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Evaluation of Serum Nitric Oxide Levels and Some
Biochemical Parameters in Patients with
Liver Cirrhosis
Hemn Jameel Majeed, Parween Abdulsamad Ismail* and Lutfia Muhammad Hassan
Department of Chemistry, University of Salahaddin, Iraq
*Corresponding author: Parween Abdulsamad Ismail, Department of Chemistry, College of Education, University of Salahaddin, Erbil,
Iraq.
To Cite This Article: Parween Abdulsamad Ismail, Evaluation of Serum Nitric Oxide Levels and Some Biochemical Parameters in Patients
with Liver Cirrhosis. 2020 - 8(1). AJBSR.MS.ID.001227. DOI: 10.34297/AJBSR.2020.08.001227.
Received: March 03, 2020; Published: March 10, 2020
Copy Right@ Parween Abdulsamad Ismail
This work is licensed under Creative Commons Attribution 4.0 License
AJBSR.MS.ID.001227.
American Journal of
Biomedical Science & Research
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ISSN: 2642-1747
Research Article
Abstract
Background:
changes in various biochemical parameters and various clinical manifestations in the patients. The objective of the current study to assessment the
level of nitric oxide and some biochemical parameters in patients with liver Cirrhosis disease.
Methods: A total of 37 cases diagnosed clinically and biochemically as Cirrhosis disease and 35 age-matched controls were enrolled in the study.
Biochemical analyses were carried out which included estimation the level of serum Nitric oxide, albumin, Aspartate Transaminase (AST), Alanine
Results:
patients in comparison with control group.
Conclusion:
Keywords: Liver Cirrhosis, Nitric Oxide, Liver Enzymes, Chronic Liver Diseases, Portal Hypertension, Cirrhotic Cardiomyopathy, Pulmonary Vascular
Abnormalities, Serum Enzymes, Chronic Active Hepatitis, Arteriovenous Inosculation
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Introduction
Chronic liver diseases may possibly classify into liver cirrhosis
and chronic active hepatitis. Liver illnesses it could be attended by
portal hypertension. Several systemic changes may occur with liver
cirrhosis and portal hypertension [1]. These abnormalities changes
syndrome, etc.). Furthermore, Liver cirrhosis is related to many
cardiovascular irregularities such us cirrhotic cardiomyopathy, and
pulmonary vascular abnormalities [2,3]. With the progression of
systems [4]. In addition, with the cirrhotic apparent, the cardiac
mitochondrial functions reduce in breathing regulator ratio and
Nitric Oxide (NO) is one of the most abundant products induced
with the catabolism of L-arginine in various mammalian cells, by the
action of enzymes that catalyze and regulate synthesis and catabolize
arginine. These induced and in certain alterations in the nitric oxide
synthase play main role in metabolic outcome of arginine in health
and disease subject [6,7]. In the beginning, the alteration of cell NO
releases was established mostly in the cardiovascular system, but
nowadays the ultimate role and twin effects (low concentration and
high concentration) had been recognized in various organizations
of human body [8]. The objective of the recent study was purposed
to determine the serum levels of Nitric Oxide in patient whom
American Journal of Biomedical Science & Research
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19
suffering with the liver cirrhosis and to exhibit their correlation
with the extra considerations such us serum albumin level and
Materials and Methods
Study Subjects
A total of thirty-seven cases which were diagnosed clinically
subjects were participated in the study. Their ages ranged from 36-
62 years. A total of thirty-seven serum samples were obtained from
individuals diagnosed with Liver Cirrhosis. Their ages ranged from
36-62 years.
Collection of Blood Samples
Approximately 5ml of venous blood was collected from
individuals. After coagulation, all samples were centrifuged at
3000rpm for 10 minutes and sera were stored at -70°C until
analyzed.
Biochemical Analysis
Assay of Nitric oxide concentration
Nitric oxide concentration has been estimated by using
sandwich enzyme immunoassay (ELISA) technique (BIOSOURCE,
Europe S.A., Belgium, Lot No.051501/B; 060601).
Principle of Human Nitric Oxide (NO) ELISA kit
This experiment was used double-sandwich ELISA technique
and the ELISA Kit provided was typical. The pre-coated antibody
was human NO monoclonal antibody and the detecting antibody
was polyclonal antibody with biotin labeled. Samples and biotin
labeling antibody were added into ELISA plate wells and washed
out with PBS or TBS. Then Avidin-peroxidase conjugates were
added to ELISA wells in order; Use TMB substrate for coloring after
reactant thoroughly washed out by PBS or TBS. TMB turns into
action of acid. The color depth and the testing factors in samples
were positively correlated.
Assay of Liver enzymes activities
Statistical Analysis of Data
Results are expressed as mean ± SD. Statistical comparisons
Results
The results are illustrated in Table 1 and Figure 1. The mean serum
NO in liver cirrhosis, and control subjects were 90.34±8.45mmol/L
and 45.01±4.27mmol/L, respectively. Statistical evaluation showed
that nitric oxide levels were elevated in case groups compared
with liver cirrhosis as compared to control samples.
Discussion
of liver mechanism process which causes the conversion from
prolonged liver disease to cirrhosis. These changes typically happen
septa with following parenchymal cell elimination and collapse of
hepatic vascular construction [9]. In addition, the disturbances of
the hepatic architecture produced by cirrhotic process increase the
issue is foremost to portal hypertension. Portal hypertension is a
most abundant and terrible obstacle of people suffering chronic
liver illness [10]. The pathological condition resulting from a portal
hypertension which has happened in consequence of destruction
to the portal veins is splanchnic overcrowding and opening of
ascites, splenomegaly etc.
