Hypoparathyroidism is an extremely rare condition due to the inadequate production of parathyroid hormone by the parathyroid glands. This condition is so rare in fact that almost all documented cases are the result of thyroid or parathyroid surgery. The parathyroid gland is actually made up of four sections, each located in a different part of the thyroid gland. The sole purpose of the parathyroid glands is to produce parathyroid hormone, which increases the body’s uptake of calcium from the large intestine. If the parathyroid glands do not produce sufficient levels of parathyroid hormone (also known as PTH) then calcium levels in the blood will fall, and a condition known as tetany will result. Tetany is an increased excitability of the nerves.
Hypoparathyroidism has many different symptoms, and not all of them will necessarily manifest themselves in any one person. The most common symptoms include uncontrollable and extremely painful spasms of the face (the Chvostek Sign), arms, and feet. Seizures are also common. Other symptoms include weakness, muscle cramps, abnormal sensations such as tingling, burning, and numbness, known as paresthesias. Other, less common symptoms include the Trousseaus Sign, which is muscle spasms caused by light to mild pressure on nerves, malformations of the teeth, malformed fingernails, and patches of skin which have lost all pigmentation. Since the symptoms of this disease are so numerous, many are also symptoms of other diseases, making it extremely difficult to identify Hypoparathyroidism.
The exact causes of Hypoparathyroidism are unknown. It can occur as a separate disorder, or in association with other endocrine system gland disorders. Occurrences related to other endocrine system disorders are often linked to thyroid, ovary or adrenal gland problems. Hypoparathyroidism can also be inherited and transmitted though autosomal recessive genes. However, damage to the parathyroid glands during thyroid surgery and the removal of the parathyroid glands themselves remain the most common causes.
Human traits, including classic genetic diseases, are caused by the interactions of two genes, one from the mother and one from the father. In order for a person to have a particular trait that is carried by a recessive gene it must be inherited from both parents. If the gene is only inherited from one side then the person will be a carrier but will not express any symptoms. The risk of transmitting a recessive genetic disorder to any one child is twenty-five percent, provided both parents are carriers of the disorder themselves.
- There are three distinct types of Hypoparathyroidism. They are:
- Deficient parathyroid hormone secretion.
- Inability to make an active form of parathyroid hormone.
- Inability of body tissues to respond to parathyroid hormone.
Deficient parathyroid hormone secretion is the easiest form of the disease to understand. A patient suffering from this condition has little or no functional parathyroid tissue, and therefore cannot synthesize sufficient levels of PTH. There are two main causes of this type of Hypoparathyroidism, as well as one rare, nutritional cause. The most common cause is the removal or damage of the parathyroid glands during thyroid surgery. During surgery to remove a cancerous thyroid gland, the parathyroid glands are often removed as well, since they are seated in the thyroid gland. Also, if a patient has hyperparathyroidism, a condition in which the parathyroid glands make too much PTH, the parathyroid glands may be removed to prevent permanent body damage from occurring.
The parathyroid glands may also fail to function correctly for no definable reason. This is referred to as “Idiopathic Hypoparathyroidism.” This is rare, and may be either congenital or acquired later in life. The congenital causes of this disease are widespread, albeit quite rare. In some families children are at a fifty percent risk of being born without functional parathyroid tissue, and this is caused by a defect in a dominant gene. In other families children may be born with a twenty-five percent risk, if the parents are carriers of a recessive gene defect. In all cases however, the genes that are affected either code for and abnormal form of PTH and the PTH receptors on cell membranes, interfere with conduction of the signal from PTH receptors to the cell nucleus, or hinder development of parathyroid glands before birth.
Also, babies whose mothers have overactive parathyroid glands may have high levels of calcium during pregnancy, and this can suppress the baby’s parathyroid glands from functioning correctly temporarily after birth.
The acquired form of Hypoparathyroidism typically occurs because the body begins to develop antibodies that identify the parathyroid glands as foreign tissue. This can occur independent of other illness, or be the result of an autoimmune disease affecting other body organs as well. An antibody that binds to the calcium sensors in the parathyroid glands has been discovered in the blood of patients with autoimmune Hypoparathyroidism. This binding tricks the parathyroid glands into believing that the blood calcium levels are high, thus stopping further production.
The most readily treatable form of Hypoparathyroidism is caused by magnesium deficiency. Magnesium is needed for synthesis of PTH, and if a person has a diet low in magnesium the body may not be able to produce sufficient levels of PTH. Once this condition is identified, it is readily treatable by increasing the dietary intake of magnesium.
- There are only a handful of confirmed cases of a patient’s body not being able to produce the correct form of PTH. As a result, there is no available information on this form of the disease, other than information to confirm its existence.
Having an actual resistance to PTH is extremely rare. Patients with this condition express all the symptoms other Hypoparathyroidism patients may have, however their bodies produce sufficient levels of PTH. The trouble is in the fact that their body tissues are unable to respond to it. In fact, no matter how much PTH is injected into the body of a person with PTH resistance, calcium levels in the blood will not rise.
Hypoparathyroidism affects both sexes in equal numbers, but is most often seen in children younger than sixteen and adults over forty. Only four people out of every one hundred thousand will develop the disease, and the only risk factors are damage to the parathyroid glands, and a family history of parathyroid or endocrine disorders.
The prognosis for a patient with Hypoparathyroidism is quite good, so long as the condition is caught early. If the disease goes too long untreated then irreversible damage to the teeth and brain may occur, and eventually even death. Complications include acute tetany, which can lead to respiratory troubles requiring a tracheotomy, which is an opening in the throat to allow for breathing. If a child has untreated Hypoparathyroidism then mental retardation and physical development problems will occur. Also, intake of high levels of Vitamin D can cause renal failure and damage to other organs.
Current treatment for Hypoparathyroidism focuses on elevating the levels of calcium in a patient’s blood, not on replacing the missing PTH. As a result, patients are given ergocalciferol and dihydrotachysterol, which are forms of Vitamin D, as well as calcium. This treatment is usually administered orally in pill form. Experimental treatment for this condition is being done as well. Currently Vitamin D3 is being tested as to its viability in replacing the use of ergocalciferol and dihydrotachysterol. However, long term effects of its use have yet to be established.
There are alternative therapies for Hypoparathyroidism, although they are not used exclusively, rather they are used to complement treatment with calcium and Vitamin D. Various other nutrients are required for the body to efficiently utilize calcium once it is in the blood stream. As a result, adjusting a patient’s diet to include foods rich in boron and Vitamin K is common. Boron enhances the body’s absorption of calcium from the intestines, and Vitamin K increases cellular absorption from the blood. Also, reducing the quantity of carbonated beverages a patient drinks is important, as the phosphates leach calcium from bones and hinder proper absorption. Discontinuing the drinking of caffeinated beverages is also advisable, as it increases the loss of calcium in urine. In terms of herbs, patients are counseled to eat traditional remedies that support normal bone growth, such as Horsetail (Equisetum avense) and Oat straw (Avena sativa).