What is Hyperparathyroidism?
Hyperparathyroidism is characterized by overactivity of one or more of the four parathyroid glands. It results in excessive secretion of parathyroid hormone (PTH). Increased PTH levels act directly on the bone and kidney tubules, causing an increase of calcium in the extracellular fluid that can't be compensated for by renal excretion or uptake into the soft tissues or skeleton.
Hyperparathyroidism is most common in women (especially those past menopause), with onset usually occurring between ages 35 and 65. The disorder is classified as primary or secondary, based on its etiology.
Causes of Hyperparathyroidism
In primary hyperparathyroidism, one or more of the parathyroid glands enlarges, increasing PTH secretion and elevating serum calcium levels. The most common cause is a single adenoma. Other causes include a genetic disorder or multiple endocrine neoplasia.
In secondary hyperparathyroidism, excessive compensatory production of PTH stems from a hypocalcemia-producing abnormality outside the parathyroid gland, which causes a resistance to the metabolic action of PTH. Some hypocalcemia-producing abnormalities are vitamin D deficiency, chronic renal failure, or osteomalacia due to laxative abuse or phenytoin.
Signs & Symptoms of Hyperparathyroidism
At least 50% of patients with primary hyperparathyroidism have no symptoms, and approximately 1% of cases go undiagnosed. When symptoms do occur, they are generally attributable to persistently high levels of calcium and may include:
Serum PTH with accompanying hypercalcemia confirms the diagnosis in primary disease.
X-rays reveal diffuse bone demineralization, bone cysts, outer cortical bone absorption, and subperiosteal erosion of the phalanges and distal clavicles in primary disease.
X-ray spectrophotometry or other microscopic examinations of the bone demonstrate increased bone turnover in primary disease.
Esophagography, thyroid scan, parathyroid thermography, ultrasonography, thyroid angiography, computed tomography scan, and magnetic resonance imaging can help to locate parathyroid lesions.
Supportive laboratory tests reveal decreased serum phosphorus levels and elevated urine and serum calcium and serum chloride in primary disease.
Hyperparathyroidism may also increase urine add and creatinine levels and increase basal acid secretion and serum immunoreactive gastri. Increased serum amylase may indicate acute pancreatitis.
In secondary hyperparathyroidism, laboratory test findings show normal or slightly decreased serum calcium levels and variable serum phosphorus levels, especially when hyperparathyroidism is due to rickets, osteomalacia, or renal disease. Other laboratory vaiues and physical examination findings are used ta identify the cause of secondary hyperparathyroidism.
Primary hyperparathyroidism may be treated by surgical removal of the adenoma or, depending on the extent of hyperplasia, removal of all but half of one gland (the remaining part is necessary to maintain normal PTH levels). Although surgery may relieve bore pain within 3 days, renal damage may be irreversible.
Preoperatively - or if surgery isn't feasible or necessary - other treatments can decrease calcium levels. Such treatments include forcing fluids; limiting dietary intake of calcium; promoting sodium and calcium excretion through forced diuresis using normal saline solution (up to 6 L in life-threatening circumstances), furosemide, or ethacrynic acid; and administering oral sodium or potassium phosphate, calctonin, or plicamycin.
To prevent postoperative magnesium and phosphate deficiencies, the patient receives l.V. magnesium and phosphate or sodium phosphate solution given orally or by retention enema. In addition, during the first 4 or 5 days after surgery when serum calcium falls to low-normal levels, supplemental calcium may be necessary; vitamin D or calcitriol also may be used to increase serum calcium levels.
The goal of treatment for patients with secondary hyperparathyroidism is to correct the underlying cause of parathyroid hypertrophy. Treatment includes vitamin D therapy or, for the patient with renal disease, aluminum hydroxide for hyperphosphatemia. The patient with renal failure requires dialysis - possibly for the rest of her life - to lower calcium levels. In the patient with chronic secondary hyperparathyroidism, the enlarged glands may not revert to normal size and function even after calcium levels have been controlled.
Glucocorticoids are effective inhibitors of bone resorption and may be particularly useful in treating hypercalcemia associated with certain cancers.
Maintaining an adequate intake of calcium may reduce risk of secondary hyperparathyroidism.
Hyperparathyroidism may be prevented by early treatment of the disease causing it. Early recognition and treatment of hyperparathyroidism may prevent hypercalcemia. Since the cause of primary hyperparathyroidism, or the adenoma which causes parathyroid enlargement, is largely unknown, there are not prescribed prevention methods.
(c)Copyright Family-health-information.com All rights reserved
Disclaimer :- The content in this web site are in no way intended to replace the professional medical care, advice, diagnosis or treatment of a doctor. The web site is build for information and educational purpose only. If you are ill from any disease or notice medical symptoms, you should consult your doctor. We will not be liable for any complications or other medical accidents arising from or in connection with the use of or reliance upon any information in this web site.