Anesthetic management in MAO-A and MAO-B deficiency: a case report
Author:
Publisher
Springer Science and Business Media LLC
Subject
Anesthesiology and Pain Medicine
Link
https://link.springer.com/content/pdf/10.1007/s00540-020-02808-5.pdf
Reference11 articles.
1. Whibley A, Urquhart J, Dore J, Willatt L, Parkin G, Gaunt L, Black G, Donnai D, Raymond FL. Deletion of MAOA and MAOB in a male patient causes severe developmental delay, intermittent hypotonia and stereotypical hand movements. Eur J Hum Genet. 2010;18(10):1095–9.
2. Saito M, Yamagata T, Matsumoto A, Shiba Y, Nagashima M, Taniguchi S, Jimbo E, Momoi MY. MAOA/B deletion syndrome in male siblings with severe developmental delay and sudden loss of muscle tonus. Brain Dev. 2014;36(1):64–9.
3. Collins FA, Murphy DL, Reiss AL, Sims KB, Lewis JG, Freund L, Karoum F, Zhu D, Maumenee IH, Antonarakis SE. Clinical, biochemical, and neuropsychiatric evaluation of a patient with a contiguous gene syndrome due to a microdeletion Xp113 including the Norrie disease locus and monoamine oxidase (MAOA and MAOB) genes. Am J Med Genet. 1992;42(1):127–34.
4. Lenders JW, Eisenhofer G, Abeling NG, Berger W, Murphy DL, Konings CH, Wagemakers LM, Kopin IJ, Karoum F, van Gennip AH, Brunner HG. Specific genetic deficiencies of the A and B isoenzymes of monoamine oxidase are characterized by distinct neurochemical and clinical phenotypes. J Clin Invest. 1996;97(4):1010–9.
5. Hayashi Y, Sumikawa K, Tashiro C, Yamatodani A, Yoshiya I. Arrhythmogenic threshold of epinephrine during sevoflurane, enflurane, and isoflurane anesthesia in dogs. Anesthesiology. 1988;69(1):145–7.
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