Clinical course of chronic viral hepatitis c in children

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Даминова S., & Маткулиева S. (2020). Clinical course of chronic viral hepatitis c in children. in Library, 20(3), 1–6. извлечено от https://inlibrary.uz/index.php/archive/article/view/14502
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Аннотация

In the following article clinical course processes of chronical hepatitis C in children is analysed.  The incidence of seropositivity is identified. The authors have analysed the arginase activity of saliva which maintained the indices of chronical hepatitis. The existence of a hematosalivation barrier  in  the  body,  the  presence  of  a  metabolism  between  blood  and  saliva,  as  well  as  the homeostatic role of these biological fluids for each other - all these facts make saliva capable in some cases of replacing blood in laboratory tests. Thus, the accumulated literature data indicate that the chronic hepatitis C virus may remain asymptomatic for a long time, but a number of extrahepatic manifestations in the oral cavity can be detected in patients.

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P u b l i s h e d b y :

T R A N S

A s i a n R e s e a r c h J o u r n a l s

AJMR:

A s i a n J o u r n a l o f

M u l t i d i m e n s i o n a l

R e s e a r c h

( A D o u b l e B l i n d R e f e r e e d & P e e r R e v i e w e d I n t e r n a t i o n a l J o u r n a l )

DOI:

10.5958/2278-4853.2020.00271.2

CLINICAL COURSE OF CHRONIC VIRAL HEPATITIS C IN CHILDREN

Daminova Sh.B*; Matkulieva S.R**

UZBEKISTAN

ABSTRACT

In the following article clinical course processes of chronical hepatitis C in children is analysed.
The incidence of seropositivity is identified. The authors have analysed the arginase activity of
saliva which maintained the indices of chronical hepatitis.

The existence of a hematosalivation

barrier in the div, the presence of a metabolism between blood and saliva, as well as the
homeostatic role of these biological fluids for each other - all these facts make saliva capable in
some cases of replacing blood in laboratory tests.

Thus, the accumulated literature data indicate

that the chronic hepatitis C virus may remain asymptomatic for a long time, but a number of
extrahepatic manifestations in the oral cavity can be detected in patients.

KEYWORDS:

Chronic Viral Hepatitis, Public Health Problem, Liver Dysfunction, Sjorgen's

Syndrome, Precancerous Conditions, Dysbiotic Processes

INTRODUCTION

Viral hepatitis C (HCV) is currently one of the urgent public health problems due to its
prevalence in the population, the high incidence of liver cirrhosis and hepatocellular carcinoma,
the development of extrahepatic manifestations that determine the difficulties in diagnosing the
disease and its treatment. According to WHO estimates, in 2015, 1.75 million new cases of HCV
infection were recorded worldwide (23.7 new cases per 100,000 people). WHO estimates that
approximately 399,000 people died from hepatitis C in 2016, mainly from liver cirrhosis and
hepatocellular carcinoma (WHO Newsletter, 2019). Hepatitis C virus causes 20% of all cases of
acute hepatitis, and chronic HCV infection is responsible for the development of 70% of cases of
chronic hepatitis, 40% of all cases of terminal cirrhosis of the liver, 60% of hepatocellular
carcinoma and 30% of the causes the patient is referred for liver transplantation [9, 10]. Of
interest is the fact that infection with hepatitis viruses, including HCV, is also possible through
the oral mucosa, for example, with kisses. It has already been proven that hepatitis B and C
viruses are transmitted by all div fluids - up to 30% hepatitis B virus and up to 5% hepatitis C
virus [29].


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Salivary transmission of hepatitis B and C viruses can be one of the non-parenteral modes of
transmission [19]. Of particular interest is the presence of the virus in the saliva of patients with
chronic viral hepatitis C (HVHS).

To date, a large number of studies have already been accumulated devoted to studying the
amount of hepatitis C virus RNA in the saliva of patients with chronic hepatitis C (HCV) [17,
28].

