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» Home » CAD » Endocrinology » Parathyroid Gland » Milk-Alkali Syndrome
Background
Milk-Alkali Syndrome is a state of hypercalcemia (elevated calcium levels), acute kidney injury, and metabolic acidosis, which usually results from consuming an inappropriate amount of milk and absorbable alkali.
This syndrome has acute-onset, gradually develops into hypercalcemia and progresses further into metastatic calcification and acute renal failure if untreated.
Epidemiology
The most prevalent cause of hypercalcemia is a milk-alkali syndrome. According to a study of patients with hypercalcemia, this syndrome is the third most common cause of malignancy and hyperparathyroidism, contributing to around 12% of cases.
The frequency depends upon the intake of calcium carbonate. The incidence has been reported more in Asian countries because of betel nut consumption. The milk-alkali syndrome is more common in postmenopausal women as there is increased calcium carbonate intake.
Anatomy
Pathophysiology
Increased calcium absorption from small intestine, is significantly regulated by calcitriol, and increased vitamin D intake contributes to the progression or exacerbation of this disorder. Hypovolemia occurs as a result of hypercalcemia effect on the kidney.
The glomerular filtration rate is decreased due to vasoconstriction, natriuresis, and a progressive suppression of the Na-K-2Cl of the medullary thick ascending limb of the nephron.
It reduces water reabsorption by suppressing the antidiuretic hormone receptors on the basolateral membrane of the kidney’s tubules. Hypovolemia increases bicarbonate reabsorption and gradually develops alkalosis. Alkalosis is caused by increased consumption of alkali, reduced glomerular filtration rate (GFR), and hypovolemic-mediated hypocalcemia.
Etiology
Calcium supplements are often prescribed to prevent onset of secondary hyperparathyroidism in patients with chronic renal disease and individuals undergoing treatment that causes bone loss, such as prolonged systemic corticosteroids. Bicarbonate consumption is not considered to be the primary cause.
The major causes of this condition also include the easy availability of over-the-counter preparations of calcium carbonate and increased use in treating patients with dyspepsia and osteoporosis.
Several incidences of this condition have been observed in pregnancy. During pregnancy, women have elevated levels of parathyroid hormone-related peptides and increased gastrointestinal calcium absorption. Calcium carbonate is often used in reflux disorders in pregnancy.
A rare cause is the consumption of significant volumes of substitutes for nicotine products, which supply a substantial amount of calcium. The syndrome is also associated with individuals in Southeast Asia who consume betel nuts. Calcium carbonate is abundant in the paste blended with the nut’s meat.
Genetics
Prognostic Factors
The prognosis of the milk-alkali syndrome is fair since the condition is reversed by inhibiting calcium carbonate alkali consumption.
The morbidity is associated with the severity and duration of alkalosis and hypercalcemia. If detected and treated early, the prognosis of this condition is good.
Clinical History
Physical Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
Medication
Future Trends
References
https://www.ncbi.nlm.nih.gov/books/NBK557500/
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» Home » CAD » Endocrinology » Parathyroid Gland » Milk-Alkali Syndrome
Milk-Alkali Syndrome is a state of hypercalcemia (elevated calcium levels), acute kidney injury, and metabolic acidosis, which usually results from consuming an inappropriate amount of milk and absorbable alkali.
This syndrome has acute-onset, gradually develops into hypercalcemia and progresses further into metastatic calcification and acute renal failure if untreated.
The most prevalent cause of hypercalcemia is a milk-alkali syndrome. According to a study of patients with hypercalcemia, this syndrome is the third most common cause of malignancy and hyperparathyroidism, contributing to around 12% of cases.
The frequency depends upon the intake of calcium carbonate. The incidence has been reported more in Asian countries because of betel nut consumption. The milk-alkali syndrome is more common in postmenopausal women as there is increased calcium carbonate intake.
Increased calcium absorption from small intestine, is significantly regulated by calcitriol, and increased vitamin D intake contributes to the progression or exacerbation of this disorder. Hypovolemia occurs as a result of hypercalcemia effect on the kidney.
The glomerular filtration rate is decreased due to vasoconstriction, natriuresis, and a progressive suppression of the Na-K-2Cl of the medullary thick ascending limb of the nephron.
