Milk-alkali syndrome

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shakiba Hassanzadeh, MD[2]

Milk-alkali syndrome (also known as calcium-alkali syndrome) is characterized by a history of excessive calcium intake and hypercalcemia, metabolic alkalosis and varying degrees of renal insufficiency. In 1915, Bertram Sippy introduced a treatment for peptic ulcer disease which was an hourly mixture of milk and cream combined with alkaline powders. In 1923, the toxic effects of Sippy’s regimen were reported for the first time. With the introduction of histamine antagonists and decrease in antacid consumption since the 1970s, the incidence of milk-alkali syndrome has decreased significantly. However, since the 1990s, there has been an increase in milk-alkali syndrome due to an increase in calcium and vitamin D consumption in postmenopausal women for osteoporosis prevention. Treatment of milk-alkali syndrome is mostly supportive and mainly includes the withdrawal of the offending agent, hydration, and intravenous volume expansion. Prognosis of milk-alkali syndrome is generally good and early diagnosis and treatment, with the withdrawal of the offending agent and supportive therapy, usually resolve the symptoms and abnormalities in milk-alkali syndrome (hypercalcemia, alkalosis and renal insufficiency).

In 1915, Bertram Sippy introduced a treatment for peptic ulcer disease which was an hourly mixture of milk and cream combined with alkaline powders.^[1] In 1923, the toxic effects of Sippy’s regimen was reported for the first time.^[2] With the introduction of histamine antagonists and decrease in antacid consumption since the 1970s, the incidence of milk-alkali syndrome has decreased significantly. However, since the 1990s, there has been an increase in milk-alkali syndrome due to increase in calcium and vitamin D consumption in postmenopausal women for osteoporosis prevention.^[3][4][5]

Milk-alkali syndrome may be classified as the following: acute (toxemic form), subacute (Cope’s syndrome) and chronic (Burnett’s syndrome).^[6]

The exact pathogenesis of milk-alkali syndrome is unknown. Hypercalcemia in milk-alkali syndrome involves several mechanisms including: intestinal absorption of calcium is increased, bone buffering of calcium becomes saturated, and renal excretion of calcium is decreased.^[5] Several factors that increase bicarbonate reabsorption and contribute to the alkalosis in milk-alkali syndrome include: volume depletion due to increased sodium and free water excretion caused by increased calcium intake, suppression of PTH, direct tubular effects of calcium and other factors that cause volume depletion or alkalosis such as vomiting or thiazide use.^[7]

Currently, the main cause of milk-alkali syndrome is calcium carbonate consumption, mostly in postmenopausal women for osteoporosis prevention or treatment or in patients on glucocorticoid therapy (for example in organ transplantation), and chronic renal disease.^[8] With the introduction of histamine antagonists and decrease in antacid consumption since the 1970s, the incidence of milk-alkali syndrome has decreased significantly. However, since the 1990s, there has been an increase in milk-alkali syndrome mostly due to increase in calcium and vitamin D consumption in postmenopausal women for osteoporosis prevention.^[3][4][5]

Milk-alkali syndrome should be differentiated from other disorders that cause hypercalcemia such as hyperparathyroidism, malignancies, hyperthyroidism, immobilization, sarcoidosis and some drugs (thiazides, vitamin D, lithium and vitamin A toxicity)^[9]

Patients with the following conditions are more susceptible to milk-alkali syndrome: Older age, preexisting chronic renal disease, concurrent vomiting (bulimia nervosa or hyperemesis gravidarum ) and use of certain drugs like thiazide, NSAIDs, and ACE inhibitors.^{[3][10][11][12][5][13][4]}

There is insufficient evidence to recommend routine screening for milk-alkali syndrome.

Most patients with milk-alkali syndrome are asymptomatic and may be incidentally diagnosed. Complications of milk-alkali syndrome may include: confusion, psychosis, renal insufficiency, pancreatitis, abnormalities in cardiac conduction, and metastatic calcification. Prognosis of milk-alkali syndrome is generally good and early diagnosis and treatment, with withdrawal of the offending agent and supportive therapy, usually resolve the symptoms and abnormalities in milk-alkali syndrome (hypercalcemia, alkalosis and renal insufficiency).^{[9][8][3][14][15][3][8][16][17]}

