Hypoparathyroidism is the pathological condition resulting from the continued lack of production of parathyroid hormone (PTH).
Parathyroid glands are usually in number of four, located at the front of the neck and back of the thyroid gland. Occasionally, one of the four glands can be situated somewhat away from the neck. And there are always 4 glands, may be between 2 and 6 glands.
These glands produce PTH, which is the hormone that regulates the level of calcium in the body. This hormone increases blood calcium. When the blood calcium level decreases (e.g., diets with little or no calcium) cells produced from these glands and blood PTH release. PTH binds to the cells of the kidney and bone to produce increased blood calcium: not eliminates both the kidney into the urine calcium and releases calcium from the bone structure.Furthermore, PTH stimulates the synthesis of vitamin D in the kidney, vitamin D increases calcium absorption in the intestine, which helps to increase the blood calcium level. In turn, makes PTH secretion by the kidneys lose phosphorus, producing the decline in blood phosphorus level. When normalized the level of blood calcium, parathyroid glands stop making PTH.
Calcium is an essential element for making our bones and teeth. But in smaller quantities than necessary and so maintained (hypoparathyroidism), that lack of calcium will prevent formation (Replace it) forming bone or teeth and there is a high risk of fractures. Similarly, when calcium in amounts greater than needed, and so maintained (hyperparathyroidism), the excess of calcium is deposited in other tissues, such as kidney, blood vessels, and joints, and the calcified or hardened. Calcification of these other tissues produces malfunction.
Therefore, it is important to maintain the level of calcium between limits “normal”, which are defined by a blood calcium concentration between 8.5 and 10.5 mg / dL (= 2’1-2’6 mmol / L ). However, there are conditions causing a decrease or absence of PTH continuously and that, accordingly, will maintain calcium figures below normal values constantly (hypocalcemia) and high phosphorus (hyperphosphatemia).
Causes of hypoparathyroidism can be divided into the three groups from a conceptual standpoint and functional:
Primary Hypoparathyroidism: This name contains all the disorders that originate in their own parathyroid glands and characterized by decreased or absent blood PTH and calcium levels resulting consistently low (hypocalcemia) and continued high levels of phosphorus ( hyperphosphatemia). The lack of blood PTH may not exist due to the parathyroid glands, the parathyroid glands or having a defect in the manufacture of PTH. The absence of parathyroid glands can be congenital (from birth), as DiGeorge syndrome, or acquired (after surgical removal of the parathyroid glands or after treatment with radiation to the neck or radioiodine). In the case of a defect in the manufacture of PTH, parathyroid glands are normal but do not make the hormone. The lack of production of PTH is known as idiopathic hypoparathyroidism, is very rare and can be isolated by a defect of the parathyroid gland function (hypoparathyroidism isolated) or family (family hypoparathyroidism) and alterations in the context of other endocrine glands like the adrenals, thyroid and pancreas (diabetes mellitus).
Secondary hyperparathyroidism: There is a lack of PTH and hypocalcemia due to a failure of the parathyroid glands caused by low blood magnesium levels (hypomagnesemia).
Pseudohypoparathyroidism (or hypoparathyroidism “not true”) PTH is produced and released into blood PTH but this is not effective because the organs where it should act (bone and kidney) unresponsive to the hormone, so that a decline occurs blood calcium. This induces a minor increase of PTH, PTH but remains ineffective. For practical purposes it is as if there were manufacturing although there PTH PTH in the blood, hence the name of pseudohypoparathyroidism. In hypoparathyroidism “true” there is little or no PTH. The pseudohypoparathyroidism is an inherited disorder characterized by signs and symptoms that are associated with hypoparathyroidism peculiar skeletal development defects.
The symptoms of hyperparathyroidism derivatives are coming decreasing blood calcium levels. In cases of minor decreases in calcium and for a long time, the symptoms will be of very low intensity. If calcium is decreased significantly or if it occurs in a short time, the symptoms will be more pronounced.
Symptoms of hypocalcemia appear in both forms of primary hyperparathyroidism (hereditary and acquired) in hypoparathyroidism and pseudohypoparathyroidism secondary to lower blood magnesium, although usually hypoparathyroidism and pseudohypoparathyroidism hereditary start in a more gradual and associated to developmental defects that are not on the other.
Typical symptoms of the hypocalcemia are:
Neuromuscular Disorders: There is an increase in the excitability of the muscles and nerves that innervate, causing muscle spasms, tingling and cramps mouth and hand and foot spasms (tetany), and may lead to convulsions (especially in children). Tetany can reveal physical examination (signs of Chvostek and Trousseau).
Mental disorders: They can range from irritability to depression, neurosis and psychosis.
Central nervous system disorders: Memory loss, parkinsonism and involuntary movements of the limbs. In almost 20% of individuals with hypocalcemia maintained intracranial calcifications can be seen by X-rays, justifying parkinsonian syndromes.
Cardiac disorders: abnormalities occur in the conduction of electrical stimulation of the heart in the form of arrhythmias, QT prolongation, T wave abnormalities, and heart blocks. Heart failure can also occur, ie, inability of the heart to pump blood.
