Hyperparathyroidism is a disease that develops due to excessive production of parathyroid hormone (PTH) by the parathyroid glands and is manifested by disorders of calcium and phosphorus metabolism. This condition is among the three most common endocrine diseases, second only to thyroid disorders and diabetes mellitus.
Depending on the underlying cause, hyperparathyroidism is classified as primary, secondary, or tertiary.
- Primary hyperparathyroidism occurs twice as often in women as in men, and up to five times more frequently in the postmenopausal period. It affects individuals aged 20–70 years, with a peak incidence between 40 and 60 years.
- Secondary hyperparathyroidism is characterized by increased secretion of parathyroid hormone due to low blood calcium levels. This form is most commonly observed in patients with chronic kidney disease.
- Tertiary hyperparathyroidism represents the final stage of parathyroid gland transformation, in which long-standing secondary hyperparathyroidism leads to autonomous hormone production and the development of an adenoma.
Meet the parathyroid glands
As a rule, there are four parathyroid glands located on the posterior surface of the thyroid gland. They are very small—approximately 5 mm in diameter and weighing up to 50 mg. The number of parathyroid glands may vary from 3 to 12.
Parathyroid hormone is essential for maintaining calcium balance in the blood. It acts on:
- bone tissue (the main reservoir containing about 99% of the body’s calcium),
- the kidneys (through which calcium is excreted),
- the intestines, where calcium absorption occurs.
The exact cause of hyperparathyroidism has not been definitively established. Predisposing factors are considered to include intoxication, certain medications (lithium, aluminum), ionizing radiation, adverse environmental conditions, and genetic predisposition.
In 80–85% of cases, primary hyperparathyroidism is associated with the development of a parathyroid adenoma.
How does hyperparathyroidism manifest?
The earliest manifestations of the disease involve disruption of processes in which calcium plays a key role—muscle contraction, nerve conduction, and blood coagulation. Patients often complain of weakness, fatigue, difficulty sitting down or standing up, and problems climbing stairs.
In some cases, muscle weakness is so pronounced that the patient becomes bedridden.
Muscle relaxation may lead to flatfoot, causing pain in the feet. Changes in the central nervous system are also observed, including drowsiness, apathy, and depression. Cardiovascular manifestations include a tendency toward bradycardia and ECG changes (shortened QT interval). Gastrointestinal symptoms include dyspepsia and constipation. From the urinary system, polyuria and polydipsia are typical (frequent urination and excessive thirst).
Due to impaired blood coagulation, hemorrhages may occur in various organs and tissues.
Significant calcium loss leads to osteoporosis, bone pain, a characteristic “waddling gait,” spontaneous fractures, loosening and loss of teeth, and spinal deformities. These changes may result in reduced height, radicular syndromes, paresthesias, paralysis of the lower limbs, and pelvic organ dysfunction.
In the kidneys, parathyroid hormone increases calcium reabsorption, creating conditions for nephrolithiasis (kidney stone formation), most commonly oxalate-phosphate and phosphate stones. Renal function may deteriorate significantly, up to the development of acute or chronic kidney failure.
In the intestines, increased calcium absorption may contribute to the development of pancreatitis and peptic ulcer disease of the stomach and duodenum.
In approximately one-third of cases, a gastric ulcer may be the only clinical manifestation of hyperparathyroidism, and it may also be asymptomatic.
Excessive calcium deposition may occur in various organs, including joints, myocardium, coronary vessels, heart valves, skin, auricles, tympanic membranes, conjunctiva, and cornea (band keratopathy—calcium phosphate deposition in the corneal capsule). In some cases, these calcifications may mimic tumors.
It should be noted that despite the wide variety of clinical manifestations, 50–80% of cases of hyperparathyroidism are asymptomatic.
How is hyperparathyroidism diagnosed?
After clinical examination, a comprehensive diagnostic evaluation is performed.
Laboratory diagnostics. At a minimum, total or ionized serum calcium levels should be measured at least three times at intervals of 14–21 days. Parathyroid hormone levels must be determined at least twice, several weeks apart. Serum phosphorus, chloride levels, and alkaline phosphatase are also assessed. Depending on clinical manifestations, the range of laboratory tests may be expanded.
Instrumental diagnostic methods.
Ultrasound examination (US) is the first-line method for visualization of the parathyroid glands. Under normal conditions, parathyroid glands are not visualized on ultrasound.
If ectopic or atypical localization of the parathyroid glands is suspected, ultrasound data may be insufficient. In such cases, computed tomography (CT), magnetic resonance imaging (MRI), and scintigraphy using technetium-99m sestamibi are performed.
Bone densitometry is used to assess bone mineral density.
Treatment of hyperparathyroidism
The effectiveness of surgical treatment reaches 95–98%.
Serum calcium and parathyroid hormone levels normalize within hours after surgery, while phosphorus and alkaline phosphatase levels normalize over several months. Bone mineral density improves within 6–12 months after surgery, peptic ulcer disease does not recur, and kidney stone formation ceases.
Patients are able to return to a fully active life.
An alternative treatment option is sclerotherapy (percutaneous injection of ethanol or calcitriol under ultrasound guidance). This method is used when surgical removal of the parathyroid glands is contraindicated due to severe comorbidities or a high risk of complications.
In subclinical hyperparathyroidism (absence of clinical manifestations) and in cases of small parathyroid lesions, active treatment is not indicated. Regular comprehensive follow-up examinations are recommended.
Why choose hyperparathyroidism treatment in Belarus?
Belarusian physicians have accumulated extensive experience in the diagnosis and treatment of hyperparathyroidism. Highly qualified specialists, many years of clinical practice, modern equipment, and advanced treatment technologies represent the key strengths of medical care in Belarus.