A Quick Synopsis of AFP's "Parathyroid Disorders"

Parathyroid DisordersTHOMAS C. MICHELS, MD, MPH, Madigan Army Medical Center, Tacoma, Washington KEVIN M. KELLY, MD, MBA, Carl R. Darnall Army Community Hospital, Fort Hood, TexasAm Fam Physician. 2013 Aug 15;88(4):249-257
http://www.aafp.org/afp/2013/0815/p249.pdf

     PTH is released from the parathyroid glands in response to low serum calcium. The PTH causes the bones to release calcium from the bones into the blood. The kidneys stop losing calcium in the urine and put it back into the system. The kidneys also convert 25-vitamin D into 1,25-vitamin D, which helps calcium absorption in the GI tract. Even though the body has four parathyroid glands, we only need one to maintain normal calcium levels.
     The most common cause of hypercalcemia is primary hyperparathyroidism, due to a single adenoma.  Lesser causes are multiglandular hyperplasia and carcinoma. Most patients are asymptomatic. Risk factors include previous neck radiation, age above 50 years, and being female.  Calcium is elevated and PTH is high or normal. The calcium/ creatinine ratio should be elevated as well. If the ratio is below 0.01, the diagnosis is familial hypocalciuric hypercalcemia. This results from a calcium receptor gene mutation, in which extra calcium in needed for PTH suppression (feedback inhibition). Patients with familial hypocalciuric hypercalcemia present with normal or high PTH, high calcium, and low urinary calcium.
     Surgery is often a curative measure for primary hyperparathyroidism. Parathyroidectomy may be considered if the creatinine clearance is less than 60 ml/min, they are younger than 50, the serum calcium is greater than 1 mg/dL above the upper limit of normal, or the T-score is less than -2.5.  Hyperparathyroid patients who are symptomatic with osteoporosis or osteopenia are candidates for surgery. The surgery will improve bone density and fracture risk. Patients who are unable or unwilling to undergo surgery should take calcimimetics (cinacalcet).
    Secondary hyperparathyroidism will have hypocalcemia, hyperphosphatemia, and low levels of 1,25 vitamin D. Causes include chronic kidney disease (where the vitamin D is synthesized as explained above), low D intake (deficiency), malabsorption, lack of sunlight, and liver disease. Secondary hyperparathyroidism can also be normocalcemic. It would present with low bone density, bone fragility, and osteoporosis. The exact cause is not known. Complications of secondary hyperparathyroidism can be treated somewhat with protein restriction, calcium supplementation, vitamin D supplementation, and calcimimetics. A referral to a nephrologist (NOOOOO!) may be necessary if kidney disease is involved.
     Hypoparathyroidism can happen from damage or removal of one or more parathyroid glands. It can happen from surgery or autoimmune destruction. Pseudohypoparathyroidism is elevated PTH due to tissue resistance. The phosphorus will be elevated as well. If the phosphorus is low, then it is most likely due to  vitamin D deficiency rather than pseudohypoparathyroidism.
     MEN syndromes should also be mentioned in this discussion. MEN is a collection ("Multiple") of "Neoplasia"s in the pancreas, pituitary, parathyroid and adrenal "Endocrine" glands. MEN 2A involves medullary thyroid cancer, pheochromocytoma, and parathyroid tumors. MEN 2B (medullary cancer, pheo, and mucosal tumors) is not mentioned here.