surg. 34 (2): 127–30. doi:10.1016/j.ejvs.2007.01.015. PMID 17400487.

[pmid15883711-36] Boedeker CC, Ridder GJ, Schipper J (2005). “Paragangliomas of the head and neck: diagnosis and treatment”. Fam. Cancer. 4 (1): 55–9. doi:10.1007/s10689-004-2154-z. PMID 15883711.

[pmid2211107-37] Gluckman JL, Robbins KT, Fried MP (1990). “Cervical metastatic squamous carcinoma of unknown or occult primary source”. Head Neck. 12 (5): 440–3. PMID 2211107.

[pmid19841343-38] Waltonen JD, Ozer E, Hall NC, Schuller DE, Agrawal A (October 2009). “Metastatic carcinoma of the neck of unknown primary origin: evolution and efficacy of the modern workup”. Arch. Otolaryngol. Head Neck Surg. 135 (10): 1024–9. doi:10.1001/archoto.2009.145. PMID 19841343.

[pmid6639441-39] Feldman PS, Kaplan MJ, Johns ME, Cantrell RW (November 1983). “Fine-needle aspiration in squamous cell carcinoma of the head and neck”. Arch Otolaryngol. 109 (11): 735–42. PMID 6639441.

[pmid26237923-40] Grénman R, Koivunen P, Minn H (2015). “[Laryngeal cancer in Finland]”. Duodecim (in Finnish). 131 (4): 331–7. PMID 26237923.

[pmid26972281-41] Guneyli S, Cinar C, Bozkaya H, Korkmaz M, Oran I (September 2016). “Endovascular management of congenital arteriovenous fistulae in the neck”. Diagn Interv Imaging. 97 (9): 871–5. doi:10.1016/j.diii.2015.08.006. PMID 26972281.

[pmid8264877-42] Gobin YP, Garcia de la Fuente JA, Herbreteau D, Houdart E, Merland JJ (November 1993). “Endovascular treatment of external carotid-jugular fistulae in the parotid region”. Neurosurgery. 33 (5): 812–6. PMID 8264877.

[pmid7606997-43] Madjar S, Weissberg D (July 1995). “Retrosternal goiter”. Chest. 108 (1): 78–82. PMID 7606997.

[pmid11893102-44] Hedayati N, McHenry CR (March 2002). “The clinical presentation and operative management of nodular and diffuse substernal thyroid disease”. Am Surg. 68 (3): 245–51, discussion 251–2. PMID 11893102.

[pmid23145396-45] Hughes K, Eastman C (August 2012). “Goitre – causes, investigation and management”. Aust Fam Physician. 41 (8): 572–6. PMID 23145396.

[pmid10972051-46] Hermus AR, Huysmans DA (August 2000). “[Diagnosis and therapy of patients with euthyroid goiter]”. Ned Tijdschr Geneeskd (in Dutch; Flemish). 144 (34): 1623–7. PMID 10972051.

[1] Parathyroid cancer. Cancer.gov (2015). http://www.cancer.gov/types/parathyroid/hp Accessed on December 29, 2015

[1] Parathyroid cancer. Canadian Cancer Society (2015). http://www.cancer.ca/en/cancer-information/cancer-type/parathyroid/parathyroid-cancer/?region=bc Accessed on December 29, 2015

[1] Parathyroid cancer. Canadian Cancer Society (2015). http://www.cancer.ca/en/cancer-information/cancer-type/parathyroid/parathyroid-cancer/?region=bc Accessed on December 29, 2015

[2] Parathyroid cancer. Cancer.gov (2015). http://www.cancer.gov/types/parathyroid/hp Accessed on December 29, 2015

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Parathyroid cancer

Overview

Historical Perspective

Pathophysiology

Causes

Differential Diagnosis

Epidemiology and Demographics

Risk Factors

Natural history, Complications and Prognosis

Diagnostic Criteria

Staging

History and Symptoms

Physical Examination

Laboratory Findings

Chest Xray

CT

MRI

Echocardiography or Ultrasound

Other Imaging Findings

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Reference

Overview

Discovery

Landmark Events in the Development of Treatment Strategies

References

Overview

Pathogenesis

Genetics

Associated Conditions

Gross Pathology

Microscopic Pathology

References

Overview

Causes

Reference

Overview

Differentiating Parathyroid cancer from other Diseases

Reference

Overview

Epidemiology and Demographics

Prevalence

Incidence

Age

Gender

Developed Countries

References

Overview

Common Risk Factors

Less Common Risk Factors

References

Overview

Screening

References

Overview

Natural History

Complications

Prognosis

References

Diagnosis

Treatment

Case Studies

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