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Hypercalcemia, or high blood calcium, is often caused by primary hyperparathyroidism or malignancy. Establishing the cause is crucial for effective treatment, which may include addressing the underlying condition and managing calcium levels.
Area of Science:
- Endocrinology
- Nephrology
- Oncology
Background:
- Hypercalcemia is a common electrolyte disturbance with diverse etiologies.
- Primary hyperparathyroidism and malignancy are the leading causes in outpatients and inpatients, respectively.
- Mild hypercalcemia may be asymptomatic but can lead to long-term complications like renal calculi.
Purpose of the Study:
- To review the causes, diagnosis, and management of hypercalcemia.
- To highlight diagnostic challenges in specific patient populations.
- To outline therapeutic strategies for acute and chronic hypercalcemia.
Main Methods:
- Clinical history and physical examination.
- Laboratory investigations including parathyroid hormone levels.
- Radiological imaging and response to therapeutic interventions.
Main Results:
- Hypercalcemia severity dictates urgency of treatment; severe cases (>3.5 mmol/L) present with significant symptoms and complications.
- Diagnosis relies on a combination of clinical assessment and targeted investigations.
- Treatment involves addressing the underlying cause (e.g., surgery for hyperparathyroidism, radiotherapy for malignancy) and direct management of calcium levels.
Conclusions:
- Prompt diagnosis and etiology determination are essential for effective hypercalcemia management.
- Initial management focuses on rehydration, followed by specific therapies like intravenous mithramycin or aminohydroxypropylidene diphosphonate (APD) for severe cases.
- Long-term management strategies vary based on the cause, with dietary modifications and specific medications being key for conditions like sarcoidosis or persistent hyperparathyroidism.
Abstract:
Hypercalcaemia can be caused by many disorders, but is most commonly due to primary hyperparathyroidism in outpatients, and to malignant disease in hospital inpatients. When mild (less than 3 mmol/L) it does not cause symptoms, but can have long term effects such as renal calculi. It is important that the aetiology of the hypercalcaemia be established, as it can reflect serious disease. In most patients the correct diagnosis can be suspected from clinical history and examination, and confirmed by laboratory tests and x-rays. The most difficult diagnostic problem is the patient with negative clinical findings, mild hypercalcaemia and mild renal impairment, when the parathyroid hormone level is normal or slightly elevated. When hypercalcaemia is severe (greater than 3.5 mmol/L), it can cause vomiting, polyuria, dehydration and renal impairment, and is then an important therapeutic problem. Therapy includes treatment of the cause, such as radiotherapy for malignant disease or surgery for primary hyperparathyroidism. In addition, it is usually necessary to treat the hypercalcaemia itself, and the initial step is always rehydration. If the plasma calcium concentration remains high, drug treatment must be added, the most effective and reliable agent being intravenous mithramycin. Aminohydroxypropylidene diphosphonate (APD), though less studied, may be equally useful in this situation. Glucocorticoids are not always effective, and phosphate may cause renal damage, particularly when given intravenously. For long term treatment of malignant hypercalcaemia, oral glucocorticoids and phosphate are often effective, and can be given in combination. When primary hyperparathyroidism cannot be corrected surgically, the hypercalcaemia (and hypercalciuria) are probably best treated with a low calcium diet and cellulose phosphate, a regimen also effective for the hypercalcaemia of sarcoidosis.