Alterations in the skin and appendages: skin appears dry and flaky, brittle nails and rough hair. You can also fall hair (alopecia). There is a higher frequency of skin infection by fungi such as Candida. These changes are usually seen only in hypoparathyroidism associated with hereditary multiple endocrine insufficiency.
Eye disorders: In long-term hypocalcemia are cataract lens changes.
In children are common dental anomalies: enamel defect, lack of dental development and delayed tooth eruption.
There may also be other changes as the particular cause of hypoparathyroidism: rickets, osteomalacia, skeletal deformities, etc..
The diagnosis of hypoparathyroidism are performed based on detection of a low blood calcium. And phosphorus values will differ depending PTH causes hypoparathyroidism. The blood test can be done clinically suspected by the patient’s physician, but occasionally, the clinic may be very mild and then be a “chance finding.”
In primary hypoparathyroidism blood calcium is low and high phosphorus, PTH with absent or low. In magnesium deficiency calcium and phosphorus in the blood are low and PTH is low or absent. There is little in the calcium and pseudohypoparathyroidism little phosphorus and PTH in blood is high, moreover, is more pronounced hypophosphatemia that hypocalcemia by the increased secretion of PTH, which is only partly effective to raise blood calcium but promotes the excretion of phosphorus by the kidney. In hypoparathyroidism magnesium deficit, the numbers of blood magnesium are logically low.
The urine should be plenty of calcium and phosphorus in low values of primary hypoparathyroidism. There pseudohypoparathyroidism in high calcium and phosphorus in urine generally is low.
If there is suspicion of a vitamin D deficiency as a cause of hypoparathyroidism, will be useful to analyze their blood levels, which are low in most cases.
The interrogation and medical examination will help you find the home of hypoparathyroidism and request additional studies. For example, the recent emergence of hypocalcemia in an adult suggests nutritional deficiency, renal or intestinal disorders that cause deficiency or ineffectiveness of vitamin D. The neck surgery, even ancient, can be associated with hypoparathyroidism develop over time. The history of a seizure disorder directed to antiepileptic drugs as a cause. Developmental defects, especially in childhood and adolescence, sometimes oriented diagnosis of pseudohypoparathyroidism. Rickets and various syndromes and neuromuscular deformities may indicate ineffective action of vitamin D deficiency either the same or by defects of metabolism.
In primary hipoparatiroidismos be used and functional imaging of the parathyroid glands in search of a partial or total lack thereof. Include ultrasound, computed tomography (CT) and magnetic resonance imaging of the neck. Dial scintigraphy with technetium (99Tc) lets us know if these glands work or not.
Other techniques may be indicated as studying bone density (lumbar spine, hip) to see the impact of hypoparathyroidism on bone.
Treatment is primarily medical and will consist (in primary hypoparathyroidism) giving the patient calcium supplements to correct symptoms that may exist. Hypoparathyroidism patients should take 2 to 3 g / day of oral elemental calcium. In severe cases that present with tetany need treatment with intravenous calcium and with the patient in the hospital.
Next to be given oral calcium vitamin D (or its active form, calcitriol), as this promotes calcium absorption in the intestine and prevents renal loss.
In general, treatment with calcium and vitamin D (or calcitriol) are sufficient to normalize calcium and phosphorus in the blood, but not to correct the excessive calcium excretion in urine and the risk of kidney stones make this entails; add a treatment with diuretics such as hydrochlorothiazide to prevent this problem.
On the other hand, if the blood phosphorus levels must remain high restrict dietary phosphorus and, if necessary, adding aluminum hydroxide treatment (which binds phosphorus in the intestine and prevent their absorption).
Treatment is similar to pseudohypoparathyroidism primary hypoparathyroidism, unless doses of calcium and vitamin D are generally lower than those needed in primary hypoparathyroidism or “true”.
Hypocalcemia associated with hypomagnesemia includes correction of blood magnesium levels.
The deficiencies of vitamin D treatment is to administer vitamin D (or calcitriol) and calcium to normalize blood calcium and vitamin D then continue (or calcitriol) exclusively.
No specific measures to prevent the occurrence of hypoparathyroidism, but may be suspected in cases of skeletal abnormalities in a child, or in cases of previous surgery or radiotherapy to the neck. Also be suspected in cases of families with decreases of calcium.
Any suspicion should be performed a blood test that includes calcium and phosphorus levels, which is usually sufficient for an early detection of the disease, and that will be confirmed with the values of PTH.
Hypoparathyroidism is a rare condition and can occur in both children and adults. It is characterized by low levels of calcium and phosphorus in the blood variables, and occasionally, by skeletal abnormalities. The symptoms are variable, depending on the numbers of calcium and the duration of the same.
The diagnosis is made by a decline in calcium levels in a blood test requested by nonspecific symptoms or clear symptoms of hypocalcemia. The diagnosis of primary hyperparathyroidism should involve the study of the glands by or functional imaging techniques to detect the absence or lack of development.
The surgical treatment is never. It is usually controlled with calcium and vitamin D in primary hipoparatiroidismos and vitamin D in the defects of this substance.
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