Hyperparathyroidism

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Definition/Description

Hyperparathyroidism is a disorder caused by oversecretion of parathyroid hormone (PTH) by one or more of the four parathyroid glands.[1] This disorder can disrupt calcium, phosphate, and bone metabolism. [1]The parathyroid glands are located in the neck on the posterior surface of each lobe of the thyroid gland. [2][3] Each of the four parathyroid glands is about the size of a grain of rice.[3] As part of the endocrine system, these glands secrete parathyroid hormone (PTH), which regulates calcium and phosphorus. [2] Hyperparathyroidism is classified into three groups: primary, secondary, or tertiary.[1] 

Primary hyperparathyroidism develops when there is an imbalance between serum calcium levels and PTH secretion.[1] Up to ten percent of these cases may be hereditary. [4]

Secondary hyperparathyroidism occurs when the glands have become enlarged due to malfunction of another organ system.[1] Causes of secondary hyperparathyroidism include; severe deficiency in vitamin D, severe deficiency in calcium, and chronic renal failure. Chronic renal failure is the most common cause of secondary hyperparathyroidism.[5] 

Tertiary hyperparathyroidism is seen in dialysis clients who have chronic secondary hyperparathyroidism.[1]  Dialysis clients who suffer from chronic renal failure lack the ability to absorb and convert vitamin D into a form that can be used by the body. This decline in vitamin D decreases the amount of calcium that can be absorbed.[5]


Hyperparathyroid Images:

www.riversideonline.com/source/images/image_popup/pthyroid.jpg

images.medicinenet.com/images/illustrations/parathyroid_glands.jpg

surgery.med.umich.edu/general/endocrine/images/content/parathyroid.jpg


Image of calcium regulation in the body:

en.wikipedia.org/wiki/File:Calcium_regulation.png

 Prevalence

Hyperparathyroidism is most prevalent in postmenopausal women over the age of 60, and is most common in the sixth decade of life.[1] [4]Incidence of hyperparathyroidism is about equal in men and women under the age of 50. Incidence increases with age and female gender.[6] The occurrence of hyperparathyroidism is highest among blacks followed by whites.[6] The condition is less prevalent in asians, hispanics, and other races.[6] The incidence of primary hyperparathyroidism in the general population is about 4 per 100,000 per year.[4] Most cases (80%) of hyperparthyroidism are discovered accidental during routine blood tests.[4]

Characteristics/Clinical Presentation

Hyperparathyroidism effects not only the endocrine system but also the central nervous system (CNS), musculoskeletal system, gastrointestinal (GI), and the gastrourinary system (GU). [2]

Individuals with this disorder commonly exhibit muscle weakness and fatigue. Other symptoms associated with hyperparathyroidism include:

  •  Loss of appetite [2]
  •  Lethargy[1]
  •  Drowsiness[1]
  •  Weight loss[2]
  •  Nausea and vomiting[2]
  •  Depression[2]
  •  Increased thirst and urination [2]
  •  Kidney stones[3]
  •  Bone and joint pain[3]
  •  Fragile bones that easily fracture (osteoporosis)[3]
  •  GI problems[2]
  •  Pancreatitis[2]
  •  Bone decalcification (hypercalcemia)[2]
  •  Psychotic paranoia[2]
  •  Frequent complaints of illness with no apparent cause[3]
  •  Paresthesias[1]
  •  Hyperactive deep tendon reflexes[1]
  •  Personality changes[1]
  •  Muscle weakness and atrophy[1]
  •  Gout[1]
  •  Myalgia[1]
  •  Abdominal pain[1]
  •  Constipation[1]
  •  Peptic ulcers[1]
  •  Renal colic[1]
  •  Hyper-calcemia[1]
  •  Kidney infections[1]
  •  Renal hypertension[1]



Associated Co-morbidities

Patients with mild PHPT had a significantly increased risk of developing cardiovascular, cerebrovascular disease, renal dysfunction and fractures.[6] Additional co-morbidities include:

Medications

Medications to treat hyperparathyroidism include:

Calcimimetics. Calcimimetics mimic calcium circulating in the blood and may trick the parathyroid glands into releasing less parathyroid hormone. It may be prescribed to treat primary hyperparathyroidism, particularly if surgery hasn't successfully cured the disorder or a person isn't a good candidate for surgery.[7]


