Background
Primary vs. secondary vs. tertiary Hyperparathyroidism.
Primary hyperparathyroidism is the most common cause of hypercalcemia in the outpatient setting.
Pathogenesis: 1) The function of the Parathyroid Hormone. 2) Vitamin D Action.
Causes of secondary hyperparathyroidism.
Diagnosis
A high or unexpectedly “normal” PTH level in the presence of a high corrected calcium generally is diagnostic of primary hyperparathyroidism. (NEJM 2011)
H&P
Risk Factors:
Common presentation. Mostly Asx or have symptoms of hypercalcemia.
DDx & Causes.
Diagnostic tests.
Diagnostic algorithm.
Treatment
Hyperparathyroidism Pearls and Links
- Patients with secondary hyperparathyroidism usually have low or normal serum calcium concentrations. If there is hypercalcemia, it’s not secondary hypercalcemia anymore. It’s either tertiary hyperparathyroidism or something else altogether. Secondary hyperparathyroidism cannot ever be associated with high blood calcium. Read more here.
- Signs and symptoms of hyperparathyroidism.
“Secondary hyperparathyroidism is most likely due to low vitamin D intake or low serum vitamin D, often in the setting of renal disease. However, the serum vitamin D level and estimated glomerular filtration rates are normal in this patient. This rules out secondary hyperparathyroidism, as well as vitamin D deficiency and renal insufficiency. Primary hyperparathyroidism is more likely in the presence of hypercalcemia and inappropriately normal or high parathyroid hormone levels. Familial hypocalciuric hypercalcemia is ruled out by a normal 24-hour urine calcium level.” ABFM
Confirm Isolated elevated calcium levels before pursuing further testing.
“Isolated elevated calcium levels should be confirmed before pursuing further testing. After calcium elevation is confirmed, immediate treatment should be undertaken if hypercalcemia is severe. Otherwise, a history and physical examination would be appropriate, as well as 25-hydroxyvitamin D, magnesium, creatinine, and PTH levels. In patients with a normal or elevated PTH level, 24-hour urine calcium and creatinine levels can help to differentiate between primary hyperparathyroidism and familial hypocalciuric hypercalcemia. If the PTH level is low, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and parathyroid hormone–related peptide levels should be checked to evaluate possible causes of hypercalcemia independent of the parathyroid. Sestamibi scintigraphy is indicated only after confirmation of hyperparathyroidism, and typically in anticipation of surgical treatment.
Ref: Michels TC, Kelly KM: Parathyroid disorders. Am Fam Physician 2013;88(4):249-257.” ABFM
“Hyperparathyroidism is usually caused by a single adenoma of one of the four parathyroid glands. A minority of cases (10%–15%) are associated with four-gland hyperplasia. Studies that localize the glands, such as a technetium scan or ultrasonography, help surgeons who are familiar with this condition achieve a cure rate of 95%–98%, with an estimated complication rate of 1%–3%. For patients <50 years old or symptomatic patients, such as those with a fragility fracture, parathyroidectomy is the treatment of choice. If a patient is older, is a poor surgical candidate, or has asymptomatic disease, long-term monitoring with treatment focused on reducing bony complications can be considered (SOR C).” ABFM
Secondary Hyperparathyroidism:
“Patients with normocalcemic hyperparathyroidism may present with low bone density, osteoporosis, or a fragility fracture. Many of these patients will probably evolve into having hyperparathyroidism” AAFP 2013
References
N Engl J Med 2011;365(25):2389-2397. Primary Hyperparathyroidism. http://www.nejm.org/doi/full/10.1056/NEJMcp1106636
BMJ 2012;344:e1013. http://www.bmj.com/content/344/bmj.e1013
http://www.aafp.org/afp/2013/0815/p249.html
http://www.aafp.org/afp/2004/0115/p333.html
http://www.parathyroid.com/secondary-hyperparathyroidism.htm