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      Comorbidity Associations with AATD Among Commercially Insured and Medicare Beneficiaries with COPD in the US

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          Abstract

          Introduction

          Alpha-1 antitrypsin deficiency (AATD) is often not identified in patients with chronic obstructive pulmonary disease (COPD) until advanced stages of disease, despite the availability of genetic testing. While clinical practice guidelines provide recommendations on patients who should be tested, more refined algorithms are needed to identify COPD patients who are likely candidates for AATD testing and to prevent delays in diagnosis and treatment. The objective of this study was to identify comorbid associations with AATD among patients diagnosed with COPD in the United States.

          Methods

          Using data from the 2012–2017 PharMetrics Plus Administrative Claims Database and 2011–2014 Medicare Fee for Service 5% Sample, patients with COPD (ICD-9-CM: 491.xx, 492.xx, or 496, ICD-10-CM J41, J42, J43, J44) and AATD (ICD-9-CM: 273.4, ICD-10-CM: E88.01) were identified. Patient demographic and diagnostic characteristics were assessed. Logistic regression models were developed to identify significant predictors of AATD.

          Results

          A cohort of 344,528 Medicare beneficiaries with COPD (of which 302 (0.09%) also had two diagnoses of AATD) and a cohort of 340,259 commercially insured patients with COPD (of which 1076 (0.3%) also had a diagnosis of AATD) were constructed. Associations with AATD identified in both models included ICD-9-CM and ICD-10-CM codes for chronic pulmonary heart disease, chronic liver disease and cirrhosis, and liver transplant.

          Discussion

          Significant associations with a diagnosis of AATD among patients with COPD were consistently represented in each of the datasets evaluated, which suggests meaningful comorbidity implications in AATD patients. These findings reinforce the need to test individuals with COPD for AATD as early as possible to help reduce the development of associated comorbid conditions.

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          Most cited references 44

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          Alpha1-antitrypsin deficiency.

          Alpha1-antitrypsin deficiency is a genetic disorder that affects about one in 2000-5000 individuals. It is clinically characterised by liver disease and early-onset emphysema. Although alpha1 antitrypsin is mainly produced in the liver, its main function is to protect the lung against proteolytic damage from neutrophil elastase. The most frequent mutation that causes severe alpha1-antitrypsin deficiency arises in the SERPINA 1 gene and gives rise to the Z allele. This mutation reduces concentrations in serum of alpha1 antitrypsin by retaining polymerised molecules within hepatocytes: an amount below the serum protective threshold of 11 micromol/L increases risk for emphysema. In addition to the usual treatments for emphysema, infusion of purified alpha1 antitrypsin from pooled human plasma represents a specific treatment and raises the concentrations in serum and epithelial-lining fluid above the protective threshold. Evidence suggests that this approach is safe, slows the decline of lung function, could reduce infection rates, and might enhance survival. However, uncertainty about the cost-effectiveness of this expensive treatment remains.
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            Liver disease in alpha1-antitrypsin deficiency detected by screening of 200,000 infants.

             T Sveger (1976)
            We prosepctively studied 200,000 newborns to determine the frequency and clinical characteristics of alpha1-antitrypsin deficiency. One hundred and twenty Pi Z, 48 Pi SZ, two PI Z-and one Pi S-infants were identified and followed to the age of six months. Fourteen of 120 Pi Z infants had prolonged obstructive jaundice, nine with severe clinical and laboratory evidence of liver disease. Five had only laboratory evidence of liver disease. Eight other Pi Z infants had minimal abnormalities in serum bilirubin and hepatic enzyme activity and variable hepatosplenomegaly. All 22 Pi Z infants with hepatic abnormalities, two thirds of whom were made, appeared healthy at six months of age. Ninety-eight Pi Z infants did not have clinical liver disease, but liver-function tests gave abnormal results in 44 of 84 at three months, and in 36 of 60 at six months of age. The number of small-for-gestational-age infants was greater (P less than 0.001) among those with clinical liver disease. None of the 48 Pi SZ infants had clinical liver disease, but 10 of 42 at three months and one of 22 at six months of age had abnormal liver function. The Pi Z and Pi SZ phenotypes are associated with covert or readily apparent hepatic dysfunction in the first three months of life.
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              Risk of cirrhosis and primary liver cancer in alpha 1-antitrypsin deficiency.

              Previous reports have suggested an association between homozygous alpha 1-antitrypsin deficiency, cirrhosis, and primary liver cancer. To assess the risk of these complications we conducted a retrospective study based on 17 autopsied cases of alpha 1-antitrypsin deficiency identified during the period 1963 to 1982 in the city of Malmö, Sweden. During the study period, autopsies were performed in 38,250, or 68.2 percent, of all patients in the city who died. From the homozygote frequency in the population, 21 of these were expected to have alpha 1-antitrypsin deficiency. The disease had been diagnosed in 20, and autopsies had been performed in 17 (1 child and 16 adults). Each autopsied case was matched with four controls selected from the same autopsy register, and the Mantel-Haenszel odds ratio (ORmh) was calculated. The results indicated a strong relation between alpha 1-antitrypsin deficiency and cirrhosis (ORmh = 7.8; 95 percent confidence limits, 2.4 to 24.7) and primary liver cancer (ORmh = 20; 95 percent confidence limits, 3.5 to 114.3). When data were stratified according to sex, these associations were statistically significant only for male patients. We conclude that men with alpha 1-antitrypsin deficiency may be at higher risk for cirrhosis and primary liver cancer. The apparent male predominance suggests the additive effects of exogenous factors.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                copd
                copd
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove
                1176-9106
                1178-2005
                05 October 2020
                2020
                : 15
                : 2389-2397
                Affiliations
                [1 ]Division of Pulmonary, Critical Care and Sleep Medicine, National Jewish Health , Denver, CO, USA
                [2 ]Department of Pulmonary and Critical Care Medicine, Medical University of South Carolina , Charleston, SC, USA
                [3 ]Global Health Economics & Outcomes Research, Grifols Shared Services of North America, Inc , Research Triangle Park, NC, USA
                [4 ]Department of Public Health Sciences, College of Health and Human Services, University of North Carolina at Charlotte , Charlotte, NC, USA
                [5 ]Department of Kinesiology, College of Health and Human Services, University of North Carolina at Charlotte , Charlotte, NC, USA
                Author notes
                Correspondence: Glenda Stone Global Health Economics & Outcomes Research, Grifols Shared Services of North America, Inc , 79 T.W. Alexander Dr, 4101 Research Commons, Research Triangle Park, NC27709, USATel +1 (919)316-6415 Email glenda.stone@grifols.com
                Article
                263297
                10.2147/COPD.S263297
                7547287
                © 2020 Sandhaus et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Figures: 1, Tables: 7, References: 46, Pages: 9
                Categories
                Original Research

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