- Milk-alkali syndrome results from ingestion of excessive amounts of calcium and absorbable alkali (e.g., bicarbonate and citrate salts).
- Historically seen during self-treatment of indigestion or reflux (heartburn)
- Also seen with treatment/prevention of postmenopausal osteoporosis, consumption of carbonated beverages and calcium salts
- Characterized by:
- Metabolic alkalosis
- ± Renal insufficiency
- System(s) affected: endocrine/metabolic; gastrointestinal (GI); renal/urologic
- Synonym(s): Burnett syndrome; Cope syndrome; milk poisoning; milk drinker syndrome; calcium alkali syndrome
- Third most common cause of hypercalcemia
- Recent increase associated with treatment for prevention of osteoporosis
Infrequent in the outpatient setting but 9–12% among hospitalized patients who have hypercalcemia
Etiology and Pathophysiology
- Cyclic process between intestines and kidneys: hypercalcemia from high-calcium intake (usually >4 g/day) believed secondary to inadequate response to calcitriol
- Hypercalcemia leads to vasoconstriction ultimately decreasing glomerular filtration.
- Activation of calcium-sensing receptors increases calcium reabsorption, absorption of bicarbonate, and natriuresis (maintaining alkalotic state).
- Blockade of antidiuretic hormone leads to increased diuresis.
- Use of calcium-containing antacids or supplements
- Chronic kidney disease
- Simultaneous vitamin D supplementation
- Thiazide diuretic therapy
- Pregnancy (increased GI calcium absorption)
- Postmenopausal women (more common overall in women)
- Nicotine substitute chewing gum in large quantities
- Avoid excess milk and/or absorbable antacids.
- Use noncarbonate salts for calcium supplementation.
- Caution in elderly treated with ACE-I/ARB, NSAIDs, and diuretic
Commonly Associated Conditions
- Peptic ulcer disease
- Hiatal hernia
- Gastroesophageal reflux
- Hypercalcemia of malignancy
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