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1.
J Vasc Surg Venous Lymphat Disord ; 12(1): 101661, 2024 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-37572778

RESUMO

OBJECTIVE: The aim of this study was to investigate the prevalence of radiological left common iliac vein (LCIV) compression among the asymptomatic population and identify possible predictors. METHODS: Contrast-enhanced abdominal and/or pelvic computed tomography scans of eligible asymptomatic patients were examined. The LCIV diameter was measured from different horizontal planes in the venous phase using PACSView. Degree of LCIV compression (Dc) was calculated by a predefined formula and graded as insignificant (Dc < 25%), mild (≥25% Dc < 50%), moderate (≥50% Dc <75%), and severe (Dc ≥ 75%). Venous stenosis was defined as a Dc of ≥50%. Comparison of variables, including gender, age, body mass index (BMI), and comorbidities was performed between the different grades of LCIV compression. RESULTS: Between November 2019 and July 2022, 1698 eligible asymptomatic patients (53.1% females; mean age, 39.3 ± 11.8 years; mean BMI, 22.9 ± 3.6 kg/m2) were reviewed. The mean Dc was 46.2% (range, 0.29%-90.4%). Insignificant, mild, moderate, and severe compression were distributed in 14.5%, 38.0%, 42.2%, and 5.2% of the cohort population, respectively. Prevalence of venous stenosis was higher in females than males (58.1% vs 42.2%; χ2 = 15.52; P < .001). Females aged ≥25 and <35 years accounted for the highest proportion of venous stenosis than other age groups and was a significant predictor (odds ratio [OR], 3.18; 95% confidence interval [CI], 1.74-7.79; P < .001). In the Asian BMI classification group, being underweight is associated with venous stenosis (OR, 4.69; 95% CI, 2.70-8.14; P < .001) and obesity may be a protective factor (OR, 0.38; 95% CI, 0.23-0.64; P < .001). There is an inverse relationship between Dc and age and BMI. CONCLUSIONS: The prevalence of radiological LCIV compression on computed tomography scans was high, but all patients were asymptomatic. Female gender, especially those aged ≥25 and <35 years, and underweight were possible predictors for venous stenosis.


Assuntos
Síndrome de May-Thurner , Doenças Vasculares , Masculino , Humanos , Feminino , Adulto , Pessoa de Meia-Idade , Veia Ilíaca/diagnóstico por imagem , Constrição Patológica/epidemiologia , Prevalência , Magreza , Síndrome de May-Thurner/diagnóstico por imagem , Síndrome de May-Thurner/epidemiologia , Estudos Retrospectivos
2.
World J Clin Cases ; 8(6): 1180-1187, 2020 Mar 26.
Artigo em Inglês | MEDLINE | ID: mdl-32258090

RESUMO

BACKGROUND: Giant paraesophageal hiatal hernias (HH) are very infrequent, and their spectrum of clinical manifestations is large. Giant HH mainly occurs in elderly patients, and its relationship with anemia has been reported. For the surgical treatment of large HH, Nissen fundoplication is the most common antireflux procedure, and the reinforcement of HH repair with a patch (either synthetic or biologic) is still debatable. CASE SUMMARY: We report on a case of giant paraesophageal HH in a middle-aged male patient with reflux symptoms and severe anemia. After performing a series of tests and diagnostic approaches, results showed a complete intrathoracic stomach associated with severe iron deficiency anemia. The patient underwent successful laparoscopic hernia repair with mesh reinforcement and Nissen fundoplication. Postoperatively, reflux symptoms were markedly relieved, and the imaging study showed complete reduction of the hernia sac. More importantly, anemia was resolved, and hemoglobin, serum iron and ferritin level were returned to the normal range. The patient kept regular follow-up appointments and remained in a satisfactory condition. CONCLUSION: This case report highlights the relationship between large HH and iron deficiency anemia. For the surgical treatment of large HH, laparoscopic repair of large HH combined with antireflux procedure and mesh reinforcement is recommended.

