Causes and pathogenesis
Primary, secondary, and tertiary hyperparathyroidism are distinguished.
Primary hyperparathyroidism is often caused by hyperplasia of all parathyroid glands (15–20%), sometimes associated with genetic syndromes (MEN). A rare cause (about 1%) is parathyroid carcinoma. This is a slow-growing but invasive tumor. The primary treatment method is surgical, as radiation therapy and chemotherapy are typically ineffective.
Secondary hyperparathyroidism occurs in response to conditions that lower blood calcium levels. The main triggers are chronic kidney disease (CKD), vitamin D deficiency, and impaired gastrointestinal calcium absorption (e.g., in celiac disease). In CKD, the pathogenesis is associated with a lack of active vitamin D ($1,25(OH)_2D$) and phosphate retention.
Tertiary hyperparathyroidism develops when an autonomous adenoma arises within hyperplastic glands against the background of a prolonged secondary process. Most commonly, this occurs in patients with CKD or severe vitamin D deficiency.
Clinical presentation
Primary hyperparathyroidism is often asymptomatic and discovered incidentally due to elevated blood calcium levels. However, particularly in young patients, prominent clinical manifestations may develop:
- Renal involvement: nephrocalcinosis and kidney stones (25–35%).
- Cardiovascular system: arterial hypertension (40–60%).
- Joints: chondrocalcinosis causing acute arthropathy (pseudogout) due to calcium pyrophosphate dihydrate (CPPD) crystals.
- Musculoskeletal system: osteoporosis, bone pain, muscle weakness.
- Gastrointestinal tract and CNS: peptic ulcer disease, pancreatitis, depressive states, and decreased concentration.
- General symptoms: lethargy, arthralgia.
Diagnostic radiology
In the vast majority (95%) of patients with asymptomatic primary hyperparathyroidism, there are no radiographic changes. Changes are visible in advanced stages or in secondary/tertiary forms.
Pathognomonic signs:
- Subperiosteal resorption: destruction of the cortical layer. The most sensitive area for early diagnosis is the radial aspect of the middle phalanges of the index and middle fingers. If erosions are absent here, searching for them elsewhere in the skeleton is futile. In advanced stages, acroosteolysis (resorption of the terminal phalanges) may occur.
- Chondrocalcinosis: deposition of CPPD crystals in cartilage (triangular fibrocartilage of the wrist, menisci of the knee joints, pubic symphysis). The combination of pubic symphysis chondrocalcinosis and nephrocalcinosis on an abdominal radiograph is a specific marker of primary hyperparathyroidism.
- Brown tumors (brown tumours): multilocular cystic lesions at sites of intense bone resorption (osteitis fibrosa cystica). On radiographs, they appear as expansile low-density areas and can mimic neoplasms.
Secondary hyperparathyroidism in the setting of CKD is characterized by osteosclerosis. A typical finding is the 'rugger jersey' spine: sclerosis of the vertebral body endplates with a radiolucent central band. Metastatic soft tissue calcification (due to phosphate retention) is also encountered in CKD.
Principles of treatment
The approach depends on the form of the disease:
- Primary hyperparathyroidism: the primary curative method is surgical removal of hyperactive tissue (success rate > 90%). If surgery is contraindicated or the patient refuses, monitoring of calcium, creatinine, and bone density is performed. Medications (calcimimetics, e.g., cinacalcet) are used to control hypercalcemia.
- Secondary hyperparathyroidism: treatment aims to compensate for the underlying disease (phosphate restriction, phosphate binders, vitamin D, calcimimetics). If conservative therapy fails, parathyroidectomy is prescribed.
Briefly: answers to topical questions
What are the causes of primary hyperparathyroidism?
Primary hyperparathyroidism is caused by neoplastic and hyperplastic processes in the parathyroid glands. The main causes of the disease include:
- Solitary adenoma — detected in 80% of cases.
- Parathyroid hyperplasia — occurs in 10–20% of patients, sometimes due to genetic factors.
- Multiple adenomas account for 2–3% of cases.
- Parathyroid carcinoma is a rare cause (about 1%), characterized by slow but invasive growth.
The condition can also be caused by diffuse hyperplasia of the glands.
Which genetic syndromes are associated with primary hyperparathyroidism?
Primary hyperparathyroidism is associated with the following hereditary conditions:
- Multiple endocrine neoplasia type 2A syndrome (MEN2A), in which it is combined with medullary thyroid carcinoma and pheochromocytoma.
- Familial hyperplasia of the parathyroid glands.
- Hyperparathyroidism-jaw tumor syndrome.
How do calcium, phosphorus, and alkaline phosphatase levels in the blood change in primary hyperparathyroidism?
In primary hyperparathyroidism, characteristic changes in electrolyte and enzyme concentrations are observed in blood serum. Laboratory parameters change as follows:
- Calcium — hypercalcemia develops.
- Phosphorus — hypophosphatemia occurs.
- Alkaline phosphatase (alkaline phosphatase) — its level increases.
These shifts are caused by the excessive secretion of parathyroid hormone, which enhances the mobilization of calcium and phosphates from bone tissue and also increases renal phosphate excretion.
Class and exam questions
Which radiological sign is the most specific for hyperparathyroidism?
Subperiosteal erosions, primarily along the radial aspect of the middle phalanges of the II and III fingers of the hand.
What is the "rugger-jersey spine" sign?
This is a striped spine pattern on X-ray that occurs in secondary hyperparathyroidism. The vertebral bodies have dense (sclerotic) endplates and a less dense central part.
What does the conservative treatment of secondary hyperparathyroidism involve?
It includes dietary phosphorus restriction, administration of phosphate binders, vitamin D preparations, and calcimimetics (e.g., cinacalcet).
What else to study on this topic
- Features of bone densitometry in hyperparathyroidism
- Differential diagnosis of brown tumors and bone metastases
- Pathogenesis of intracortical resorption (cortical "tunneling")
- Impact of vascular calcification on DXA results
- Surgical treatment of parathyroid carcinoma
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