The exact incidence and prevalence of milk-alkali syndrome is not known.^[18] With the introduction of histamine antagonists and decrease in antacid consumption since the 1970s, the incidence of milk-alkali syndrome has decreased significantly. However, since the 1990s, there has been an increase in milk-alkali syndrome due to increase in calcium and vitamin D consumption in postmenopausal women for osteoporosis prevention.^[3][4][5] Milk-alkali syndrome is the third most common cause of hypercalcemia in hospitalized patients after primary hyperparathyroidism and malignancies.^[10]

Milk-alkali syndrome is diagnosed by a history of excessive calcium consumption, hypercalcemia, metabolic alkalosis and variable degrees of renal insufficiency. ^[3]

In patients with milk-alkali syndrome, there is a history of excessive calcium and absorbable alkali consumption.^[3] Symptoms of milk-alkali syndrome may inculde: dizziness, vertigo, confusion, apathy, nausea, vomiting, anorexia, distaste for milk, headache, anorexia, pruritus, polydipsia, polyuria, myalgia, tremor, psychosis, and abnormal calcifications (keratopathy, renal calcinosis).^[14][15]

The following should be considered in the physical examination of milk-alkali syndrome: vertigo, confusion, apathy, nausea, vomiting, pruritus, polydipsia, polyuria, myalgia, tremor, psychosis, and abnormal calcifications (keratopathy, renal calcinosis).^[14][15][3]

The following laboratory findings are usually seen in milk-alkali syndrome: hypercalcemia, metabolic alkalosis, variable degrees of renal insufficiency, low or normal phosphorus, low Vitamin D, and low PTH.^{[8][3][19][4]}

Milk-alkali syndrome causes hypercalcemia and hypercalcemia may cause the following findings on electrocardiogram (ECG): shortened QT interval (the most common finding), shortened ST segment, PR prolongation, increased amplitude of QRS complex, decreased amplitude of T wave, T wave notching, transient ST segment elevation, bradycardia, sinus arrest, and ventricular arrhythmias.^{[20][21][22][23][24][25]}

X-ray is not useful in the diagnosis of milk-alkali syndrome. However, X-ray may be useful in excluding other causes of hypercalcemia. Renal calcium deposits are not seen on X-ray in milk-alkali syndrome.^[3]

Echocardiography is not useful in the diagnosis of milk-alkali syndrome. Ultrasound is not useful in the diagnosis of milk-alkali syndrome. However, ultrasound may be helpful in excluding other causes of hypercalcemia.

CT scan is not useful in the diagnosis of milk-alkali syndrome. However, CT scan may be helpful in excluding other causes of hypercalcemia.

MRI is not useful in the diagnosis of milk-alkali syndrome. However, MRI may be helpful in excluding other causes of hypercalcemia.

There are no other imaging findings associated with milk-alkali syndrome.

There are no other diagnostic studies associated with milk-alkali syndrome.

Treatment of milk-alkali syndrome is mostly supportive and mainly includes withdrawal of the offending agent, hydration and intravenous volume expansion. However, other treatments such as therapy with calcium supplements (in temporary hypocalcemia) and hemodialysis (in acute or chronic irreversible renal insufficiency) may be required.^[8][3]

Surgical intervention is not recommended for the routine management of milk-alkali syndrome.

Effective measures for the primary prevention of milk-alkali syndrome includes public education about the potential adverse effects of calcium supplements. Calcium intake less than 2 g/daily is usually safe, however, 1.2 to 1.5 g/daily of calcium intake should be taken by individuals with risk factors for milk-alkali syndrome.^{[3][10][11][12][5][13][4]}

There are no established measures for the secondary prevention of milk-alkali syndrome.

There is insufficient evidence about the cost-effectiveness of therapy in milk-alkali syndrome.

No further or investigational therapies have been suggested in milk-alkali syndrome.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shakiba Hassanzadeh, MD[2]

In 1915, Bertram Sippy introduced a treatment for peptic ulcer disease which was an hourly mixture of milk and cream combined with alkaline powders. In 1923, the toxic effects of Sippy’s regimen. were reported for the first time. With the introduction of histamine antagonists and decrease in antacid consumption since the 1970s, the incidence of milk-alkali syndrome has decreased significantly. However, since the 1990s, there has been an increase in milk-alkali syndrome due to an increase in calcium and vitamin D consumption in postmenopausal women for osteoporosis prevention.

