| disease | Milk-Alkali Syndrome |
| alias | Milk-Alkali Syndrome, Milk-alkali Syndrome |
Milk-Alkali Syndrome refers to a clinical syndrome characterized by hypercalcemia, alkalosis, and varying degrees of renal impairment caused by long-term consumption of large amounts of milk or calcium supplements along with absorbable alkali. It was previously common in the medical treatment of peptic ulcer patients, but has become rare due to improvements in treatment regimens, such as the use of insoluble alkaline medications.
bubble_chart Etiology
Long-term consumption of calcium- and phosphorus-rich milk and the intake of large amounts of easily absorbable alkaline agents are the causes of this syndrome. Frequent vomiting and pre-existing kidney diseases make individuals more susceptible to triggering or worsening this condition. Milk is rich in calcium and phosphorus, and prolonged excessive consumption inevitably leads to an increase in these minerals in the body. Additionally, the simultaneous intake of large amounts of readily absorbable alkaline agents causes alkalosis, which enhances intestinal calcium absorption. This results in the deposition of calcium and phosphorus ions in soft tissues, primarily in the kidneys and eyes, though other areas such as the skin, blood vessels, lungs, and brain may also be affected, leading to structural and functional damage in the corresponding tissues and organs.
bubble_chart Clinical Manifestations
The main manifestations include muscle weakness, loss of appetite, nausea vomiting, excessive thirst and polyuria, weight loss, headache dizziness, drowsiness, and renal colicky pain, primarily caused by hypercalcemia, alkalosis, and soft tissue calcification. Based on the course of the disease, it can be divided into the late stage [third stage]:
1. Acute phase (Mcmillan syndrome): Symptoms develop within a week after consuming milk and large doses of easily absorbable alkali, but without ocular involvement. Symptoms usually resolve rapidly after discontinuing milk and alkali, and renal function also recovers.2. Subacute phase (Cope syndrome): Band keratopathy and conjunctival microcalcifications appear, and systemic soft tissue calcification may also occur. Symptoms gradually disappear after discontinuing milk and alkali, with slower recovery of renal function, but full recovery is possible.
3. Chronic phase (Burnett syndrome): Symptoms worsen further, with extensive and severe soft tissue calcification and significant renal impairment. Blood calcium levels may return to normal after discontinuing milk and alkali, but renal insufficiency cannot fully recover.
1. History of long-term consumption of milk and intake of alkaline medications.
2. Elevated serum calcium, mostly above 2.56 mmol/L.
3. Presence of metabolic alkalosis, with blood CO₂ combining power and pH both higher than normal.
4. Impaired renal function, such as increased nocturia, low urine specific gravity, elevated blood urea nitrogen, and creatinine.
5. Manifestations of soft tissue calcification.
6. Condition may improve after discontinuation of milk and alkaline agents. {|105|}
bubble_chart Treatment Measures
Treatment should involve discontinuing milk and alkali agents, adopting a low-calcium diet, correcting alkalosis and hypokalemia, and actively preventing and treating urinary tract infections. For those with severe renal impairment, hemodialysis may be performed, and kidney transplantation can be considered if conditions permit. The prognosis of this syndrome primarily depends on the severity of kidney damage.
The prognosis primarily depends on the severity of renal damage.
It needs to be differentiated from hypercalcemia or calcinosis caused by primary hyperparathyroidism, vitamin D intoxication, sarcoidosis, malignant tumor metastasis, and other conditions.
