Hyperparathyroidism refers to excessive production of parathyroid hormone. The parathyroid glands are located at the front and base of the neck at the 4 corners of the thyroid gland. The glands produce parathyroid hormone (PTH), which regulates calcium and phosphorus balance in the body.

Am Fam Physician. 2013. Disorders of the parathyroid glands most commonly present with abnormalities of serum calcium. Patients with primary hyperparathyroidism, the most common cause of hypercalcemia in outpatients, are often asymptomatic or may have bone disease, nephrolithiasis, or neuromuscular symptoms. Patients with chronic kidney disease may develop secondary hyperparathyroidism with resultant chronic kidney disease-mineral and bone disorder. Hypoparathyroidism most often occurs after neck surgery; it can also be caused by autoimmune destruction of the glands and other less common problems. Evaluation of patients with abnormal serum calcium levels includes a history and physical examination; repeat measurement of serum calcium level; and measurement of creatinine, magnesium, vitamin D, and parathyroid hormone levels. The treatment for symptomatic primary hyperparathyroidism is parathyroidectomy. Management of asymptomatic primary hyperparathyroidism includes monitoring symptoms; serum calcium and creatinine levels; and bone mineral density. Patients with hypoparathyroidism require close monitoring and vitamin D (e.g., calcitriol) replacement.

Primary Hyperparathyroidism
Increased secretion of parathyroid hormone occurs because one or more of the glands have become enlarged. The effects of increased calcium are seen in several body systems including the skeletal, gastrointestinal, renal (kidney), muscular, and central nervous system. The disease is most common in people over 60, but can also be seen in younger adults. Women are more likely to be affected than men. Primary hyperparathyroidism (PHPT) is characterized by excessive parathyroid hormone secretion in respect to calcium homeostasis needs, due to parathyroid adenoma (80% of cases), hyperplasia (15-20%), or carcinoma (1-2%).
     Hyperparathyroidism symptoms and signs include hypercalcemia which may cause fatigue, anorexia, thirst, and polyuria. Vague neurological and psychiatric symptoms, such as weakness, anxiety, depression, paresthesias, and muscular cramps may ameliorate after parathyroidectomy. Recent reports indicate increased cardiovascular mortality in primary hyperparathyroidism patients.

Diagnosis of Hyperparathyroidism
Diagnosing this condition is based on the detection of hypercalcemia, together with inappropriately high serum parathyroid hormone levels. Preoperative localization of the diseased glands is mandatory in persistent or recurrent primary hyperparathyroidism, when minimally invasive surgery is planned. High resolution ultrasonography and SPECT double-phase 99m Tc-sestamibi scintigraphy are the most commonly employed techniques. Intraoperatory parathyroid hormone assay may confirm successful surgery when serum concentrations decrease more than 50%.

Hyperparathyroidism treatment
Surgical therapy is indicated in patients with renal or skeletal complications, such as in those with previous parathyrotoxic crisis. Many surgeons in recent years adopted minimally invasive parathyroidectomy. Medical treatment is an option for patients unwilling or unfitted for surgery because of severe concomitant diseases. Employed therapy includes estrogens, SERMs, bisphosphonates and calcimimetics.

Secondary hyperparathyroidism
This condition is characterized by parathyroid gland hyperplasia resulting from end-organ resistance to parathyroid hormone. The excess secretion of PTH depresses calcium levels. The most important cause of secondary hyperparathyroidism is chronic renal insufficiency.
     Secondary hyperparathyroidism can be due to disorders of vitamin D metabolism, disorders of phosphate metabolism, and calcium deficiency (either lack of calcium in the diet or excessive calcium loss in the urine). Women who supplement their diets with modest amounts of calcium have a lower risk for this hormone disorder.

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I was most interested in reading your site, however there doesn’t appear to be anything at all relating to Primary or Secondary Hyperparathyroidism supplements that may be of some benefit, even when a tumour is present. Also, there is no mention of 2-AEP Calcium and 2-AEP Magnesium Supplements. With no clear diagnosis re the type of Hyperparathyroidism (likely Primary), I am now going to ‘trial’ myself on all the following, for 3 months. If the high PTH levels fall to normal (or near normal), and the calcium loss from the bones, through the urine (have severe Osteoporosis, exacerbated by the high PTH levels), is curtailed and retained, I will advise you of any positive results, which may assist other readers. The following regime is what I have been taking for quite some time, and now intend adding / trialling 3 mg of a Boron supplement/day, for 3 months, with a possible break of 2 days/week, so as not to overdo it!1x 500 mg 2-AEP Calcium/1x 500 mg 2-AEP Magnesium/2 drops Vitamin K2/1x Activated B6 with B12/Folate/1x Picmins/1,000 i.u. Vitamin D (1 drop) per day, and will now add the 3 mg of Boron/day. A mainly alkaline diet regime (for years), no pharmaceutical meds./exercise regularly/vegetarian, 68 years of age and not overweight. Take about 2 dessertspoons of Apple Cider Vinegar/day to assist with gut absorption of what I ingest. Blood calcium levels are normal and Vitamin D is perfect! Being very pro-active in trying to manage the above conditions, nothing to this point is working, am constantly losing bone, and any operation to remove a tumour is likely out of the question, due to previous thyroid surgery (50 years ago) and scar tissue! I don’t know if there’s something I am missing in my regime, or not, and having consulted with 4 Specialists, they are all but useless in helping to resolve these 2 conditions, and of course, do not address anything nutritionally or naturally! Should you have anything to contribute, with regard to healing or modifying the effects, especially of the Hyperparathyroidism, I would be most appreciative. Maybe mal-absorption is also an issue, but no-one has investigated this possibility!