• In 1915, Bertram Sippy introduced a treatment for peptic ulcer disease which was an hourly mixture of milk and cream combined with alkaline powders (magnesium oxide, sodium bicarbonate, and bismuth subcarbonate).^[1]
• In 1923, Hardt and Rivers reported toxic effects of Sippy’s treatment regimen, and reported azotemia and increase in sodium bicarbonate in patients that had signs of toxemia (headaches, nausea, vomiting, dizziness, and distaste for milk).^[2]
• In 1936, Cope found hypercalcemia, hyperphosphatemia, azotemia, and increased bicarbonate in patients on alkali therapies for gastric ulcers.
• In 1949, Burnett described a syndrome with hypercalcemia without hypercalciuria or hypophosphatemia, renal insufficiency and calcinosis in patients consuming milk and alkali. The renal insufficiency did not resolve after the withdrawal of the milk and alkali therapy and most patients progressed to chronic renal disease.^[3]
• In 1963, Punsar and Somer classified milk-alkali syndrome into 2 categories:^[4]
  • Cope syndrome (acute)
  • Burnett syndrome (chronic)

• Histamine-2 blockers and proton pump inhibitors (PPIs) were introduced in in 1976 and 1989, respectively. This has led to a significant decrease in the ‘classic’ milk-alkali syndrome that mostly affected middle-aged men who consumed the ‘Sippy Powder’ for peptic ulcer disease.^[5][6][7]

• Since the 1990s, there has been an increase in the ‘modern’ milk-alkali syndrome due to an increase in calcium and vitamin D consumption in postmenopausal women for osteoporosis prevention.^[6][7][8]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shakiba Hassanzadeh, MD[2]

Milk-alkali syndrome may be classified as the following: acute (toxemic form), subacute (Cope’s syndrome), and chronic (Burnett’s syndrome).

In all types of milk-alkali syndrome there are increases in calcium, BUN, creatinine, and there are normal or increased phosphorus. Milk-alkali syndrome may be classified as the following:^[1]

• The acute or toxemic form occurs about one week after treatment with milk and alkali.
• They have symptoms of acute hypercalcemia such as:
  • Headache, dizziness
  • Lethargy
  • Nausea, vomiting
  • Anorexia  
  • Weakness
  • Mental changes such as psychosis

• Acute renal insufficiency

• Metabolic alkalosis
• Withdrawal of milk and alkali resolves the symptoms and renal function to normal, rapidly.

• Usually seen in patients that have taken milk and alkali intermittently for years.
• Patients have symptoms of both acute and chronic hypercalcemia and respond to medication withdrawal with gradual improvement. Renal function improves gradually but significantly.

• Patients have a long history of high milk and alkali consumption.
• They have symptoms of chronic hypercalcemia such as:
  • Occasional nausea, vomiting, anorexia and mental changes  
  • Asthenia  
  • Polyuria
  • Polydipsia
  • Pruritus
  • Myalgia
• Metastatic calcifications (band keratopathy and nephrocalcinosis)
• Laboratory abnormalities are similar to those in the acute syndrome, but the response to the withdrawal of milk and alkali is quite different.
• Myalgia and pruritus improves slowly as calcium level slowly normalizes.
• Calcium levels resolve to a normal level, gradually and some abnormal calcification decrease.
• There is usually minimal or no improvement in renal function, as many patients continue to have chronic renal failure.^[2][3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shakiba Hassanzadeh, MD[2]

The exact pathogenesis of milk-alkali syndrome is unknown. Hypercalcemia in milk-alkali syndrome involves several mechanisms including: intestinal absorption of calcium is increased, bone buffering of calcium becomes saturated, and renal excretion of calcium is decreased. Several factors that increase bicarbonate reabsorption and contribute to the alkalosis in milk-alkali syndrome include: volume depletion due to increased sodium and free water excretion caused by increased calcium intake, suppression of PTH, direct tubular effects of calcium and other factors that cause volume depletion or alkalosis such as vomiting or thiazide use.

• The exact pathogenesis of milk-alkali syndrome is unknown.
• Consumption of excessive amounts of calcium and absorbable alkali causes milk-alkali syndrome.^[1]

The pathogenesis of milk-alkali syndrome involves the kidneys, bones, and intestines.^[2]

• Hypercalcemia involves the following:^[3]
  • Intestinal absorption of calcium is increased.
  • Bone buffering of calcium becomes saturated.
  • Renal excretion of calcium is decreased.

