Chronic obstructive pulmonary disease and abdominal aortic aneurysms

Laarhoven, Cornelis J. H. M. van; Borstlap, A. C. W.; Henegouwen, D.P. van Berge; Palmen, F.M.L.H.G.; Verpalen, M. C. P. J.; Schoemaker, Marinus C.

doi:10.1016/s0950-821x(05)80254-3

Cited by 76 publications

(54 citation statements)

References 26 publications

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“…There might be differences between the sexes in susceptibility to disease in subjects with this polymorphism. It has also been demonstrated that patients with severe COPD have a significantly higher prevalence of aneurysms compared to mild or moderate COPD patients [14]. Therefore, this polymorphism might be conserved for both COPD and aneurysms.…”

Section: Discussionmentioning

confidence: 95%

Tissue inhibitor of metalloproteinases-2 gene polymorphisms in chronic obstructive pulmonary disease

Hirano¹,

Sakamoto²,

Uchida³

et al. 2001

European Respiratory Journal

106

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Proteinase/antiproteinase imbalance is the most widely accepted theory for development of chronic obstructive pulmonary disease (COPD). Mutations of tissue inhibitor of metalloproteinases-2 (TIMP-2) that downregulate its activity may increase the activities of matrix metalloproteinases and result in the degradation of the lung matrix.Polymorphisms of the TIMP-2 gene were investigated in 88 COPD patients and 40 control subjects. The variations were examined by single-strand conformational polymorphism analysis followed by sequencing.Two polymorphisms were identified,z853 G/A and -418 G/C nucleotide substitutions. There was a significant deviation in the genotypic frequencies at z853 and the allele frequencies for G were significantly higher in the COPD patient group than in the control group. For locus -418, the allele frequencies for C in the COPD patient group also tended to be higher than those in the control group. The z853 G/A nucleotide substitution was a silent variant. The -418 G/C substitution was located in the consensus sequence for the Sp1 binding site.These polymorphisms may be associated with the development of chronic obstructive pulmonary disease, decreasing the transcription and stability of the messenger ribonucleic acid, and available as genetic markers of susceptibility to the disease.

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Section: Discussionmentioning

confidence: 95%

Tissue inhibitor of metalloproteinases-2 gene polymorphisms in chronic obstructive pulmonary disease

Hirano¹,

Sakamoto²,

Uchida³

et al. 2001

European Respiratory Journal

106

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show abstract

“…17 The etiology of these, albeit multifactorial, is thought to represent a defect in collagen and elastin metabolism. Patients with emphysema have a higher incidence of AAA than the healthy population 18 and are at greater risk of AAA rupture. 19 Histopathology of both diseases confirms decreased elastin concentration in the aortic and lung tissue.…”

mentioning

confidence: 99%

Evidence from cross-sectional imaging indicates abdominal but not thoracic aortic aneurysms are local manifestations of a systemic dilating diathesis

Nordon

Brar

Taylor

et al. 2009

Journal of Vascular Surgery

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A clear understanding of the pathophysiology of aortic aneurysms is essential. Observational studies have raised the suspicion that abdominal aortic aneurysms are a local representation of a systemic disease of the vasculature. Whether aneurysms of the thoracic aorta have a similar systemic tendency is unknown. Validation of this will open broader avenues of research clarifying understanding of the initiating factors of aneurysms and whether all aneurysms distributed through the arterial tree share the same etiology. This may in turn identify systemic treatments that eventually may allow targeted pharmaceutical management of small aortic aneurysms.

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“…Major risk factors for the AAA development include an age of >65 years, smoking, HT, and a presence of a vascular disease [1][2][3]. In recent years, COPD has been accepted to be a predisposing factor for AAA development [4,[6][7][8].…”

Section: Discussionmentioning

confidence: 99%

“…They suggested that COPD was more frequent in patients with a ruptured aneurysm. Van Laarhoven et al [7] examined 362 COPD patients aged >65 years and reported a higher AAA prevalence, with a rate of 9.9%. AAA prevalence was statistically higher in more severe COPD patients (FEV 1 <55%) than in milder COPD patients.…”

Section: Discussionmentioning

confidence: 99%

“…Recent epidemiological studies have shown that considerable chronic comorbidities, mainly cardiovascular diseases, contributed to COPD [4,5]. Although several studies suggest that COPD is associated with AAA development and engenders an additional risk factor for AAA rupture when smaller aneurysms are present, the literature regarding a potential association between the presence of COPD and AAA remains limited [4,[6][7][8]. Furthermore, there is no prevalence study that reflects an epidemiological status of Turkey.…”

Section: Introductionmentioning

confidence: 99%

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What are the Prevalence of Abdominal Aortic Aneurysm in Patients with Chronic Obstructive Pulmonary Diseases and the Characteristics of These Patients?

et al. 2017

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Objective: To determine the prevalence of abdominal aortic aneurysm (AAA) in patients with chronic obstructive pulmonary disease (COPD) and to assess the characteristics of these patients.Materials and Methods: Stable COPD patients (age, >40 years) were included in the study between January 2014 and June 2014. Patients with acute exacerbations and a previous lung resection were excluded. Data regarding demographic characteristics were recorded. The modified Medical Research Council (mMRC) dyspnea scale was used to assess the severity of breathlessness. The COPD Assessment Test (CAT) was performed. Abdominal aortic diameter was measured using abdominal ultrasonography (AUS), and AAA was diagnosed as an aortic diameter of ≥30 mm at the renal artery level.Results: In total, 82 patients were examined. AAA was detected in five (6.1%) patients. Diabetes mellitus, hypertension, and coronary artery disease were present in four patients with AAA. The average mMRC score was 3.2±0.4, and the mean CAT score was 18.4±6.0. Aneurysmal diameter was >50 mm in four patients and 37 mm in one patient. Statistically significant differences were found between patient with AAA and those without AAA with respect to the mean abdominal aortic diameters at the renal artery and iliac artery levels (p=0.012 and 0.002, respectively). Conclusion:Our findings suggest that AAA is associated with COPD, with a prevalence rate of 6.1%. AAA is usually asymptomatic until a clinical status of rupture, which is associated with a higher mortality risk. Early diagnosis of AAA is lifesaving. In COPD patients, AAA might be easily determined using AUS, which is a noninvasive and relatively cheap procedure. Sonuç: Çalışmamızda KOAH hastalarında AAA prevelansı %6,1 bulunmuş olup AAA ile KOAH hastalığının ilişkili olabileceğini düşündürmektedir. AAA yüksek mortalite riski taşıyan ve rüptür gelişimine kadar genellikle asemptomatik seyreden bir hastalıktır. Erken tanı hayat kurtarıcıdır. KOAH hastalarında AAA tanısı non invaziv ve nisbeten ucuz bir yöntem olan AUS ile kolaylıkla konulabilir.

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Chronic obstructive pulmonary disease and abdominal aortic aneurysms

Cited by 76 publications

References 26 publications

Tissue inhibitor of metalloproteinases-2 gene polymorphisms in chronic obstructive pulmonary disease

Tissue inhibitor of metalloproteinases-2 gene polymorphisms in chronic obstructive pulmonary disease

Evidence from cross-sectional imaging indicates abdominal but not thoracic aortic aneurysms are local manifestations of a systemic dilating diathesis

What are the Prevalence of Abdominal Aortic Aneurysm in Patients with Chronic Obstructive Pulmonary Diseases and the Characteristics of These Patients?

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