Furthermore, concerning splanchnic arteriolar vasodilatation
which will causes portal hypertension facilitated by NO and act
retention due to stimulating antidiuretic hormone [2]. Our study
showed increased serum concentration of Nitric Oxide in patients
with cirrhosis. Several investigators also demonstrated that serum
NO concentrations are increased in hepatic cirrhosis [11-13].
The best explanation for increasing the NO concentrations is that
differences in serum nitrite and nitrate levels The initial cause of
venous hypertension, which increases shear stress and up-regulates
endothelial nitric oxide synthase, no doubt involved to nitric oxide
overproduction [14,15]. The anatomic sites of the enhanced NO
synthesis and release remain unclear. Evidence suggests that the
activity of NO synthase activity may be upregulated at different
sites, including the jejunum, gastric mucosa, and esophageal
mucosa [16-19].
The levels of nitric oxide are higher in portal venous plasma
than in peripheral venous plasma in patients with cirrhosis,
suggesting elevated splanchnic production of nitric oxide [12]. The
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activity of nitric oxide synthase in polymorphonuclear cells and
monocytes was elevated in patients who had cirrhosis. These cells
that provides evidence that this type of the enzyme may have a
role in peripheral vasodilatation in patients with cirrhosis [19].
Nitric Oxide which has been recognized as the utmost important
vasodilator of hepatic vascular nature regulation is formed by
endothelial cells. It is generally formed from the metabolism of
guanidine group of arginine [20,2]. In the recent study, our results
cirrhotic group than in the control group (Figure 1).
Figure 1: Mean values of serum NO in control and patients with liver Cirrhosis groups.
The various studies all agreed that serum NO concentrations
are raised in liver cirrhosis [1,2,5]. Despite the anatomic and the
mechanisms of the enhanced NO releases during cirrhosis is
that at different sites, such as esophageal mucosa, gastric mucosa,
and jejunum, NO synthase activity can be uncontrolled, and the
activity of erythrocyte adversely related with the serum level of
NO in liver cirrhotic patients [21]. The activity of serum ADA is
compared to normal healthy individuals in all age groups. The data
are in line with earlier results respectively [22,23]. The diagnosis
of organ disease is aided by estimation of several non-functional
plasma enzymes characteristic of that tissue or organ. The quantity
of enzymes produced depends on the degree of cellular damage,
the concentrations of the intracellular enzymes and the mass of
affected tissue.
The cause of the damage (viral infection, hypoxia, surgical,
chemical, or mechanical trauma) has no bearing on the enzymes
released into blood circulation. The levels of the enzymes released
yield mitochondrial enzymes as well. The use of appropriate
normal ranges is important in assessing abnormal levels of plasma
enzymes. Concerning liver injury, not liver normally functions are
referred to measurements each of the Aspartate Aminotransferase
(ALP). These laboratory measurement parameters are extremely
reproducible. Therefore, hepatic cirrhosis as a last stage of liver
disease or hepatic illnesses is required to assess and potential
evaluation of AST, ALT and ALP.
or ALP fractionation may trust an elevated ALP level of hepatic
origin. Despite, AST is elevated in the liver dysfunctions, but it
damage, because it is present in other organs rather than liver
ALT and AST in hepatic cirrhosis patients as compared to control
injury in both intra and extra hepatic failure, due to it is existence
of liver disease such as viral hepatitis, cholestasis and alcoholic
upper than normal values [25]. However, in our study persistence
as an indicator of cirrhosis.
Table 1: (Mean ± SD) of Biochemical parameters in liver cirrhotic patients and control group.
Parameters Control Patients P-value
Albumin(gm/dl) 4.8±0.68 2.43±0.47
63±11.67 187±35.09
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ADA(IU/L) 15.07±1.92 48.01±6.40
ALP(IU/L) 274±18.50 340±25.01
ALT(IUL) 30.5±7.22 70.02±27.35
AST(IUL) 27.91±5.71 80±27.12
and ALP considered as a feature diagnostic of hepatic diseases,
subsequently enzymes are secreted into the bloodstream after the
worsening of the liver organ. Despite releasing these mitochondri-
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and lipoproteins are used to estimate the status of liver function,
while an elevation of transaminase enzyme more than two times
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totoxicity [26]. In this study, all the ADA, ALP and alanine trans-
aminase as well as aspartate transaminase enzymes raised from
(15.07±1.92, 274±18.50, 30.5±7.22 & 27.91±5.71) to (48.01±6.40,
340±25.01, 70.02±27.35 and 80±27.12) respectively.
Albumin is a family of spherical proteins produced in the liver
and is closely attendant with the systems of pathophysiology in
different forms of liver disease. Therefore, it has an important role
the current study shows considerably decrease concentration
of serum albumin in patient group (Table 1). This could cause by
the changing qualitatively in albumin structure and not purely a
quantitative decrease which is responsible for the defeat of it is
in liver disease. Albumin, bilirubin, and time of prothrombin
Conclusion
Increased levels of nitric oxide contributed to the hemodynamic
changes occur in patients of liver cirrhosis. Indicate that nitric oxide
has a pathophysiological role in liver cirrhosis.
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