Hormone replacement therapy. Hormone replacement therapy (HRT) does not address the underlying causes of excess PTH but helps to prevent bone from demineralizing as a result of excess PTH in the blood. HRT is used for menopausal women or for individuals who are exhibiting signs of osteoporosis. Estrogen and progestin are commonly used in combination for this treatment option.[7]


Bisphosphonates- Bisphosphonates prevents the loss of calcium from bones decreasing the risk for development of osteoporosis which is caused by hyperparathyroidism.[7]


Calcitonin- Calcitonin is used in the treatment of osteoporosis.[8] It binds to osteoclasts and inhibits their action, helping to prevent the breakdown of bone.[8]

Diagnostic Tests/Lab Tests/Lab Values

Diagnostic tests/Labs:

  • Blood tests are used to indicate how much calcium, PTH and phosphorus are in the blood. If an elevated amount of any of these is found in the blood it may be indicative of overactivity of the parathyroid glands.[7]

Other tests once diagnosis has been made:

  •  Bone mineral density test (bone densitometry). Dual energy X-ray absorptiometry, or a DXA scan, is commonly used to measure bone mineral density. This test measures how many grams of calcium and other minerals are packed into a segment of bone. [7]
  •  Urine tests. A 24-hour collection of urine can be used to measure kidney function and how much calcium is expelled in urine. This test may help in determining if kidney dysfunction or parathyroid disorder is the primary cause of bone demineralization. [7]
  •  Imaging tests of kidneys. Used to determine presence of kidney stones or other kidney abnormalities.[7]


Images:

Dual energy X-ray absorptiometry

Kidney Stone Imaging

Kidney Stone X-ray

Etiology/Causes

Primary hyperparathyroidism is often caused by an adenoma of the parathyroid gland.[1]


Systemic Involvement [2] [9]


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Medical Management (current best evidence)

Treatment for primary hyperparathyroidism is surgical removal of affected parathyroid gland, management of any bone or organ damage, and use of medication to protect bones prior to surgery or when parathyroidectomy is not an option. [1]

Surgical Images:

Skin incision

Adenoma

Physical Therapy Management (current best evidence)

Therapists may observe skeletal, articular and neuromuscular impairments associated with hyperparathyroidism. [1][3] In the acute phase, therapists should exercise caution with patients as they are at an increased risk for bone fracture.[1] After surgery, patients should be encouraged to ambulate as soon as possible to prevent further demineralization.[1] Encourage and aid patients in setting up their homes to avoid or minimize fall risks.[1]

Alternative/Holistic Management (current best evidence)

Eating a healthy and well balanced natural diet, avoiding coffee, tea, alcohol, tobacco, and carbonated beverages, exercising regularly, and drinking plenty of water may help to reduce the symptoms of hyperparathyroidism.[10] Some herbal supplements have been used for the treatment of hyperparathyroidism including chaste tree and dandelion.[10]  Some holistic medical practitioners also treat hyperparathyroidism.[10] Vitamin supplements including calcium, vitamin D, Ipriflavone (soy isoflavones) standardized extract and Omega-3 fatty acids have been used to help treat this disorder.[10] Alternative treatments for hyperparathyroidism have not been proven effective for the management of hyperparathyroidism. Alternative/holistic treatment options should be discussed with a qualified healthcare practitioner prior to initiation.


Image of My Plate Dietary Guidelines:

http://en.wikipedia.org/wiki/File:USDA_MyPlate_green.jpg

Differential Diagnosis


Adrenal insufficiency [11]


Certain malignant tumors or myelomas[11] 


Excessive calcium or vitamin D ingestion[11] 


Familial hypocalciuric hypercalcemia[11] 


Hyperthyroidism[11]


Malnutrition[11] 

Case Reports/ Case Studies

A patient with persistent primary hyperparathyroidism due to a second ectopic adenoma.[12]

A 33 year old woman was diagnosed with hyperparathyroidism and treated with parathyroidectomy. Post-operatively the patient’s serum calcium and PTH levels decreased but did not normalize and continued to present with kidney stones.


