Hyperparathyroidism
What are the consequences of hyperparathyroidism on the body? All the information about this disorder.
Symptoms and Causes
Hyperparathyroidism refers to the excessive production of parathyroid hormone due to the overactivity of one or more parathyroid glands.
The parathyroid glands are very small glands located behind the thyroid gland. Generally, there are four glands situated at the corners of the thyroid, although their number and exact location can vary significantly. The function of parathyroid hormone is to regulate calcium and phosphate concentrations in the blood and tissues by influencing their intestinal absorption, renal excretion, and the release of calcium and phosphate from the bones. When the glands secrete excessive amounts of parathyroid hormone, calcium levels rise.
Symptoms
Hyperparathyroidism often presents no symptoms. When they do occur, they result from elevated calcium levels in the blood. Common symptoms include:
- Fatigue or lethargy.
- Excessive urination.
- Abdominal pain.
- Nausea and vomiting.
- Constipation.
- Loss of appetite.
- Bone pain.
- Difficulty concentrating.
- Memory loss.
- Depressed mood.
- Confusion.
- Psychosis: delusions or hallucinations.
Causes
Depending on the underlying cause, hyperparathyroidism is classified into three types:
- Primary hyperparathyroidism: The most common type, caused by an abnormality in the parathyroid glands. It leads to hypercalcemia, hypophosphatemia, and excessive bone resorption. Possible causes include:
- Presence of an adenoma (benign tumor) in one of the glands, the most common cause.
- Enlargement of the glands due to hyperplasia (cell proliferation).
- Presence of carcinoma, typically affecting only one gland, though it is very rare.
These abnormalities usually occur spontaneously but can sometimes be linked to multiple endocrine neoplasia syndrome, a hereditary disorder caused by genetic mutations.
- Secondary hyperparathyroidism: Occurs due to a decrease in calcium levels caused by a non-parathyroid disorder, leading to excessive parathyroid hormone secretion to regulate calcium levels. Conditions that cause hypocalcemia include:
- Chronic kidney disease: Leads to reduced synthesis of active vitamin D, which is necessary for calcium absorption. The lack of vitamin D results in hypocalcemia, making this the most common cause of secondary hyperparathyroidism.
- Calcium deficiency: Due to insufficient dietary intake or malabsorption.
- Vitamin D deficiency: Caused by inadequate sun exposure or insufficient dietary intake.
- Tertiary hyperparathyroidism: Occurs when secondary hyperparathyroidism persists and becomes chronic, causing parathyroid hormone secretion to continue independently of calcium levels in the blood. It is common in cases of end-stage chronic kidney disease.
Risk Factors
The likelihood of developing hyperparathyroidism increases in the following cases:
- Menopause: Primary hyperparathyroidism is more common in postmenopausal women.
- Radiation therapy to the neck: Primary hyperparathyroidism may develop decades after radiation exposure.
- Lithium treatment: Lithium alters parathyroid function, potentially exacerbating preexisting hyperparathyroidism or causing parathyroid hyperplasia.
- Inadequate calcium intake.
- Low sun exposure.
Complications
As with symptoms, hyperparathyroidism complications arise from prolonged hypercalcemia. High calcium concentration in urine frequently leads to kidney stone formation, which can be very painful. Additionally, increased parathyroid hormone levels stimulate osteoclast activity, the cells responsible for bone resorption. This leads to osteoporosis, a loss of bone mass that weakens bones, making them more prone to fractures and deformities.
Hyperparathyroidism also results in soft tissue calcification, which can progress to arterial and valvular calcifications, potentially leading to hypertension, tachycardia, and cardiac arrest. When calcium levels exceed 15 mg/dL, neurological impairment may result in coma.
Prevention
There are no specific measures to prevent hyperparathyroidism, but periodic blood tests can help detect the disease early, especially in individuals with a family history of hypercalcemia or endocrine disorders.
Which Doctor Treats Hyperparathyroidism?
Hyperparathyroidism is evaluated and treated in the endocrinology unit.
Diagnosis
Hyperparathyroidism is usually suspected when high calcium levels are detected in a routine blood test performed for other reasons. To confirm the diagnosis, the following tests are performed:
- Blood tests: Measure parathyroid hormone levels. Phosphate levels are also assessed (normal or low in primary hyperparathyroidism, high in secondary hyperparathyroidism) as well as vitamin D levels to rule out deficiency as a cause.
- Urine tests: Checking calcium and phosphate concentrations in urine helps confirm the diagnosis.
- Imaging studies: Used to identify glandular abnormalities responsible for primary hyperparathyroidism (adenomas, hyperplasias, or carcinomas). A technetium-99 sestamibi scan is commonly performed, as this radioactive compound accumulates in abnormal parathyroid cells and is visible through a gamma camera.
Additional tests may be performed to assess the effects of hyperparathyroidism on the body:
- Dual-energy X-ray absorptiometry (DXA): Measures bone mineral density.
- Abdominal ultrasound: Detects kidney stones.
Treatment
If hyperparathyroidism-induced hypercalcemia is mild, there is no kidney involvement, and bone density is normal, no treatment is required; periodic monitoring is sufficient to assess kidney function and calcium levels. For more advanced hyperparathyroidism, treatment options include:
- Parathyroidectomy: Surgery to remove the affected parathyroid glands in cases of primary hyperparathyroidism. If all glands are affected, a portion of healthy parathyroid tissue is preserved to maintain parathyroid function and prevent hypoparathyroidism. This tissue can be left in its original location or reimplanted elsewhere, such as in the sternocleidomastoid muscles or under the forearm skin.
- Medication: In secondary hyperparathyroidism due to kidney failure, medications are used to regulate calcium, phosphate, and vitamin D levels.
- Cinacalcet: A calcimimetic drug that lowers parathyroid hormone levels by mimicking circulating calcium.
- Active vitamin D.
- Phosphate binders, such as calcium carbonate, calcium acetate, or lanthanum, which reduce dietary phosphate absorption.
