Journals / Turkish Journal of Gastroenterology / 2000 / Cilt: 11 - Sayı: 2

Dekompanse kronik karaciğer hastalığında nitrik oksit artışı

Increased endogenous nitric oxide in decompensated chronic liver disease

Pages
103–107
DOI
—
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Conclusions: These findings suggest that production of endogenous NO is increased in patients with cirrhosis, particularly in decompanseted patients.

📌 3 Key Takeaways

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Objective & Hypothesis:Background/Aims: Nitric oxide (NO) is reported to play a role in the pathogenesis of portal hypertension (PH).
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Key Findings & Data:NO is an extremely unstable molecule and rapidly degrades to nitrite ($NO_{2}$) and nitrate ($NO_{3}$ .
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Conclusion & Impact:Conclusions: These findings suggest that production of endogenous NO is increased in patients with cirrhosis, particularly in decompanseted patients.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Kronik hastalık · Nitrik oksit · Karaciğer hastalıkları

Abstract

Background/Aims: Nitric oxide (NO) is reported to play a role in the pathogenesis of portal hypertension (PH). NO is an extremely unstable molecule and rapidly degrades to nitrite ($NO_{2}$) and nitrate ($NO_{3}$ . Methods: In this study, serum $NO_{2}$/$NO_{3}$ (NOx) as an index of endogenous NO production was measured in 40 chronic liver disease patients (13 women, 27 men; mean age: 51±1). Etiology was viral in 31 patients, alcohol in six, auto immunity in one and unknown in two patients. NOx was determined in chronic liver disease patients, and the relationship between NOx and severity of disease was also evaluated. Patients were evaluated for the presence of portal hypertension. Twelve healthy subjects (five women, seven men; mean age 51±3) were used as a control group. The concentration of $NO_{2}$ was determined spectrophotometrically and $NO_{3}$ was obtained after reduction to $NO_{2}$ with Griess reaction. Results: NOx found to be no different between the control and chronic active hepatitis group. Cirrhotic patients had a higher NOx level than that of the chronic active hepatitis group and control group (p<0.01). Patients with ascites and/or esophageal varices had a higher NOx level than that of patients without ascites and/or esophageal varices (p<0.05). Conclusions: These findings suggest that production of endogenous NO is increased in patients with cirrhosis, particularly in decompanseted patients.

Özet

Amaç: Portal hipertansiyon patogenezinde nitrik oksit (NO)'in rolü olduğu düşünülmektedir. NO çok labil bir molekül olup, hızla nitrit (NO2) ve nitrata (NO3) dönüşmektedir. Yöntem: Çalışmamızda 40 kronik karaciğer hastasında (13 kadın, 27 erkek; yaş ort:51±1) endojen NO göstergesi olarak NO2/NO3(NOx) ölçülmüştür. Etyoloji 31 hastada viral, 6 hastada alkol, 1 hastada otoimmünite ve 2 hastada kriptojenik olarak saptanmıştır. Hastalar portal hipertansiyon varlığı açısından değerlendirilmişler ve NOx ile hastalık şiddeti arasındaki ilişki de aranmıştır. Oniki sağlıklı kişi (5 kadın, 7 erkek; yaş ort: 51±3) kontrol grubu olarak kullanılmıştır. $NO_{2}$ direkt olarak, $NO_{3}$ modifiye Griess yöntemiyle $NO_{2}$ ye indirgendikten sonra spektrofotometrik olarak ölçülmüştür. Bulgular: NOx, kontrol grubu ve kronik aktif hepatit grubu arasında farklılık göstermemiştir. Sirotik grupta Nox her iki gruptan da yüksek saptanmıştır (p< 0.05). Sonuç: Bu bulgular, sirotik hastalarda özellikle dekompanse olanlarda NO'nun arttığını düşündürmektedir.

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Cite This Article

ÖZAKYOL, A. H., DEMİR, T. A., SARIÇAM, T., VARDARELİ, E., YAVUZ, H., GÜRAY, T., ERNOĞLU, E. (2000). Dekompanse kronik karaciğer hastalığında nitrik oksit artışı. Turkish Journal of Gastroenterology, Cilt: 11 - Sayı: 2, 103–107. https://ajindex.com/articles/410460

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