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- 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 for indigestion or “heartburn”
- Also seen with treatment/prevention of postmenopausal osteoporosis, consumption of carbonated beverages and calcium salts
- Characterized by the following:
- Metabolic alkalosis
- ± Renal insufficiency
- System(s) affected: endocrine/metabolic; gastrointestinal; 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
- Avoid excess milk and/or absorbable antacids.
- Use noncarbonate salts for calcium supplementation.
Etiology and Pathophysiology
- Cyclic process between intestines and kidneys: hypercalcemia from high-calcium intake (usually >4 g/day) coupled with increased renal calcium reabsorption due to metabolic alkalosis (by sensitizing calcium-sensing receptor in the kidney)
- Hypercalcemia leads to suppression of parathyroid hormone–reduced urinary calcium excretion (by inducing volume depletion). An increase in the reabsorption of bicarbonate also maintains the metabolic alkalosis.
- Use of calcium-containing antacids or supplements
- Chronic kidney disease
- Simultaneous vitamin D supplementation
- Thiazide diuretic therapy
- Pregnancy (increased GI calcium absorption)
- Postmenopausal woman
- More common in women than men
Commonly Associated Conditions
- Peptic ulcer disease
- Gastroesophageal reflux
- Hiatal hernia
- Hypercalcemia of malignancy