Hypercalcemia is a common problem encountered on internal medicine, with a long list of etiologies. Despite this, the large majority are related to (>;90%) malignancy and hyperparathyroidism.
The categories of causes can be broken down in multiple ways, but it may help to think of it based on the mechanism by which the calcium is increased.
1. Bone resorption
- primary hyperparathyroidism and tertiary hyperparathyroidism.
- malignancy - direct boney destruction and osteolysis with metastasis.
- PTHrP production by SCC
- osteoclasts activating factors (OAF) and RANKL production in
multiple myeloma
- thyrotoxicosis - with increased metabolic rate and bone resorption
- Pagets disease of the bone with immobility
- hypervitaminosis A
2. Increased calcium absorption
- milk alkali syndrome - secondary to over supplimentation, can be worsened in
context of kidney disease
- hypervitaminosis D - can be endogenous or exogenous
- endogenous - secondary to granulomatous disease (sarcoidosis) or
lymphoma
3. Miscellaneous
- Drugs - lithium, HCTZ, theophylline toxicity
- Adrenal insufficiency - multiple mechanisms including volume contraction
- familial hypocalciuric hypercalcemia - autosomal dominant mutation in sensory
receptor of parathyroid cells
Initial evaluation should consist of confirmation on accurate calcium level (corrected for albumin), followed by PTH level. Hyperparathyroidism is more common in patients with malignancy and a hence a history of cancer shouldn't negate the ordering of a PTH level.
Treatment includes fluid resuscitation, bisphosphonate therapy, discontinuation of offending meds and rarely, if ever, lasix and calcitonin. Following medical management, the correction of the underlying problem needs to be addressed.
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