• Intestines absorb the high quantities of consumed calcium and cause hypercalcemia.
• Bones have a limited capacity of calcium buffering and the variations in this capacity may contribute to hypercalcemia.
• Hypercalcemia causes vasoconstriction in the kidneys, which decreases glomerular filtration rate (GFR) and calcium excretion in the kidneys.^[3]
• Hypercalcemia activates calcium-sensing receptors (CaSRs) in different areas and the following effects happen:^[4]
  • Renal tubules
    • Thick ascending loop of Henle:
      • Reabsorption of sodium chloride is blocked, which leads to diuresis and an increase in calcium excretion in the kidneys. These, in turn, result in volume depletion and metabolic alkalosis.
    • Distal convoluted tubules (luminal membrane) :
      • Calcium reabsorption through transient receptor potential vanilloid member 5 (TRPV5) channels is increased.
    • Collecting duct (luminal membranes):
      • Expression of aquaporin 2 water channels is decreased, and that decreases water reabsorption and dilutes the urine.
• 25-hydroxylation of vitamin D in the kidneys is reduced by excessive calcium consumption, which decreases calcium absorption in the intestine.^[1]
• Hypercalcemia inhibits parathyroid hormone (PTH) which decreases bone turnover and the capacity of the bone for calcium buffering and increases the excretion of calcium in the kidneys.^[3]
• Hypercalcemia causes nausea and vomiting, which in turn deteriorate volume depletion and metabolic alkalosis.^[3]

• Increases the affinity of the CaSRs to calcium, which increases natriuresis.  
• Stimulates TRPV5 which increases calcium reabsorption and worsens hypercalcemia.^[5][4]
• Several factors that increase bicarbonate reabsorption and contribute to the alkalosis in milk-alkali syndrome include:^[6]
  • Volume depletion due to increased sodium and free water excretion caused by increased calcium intake
  • Suppression of PTH 
  • Direct tubular effects of calcium  
  • Other factors that cause volume depletion or alkalosis such as vomiting or thiazide use

• There is limited evidence on the renal histopathological findings of milk-alkali syndrome.^[1]
• The following findings on autopsies have been reported:^{[7][8][9][10]}
  • Nephrocalcinosis
  • Glomerulus hyalinization (partial to complete)
  • Thickened Bowman’s capsule
  • Atrophy of the tubules
  • Vascular changes
  • Diffuse lymphocytic infiltration

• The following findings on biopsies have been reported:^[11][12][13]
  • Focal calcification in the renal tubules
  • Degeneration of the tubular epithelium
  • Granular material (presumably calcium laden) in and around the collecting tubules
  • Hyalinization of some glomeruli
  • Thickened basement membrane

• It has been suggested that the prognosis of milk-alkali syndrome is associated with the severity of the histologic changes on the biopsies and that renal calcium deposition are usually not detectable on x-ray.^[13]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shakiba Hassanzadeh, MD[2]

Currently, the main cause of milk-alkali syndrome is calcium carbonate consumption, mostly in postmenopausal women for osteoporosis prevention or treatment or in patients on glucocorticoid therapy (for example in organ transplantation), and chronic renal disease.With the introduction of histamine antagonists and decrease in antacid consumption since the 1970s, the incidence of milk-alkali syndrome has decreased significantly. However, since the 1990s, there has been an increase in milk-alkali syndrome mostly due to increase in calcium and vitamin D consumption in postmenopausal women for osteoporosis prevention.

With the introduction of histamine antagonists and decrease in antacid consumption since the 1970s, the incidence of milk-alkali syndrome has decreased significantly. However, since the 1990s, there has been an increase in milk-alkali syndrome mostly due to increase in calcium and vitamin D consumption in postmenopausal women for osteoporosis prevention.^[1][2][3]

Currently, the main causes are:^[4]

• Calcium carbonate consumption in:
  • Postmenopausal women for osteoporosis prevention or treatment.
  • Patients on glucocorticoid therapy:
    • Organ transplantation
    • Autoimmune disorders
    • Inflammatory disorders
  • Chronic renal disease
• Betel nut chewers in the Far East (due to the lime paste (calcium oxide and calcium hydroxide) consumed during betel nut chewing).^[5]
• There have been reports of milk-alkali syndrome in pregnant women.^[6][7]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Milk-alkali syndrome must be differentiated from other causes of hypercalcemia.

