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Is it my parathyroid?

The parathyroid glands are located in the neck in close proximity to the thyroid gland and secrete parathyroid hormone. Understanding the entire system of calcium regulation helps to make sense of the possible associated diseases.  

Normal calcium metabolism 
Blood calcium is similar to an electrical current and needs to be tightly and quickly regulated.  Similar to mechanisms to prevent electrical surges and outages, the body has a number of hormones that regulate the level of blood calcium. The major hormones involved in this regulation are parathyroid hormone (PTH) and the vitamin D hormones. The minute-to-minute regulation of blood calcium is mainly controlled by PTH which controls both the kidneys' ability to leak calcium into the urine and the bone's ability to dissolve to release calcium into the blood.  Activated-vitamin D controls the long term levels of calcium in the blood primarily by controlling the amount of calcium absorbed from oral intake of calcium. The below figure explains further how calcium is regulated. Make an appointment with the the endocrinologists to better explain your calcium regulation problems.  Read about the basics of the parathyroid glands here


Normal calcium metab0lism


Parathyroid Related Diseases

Certain diseases can cause calcium levels to be too high or too low in relation to the parathyroid hormone level. These conditions can all be diagnosed fairly reliably with simple blood testing. The below figure shows the most common diseases that are associated with parathyroid disease. Please schedule an appointment with your Houston endocrinologist to discuss hyperparathyroidism before planning a surgery. There are a number of caveats to interpreting the graph: need a normal albumin level, need to evaluate for familial hypocalciuric hypercalcemia in some cases, upper-normal calcium levels can be early primary hyperparathyroidism, etc.


If parathyroid disease is diagnosed, there are several different types:

Primary Hyperparathyroidism: a condition of excess parathyroid hormone secretion caused by one or more abnormal parathyroid glands causing an eventual elevation in the blood calcium levels. There are patients with symptomatic and asymptomatic primary disease. Although most commonly caused by a parathyroid adenoma, it is also found in endocrine syndromes like MEN1 and MEN2a.

Secondary Hyperparathyroidism: this is an excess of the parathyroid hormone secretion from otherwise normal parathyroid glands caused by non-parathyroid disease. A common cause of this would be low vitamin D levels or kidney disease.

Tertiary Hyperparathyroidism: this is an excess of parathyroid hormone secretion from permanently enlarged parathyroid glands caused by long standing, untreated, secondary hyperparathyroidism. This is commonly found in patients with end stage kidney disease.

Hypoparathyroidism: this is a deficiency of parathyroid hormone which can cause hypocalcemia (low calcium levels). The most common cause is a complication of neck surgery which damages the parathyroid glands. Pseudohypoparathyroidism and pseudo-pseudohypoparathyroidism are rare parathyroid diseases. 


Parathyroid-Related Diseases
The key to understanding the parathyroid system is relationship of a simultaneously drawn parathyroid hormone level and calcium level. In NORMAL calcium metabolism (shown by the blue box) as calcium levels rise then parathyroid levels should begin to reduce, and as calcium levels drop then parathyroid hormone levels should drop. 

Non parathyroid related hypercalcemia

Although primary hyperparathyroidism is the most common cause of high calcium levels, if parathyroid disease is not confirmed then the physician needs to evaluate for other causes of hypercalcemia


Clinical Symptoms of Primary Hyperparathyroidism (hypercalcemia)

Symptomatic
The symptoms of hyperparathyroidism can be vague and worsen gradually over many years. Thus, hyperparathyroidism was classically diagnosed very late into the disease process. The symptoms fit into the spectrum of "stones, groans, bones, and psychic overtones."  In reality these symptoms only occur in a small minority (<20%) of patients with primary hyperparathyroidism. Patients may also present with objectively measurable medical problems including calcium kidney stones (calcium phosphate or calcium oxalate), peptic ulcer disease, osteoporosis, pancreatitis, and mental status changes. Hypercalcemic crisis (severe confusion, come, associated dehydration) is rare. These symptoms and signs would have alerted a physician to order a calcium level which would confirm the diagnosis if it was elevated. These calcium levels had probably been high for many years prior to the onset of symptoms. Notably, the severity of symptoms is not directly correlated with the degree of elevation of calcium.

Asymptomatic
Since the 1960's lab testing when lab testing became automated, a calcium level has become part of lab chemistry panels. Over the next several decades the incidence of primary hyperparathyroidism increased significantly because it was being found early with elevated serum calcium levels on these panels.There are usually no objectively measurable signs or symptoms when hyperparathyroidism is diagnosed in this manner. Since these patients have non-quantifiable symptoms they are considered "asymptomatic."2  Some of the subjective symptoms patients may complain of are vague pains, mood swings, muscle weakness, memory difficulty. The presence of these vague symptoms does not diagnose hyperparathyroidism and will not necessarily improve with parathyroid surgery.  More than 80% of patients with primary hyperparathyroidism are considered 'symptomatic' at the time of diagnosis.  

 Symptomatic Hyperparathyroidism Asymptomatic Hyperparathyroidism1
Calcium kidney stones Pain in bones
 Peptic ulcer disease in association with MEN1 Feeling tired easily
 Pancreatitis Depressed mood                
 Osteoporosis Pain in abdomen
 Muscle weakness Forgetfulness
 Confusion Irritability



References
1. Pasieka et al. World J Surgery 2002; 26:942-949
2. Silverberg SJ, Bilezikian JP, Bone HG, et al.  J Clin Endocrinology Metabolism. 1999;84:2275-2285
3. Bilezikian JP et al. New England Journal of Medicine. 2004;350:1746-1751