Milk-alkali syndrome in a middle-aged woman after ingesting large doses of calcium carbonate: a case report
© Grubb et al.; licensee Cases Network Ltd. licensee BioMed Central Ltd. 2009
Received: 7 June 2009
Accepted: 28 August 2009
Published: 16 September 2009
Most cases of hypercalcaemia are secondary to malignancy or primary hyperparathyroidism. Here we report a case of hypercalcaemia that we have attributed to milk-alkali syndrome.
A 51-year-old Caucasian woman with a past history of thyroidectomy and parathyroidectomy secondary to thyroid cancer developed an altered mental state and had an extremely high calcium concentration of 22.8 mg/dl (5.7 mmol/l). Investigations included work up for malignancy and hyperparathyroidism. However, the hypercalcaemia was attributed to ingestion of large doses of calcium carbonate, leading to milk-alkali syndrome. She was managed with intravenous fluids and withdrawal of calcium carbonate. The patient responded well to treatment, with normalization of the calcium concentration and clinical improvement.
We present this case to remind clinicians of the importance of detailed history taking and of milk-alkali syndrome as a cause of hypercalcemia.
Most cases of hypercalcemia are secondary to malignancy or primary hyperparathyroidism . Milk-alkali syndrome accounts for about 12% of cases and ranks third among the causes of hypercalcemia  This syndrome is caused by ingestion of large amounts of calcium along with absorbable alkali. The occurrence of milk-alkali syndrome had fallen with the use of non-alkali therapies for peptic ulcer disease . However, recently the incidence has increased secondary to the use of calcium carbonate for the prevention and treatment of osteoporosis and hyperphosphataemia in patients with chronic kidney disease . We report a case of milk-alkali syndrome secondary to ingestion of calcium carbonate.
Pertinent laboratory values
22.8 mg/dL (5.7 mmol/L)
4.6 g/dL (46 g/L)
8.5 g/dL (85 g/L)
10.6 × 109/L
4.8-10.8 × 109/L
10.9 g/dL (109 g/L)
Blood urea nitrogen
2.1 mg/dL (186 µmol/L)
1.5 mg/dL (0.62 mmol/L)
2.9 mg/dL (0.94 mmol/L)
0.65 ug/dL (8.4 pmol/L)
Symptoms in hypercalcaemia may be secondary to the raised calcium concentration itself or to the underlying cause. Hypercalcaemia usually becomes symptomatic at a concentration of 12-14 mg/dl (3.0-3.5 mmol/l) . The symptoms are predominantly related to the gastrointestinal and renal tracts and the nervous and musculoskeletal systems. These include abdominal pain, reduced appetite, nephrolithiasis, depressed mood, headache, confusion, lethargy, and muscle weakness . Of all cases of hypercalcaemia 80-90% are secondary to malignancy or primary hyperparathyroidism, but many other disorders can cause hypercalcaemia . A few that are important to remember include milk-alkali syndrome, vitamin D intoxication, and granulomatous diseases such as sarcoidosis. Milk-alkali syndrome is now the third most common cause and accounts for about 12% of cases . The initial diagnostic work-up for hypercalcaemia includes serum PTH, phosphorus, 25-OH-cholecalciferol and 1,25 OH2-cholecalciferol, and urinary calcium.
Our patient had profound symptomatic hypercalcaemia, which caused lethargy, cognitive disturbance, and muscle weakness. Work-up for malignancy was negative and she gave a history of calcium and alkali ingestion. The clinical laboratory data were characteristic of milk-alkali syndrome and we excluded other causes of hypercalcemia .
In the early 20th century, calcium-containing antacids and milk were used to treat peptic ulcer disease. Sometimes this therapy was associated with toxicity [6, 7]. Hardt and Rivers identified the milk-alkali syndrome in 1923 and reported that it caused headache, nausea, vomiting, dizziness, musculoskeletal pains, and weakness . Today, this syndrome continues to occur in patients who have ingested large amounts of calcium, in excess of 4 g/day with absorbable alkali, particularly as calcium carbonate [4, 6]. The milk-alkali syndrome had become less frequent with the use of non-alkali therapies for peptic ulcer disease, but the incidence has recently increased, probably secondary to the use of calcium carbonate for osteoporosis and hyperphosphataemia in patients with chronic kidney disease .
The syndrome can present in three ways: acute, subacute, and chronic. The acute presentation includes weakness, myalgia, irritability, and apathy. Advanced or chronic milk-alkali syndrome, otherwise known as Burnett's syndrome, involves severe hypercalcaemia, phosphate retention, and irreversible renal insufficiency. This presentation can be accompanied by ectopic calcification. Subacute presentation, as in our patient, causes reversible renal insufficiency and usually improves over a period of weeks after withdrawal of oral calcium and alkali. Conservative treatment and supportive measures such as intravenous fluids should also be given .
In patients with hypercalcaemia, after common causes such as hyperparathyroidism or malignancy have been ruled out, it is important to remember the milk-alkali syndrome as an increasingly common cause of hypercalcaemia. A detailed history, including the use of over-the-counter medications, should be taken in all patients .
At our institution, the UT College of Medicine Chattanooga and Erlanger we have an Institutional Review Board (IRB) to review projects and ensure the protection of human subjects involved. The Chairman of the IRB is B W Ruffner, M.D. Our manuscript has been approved by our Institutional Review Board.
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