Liver dysfunction can manifest itself with various changes in the oral cavity, namely, in the form
of ictericity of the mucous membrane, bleeding disorders, the presence of petechiae, a tendency
to hematomas, gingivitis, gingival bleeding (even in response to minimal trauma), hepatic odor
from the mouth, cheilitis, smooth and atrophic tongue, xerostomia, perioral rash, soreness of the
oral cavity [30].

According to various authors, patients with hepatitis C are prone to tooth decay, suffer from a
loss of self-esteem due to poor aesthetics of the oral cavity, and sometimes experience
difficulties with nutrition due to an unsatisfactory state of the oral cavity. All this leads to a
decrease in the quality of life [22].

In a study by Coates E.A. et al. (2000) studied the state of the oral cavity in patients with chronic
hepatitis C compared with patients without HCV markers. Patients were between 25 and 50
years old. Although there were no significant differences between the groups, nevertheless,
HCV-infected patients were more likely to have problems associated with the state of
periodontal structures. So, in half of patients with HCV there was a decrease in the amount of
saliva secreted. 71% of patients with HCV showed a decrease in quality of life due to the
presence of significant pain in the oral cavity [22].

In recent years, the relationship between HCV and the development of lichen planus, which also
affects the mucous membrane of the oral cavity, has been proven, and the frequency of
occurrence varies depending on the geographical region. So, the most typical development of
this pathology is for the South European region and Japan [18, 20].

Given that seropositivity for anti-HCV in patients with lichen planus is much higher, for
example, in Israel, all patients with lichen are regularly tested for antibodies to HCV [33].

HCV is known to affect the salivary glands, but the exact nature of this effect remains to be fully
understood. It is believed that hepatitis C virus causes shergen-like syndrome. There are
suggestions that HCV is the cause of Sjogren’s syndrome, but this is controversial. It is unclear
whether the virus can cause a similar pathological condition; primary Sjogren's syndrome or
HCV is directly responsible for the development of Sjogren's syndrome in a specific subgroup of
patients [21].

Increased prevalence of HCV infection in patients with squamous cell carcinoma of the oral
cavity was discovered back in 1995 by Nagao Y. and coauthor [26]. A 2004 study in the United
States showed that 21% of 99 patients with squamous cell carcinoma had HCV markers [27].

It has been shown that HCV does not affect the survival of such patients [24].

In another study from Japan [32], the authors found an increase in the incidence of HCV in
patients with oral cancer, but this difference was not significant after the data were adjusted for
age.


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However, HCV is a common cause of cirrhosis, which, in turn, can be an independent risk factor
for oral cancer [31].

On the other hand, it has been shown that precancerous conditions such as leukoplakia and oral
epithelial dysplasia are not associated with HCV infection [20, 25].

Special attention should be paid to the issues of periodontal tissue lesions in HCV.

The pathogenesis of periodontal diseases is based on serious violations of microbiocenosis in
combination with dysfunction of the div's immune system against the background of
generalized inflammatory, dystrophic and vascular changes [5].

It is known that the development of periodontal pathology is influenced by concomitant chronic
diseases of the liver and hepatobiliary system, which currently have a predominantly viral nature
[2, 3, 7].

According to a study by Farghaly A.G. et al. (1998), cases of periodontal disease were noted
more often in children with hepatitis markers than in the group of patients in whom hepatitis
markers were not detected. At the same time, hepatitis C markers were detected more often than
hepatitis B markers (26% and 13% versus 22% and 8%, respectively). Also, in patients with
periodontal disease, unstimulated saliva showed a higher degree of detection of HBsAg, anti
HBc, anti-HCV or both anti-HCV and / or anti-HBc than in the control group (100% versus
66.7%, 50% against 23.5%, 23.1% against 0.0% and 42.3% against 18.2%, respectively) [23].

As one of the pathogenetic factors that can induce numerous clinical and laboratory phenomena
described in CVHB and CVHV, a number of researchers consider endotoxin of gram-negative
bacteria, causing the development of a complex of pathophysiological, immunological and other
biological processes [6, 11, 12].

The main anti-endotoxin barrier is the liver [2, 6].

