Milk-alkali syndrome


In medicine, milk-alkali syndrome is characterized by high blood calcium and metabolic alkalosis caused by taking in too much calcium and absorbable alkali; common sources of calcium and alkali are dietary supplements taken to prevent osteoporosis and antacids. If untreated, milk-alkali syndrome may lead to kidney failure or death.
It was most common in the early 20th century, but since the 1990s, there has been an increase in the number of cases reported, linked to the increased use of calcium supplements to address or prevent osteoporosis.

Signs and symptoms

The most common symptoms are poor appetite, dizziness, headache, confusion, psychosis, and dry mouth; laboratory tests may show that a person with milk-alkali syndrome has high blood calcium, kidney failure, and metabolic alkalosis.

Causes

Milk-alkali syndrome is caused by taking too much calcium and absorbable alkali.

Mechanism

The mechanism by which ingesting too much calcium and alkali leads to milk-alkali syndrome is unclear, since the human body tightly regulates levels of calcium. Impaired kidney function is a risk factor but even people with healthy kidneys can develop the syndrome.

Diagnosis

To diagnose milk-alkali syndrome, primary hyperparathyroidism has to be excluded. Usually the PTH is suppressed. Phosphorus levels are usually decreased while creatinine and bicarbonate levels are elevated.

Treatment

Treatment involves having the person stop taking any calcium supplements and any other alkali agents they have been taking, and hydration.
In severe cases, hospitalization may be required, in which case saline may be administered intravenously.
If kidney failure is advanced then treatment for that is required, namely chronic dialysis.

Outcomes

In mild cases, full recovery is expected. In severe cases, permanent kidney failure or death may result.

Epidemiology

Among people hospitalized with high blood calcium, milk-alkali syndrome is the third most common cause, after hyperparathyroidism and cancer.

History

The name "milk-alkali syndrome" derives from a reaction that arose to a treatment for gastric ulcers created in the early 1900s by Bertrand Sippy; Sippy prescribed his patients milk and alkali on the theory that ulcers were caused by excessive gastric acid. However within a few decades, an acute hypercalcemia syndrome with a relative good outcome was identified by Cuthbert Cope in 1936, and in 1949 Charles H. Burnett identified a similar but more severe syndrome, with chronically high blood calcium levels and poor outcomes.
When the true cause of most gastric ulcers was identified and drugs other than antacids were developed to treat heartburn – namely acid-reducing drugs like H2-receptor antagonists or proton pump inhibitors – the incidence of milk-alkali syndrome greatly diminished. However, as a result of increased osteoporosis awareness and the routine use of calcium supplements to prevent it, the incidence has again increased.