Milk-alkali syndrome epidemiology and demographics
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shakiba Hassanzadeh, MD[2]
Overview
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.
Epidemiology and Demographics
Incidence
- 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]
Prevalence
- 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]
Age
- 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]
Gender
- 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]
References
- ↑ Patel AM, Adeseun GA, Goldfarb S (2013). “Calcium-alkali syndrome in the modern era”. Nutrients. 5 (12): 4880–93. doi:10.3390/nu5124880. PMC 3875933. PMID 24288027.
- ↑ 2.0 2.1 2.2 2.3 2.4 Medarov BI (2009). “Milk-alkali syndrome”. Mayo Clin Proc. 84 (3): 261–7. doi:10.1016/S0025-6196(11)61144-0. PMC 2664604. PMID 19252114.
- ↑ 3.0 3.1 3.2 Arroyo M, Fenves AZ, Emmett M (2013). “The calcium-alkali syndrome”. Proc (Bayl Univ Med Cent). 26 (2): 179–81. doi:10.1080/08998280.2013.11928954. PMC 3603742. PMID 23543983.
- ↑ Felsenfeld AJ, Levine BS (2006). “Milk alkali syndrome and the dynamics of calcium homeostasis”. Clin J Am Soc Nephrol. 1 (4): 641–54. doi:10.2215/CJN.01451005. PMID 17699269.
- ↑ Beall DP, Scofield RH (1995). “Milk-alkali syndrome associated with calcium carbonate consumption. Report of 7 patients with parathyroid hormone levels and an estimate of prevalence among patients hospitalized with hypercalcemia”. Medicine (Baltimore). 74 (2): 89–96. doi:10.1097/00005792-199503000-00004. PMID 7891547.
- ↑ 6.0 6.1 6.2 6.3 Beall DP, Henslee HB, Webb HR, Scofield RH (2006). “Milk-alkali syndrome: a historical review and description of the modern version of the syndrome”. Am J Med Sci. 331 (5): 233–42. doi:10.1097/00000441-200605000-00001. PMID 16702792.
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