Milk-alkali syndrome must be differentiated from other causes of hypercalcemia.^{[1][2][3][4][5][6][7]}

Differential diagnosis of milk-alkali syndrome on the basis of hypercalcemia
Disorder		Mechanism of hypercalcemia	Clinical features	Laboratory findings				Imaging & diagnostic modalities
				PTH	Calcium	Phosphate	Other findings
Hyperparathyroidism	Primary hyperparathyroidism	Increase in secretion of parathyroid hormone (PTH) from a primary process in parathyroid gland. Parathyroid hormone causes increase in serum calcium.	Usually asymptomatic Hypercalcemia detected on routine biochemical panel	↑	↑	↓/Normal	Normal/↑ calcitriol	Findings of bone resorption: X-ray Dual energy X-ray absorptiometry (DXA) Preoperative localization of hyperfunctioning parathyroid gland: Non-Invasive Tc-99m sestamibi scintigraphy Neck ultrasound 4D-CT SPECT(P-SPECT) PET MRI Invasive: Super sensitive venous sampling Selective arteriography Angiography Predicting post-operative success: Intraoperative parathyroid hormone monitoring
	Secondary hyperparathyroidism	Increase in secretion of parathyroid hormone (PTH) from a secondary process. Parathyroid hormone causes increase in serum calcium after long periods.	May present with history of: Chronic renal failure Vitamin D deficiency	↑	↓/Normal	↑	—
	Tertiary hyperparathyroidism	Continuous elevation of parathyroid hormone (PTH) even after successful treatment of the secondary cause of elevated parathyroid hormone. Parathyroid hormone causes increase in serum calcium.	Usually present with history of kidney transplant Usually hyperplasia of all four parathyroid glands	↑	↑	↑	—
Familial hypocalciuric hypercalcemia		This is a genetic disorder caused my mutation in calcium-sensing receptor gene.	A benign condition Does not require treatment	Normal/↑	Normal/↑	—	—	Urinary calcium/creatinine clearance ratio
Malignancy	Humoral hypercalcemia of malignancy	Tumor cells secretes parathyroid hormone-related protein (PTHrP) which has similar action as parathyroid hormone.	Most common cause of malignancy related hypercalcemia Usually present with solid tumors	—	↑	↓/Normal	↑ PTHrP Normal/↑ calcitriol	Chest X-ray CT scan MRI
	Osteolytic tumors	Multiple myeloma produces osteolysis of bones causing hypercalcemia. Osteolytic metasteses can cause bone resorption causing hypercalcemia.	Commonly present in multiple myeloma and breast cancer	↓	↑	—	—	DXA X-ray Mammography Ultrasound ESR Serum protein electrophoresis
	Production of calcitirol	Some tumors has ectopic activity of 1-alpha-hydroxylase leading to increased production of calcitriol. Calcitriol is active form of vitamin D and causes hypercalcemia.	Commonly present in lymphomas and in some ovarian germ cell tumors	—	↑	—	↑ Calcitriol	CT scan MRI
	Ectopic parathyroid hormone	Some tumors leads to ectopic production of parathyroid hormone.	In rare instances, small cell carcinoma of lung may produce hypercalcemia by this process	↑	↑	↓/Normal	Normal/↑ calcitriol	Chest X-ray CT scan MRI
Medication induced	Lithium	Lithium lowers urinary calcium and causes hypercalcemia. Lithium has been reported to cause an increase in parathyroid hormone and enlargement if parathyroid gland after weeks to months of therapy.	History of mood disorder	↑	↑	—	—	Lithium levels
	Thiazide diuretics	Thiazide diuretics lowers urinary calcium excretion and causes hypercalcemia.	History of cardiac disorder Rarely causes hypercalcemia	—	↑	—	—	—
Nutritional	Milk-alkali syndrome	Hypercalcemia is be caused by high intake of calcium carbonate.	History of High milk intake Excess calcium intake for treating: Osteoporosis Dyspepsia May lead to metabolic alkalosis and renal insufficiency.	—	↑	—	—	Renal function tests
	Vitamin D toxicity	Excess vitamin D causes increased absorption of calcium from intestine causing hypercalcemia.	History of: Excess intake vitamin D Excess milk fortified with vitamin D[8] Topical application of vitamin D analogue calcipotriol[9]	—	↑	—	↑ Vitamin D (calcidiol and/or calcitriol)	—
Granulomatous disease	Sarcoidosis	Hypercalcemia is causes by endogeous production of calcitriol by disease-activated macrophages.	History of: Cough Dyspnea Chest pain Tiredness or weakness Fever Weight loss	—	↑	—	↑ Calcitriol ↑ ACE levels	Chest X-ray Biopsy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shakiba Hassanzadeh, MD[2]

The exact incidence and prevalencef of milk-alkali syndrome is not known. With the introduction of histamine antagonists and decrease in antacid consumption since the 1970s, the incidence of milk-alkali syndrome has decreased significantly. However, since the 1990s, there has been an increase in milk-alkali syndrome due to an increase in calcium and vitamin D consumption in postmenopausal women for osteoporosis prevention. Milk-alkali syndrome is the third most common cause of hypercalcemia in hospitalized patients after primary hyperparathyroidism and malignancies.