It reduces water reabsorption by suppressing the antidiuretic hormone receptors on the basolateral membrane of the kidney’s tubules. Hypovolemia increases bicarbonate reabsorption and gradually develops alkalosis. Alkalosis is caused by increased consumption of alkali, reduced glomerular filtration rate (GFR), and hypovolemic-mediated hypocalcemia.
Calcium supplements are often prescribed to prevent onset of secondary hyperparathyroidism in patients with chronic renal disease and individuals undergoing treatment that causes bone loss, such as prolonged systemic corticosteroids. Bicarbonate consumption is not considered to be the primary cause.
The major causes of this condition also include the easy availability of over-the-counter preparations of calcium carbonate and increased use in treating patients with dyspepsia and osteoporosis.
Several incidences of this condition have been observed in pregnancy. During pregnancy, women have elevated levels of parathyroid hormone-related peptides and increased gastrointestinal calcium absorption. Calcium carbonate is often used in reflux disorders in pregnancy.
A rare cause is the consumption of significant volumes of substitutes for nicotine products, which supply a substantial amount of calcium. The syndrome is also associated with individuals in Southeast Asia who consume betel nuts. Calcium carbonate is abundant in the paste blended with the nut’s meat.
The prognosis of the milk-alkali syndrome is fair since the condition is reversed by inhibiting calcium carbonate alkali consumption.
The morbidity is associated with the severity and duration of alkalosis and hypercalcemia. If detected and treated early, the prognosis of this condition is good.
https://www.ncbi.nlm.nih.gov/books/NBK557500/
Milk-Alkali Syndrome is a state of hypercalcemia (elevated calcium levels), acute kidney injury, and metabolic acidosis, which usually results from consuming an inappropriate amount of milk and absorbable alkali.
This syndrome has acute-onset, gradually develops into hypercalcemia and progresses further into metastatic calcification and acute renal failure if untreated.
The most prevalent cause of hypercalcemia is a milk-alkali syndrome. According to a study of patients with hypercalcemia, this syndrome is the third most common cause of malignancy and hyperparathyroidism, contributing to around 12% of cases.
The frequency depends upon the intake of calcium carbonate. The incidence has been reported more in Asian countries because of betel nut consumption. The milk-alkali syndrome is more common in postmenopausal women as there is increased calcium carbonate intake.
Increased calcium absorption from small intestine, is significantly regulated by calcitriol, and increased vitamin D intake contributes to the progression or exacerbation of this disorder. Hypovolemia occurs as a result of hypercalcemia effect on the kidney.
The glomerular filtration rate is decreased due to vasoconstriction, natriuresis, and a progressive suppression of the Na-K-2Cl of the medullary thick ascending limb of the nephron.
It reduces water reabsorption by suppressing the antidiuretic hormone receptors on the basolateral membrane of the kidney’s tubules. Hypovolemia increases bicarbonate reabsorption and gradually develops alkalosis. Alkalosis is caused by increased consumption of alkali, reduced glomerular filtration rate (GFR), and hypovolemic-mediated hypocalcemia.
Calcium supplements are often prescribed to prevent onset of secondary hyperparathyroidism in patients with chronic renal disease and individuals undergoing treatment that causes bone loss, such as prolonged systemic corticosteroids. Bicarbonate consumption is not considered to be the primary cause.
The major causes of this condition also include the easy availability of over-the-counter preparations of calcium carbonate and increased use in treating patients with dyspepsia and osteoporosis.
Several incidences of this condition have been observed in pregnancy. During pregnancy, women have elevated levels of parathyroid hormone-related peptides and increased gastrointestinal calcium absorption. Calcium carbonate is often used in reflux disorders in pregnancy.
A rare cause is the consumption of significant volumes of substitutes for nicotine products, which supply a substantial amount of calcium. The syndrome is also associated with individuals in Southeast Asia who consume betel nuts. Calcium carbonate is abundant in the paste blended with the nut’s meat.
The prognosis of the milk-alkali syndrome is fair since the condition is reversed by inhibiting calcium carbonate alkali consumption.
The morbidity is associated with the severity and duration of alkalosis and hypercalcemia. If detected and treated early, the prognosis of this condition is good.
https://www.ncbi.nlm.nih.gov/books/NBK557500/
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