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      Angiotensin-converting enzyme polymorphism affects outcome of local Chinese with acute lung injury


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          Acute Lung Injury (ALI) with genetic predisposition is fatal. Relationship between angiotensin-converting enzyme insertion/deletion (ACE I/D) polymorphism and the prognosis of local Chinese patients with ALI was investigated; meanwhile, the mechanisms involved were explored.


          101 ALI patients, 408 non-ALI patients and 236 healthy blood donors were enrolled. ACE I/D polymorphism was detected by polymerase chain reaction, then ACE genotype (II, ID, DD) and allele (I, D) frequencies were compared. Clinical data of ALI patients was calculated. Also, peripheral blood mononuclear cells (PBMC) were isolated from healthy volunteers with different ACE genotypes. Lipopolysaccharide (LPS)-induced ACE gene mRNA expression and ACE activity was measured.


          There was no significant difference in the frequencies of the genotypes and alleles. Acute Physiology and Chronic Health Evaluation (APACHE) II score was higher in DD subgroup than in II subgroup (19.7 ± 8.7 and 15.6 ± 6.2; P < 0.05). The 28-day mortality was significantly different (17.4%, 26.8%, and 64.3% for II, ID, and DD; P = 0.013). DD genotype was the independent prognostic factor for 28-day outcome. Furthermore, LPS-induced ACE mRNA expression and ACE activity from PBMC in DD genotype subgroup were both significantly higher than those in the other two subgroups.


          ACE I/D polymorphism is a prognostic factor for ALI. Patients with the DD genotype have higher mortality of ALI. Polymorphism influences the expression of ACE gene in LPS-stimulated PBMC, DD genotype leads to higher level of mRNA and enzyme activity. It may be one of the mechanisms involved.

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          ACE1 polymorphism and progression of SARS

          We have hypothesized that genetic predisposition influences the progression of SARS. Angiotensin converting enzyme (ACE1) insertion/deletion (I/D) polymorphism was previously reported to show association with the adult respiratory distress syndrome, which is also thought to play a key role in damaging the lung tissues in SARS cases. This time, the polymorphism was genotyped in 44 Vietnamese SARS cases, with 103 healthy controls who had had a contact with the SARS patients and 50 controls without any contact history. SARS cases were divided into either non-hypoxemic or hypoxemic groups. Despite the small sample size, the frequency of the D allele was significantly higher in the hypoxemic group than in the non-hypoxemic group (p = 0.013), whereas there was no significant difference between the SARS cases and controls, irrespective of a contact history. ACE1 might be one of the candidate genes that influence the progression of pneumonia in SARS.
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            Polymorphism of the angiotensin-converting enzyme gene affects the outcome of acute respiratory distress syndrome.

            There has been increasing evidence that angiotensin II may play an important role in the pathogenesis and in the evolution of acute lung injury. It was therefore hypothesized that polymorphisms of the angiotensin-converting enzyme gene affects the risk and outcome of acute respiratory distress syndrome (ARDS). Prospective, observational study. The ARDS group consisted of 101 patients treated at the medical intensive care unit; the control groups consisted of 138 "at-risk" patients treated at the medical intensive care unit due to acute respiratory failure but did not meet the ARDS criteria throughout the hospital course, and 210 non-at-risk subjects. None. The ARDS patients and control subjects were genotyped for the insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme gene. Association of the polymorphism and the risk and the outcome of ARDS was analyzed. There was no significant difference in the frequencies of the genotypes between the ARDS, at-risk, and non-at-risk groups. The 28-day mortality rates were significantly different between the three angiotensin-converting enzyme genotypes (42%, 65%, and 75% for II, ID, and DD, respectively; p = .036). Survival analysis showed that the II genotype favorably affected 28-day survival (hazard ratio, 0.46; 95% confidence interval, 0.26-0.81; p = .007), whereas ARDS caused by hospital-acquired pneumonia had a negative effect (hazard ratio, 2.34; 95% confidence interval, 1.25-4.40; p = .008). The II genotype (hazard ratio, 0.53; 95% confidence interval, 0.32-0.87; p = .012) and ARDS caused by hospital-acquired pneumonia (hazard ratio, 2.13; 95% confidence interval, 1.24-3.68; p = .006) were also significant prognostic factors for the in-hospital mortality. The angiotensin-converting enzyme I/D polymorphism is a significant prognostic factor for the outcome of ARDS. Patients with the II genotype have a significantly better chance of survival. This study did not show an increased risk for ARDS in Chinese patients with the D allele.
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              ACE I/D but not AGT (-6)A/G polymorphism is a risk factor for mortality in ARDS.

              The intrapulmonary renin-angiotensin system via tissue concentration of angiotensin II or bradykinin may have multiple effects on pulmonary pathophysiology. Therefore, it was investigated whether the presence of the D allele of the angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism or the A allele of angiotensinogen (AGT) promoter polymorphism (-6)A/G are independent risk factors for 30-day survival in acute respiratory distress syndrome (ARDS) patients. In a prospective study, adults (Germans of Caucasian ethnicity) with ARDS (n = 84) were recruited from the current authors' intensive care unit and genotyped for the ACE I/D and the AGT (-6)A/G polymorphisms, as were 200 healthy Caucasian controls. Mortality was increased in the ACE DD genotype compared with the I allele, and the ACE I/D polymorphism was an independent prognostic factor for 30-day survival. Patients with a homozygous DD genotype were at highest risk for death (hazard ratio 5.7; 95% confidence interval 1.7-19.2) compared with the II genotype. In contrast, the AGT (-6)A/G polymorphism was neither associated with an increased risk for development of ARDS nor with outcome. In patients with acute respiratory distress syndrome, the angiotensin-converting enzyme insertion/deletion polymorphism but not the angiotensinogen (-6)A/G promoter polymorphism is an independent risk factor with a pronounced effect on 30-day survival.

                Author and article information

                Respir Med
                Respir Med
                Respiratory Medicine
                Elsevier Ltd.
                13 July 2011
                October 2011
                13 July 2011
                : 105
                : 10
                : 1485-1490
                Department of Critical Care Medicine, Nanjing Zhong-Da Hospital, Southeast University School of Medicine, 87 Ding jia Qiao, Nanjing 210009, China
                Author notes
                []Corresponding author. Tel.: +86 2583272201. yiyiyang2004@ 123456yahoo.com.cn
                Copyright © 2011 Elsevier Ltd. All rights reserved.

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

                : 25 February 2011
                : 20 June 2011

                angiotensin-converting enzyme,polymorphism,acute lung injury,outcome


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