Diplopia associated with hyperparathyroidism: report of a case.[13]

A 60 year old man presented with diplopia as well as common symptoms of hyperparathyroidism. He was diagnosed with primary hyperparathyroidism and a search for the cause of the diplopia continued. After undergoing thyroidectomy his double vision was relieved as his serum calcium levels returned to normal.


Primary hyperparathyroidism presenting as recurrent acute pancreatitis: A case report and review of literature[1]

A 32 year old man presents with repetitive episodes of pancreatitis. Patient was treated by parathyroidectomy and recurrence of abdominal pain ceased and serum calcium levels normalized.

Resources

add appropriate resource here

American Academy of Otolaryngology-Head and Neck Surgerys

American Association of Clinical Endocrinologists

American Association of Endocrine Surgeons

The American Society for Bone and Mineral Research

The Endocrine Society

The Paget Foundation for Paget’s Disease of Bone and Related Disorders

Recent Related Research (from Pubmed)

see tutorial on Adding PubMed Feed

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References

  1. 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 1.21 1.22 1.23 1.24 1.25 1.26 1.27 1.28 1.29 1.30 1.31 1.32 1.33 1.34 1.35 Goodman C, Fuller K.. Pathology: Implications for the Physical Therapist, 3rd ed. St. Louis, Missouri: Saunders Elsevir; 2007.
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 Goodman C, Snyder T. Differential Diagnosis for Physical Therapists: Screening for Referral, 5th ed. St. Louis, Missouri: Saunders Elsevir; 2013.
  3. 3.0 3.1 3.2 3.3 3.4 3.5 3.6 Mayo Clinic Staff. Diseases-conditions/hyperparathyroidism/basics/symptoms. http://www.mayoclinic.org (accessed January 16, 2014).
  4. 4.0 4.1 4.2 4.3 Skugor, M. Milas, M. Hypercalcemia [Internet].Accessed 2014 Apr 3. Available from: http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/endocrinology/hypercalcemia/
  5. 5.0 5.1 Mayo Clinic Staff. Diseases/conditions/hyperparathyroidism/basics/causes/ http://www.mayoclinic.org (accessed January 16, 2014)
  6. 6.0 6.1 6.2 6.3 6.4 Yeh M, Ituarte P, Adams A, et al. . Incidence and prevalence of primary hyperparathyroidism in a racially mixed population.. The Journal Of Clinical Endocrinology And Metabolism 2013; (98(3)): 1122-1129.
  7. 7.0 7.1 7.2 7.3 7.4 7.5 7.6 Mayo Clinic Staff. Diseases-conditions/hyperparathyroidism/treatment. http://www.mayoclinic.org (accessed January 16, 2014).
  8. 8.0 8.1 Gladson B. Pharmacology for Rehabilitation Professionals, 2nd ed. St. Louis: Elseivier Saunders; 2011.
  9. Vestergaard P,Mosekilde L. Cohort study on effects of parathyroid surgery on multiple outcomes in primary hyperparathyroidism.BJM 2003;327(7174):530-534.
  10. 10.0 10.1 10.2 10.3 (2013) Hyperparathyroisism, Available at: http://umm.edu/health/medical/altmed/condition/hyperparathyroidism (Accessed: January 17, 2014.)
  11. 11.0 11.1 11.2 11.3 11.4 11.5 Hyperparathyroidism: differential diagnosis, Available at: http://www.google.com/url?q=http%3A%2F%2Fwww.mdguidelines.com%2Fhyperparathyroidism%2Fdifferential-diagnosis&sa=D&sntz=1&usg=AFQjCNH8A5bwzEOzyVFe_WOquB5mwXbrsQ (Accessed: 16th January 2014)
  12. Hamdy N. A patient with persistent primary hyperparathyroidism due to a second ectopic adenoma. Natural Clinical Practice Endocrinology and Metabolism. [Serial on the Internet].2007 [cited 2014 Jan. 17];3:311-315. Available from:fckLRhttp://www.nature.com/nrendo/journal/v3/n3/full/ncpendmet0448.html
  13. Forman B.H., Ciardiello K., Landau S.J., Freedman J.K. (1995) 'Diplopia associated with hyperparathyroidism: report of a case', Yale J Biol Med, 68(5-6), pp. 215-217 [Online]. Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2588946/ (Accessed: 17th January 2014).