The numerous glands in the human body hold varying functions. For the most part, however, their role is to secrete hormones to help regulate homeostasis. They can be categorized based on their location, what they secrete, or what organ system they control. Some common gland disorders, for instance those involving the thyroid, are often seen in the insurance industry. On the other hand, Parathyroid disorders are not as prevalent and therefore make an interesting topic for a medical underwriter to review.
The parathyroid comprises four tiny glands, each about 3–4 mm in diameter, which are located right behind the thyroid. These glands produce a hormone called parathyroid hormone (PTH) that helps regulate calcium levels in the body. Calcium (Ca+) is a known electrolyte with a variety of essential functions. The body must precisely control the levels of calcium for muscle contractions, normal functioning of enzymes, blood clotting, and normal heart rhythm. If one does not consume enough calcium, too much of it moves out of the bones, potentially causing complications such as osteoporosis.
Having low levels of calcium is called hypocalcemia. While hypocalcemia is asymptomatic in the early stages, some people may experience symptoms including fatigue; muscle spasms and stiffness; low blood pressure; memory issues; and even mood changes such as depression and anxiety. In long-term or severe cases, individuals may experience eczema, brittle nails, seizures, congestive heart failure, and arrhythmias.
Causes of hypocalcemia
Some causes of hypocalcemia are a lack of response to PTH, a lack of parathyroid glands (i.e., DiGeorge syndrome), vitamin D deficiency, kidney dysfunction, pancreatitis, some antibiotics, and certain anticonvulsant drugs. Still, the most common cause of low calcium is hypoparathyroidism, which occurs when the body produces abnormally low amounts of PTH. Again, PTH is essential in maintaining the body’s calcium balance. It raises calcium levels in the body in a few ways. Since about 99% of the body’s calcium is stored in the bones, PTH can break down bone to release calcium. It can also increase the body’s ability to absorb calcium from the food we eat and increase the kidney’s ability to retain calcium that would otherwise be discarded in the urine. In contrast to hypoparathyroidism producing low levels of PTH, hyperparathyroidism involves the parathyroid glands becoming overactive and secreting excess amounts of PTH. This excess causes calcium levels in the blood to rise, resulting in hypercalcemia.
Primary Hyperparathyroidism (PHPT)
Hyperparathyroidism can be classified into two types: primary and secondary. In primary hyperparathyroidism (PHPT) the glands secrete excess PTH, which in 80–85% of cases is caused by a solitary parathyroid adenoma (making up the rest of the cases are diffuse glandular hyperplasia and multiple adenomas along with a small percentage caused by multiple endocrine neoplasia [MEN]). The incidence rate of hypercalcemia brought on by elevated PTH is about 1-4% of the general population, is roughly 2–3 times higher in women, and is more likely to occur among those 55 and older. Although most individuals are asymptomatic, joint and muscle pain; nausea; pancreatitis; and cardiovascular disease are all associated with PHPT.
Secondary hyperparathyroidism (SHPT)
Secondary hyperparathyroidism (SHPT), on the other hand, occurs when a disease outside of the parathyroid glands causes the glands to become hyperactive. Kidney failure and vitamin D deficiency are two of the more common causes. A failing kidney that cannot produce sufficient vitamin D or remove the phosphorus out of the body leads to low calcium levels. Over time, low calcium levels cause the parathyroid glands to enlarge and become overactive. Aside from bone pain, a symptom sometimes seen with SHPT is calciphylaxis in which calcium deposits forming in the skin, blood vessels, and muscles cause lesions, ulcers, and eventually necrosis. Less than 8% of individuals with SHPT will develop tertiary hyperparathyroidism. It typically occurs in individuals with a long history of SHPT, even when the initial cause of the low blood calcium has been corrected. Usually, these individuals have chronic renal failure as well.
Diagnosis of parathyroid gland disorders
The diagnosis of parathyroid gland disorders is based on vitamin D, PTH, and calcium levels in the blood. These tests include measuring calcium bound to albumin and the albumin in the blood. Blood and urine tests are also performed to evaluate kidney function by assessing magnesium, phosphate, and serum creatinine levels. In cases of primary hyperparathyroidism, hypercalciuria (calcium/creatinine ratio > 0.02), and elevated cAMP (cyclic adenosine monophosphate) in the urine may be tested, too. In secondary hyperparathyroidism, the focus is largely on identifying the underlying disease. Skeletal bone density tests, for example dual-energy x-ray absorptiometry (DXA), may be used to assess any bone abnormalities while an abdominal ultrasound is used to investigate kidney function and other impairments that may be causing the abnormalities.
Treatment for parathyroid disorders
The treatment for parathyroid disorders depends on the diagnosis but in most cases is accompanied by the watchful waiting method. Surgical removal, ultrasound guided chemical, or heat ablation can cure about 95% of PHPT cases if the cause is a tumor or enlarged gland. Medication such as calcimimetics, hormone replacement therapy, and biophosphonates may also be used to reduce the effects of osteoporosis. Individuals diagnosed with hypoparathyroidism may have to take supplements, often for the rest of their lives, which include calcium, phosphorus, magnesium, and PTH to help stabilize the calcium levels. Additionally, lifestyle modifications – quitting smoking, exercising, and treatment compliance – can eventually reduce the PHPT mortality risk to that of the general population.
While Parathyroid disorders may not be prevalent, this overview of causes, diagnosis and treatment, provides life underwriters with a better understanding should cases come across their desk.
Featured Underwriter: Garen Markarian
Garen joined LOGiQ3 as an underwriter in January 2016. In addition to over 10 years of experience in the insurance industry, he has completed the LOGiQ3 Underwriting Training Program. He has an undergrad degree in Neuroscience from The University of Toronto, and a post-grad diploma as a CRA from The Michener Institute.