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Alpha-1 antitrypsin deficiency (A1AD or AATD) is a genetic disorder that may result in lung disease or liver disease. [1] Onset of lung problems is typically between 20 and 50 years of age. [ 1 ] This may result in shortness of breath , wheezing , or an increased risk of lung infections .
Alpha-1 antitrypsin or α 1-antitrypsin (A1AT, α 1 AT, A1A, or AAT) is a protein belonging to the serpin superfamily. It is encoded in humans by the SERPINA1 gene.A protease inhibitor, it is also known as alpha 1 –proteinase inhibitor (A1PI) or alpha 1-antiproteinase (A1AP) because it inhibits various proteases (not just trypsin). [5]
About Alpha-1 Antitrypsin (AAT) and AAT Deficiency Alpha-1 antitrypsin deficiency is an autosomal disorder that results in disease of the lungs and liver, and afflicts roughly 10,000 patients ...
In medicine, protease inhibitor is often used interchangeably with alpha 1-antitrypsin (A1AT, which is abbreviated PI for this reason). [3] A1AT is indeed the protease inhibitor most often involved in disease, namely in alpha-1 antitrypsin deficiency.
John W. Walsh (February 4, 1949 – March 7, 2017) was an American non-profit leader and patient advocate.After being diagnosed with alpha-1 antitrypsin deficiency, he co-founded the Alpha-1 Foundation and AlphaNet, both of which serve people diagnosed with that condition, and the COPD Foundation, which serves people with chronic obstructive pulmonary disease.
The alpha-1 fraction does not disappear in alpha 1-antitrypsin deficiency, however, because other proteins, including alpha-lipoprotein and orosomucoid, also migrate there. As a positive acute phase reactant, AAT is increased in acute inflammation. [citation needed] Bence Jones protein may bind to and retard the alpha-1 band. [citation needed]
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