Burnett Syndrome

Classification according to ICD-10
E83.5	Disorders of calcium metabolism
ICD-10 online (WHO version 2019)

The milk-alkali syndrome , also called milk-alkali syndrome called, is after the American physician Charles Hoyt Burnett named (1913-1967) calcium - metabolic disorder due to an oversupply of easily absorbable alkalis (eg as bicarbonates.) And calcium ( e.g. about milk).

Burnett's syndrome manifests itself clinically with nausea and vomiting , dizziness and gait disorders ( ataxia ). An alkalosis occurs , an increase in the calcium content in the blood ( hypercalcaemia ) without increased calcium excretion in the urine and without a decrease in the phosphate content in the blood. The increased calcium level leads to calcinosis with calcium salt deposits in the conjunctiva , possibly also in the cornea ("band keratitis" of the eyelid fissure), as well as in the renal tubules with the risk of developing renal insufficiency .

Historical

In 1915 Bertram Sippy introduced a treatment for gastric ulcer for the first time . This consisted of the hourly intake of milk, cream and alkali powder . This therapy improved symptoms but did not cure them. Increasingly serious side effects have been reported after the introduction of milk-alkali treatment, in particular kidney failure , alkalosis and hypercalcemia . These side effects were particularly common in men with gastric ulcer. Deaths have even been reported. With the introduction of better therapeutic options for gastric and duodenal ulcers , the frequency of the milk-alkali syndrome initially decreased.

In the last 15 years, however, the number of diseases has increased again, especially in women who consume more than the recommended dose of 1200 to 1500 mg of calcium per day for the prevention or treatment of osteoporosis .

Pathogenesis

The metabolic alkalosis stimulates calcium transport in the tubules of the kidney . Together with an increased supply of calcium, this leads to an increase in the calcium level in the blood. The hypercalcemia leads to a narrowing of the blood vessels ( vasoconstriction ) in the kidney, the kidney performance decreases and with it the ability of the kidney to excrete excess calcium. The level of the parathyroid hormone (parathyroid hormone) drops. If the course is chronic, calcium deposits can form in the tissues, especially in the kidneys.

diagnosis

The most important note is a history of increased consumption of calcium and alkali salts. The laboratory diagnosis results in an increased level of calcium (hypercalcemia), a metabolic alkalosis and impaired renal function . In the classic milk-alkali syndrome due to massive intake of milk and alkali, the phosphate level is increased ( hyperphosphataemia ), in the "modern" milk-alkali syndrome due to excessive calcium carbonate doses , the phosphate level is usually normal. The parathyroid hormone is low. Often there is a lack of volume.

therapy

Stopping the calcium supply and intravenous infusion of physiological saline solution leads to a decrease in calcium uptake in the renal tubule system (by inhibiting passive tubular reabsorption) and thus to a rapid normalization of the calcium level.

literature

• P. Olschewski, JP Nordmeyer, T. Scholten: The milk-alkali syndrome - a rare differential diagnosis of hypercalcemia. In: Dtsch med Wochenschr. 1996, 121 (33), pp. 1015-1018.
• AJ Felsenfeld, BS Levine: Milk alkali syndrome and the dynamics of calcium homeostasis . In: Clin J Am Soc Nephrol . No. 1 , 2006, p. 641-654 , PMID 17699269 ( asnjournals.org ).
• Ilan Gabriely: Back to Basics . In: N Engl J Med . No. 358 , 2008, p. 1952-1956 ( abstract ).

This article is about a health issue. It is not used for self-diagnosis and does not replace a diagnosis by a doctor. Please note the information on health issues !