Parathyroids and You
Parathyroids rarely go wrong, but when they do, they can cause osteoporosis, kidney stones and other problems.
People have four parathyroid glands (often referred to simply as parathyroids), usually located on the thyroid gland in the neck. Occasionally someone is born with one or more of the parathyroids located elsewhere: within the thyroid, or in the thymus, or somewhere else in the vicinity. Despite their similar names and adjacent locations, the thyroid and parathyroids are entirely different–they produce different hormones for different purposes.
Parathyroids are only about the size of peppercorns. They make parathyroid hormone (PTH), one of the most powerful hormones involved in regulating blood levels of calcium. (Calcium is involved in basic metabolism. See my article about bone density, bone loss and osteoporosis for a more detailed explanation of how your body stores and manages calcium.)
PTH helps to control:
- The amount of calcium circulating in the bloodstream
- Destruction of bone to release calcium into the bloodstream so it can be used for metabolism, muscle control, and blood clotting
- Absorption of calcium from food by the intestines, and
- Disposal of excess calcium (circulating in the blood but more than needed for metabolism, nerve function or muscle function) in urine
- Disposal of excess phosphorus (also released by bone destruction) in urine
When something goes wrong with the parathyroids, all of that is thrown out of balance.
When It Goes Wrong, It Usually Works Too Hard
Parathyroid malfunction is not very common. When it does happen, it's much more likely to be hyperactive (working too hard, making much parathyroid hormone). Hypoactivity (not working hard enough, not making enough PTH) is very unusual.
In about 3 to 5 people per 20,000, at least one parathyroid gland is hyperactive (works too hard). This translates to about 100,000 people developing this disorder every year in the USA. About two out of every three patients are women.
Hyperparathyroidism can be
- Primary, which means the cause of the problem is in the parathyroids, or
- Secondary, which means something outside the parathyroids (such as kidney failure, low calcium intake, gastrointestinal disorders, or vitamin D deficiency) prompted them to become overly active, or
- Tertiary, excessive production of PTH after longstanding secondary hyperparathyroidism, typically after a successful renal (kidney) transplant
Regardless of whether the cause is primary, secondary or tertiary, too much parathyroid hormone causes calcium to be removed from bones and raises the calcium concentration in the bloodstream.
Too much calcium in the blood can lead to kidney stones and loss of bone mass. (See articles about osteoporosis for more detail about why loss of bone density is highly undesirable.) Calcium is also vital for metabolism, nerve conduction and muscle operation. Loss of bone mass and development of kidney stones take a while. By the time you suffer a bone fracture or kidney stone attack, calcium levels have been too high in your bloodstream for a long time. If you have hyperparathyroidism, some symptoms you might notice include fatigue, weakness, constipation, loss of appetite, nausea, vomiting, increased thirst or increased urination. You can also become depressed or confused, or exhibit subtle mental changes such as memory problems or difficulty concentrating that you may not recognize yourself. You could become more prone to peptic ulcers, and in rare cases pancreatitis can occur.
Somehow, excessive PTH levels need to be brought back down to normal.
Note: A hyperactive parathyroid gland is not the only possible reason for elevated levels of calcium in the blood. For example, dialysis patients must consume "binders" with anything that contains substantial calcium, such as Tums. This is because their kidneys are not functioning and cannot clean extra calcium out of their blood.
Underactive parathyroids are uncommon, but can occur. This causes abnormally low levels of calcium in the blood, which in turn interferes with metabolism, muscle control and blood clotting. Hypoparathyroidism can occur when someone is born without parathyroids (causing DiGeorge syndrome), suffers damage to the parathyroids or must have them surgically removed, has another disorder that forces low PTH production such as low blood levels of magnesium or metabolic alkalosis, or in rare cases has two copies of a specific recessive gene that causes hypoactive parathyroids.
Symptoms of underactive parathyroids include weakness, headaches, muscle cramps, brittle nails, weakened tooth enamel, painful menstruation, abdominal pain, dry hair, dry scaly skin, excessive nervousness, and increased excitability of nerves. The overly excitable nerves can cause tingling lips, toes and fingers–or twitching and spasms of muscles such as those of the hands, feet, arms, and face, which is called tetany.
Most Common Reasons for Hyperactivity
Hyperactivity of a parathyroid is often caused by a benign tumor on a parathyroid gland. About 85% of primary hypoparathyroid cases occur because of a single benign adenoma. About 15% of cases involve multiple adenomas or hyperplasia. It is rare for primary hyperparathyroidism to be caused by a cancerous tumor on a parathyroid gland.
When the cause is a tumor, the feedback mechanism that controls the parathyroids is apparently disrupted. When the cause is hyperplasia, an increase in the number of cells producing hormone apparently occurs.
In the April 18, 1997 issue of the journal Science, the USA National Institutes of Health announced that a gene can cause benign tumors on the parathyroids. The same gene can also cause benign tumors on the pituitary glands, and islet cell tumors that progress to pancreatic cancer. This gene is designated as causing multiple endocrine neoplasia, type 1 (MEN1). it is a tumor suppressor gene (a gene that inhibits the growth of abnormal cells) by producing a protein called menin.
