Additionally, hypercalcemia can decrease the reabsorption of water in the kidneys collecting ducts by suppressing antidiuretic hormone (ADH) receptors, contributing to more hypovolemia. Hypercalcemia also results in lower parathyroid hormone (PTH) levels via a negative feedback loop, in which calcium-sensing receptors in the PTH gland are activated by the elevated calcium levels to inhibit PTH production, thus decreasing renal reabsorption of calcium.Hypovolemia then leads to metabolic alkalosis (increase in blood pH) by stimulating bicarbonate reabsorption in order to maintain extracellular volume. In summary, the symptoms of alkalosis is the net result of over-consumption of absorbable alkali, hypercalcemia-induced hypovolemia, and impaired glomerular filtration rate. Alkalosis, in turn, increases calcium-reabsorption from the distal tubules of the nephron, thus exacerbating the hypercalcemia and hypovolemia.Altogether, these result in a cycle of hypercalcemia, alkalosis, and renal injury characteristic of MAS. Diagnosis
Prior to an official diagnosis of milk-alkali syndrome, other causes of hypercalcemia must be ruled out. Other causes of hypercalcemia can include elevated vitamin D levels, hyperthyroidism, and hyperparathyroidism. Physical Examination:Symptoms such as vertigo, confusion, apathy, nausea and vomiting, anorexia, tremors, psychosis, myalgia, polyuria, abnormal calcifications such as renal calcifications, and pruitus could be observed in people. Lab work:
Lab work must be done to diagnose milk-alkali syndrome. Lab workup includes serum calcium levels, parathyroid hormone (PTH), phosphorus, creatinine, blood urea nitrogen (BUN), magnesium, and vitamin D levels. Primary hyperparathyroidism has to be excluded. Diagnosis is made by looking at past medical history and laboratory studies. Serum calcium levels: high serum calcium levels. PTH: low serum PTH levels are indicative of MAS.
Milk-alkali syndrome (MAS), also referred to as calcium-alkali syndrome, is the third most common cause of hypercalcemia. Milk-alkali syndrome is characterized by elevated blood calcium levels, metabolic alkalosis, and acute kidney injury.Milk-alkali syndrome can be caused by the excessive intake of calcium and absorbable alkali. Sources of calcium and alkali include dietary supplements taken for the prevention of osteoporosis or hyperparathyroidism and antacids taken for peptic ulcer disease. Common acute symptoms of milk-alkali syndrome include nausea and vomiting, dry mouth, confusion, lethargy, and distaste for milk. If left untreated, milk-alkali syndrome may lead to kidney failure or even death. Signs and symptoms
The signs and symptoms of milk-alkali syndrome can develop after only a few days and up to several months following the initial ingestion of absorbable calcium and alkali. However, the severity of signs and symptoms of milk-alkali syndrome is largely dependent upon the duration and quantity of calcium and alkali ingested.Acute milk-alkali syndrome is characterized by several biochemical alterations, mainly alkalosis, hypochloremia, hypokalemia, and hypercalcemia. In the acute phase of milk-alkali syndrome (Cope syndrome), the first symptoms of toxicity are nausea, vomiting, anorexia, headache, dizziness, vertigo, apathy, weakness, confusion, irritability, dry mouth, and repulsion to milk. In individuals with chronic milk-alkali syndrome (Burnett syndrome), symptoms may include muscle aches, psychosis, tremor, polyuria (producing large volumes of dilute urine), polydipsia (intense thirst), pruritus (itchy sensation on skin), band keratopathy and abnormal calcifications.