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!