With the development of dysbiotic processes in the oral cavity, as well as with other pathological
processes in the gastrointestinal tract, the intake of endotoxin into the systemic circulation
increases, which can cause an increase in intoxication syndrome and aggravation of chronic
inflammation in the tissues [6, 11].

In his research, Fazylova Yu.V. showed that the level of specific antiendotoxin antibodies in
patients with CVD against CVHB and CVHC is an integral indicator of immunological
deficiency and indicates the development of systemic endotoxemia as a result of microbial
aggression associated with the severity and prevalence of periodontal disease and activity of
chronic viral hepatitis [14].

Of particular scientific interest is the study conducted by S. Kolesov. et al. [8], dedicated to the
study of salivary arginase activity in children with HVHV and KhVGS.

As you know, arginase catalyzes the hydrolysis of arginine with the formation of ornithine and
urea. Since disruption of urea synthesis leads to an increase in the amount of ammonia in tissues,
it is generally accepted that the level of arginase activity reflects the degree of detoxifying liver
function [4, 15].

In addition, there is evidence that in clinical studies, the determination of arginase in blood
serum can be used as a specific marker that allows you to detect liver damage at an earlier stage


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than in the study of aminotransferases, which is important for the correct treatment of liver
diseases including chronic hepatitis.

It should be especially noted that at present, an increase in researchers' interest in arginase can be
expected, since it is proved that this enzyme can act as a limiting factor in the formation of nitric
oxide in the div, a unique messenger whose biological role is very large: the physiological
effect of NO varies from modulation of the vascular system to the regulation of immune
processes and control of neuronal functions [1].

In addition to the liver, arginase activity was also found in other organs, tissues and substrates of
the div, including saliva [16]. The existence of a hematosalivation barrier in the div, the
presence of a metabolism between blood and saliva, as well as the homeostatic role of these
biological fluids for each other - all these facts make saliva capable in some cases of replacing
blood in laboratory tests. Especially attractive is the use of saliva for pediatric practice, since
obtaining oral secretions is accessible and non-traumatic.

According to the results obtained by the authors, the average values of arginase I (liver arginase)
in the blood serum of children with chronic viral hepatitis B and chronic viral hepatitis C were
added 8.01 and 10.35 ng / ml, respectively. The average values of the arginase activity of saliva
in the group of children with chronic viral hepatitis B turned out to be two times higher than the
level of this indicator in patients with chronic viral hepatitis C and amounted to 82.34 and 33.24
mmol / hr / ml, respectively. The authors concluded that the arginase activity of saliva is due to
the enzymatic activity of the arginase isoenzyme from the salivary glands and is not related to
the activity of arginase I (liver arginase). The decrease in the arginase activity of saliva in
children with chronic viral hepatitis C, apparently, is an extrahepatic manifestation of chronic
viral hepatitis C, and is characterized by changes in the dental status characteristic of this
disease.

It is known that half of patients with chronic hepatitis C have extrahepatic manifestations of the
disease, including damage to the oral cavity: they have a high incidence of symptoms of
periodontal disease, there has been a periodontal disease and gingivitis (and in patients with
chronic hepatitis C, these diseases represented mainly by generalized forms of severe and
moderate) [13], lymphocytic sialadenitis.

The authors of the study believe that the need to combat infection is a biochemical mechanism
that ensures a decrease in salivary arginase activity during periodontal lesions of the oral cavity.
According to literature [1], arginine, not utilized by arginase, is used for the synthesis of nitric
oxide, one of the functions of which is both direct participation in the fight against infection and
stimulation of the immune response to it. Due to this, a peculiar dynamic relationship between
aggression factors (oral infection) and the div's defensive reactions is established in the
patient’s div.

Thus, the accumulated literature data indicate that the chronic hepatitis C virus may remain
asymptomatic for a long time, but a number of extrahepatic manifestations in the oral cavity can
be detected in patients. In this regard, the dentist plays an active role in detecting HCV infection.
Further research is needed to identify a possible relationship between oral pathology and HCV.

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