Milk-alkali syndrome (MAS), also referred to as calcium-alkali syndrome, is the third most common cause of hypercalcemia. Milk-alkali syndrome is characterized by elevated blood calcium levels, metabolic alkalosis, and acute kidney injury.Milk-alkali syndrome can be caused by the excessive intake of calcium and absorbable alkali. Sources of calcium and alkali include dietary supplements taken for the prevention of osteoporosis or hyperparathyroidism and antacids taken for peptic ulcer disease. Common acute symptoms of milk-alkali syndrome include nausea and vomiting, dry mouth, confusion, lethargy, and distaste for milk. If left untreated, milk-alkali syndrome may lead to kidney failure or even death. Signs and symptoms
The signs and symptoms of milk-alkali syndrome can develop after only a few days and up to several months following the initial ingestion of absorbable calcium and alkali. However, the severity of signs and symptoms of milk-alkali syndrome is largely dependent upon the duration and quantity of calcium and alkali ingested.Acute milk-alkali syndrome is characterized by several biochemical alterations, mainly alkalosis, hypochloremia, hypokalemia, and hypercalcemia. In the acute phase of milk-alkali syndrome (Cope syndrome), the first symptoms of toxicity are nausea, vomiting, anorexia, headache, dizziness, vertigo, apathy, weakness, confusion, irritability, dry mouth, and repulsion to milk. In individuals with chronic milk-alkali syndrome (Burnett syndrome), symptoms may include muscle aches, psychosis, tremor, polyuria (producing large volumes of dilute urine), polydipsia (intense thirst), pruritus (itchy sensation on skin), band keratopathy and abnormal calcifications.
This can be attributed to the greater availability of over-the-counter calcium carbonate supplements to treat osteoporosis and dyspepsia, as well as the growing awareness among consumers of the potential health benefits of calcium intake. Calcium carbonate is also often prescribed to people with chronic kidney disease for the prevention of secondary hyperparathyroidism and to people receiving prolonged corticosteroid therapy that may lead to bone loss, putting them at a higher risk of calcium over-consumption and developing MAS.Other drugs reported to be associated with the development of MAS include thiazide diuretics, which causes increased reabsorption of calcium in the kidneys and hypovolemia that leads to contraction alkalosis. Angiotensin-converting enzyme (ACE) inhibitors and non-steroidal anti-inflammatory drugs (NSAIDs) are also drugs associated with MAS because they decrease glomerular filtration rate (GFR) and thus reduce calcium excretion. Taking medications such as aluminum hydroxide and magnesium hydroxide, which are absorbable alkali, can also contribute to MAS in those who already consume a large amount of calcium.Pregnant individuals have an increased risk for developing MAS due to hyperemesis (which can cause hypovolemia) and enhanced gastrointestinal calcium absorption as a result of higher levels of prolactin or placental lactose signaling (resulting in hypercalcemia). Calcium carbonate is also commonly used in pregnant individuals to treat acid reflux, further putting them at risk for overconsumption of calcium and developing MAS. Mechanism
The mechanism of how milk-alkali syndrome develops from ingesting too much of calcium and absorbable alkali is still unclear.