• The exact incidence of milk-alkali syndrome is not known.^[1]

• With the introduction of histamine antagonists and decrease in antacid consumption since the 1970s, the incidence of milk-alkali syndrome has decreased significantly. However, since the 1990s, there has been an increase in milk-alkali syndrome due to increase in calcium and vitamin D consumption in postmenopausal women for osteoporosis prevention.^[2][3][4]

• The exact prevalence of milk-alkali syndrome is not known.

• Milk-alkali syndrome is the third most common cause of hypercalcemia in hospitalized patients after primary hyperparathyroidism and malignancies. ^[5]

• Currently, the ‘modern’ milk-alkali syndrome mostly affects postmenopausal women who consume calcium supplements for osteoporosis prevention. ^[6][2]

• The ‘classic’ milk-alkali syndrome mostly affected middle aged men who consumed the ‘Sippy Powder’ for peptic ulcer disease, and has disappeared with the introduction of histamine-2 blockers and proton pump inhibitors (PPIs) in 1976 and 1989, respectively.^[6][2][3]

• Currently, the ‘modern’ milk-alkali syndrome mostly affects postmenopausal women who consume calcium supplements for osteoporosis prevention.^[6][2]

• The ‘classic’ milk-alkali syndrome mostly affected middle aged men who consumed the ‘Sippy Powder’ for peptic ulcer disease, and has disappeared with the introduction of histamine-2 blockers and proton pump inhibitors (PPIs) in 1976 and 1989, respectively.^[6][2][3]

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shakiba Hassanzadeh, MD[2]

Patients with the following conditions are more susceptible to milk-alkali syndrome: Older age, preexisting chronic renal disease, concurrent vomiting (bulimia nervosa or hyperemesis gravidarum ) and use of certain drugs like thiazide, NSAIDs, and ACE inhibitors.

Patients with the following conditions are more susceptible to milk-alkali syndrome:^{[1][2][3][4][5][6][7]}

• Older age
• Preexisting chronic renal disease
• Concurrent vomiting:
  • Bulimia nervosa
  • yperemesis gravidarum

• Use of some drugs
  • Thiazide
  • NSAIDs
  • ACE inhibitors.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shakiba Hassanzadeh, MD[2]

There is insufficient evidence to recommend routine screening for milk-alkali syndrome.

There is insufficient evidence to recommend routine screening for milk-alkali syndrome.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shakiba Hassanzadeh, MD[2]

Most patients with milk-alkali syndrome are asymptomatic and may become incidentally diagnosed. Complications of milk-alkali syndrome may include: confusion, psychosis, renal insufficiency, pancreatitis, abnormalities in cardiac conduction, and metastatic calcification. Prognosis of milk-alkali syndrome is generally good and early diagnosis and treatment, with the withdrawal of the offending agent and supportive therapy, usually resolve the symptoms and abnormalities in milk-alkali syndrome (hypercalcemia, alkalosis and renal insufficiency).

Milk-alkalai syndrome and its features (hypercalcemia, alkalosis, and renal insufficiency) may be incidentally diagnosed since most patients are asymptomatic.^[1]

Complications of milk-alkali syndrome may include:^{[2][3][4][5][6][7]}

• Confusion
• Psychosis
• Variable degrees of renal insufficiency
• Pancreatitis
• Reversible abnormalities in cardiac conduction
• Tremor
• Metastatic calcification
  • Ocular calcification in the cornea (keratopathy) and in the conjunctiva (conjunctivitis)
  • Renal calcinosis
  • In less common sites such as central nervous system, lungs, liver, adrenal glands, bone, periarticular and subcutaneous tissue

• Prognosis of milk-alkali syndrome is generally good.^[1]
• Early diagnosis and treatment, with withdrawal of the offending agent and supportive therapy, usually resolve the symptoms and abnormalities in milk-alkali syndrome (hypercalcemia, alkalosis and renal insufficiency).^[5][4]

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