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{{Milk-alkali syndrome}} | {{Milk-alkali syndrome}} | ||
{{CMG}} | {{CMG}} {{AE}} {{SHA}} | ||
== Historical Perspective == | == Historical Perspective == | ||
===Eponym=== | ===Eponym=== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shakiba Hassanzadeh, MD[2]
Historical Perspective
Eponym
It is named for Charles Hoyt Burnett.[1][2]
Discovery
- There is limited information about the historical perspective of milk-alkali syndrome.
- In 1915, Sippy designed an antacid regimen to neutralize gastric acidity and promote the healing of peptic ulcer disease.
- The regimen included the hourly administration of milk or cream with Sippy powders (a powder containing 600 mg of magnesium carbonate and 600 mg sodium bicarbonate alternating with a powder containing 600 mg of bismuth subcarbonate and 1200 to 1800 mg of sodium bicarbonate)
- Toxic reactions associated with alkalosis and renal insufficiency were noted shortly thereafter, but the plasma calcium concentration was not measured.
- In 1936, a report associated hypercalcemia with the alkalosis and renal failure in patients treated with the Sippy regime.[3]
Overview
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. was 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.
Historical Perspective
- 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).[4]
- 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).[5]
- 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.[6]
- In 1963, Punsar and Somer classified milk-alkali syndrome into 2 categories:[7]
- 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.[8][9][10]
- 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.[9][10][11]
References
- ↑ Template:WhoNamedIt
- ↑ Burnett CH, Commons RR, Albright F, Howard JE (1949). "Hypercalcemia without hypercalcuria or hypophosphatemia, calcinosis and renal insufficiency; a syndrome following prolonged intake of milk and alkali". N. Engl. J. Med. 240 (20): 787–94. PMID 18126919.
- ↑ Beall DP, Scofield RH (March 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. PMID 7891547.
- ↑ Sippy BW (1983). "Landmark article May 15, 1915: Gastric and duodenal ulcer. Medical cure by an efficient removal of gastric juice corrosion. By Bertram W. Sippy". JAMA. 250 (16): 2192–7. doi:10.1001/jama.250.16.2192. PMID 6352976.
- ↑ HARDT, LEO L. (1923-02-01). "TOXIC MANIFESTATIONS FOLLOWING THE ALKALINE TREATMENT OF PEPTIC ULCER". Archives of Internal Medicine. American Medical Association (AMA). 31 (2): 171. doi:10.1001/archinte.1923.00110140023003. ISSN 0003-9926.
- ↑ BURNETT CH, COMMONS RR (1949). "Hypercalcemia without hypercalcuria or hypophosphatemia, calcinosis and renal insufficiency; a syndrome following prolonged intake of milk and alkali". N Engl J Med. 240 (20): 787–94. doi:10.1056/NEJM194905192402001. PMID 18126919.
- ↑ PUNSAR S, SOMER T (1963). "The milk-alkali syndrome. A report of three illustrative cases and a review of the literature". Acta Med Scand. 173: 435–49. PMID 13972538.
- ↑ 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.
- ↑ 9.0 9.1 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.
- ↑ 10.0 10.1 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.