What is the difference between primary hyperparathyroidism and secondary

Severe secondary hyperparathyroidism can lead to calciphylaxis which is a life threatening condition. Calciphylaxis can lead to soft-tissue wounds that won't heal until the hyperparathyroidism is controlled.

Chronic non-healing wounds can lead to widespread infection sepsis and death. In many patients who have undergone kidney transplants, parathyroid function returns to normal. In some patients, the parathyroid glands have functioned abnormally for so long while patients have kidney failure and are on dialysis, that parathyroid gland function never returns to normal.

It is critically important to protect the transplanted kidney from any negative effects excess parathyroid hormone may have on the kidney kidney stones, decreased function, dehydration that often accompanies high calcium levels. Hypercalcemia should be confirmed by repeated measurements of serum calcium concentrations, because all patients with primary hyperparathyroidism do not have demonstrable hypercalcemia every time the serum calcium level is measured.

Use of thiazide diuretics should be discontinued two weeks before a serum calcium level measurement is repeated. Information from references 2 through 5 , 9 and The total calcium level can be corrected for low albumin levels by adding 0. Ionized calcium levels are unaffected by altered serum albumin levels. The NIH consensus panel 9 did not recommend routine testing of the ionized calcium level for confirmation of hypercalcemia, because most physicians do not have access to a facility that can produce an accurate measurement.

The rightsholder did not grant rights to reproduce this item in electronic media. For the missing item, see the original print version of this publication. Intact PTH the entire 1 through 84 amino acid sequence can be measured by immunoradiometric assay or immunochemical assay. In approximately 10 percent of patients, the PTH level is not elevated but is in the upper one half of normal range.

Once the diagnosis of primary hyperparathyroidism is confirmed biochemically, bone mineral density should be measured in three sites lumbar spine, hip, forearm , and the patient should be evaluated for renal complications.

Other possible causes of hypercalcemia must be considered in the differential diagnosis of primary hyperparathyroidism 3 , 4 , 5 , 11 Table 1. Symptomatic primary hyperparathyroidism nephrolithiasis, nephrocalcinosis, osteitis fibrosa cystica. Creatinine clearance reduced by more than 30 percent compared with age-matched persons.

Medical surveillance not desirable or possible. Surgery requested by patient. Information from reference 9. The standard surgical approach is bilateral neck exploration, with identification of all four parathyroid glands. Technetium Tc 99m sestamibi scanning is the most accurate technique 80 to 90 percent sensitivity for localizing abnormal parathyroid glands. An intraoperative rapid PTH test that can be performed in minutes is available to detect any remaining abnormal glands.

If the intraoperative PTH level falls by more than 50 percent, surgery should be terminated. Immediate postoperative management focuses on establishing the success of the surgery and monitoring the patient for complications such as symptomatic hypocalcemia, bleeding, vocal cord paralysis, and laryngospasm.

The serum calcium concentration typically reaches a nadir within 24 to 36 hours after surgery. The serum PTH level is in the normal range within 30 hours, although the secretory response to hypocalcemia may not return to normal for weeks. The patient should maintain a low-calcium diet until the serum calcium concentration is normal. Ampules of injectable calcium and other seizure precautions should be maintained at the bedside for emergency use.

Outpatient monitoring of serum and urinary calcium levels at frequent intervals may be necessary. Less common causes are a failure to recognize and adequately treat parathyroid malignancy or an incorrect diagnosis of primary hyperparathyroidism. Asymptomatic patients who meet the criteria suggested by the NIH guidelines may be candidates for medical monitoring rather than surgical intervention with parathyroidectomy 9 , 23 Table 3.

Recommended surveillance includes biannual measurement of serum calcium levels, annual measurement of serum creatinine levels, and annual bone density testing. Normal renal status i. Normal bone status i. There are no clinical factors that predict the prognosis of patients with asymptomatic hyperparathyroidism. Recommendations include modest intake of calcium 1, to 1, mg per day and vitamin D to IU per day. Theoretically, low calcium intake could stimulate PTH production. Currently, no medical therapies are available to effectively cure primary hyperparathyroidism.

In postmenopausal women, estrogen may reduce PTH-stimulated bone resorption. The effects of newer oral bisphosphonates, calcimimetics, and raloxifene are being studied.

Bisphosphonates should be used with caution in patients with renal failure. Whenever possible, the underlying cause of secondary hyperparathyroidism should be removed. The goal of medical management is to normalize calcium levels.

Supplementation of vitamin D and calcium is necessary. Patients with end-stage renal disease also need phosphate binders to decrease hyperphosphatemia.

Parathyroidectomy may be necessary in patients who develop tertiary hyperparathyroidism and severe metabolic bone disease. Already a member or subscriber? Log in. Interested in AAFP membership?

Learn more. She completed a residency in family medicine at the Medical University of South Carolina, Charleston. Address correspondence to Edna D. Taniegra, M. Markham, , Little Rock, AR — e-mail: edtaniegra uams. Reprints are not available from the author.

The author indicates that she does not have any conflicts of interest. Sources of funding: none reported. Medical and surgical management of hyperparathyroidism. Mayo Clin Proc. Silverberg SJ. Natural history of primary hyperparathyroidism.

Endocrinol Metab Clin North Am. Primary hyperparathyroidism in pregnancy: evidence-based management. Obstet Gynecol Surv. Potts JT Jr. Diseases of the parathyroid gland and other hyper- and hypocalcemic disorders. In some people with long-term end-stage kidney disease, the parathyroid glands enlarge and begin to release PTH on their own, and PTH doesn't go down with medical treatment. This is called tertiary hyperparathyroidism, and people with this condition may require surgery to remove parathyroid tissue.

Complications of hyperparathyroidism are mainly related to the long-term effect of too little calcium in your bones and too much calcium in your bloodstream. Common complications include:. Mayo Clinic does not endorse companies or products. Advertising revenue supports our not-for-profit mission. This content does not have an English version.

This content does not have an Arabic version. Overview Parathyroid glands Open pop-up dialog box Close. Parathyroid glands The parathyroid glands, which lie behind the thyroid, manufacture the parathyroid hormone, which plays a role in regulating your body's levels of the minerals calcium and phosphorus. Request an Appointment at Mayo Clinic. Share on: Facebook Twitter. Show references Primary hyperparathyroidism. Accessed Jan. El-Hajj Fuleihan G, et al.

Pathogenesis and etiology of primary hyperparathyroidism. Primary hyperparathyroidism: Diagnosis, differential diagnosis, and evaluation. Ferri FF. In: Ferri's Clinical Advisor Elsevier; Kliegman RM, et al. In: Nelson Textbook of Pediatrics. Silverberg SJ, et al. Primary hyperparathyroidism: Management. Hormone replacement therapy. IBM Micromedex. Smoking and bone health.