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| Journal of the New Zealand Medical Association,
21-September-2007, Vol 120 No 1262
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Modern milk alkali syndrome—a preventable
serious condition
Binay K Shah, Sharath Gowda, Hejmadi Prabhu, Jeffrey Vieira,
Harish C Mahaseth
In the post H2-blocker era,
milk alkali syndrome has become very rare. However, with growing use of
over-the-counter (OTC) calcium preparations, a resurgence of this disorder has
been noticed. We report a case of severe hypercalcaemia resulting from overuse
of calcium preparations.
Case reportA 47-year-old female from an adult home (residential care
home / rest home) was brought to the emergency room with history of abdominal
pain, loss of appetite, lethargy, and constipation.
Her past medical history was significant for Down’s
syndrome and hypothyroidism. Her home medications were risperidol,
levothyroxine, alendronate 70 mg once a week; two calcium preparations (one
containing calcium carbonate 500 mg and vitamin D 200 IU, and the other
containing calcium carbonate 500mg) each three times a day; and raloxifene 60 mg
once a day. It was not clear from the adult home notes why the patient was
taking two calcium preparations: raloxifene and alendronate.
ER vitals (vital signs) were normal and the physical
examination was unremarkable. Her lab results at admission revealed sodium 148
mmol/L (normal range: 135–145 mmol/L), potassium 3.3 mmol/L (3.5–5.3
mmol/L), chloride 104 mmol/L (97–107 mmol/L), bicarbonate 33 mmol/L
(22–33 mmol/L), blood urea nitrogen (BUN) 25 mg/dl (5–19
mg/dL), creatinine 4.1 mg/dL (0–1.1 mg/dL), glucose 79 mg/dL, calcium more
than 16.5 mg/dL (8.5–10.3 mg/dL), and albumin 3.8 g/dL; liver function
tests and thyroid-stimulating hormone (TSH) were normal.
Intact parathyroid hormone (PTH) was 8.9 pg/mL (10–69
pg/mL) and serum protein electrophoresis and urine protein electrophoresis were
normal. Renal sonogram showed no abnormality.
The patient was treated with intravenous (IV) fluids and
furosemide for hypercalcaemia secondary to milk alkali syndrome. Her serum
calcium normalised in 2 days and renal function returned to normal.
DiscussionThe commonest cause of hypercalcaemia is hyperparathyroidism
in outpatient settings and malignancy in inpatient settings. Milk alkali
syndrome was a common cause of hypercalcaemia when peptic ulcer disease was
treated with Sippy regimen1 consisting of
hourly administration of milk and cream with a mixture of bicarbonate containing
salts that included calcium carbonate.
Renal failure and alkalosis as toxicities of Sippy regimen
was recognised by Hardt and Rivers in 1923.2
The hypercalcaemia which is now known to be central to the milk alkali syndrome
was first described by Cope in 1936.3 With the
advent of H2 antagonists and proton pump
inhibitors, the use of antacids to treat peptic ulcer disease declined
dramatically and the incidence of the syndrome fell to 2% of all patients
admitted with hypercalcaemia during 1985 to
1989.4
Recently, there has been resurgence of the cases of milk
alkali syndrome due to common use of calcium therapy for osteoporosis,
readily-available OTC calcium carbonate preparations, and use of calcium
carbonate to minimise secondary hyperparathyroidism in patients with chronic
renal failure.
In a recent study during surveillance period from 1998 to
2003, milk alkali syndrome was the third most common cause of hypercalcaemia
(8.8%) and the second most common cause of severe hypercalcaemia (>14
mg/dL).5 Therefore, with the increased use of
calcium carbonate for treatment of osteoporosis, an increased awareness of the
milk alkali syndrome is necessary.
There is no correlation between reported intakes and the
severity of the hypercalcaemia or other manifestations of the
disease.4 In susceptible patients, milk alkali
syndrome begins with development of hypercalcaemia. High serum calcium produces
a decrease in glomerular filteration rate and along with increased alkali
intake, causes metabolic alkalosis and further decreases calcium
excretion.6 Nausea and vomiting further
dehydrates the patient thereby worsening the effects of hypercalcaemia, renal
failure, and metabolic alkalosis. Our patient was taking calcium preparation 3
grams/day.
Symptomatic patients and patients with serum calcium levels
above 13.5 mg/dL generally warrant aggressive intervention. Treatment initially
consists of IV normal saline and a loop
diuretic.7
This case highlights a serious complication of a
nonprescription drug when used inadvertently. Milk alkali syndrome is likely to
become more common with increased use of calcium preparations for osteoporosis.
It can easily be recognised by taking a thorough medication history.
Similarly before prescribing “safe” medications
such as calcium preparations, we should carefully assess other similar
medications that the patient may be taking.
Author information: Binay K Shah, Fellow,
Haematology/Oncology Department; Sharath Gowda, Fellow, Geriatrics; Hejmadi
Prabhu, Chief Resident, Department of Internal Medicine; Jeffrey Vieira, Program
Director, Internal Medicine residency program; Harish C Mahaseth, Resident,
Department of Internal Medicine; Long Island College Hospital, Brooklyn,
NY, USA
Correspondence: Dr Binay K Shah, University
of Illinois at Chicago Hospital, 840 S. Wood St., (M/C 713), Room 820E,
Chicago, IL 60612, USA. Fax: +1 773 856 3090; email: binay.shah@gmail.com
References:
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