3.
Exp Ther Med ; 18(2): 1375-1383, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31316626

RESUMO

Although the underlying mechanism of stress remains unknown, it has been associated with the pathophysiology of gastroesophageal reflux diseases, the development of which appear to be accelerated by oxidative stress and fibrosis. The aim of the current study was to investigate the effect of chronic restraint stress on esophageal oxidative stress and fibrosis, as well as the impact of oxidative stress in a murine model whereby 8-week old C57BL/6J male mice were subjected to intermittent chronic restraint stress for a two-week period. The current study demonstrated that chronic restraint stress significantly reduced the body weight of mice compared with the control group. Although chronic restraint stress did not significantly alter the levels of triglycerides or cholesterol, free fatty acid concentration was significantly increased compared with the control group. Furthermore, chronic restraint stress significantly upregulated the expression levels of several fibrotic biomarkers including collagen type I, transforming growth factor ß-1, α-smooth muscle actin and SMAD-3 compared with the control group. In addition, the expression levels of the reactive oxygen species (ROS) NADPH oxidase-4 and malondialdehyde were significantly increased, while the expression levels of nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 were significantly decreased in esophageal tissue from mice in the chronic restraint stress group compared with the control group. In conclusion, chronic restraint stress may induce esophageal fibrosis by accumulating ROS and increasing fibrotic gene expression in a murine model.

4.
Mol Med Rep ; 19(6): 5386-5396, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-31059059

RESUMO

Stress is a pivotal factor for inflammation, reactive oxygen species (ROS) production and formation of visceral hypersensitivity (VH) in the process of gastroesophageal reflux disease (GERD). In the present study, the effects of stress on esophageal inflammation, oxidative stress and VH were investigated in a chronic restraint stress mouse model. C57BL/6J male mice were subjected to 2 weeks of intermittent restraint stress, and histopathological analysis revealed that stress induced esophageal inflammation and fibrosis, while no distinct changes were detected in non­stressed control mice. In addition, increased NADPH oxidase 4 expression was observed in the plasma and esophagus of stressed mice, indicating accumulation of ROS. The expression levels of antioxidants, including Mn­superoxide dismutase (MnSOD), Cu/Zn­SOD, catalase and glutathione peroxidase, were also analyzed using reverse transcription­quantitative polymerase chain reaction (RT­qPCR). In addition, transient receptor potential vanilloid 1 (TRPV­1) and protease­activated receptor 2 (PAR­2), which are crucial receptors for VH, were measured by immunohistochemistry and RT­qPCR. The results demonstrated that stress markedly reduced antioxidant expression, while it significantly upregulated TRPV­1 and PAR­2 expression levels in the mouse esophagus. Finally, 2 weeks of restraint stress significantly increased the esophageal and plasma levels of inflammatory cytokines, including interleukin (IL)­6, IL­8, interferon­Î³ and tumor necrosis factor­α. Taken together, the present study results indicated that stress­induced esophageal inflammation and ROS generation involves VH.


Assuntos
Esôfago/patologia , Inflamação , Receptor PAR-2/metabolismo , Canais de Cátion TRPV/metabolismo , Animais , Catalase/genética , Catalase/metabolismo , Citocinas/sangue , Citocinas/genética , Citocinas/metabolismo , Modelos Animais de Doenças , Células Epiteliais/citologia , Células Epiteliais/metabolismo , Esôfago/citologia , Esôfago/metabolismo , Humanos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , NADPH Oxidase 4/genética , NADPH Oxidase 4/metabolismo , Interferência de RNA , RNA Interferente Pequeno/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Receptor PAR-2/genética , Estresse Fisiológico , Superóxido Dismutase/genética , Superóxido Dismutase/metabolismo , Canais de Cátion TRPV/antagonistas & inibidores , Canais de Cátion TRPV/genética , Regulação para Cima
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