Discovery of this genetic cause led to the discovery of more. Additional genes implicated in hyperparathyroidism include MEN2a and hyperparathyroid-jaw tumor (HPT-JT).
Other familial causes include familial isolated hyperparathyroidism (FIHPT), familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism.
Treatment for Hyperactive Parathyroids
If you have primary hyperparathyroidism, you should maintain a moderate daily calcium intake (800-1000 mg) and an appropriate vitamin D intake. Women generally need more than men. Avoid letting yourself get dehydrated or too sedentary. Also avoid medications such as diuretics, thiazides, and lithium. Tell your pharmacist about your hyperactive parathyroid, and your pharmacist can protect you against inadvertently getting a medication that would be harmful.
Many cases of hyperparathyroidism are treated entirely with medication and dietary restrictions, especially when the case is mild. Nearly all secondary hyperparathyroidism is treated this way. However, many other cases are treated surgically.
Surgery is typical treatment for tertiary hyperparathyroidism. The USA National Institutes of Health (NIH) guidelines were revised in 2002 and now suggest surgery for primary hyperparathyroidism when the following criteria are met:
- Serum calcium 1 mg/dL above the upper limit of the reference range
- 24-hour urinary calcium excretion greater than 400 mg
- 30% reduction in creatinine clearance
- Bone mineral density T-score below -2.5 at any site in the skeleton
- Patient is younger than 50 years of age
In about 70% to 80% of cases with a single malfunctioning gland, preoperative scans can identify the parathyroid that is malfunctioning so that surgery only disturbs the area around the faulty gland, not the remaining glands. There are other techniques for zeroing in on the malfunctioning gland or glands while surgery is in progress. However, if you are undergoing parathyroid surgery in a hospital that is not highly practiced in these techniques, traditional techniques will generally require longer post-operative recovery but provide a comparable result.
Many doctors hesitate to recommend surgery, especially if there are no overt (noticeable) symptoms such as kidney stones. There has been disagreement about whether surgery really does enough good to be worthwhile.
The 21 October, 1999 issue of New England Journal of Medicine published findings from a study at Columbia University College of Physicians and Surgeons in New York. This study identified 121 people with high concentrations of calcium in the blood, about half of whom (61) chose surgery. After studying the sample patients for 10 years, the study found that surgery provided relief for multiple symptoms. Before surgery, 12 patients had kidney stones; none of the surgical patients had any kidney stones in the 10 years following surgery. By contrast, of the non-surgical patients, 8 had kidney stones before the study began and 6 of those had a recurrence while the study was in progress.
Also, surgical patients gained bone density after surgery, averaging a 12% gain in vertebrae and 14% in hip bones. Average bone density in non-surgical patients remained unchanged. However, 11 of the non-surgical patients lost bone mass, 5 of them women who entered menopause during the study. Fourteen of the non-surgical patients showed other signs that their hyperparathyroidism was worsening.
For secondary hyperparathyroidism, non-surgical treatment is the first choice, and surgery is not common. As an example, here are some non-surgical treatments for secondary hyperparathyroidism that results from chronic kidney disease:
- Restricting phosphate intake in food if PTH is elevated despite sufficient adequate vitamin D (>30 ng/mL)
- Phosphate binders such as calcium carbonate, calcium acetate, sevelamer hydrochloride or lanthanum carbonate if phosphate levels remain high despite dietary restrictions
- Restricted intake of calcium supplements, less than 2 g/day
- Supplements of vitamin D or its analogs, such as calcitriol, paricalcitol, doxercalciferol, maxacalcitol, and falecalcitriol
- Calcimimetics (drugs that reduce production of PTH) such as cinacalcet
Treatment for Hypoactive Parathyroids
Treatment is straightforward. Most patients simply need to take calcium and vitamin D supplements for the rest of their lives and eat a diet high in calcium but low in phosphorus. As with hyperparathyroid patients, tests should be done on a regular basis to make sure blood levels of calcium and phosphorus are good. If a patient has an attack of blood calcium levels so low as to be life-threatening, or prolonged muscle contractions, a calcium solution is administered intravenously and the heart is monitored closely. After the attack passes, treatment by diet and oral supplements resumes.
Official Sources of More Information
I am not a health care professional. Years ago I was a volunteer sysop in a highly regarded forum for people with chronic illnesses. My health-related articles came from efforts there to translate complex medical information so it is easier to understand. If you want more complete and technical material, try these links.
USA National Endocrine and Metabolic Diseases Information Service (NEMDIS), a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health (NIH). This is current USA standard medical information about hyperparathyroidism: what it is and how it can be treated.
MedicineNet. Sometimes MedicineNet is easier to understand than NIH.
Do you have a burning desire to know more than short articles can tell you? Here are some books that can help quench that thirst for knowledge. The more serious you are, the more expensive the book may seem–but used copies are often available at low prices.
The Official Patient’s Sourcebook on Parathyroid Cancer: A Revised and Updated Directory for the Internet Age
The Bone and Mineral Manual: A Practical Guide
Endocrinology at a Glance
Greenspan’s Basic and Clinical Endocrinology, Ninth Edition (LANGE Clinical Medicine)