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CHANGES IN PLATELETS IN PATIENTS WITH CHRONIC HEPATITES AND
LIVER CIRRHOSIS OF VIRAL ETIOLOGY
Tuychiev Laziz N.
Department of Infectious and Pediatric Infectious Diseases
Tashkent Medical Academy
https://orcid.org/0000-0003-2312-8640
Rakhmatullaeva Shakhnoza B.
Department of Infectious and Pediatric Infectious Diseases
Tashkent Medical Academy
https://orcid.org/0000-0001-7257-2081
Akhmedova Oydin A.
Department of Infectious and Pediatric Infectious Diseases
Tashkent Medical Academy
Sadikov Khumaun-Mirzo A.
Department of Infectious and Pediatric Infectious Diseases
Tashkent Medical Academy
Sadikovhumayunmirzo@gmail.com
https://orcid.org/0000-0001-7071-9393
Summary:
In liver cirrhosis, the normal functioning of hemostasis is disrupted, which leads
to an increased risk of both thrombosis and bleeding. The study of platelet changes in such
patients helps to understand the pathogenesis of these disorders and contributes to improved
diagnostics and therapy.
Purpose of the study.
To assess the dynamics of platelet levels in patients with chronic
viral hepatitis and liver cirrhosis.
Materials and methods.
The study included 140 patients with chronic diffuse liver diseases,
including 70 patients with liver cirrhosis of viral etiology, 20 patients with liver cirrhosis of
unknown etiology and 50 patients with chronic viral hepatitis of moderate activity.
Results and discussion.
As can be seen from the table, in liver cirrhosis of HBV and
HBV+HDV etiology there is thrombocytopenia, erythrocytopenia and leukopenia.
The study of platelet indices of the hemogram performed on a hematology analyzer showed
that patients with cirrhosis have significant violations of the mean platelet volume (MPV),
platelet distribution width (anisocytosis) (PDV) and platelet crit (PCT).
The performed hematological studies of platelets in patients with liver cirrhosis and chronic
hepatitis of viral etiology showed significant disturbances in the number of blood cells of
platelets in liver cirrhosis and unexpressed changes in chronic hepatitis.
Key words:
chronic hepatitis, liver cirrhosis, platelet, blood test.
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The problem of viral hepatitis (especially B and C) is one of the most actual in infectology.
Chronic viral hepatites can progress into liver cirrhosis which increases the risk to the health
and life of patients [2; 5].
One of the characteristic complications of chronic hepatic disorders is a decrease in the
platelet level, which is associated with several factors, including hypersplenism, impaired
platelet synthesis in the liver and their increased destruction [4; 6]. Thrombocytopenia can
contribute to an increased risk of bleeding, that significantly worsens the clinical condition
of patients.
In liver cirrhosis, the normal functioning of hemostasis is disrupted, which leads to an
increased risk of both thrombosis and bleeding. The study of platelet changes in such
patients helps to understand the pathogenesis of these disorders and contributes to improved
diagnostics and therapy. Understanding the mechanism of platelet changes in patients with
chronic hepatitis and cirrhosis allows us to identify patients with a high risk of
complications (for example, esophageal varices, gastric and intestinal bleeding). This
requires regular monitoring of platelet counts and other hemostasis markers [1;3].
Modern treatment methods of chronic viral hepatites (e.g. antiviral therapy) and liver
cirrhosis may affect platelet level. The researches in that area helps to develop the strategies
to improve therapy and reduce the complications.
The changes in platelet level can also affect the prognosis of the disease and the quality of
patients’ life. Early detection of changes in the hemostasis system can help in more timely
intervention and improvement of the condition of patients.
Thus, the study of platelet changes in patients with chronic hepatitis and liver cirrhosis of
viral etiology is vital, since the study of these changes is important for improving the quality
of diagnosis, treatment and prevention of complications in this category of patients.
Purpose of the study.
To assess the dynamics of platelet levels in patients with chronic
viral hepatitis and liver cirrhosis.
Materials and methods.
Clinical studies were conducted in the infectious diseases
department of the multidisciplinary clinic of the Tashkent Medical Academy from 2015 to
2024. The study included 140 patients with chronic diffuse liver diseases, including 70
patients with liver cirrhosis of viral etiology, 20 patients with liver cirrhosis of unknown
etiology and 50 patients with chronic viral hepatitis of moderate activity.
When diagnosing liver cirrhosis and chronic hepatitis of viral etiology, anamnesis data (for
example, indications of blood transfusion, treatment at the dentist, etc.), characteristic
clinical syndromes (hemorrhagic, anemic, asthenoneurotic, icteric and others), as well as the
results of laboratory and instrumental studies were taken into account. A mandatory
condition for inclusion in the study was the presence of hepatitis virus markers determined
by ELISA and PCR blood tests, with the detection of hepatitis B virus (HBV) DNA and
hepatitis C virus (HCV) and D (HDV) RNA, as well as determination of their genotypes. In
patients with chronic hepatitis and liver cirrhosis of viral etiology, the viral load exceeded
1,000,000 IU / ml.
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The diagnosis of liver cirrhosis and the degree of liver failure were established taking into
account the recommendations of the World Health Organization (WHO, 2008) and the
Child-Pugh classification based on diagnostic criteria.
Ultrasound examination (US), multi-layer computed tomography (MSCT) and liver
fibroscan were performed to assess the degree of fibrosis in patients with liver cirrhosis.
Only patients with chronic hepatitis and liver cirrhosis who did not receive antiviral therapy
were included in the study.All patients examined by us were divided into 6 groups: group I
included 20 patients with decompensated cirrhosis of the liver of viral etiology HBV, class
B according to the Child-Pugh classification, group II - 20 patients with decompensated
cirrhosis of the liver of viral etiology HBV + HDV, class B according to the Child-Pugh
classification, group III - 30 patients with decompensated cirrhosis of the liver of viral
etiology HCV, class B according to the Child-Pugh classification, group IV - 20 patients
with decompensated cirrhosis of unknown etiology, class B according to the Child-Pugh
classification, group V - 25 patients with moderate chronic viral hepatitis B, group VI - 25
patients with moderate chronic viral hepatitis C.
Among the 140 patients included in the study, 78 were men (55.7%), 62 were women
(44.2%). The age of patients ranged from 21 to 69 years, the average age was 48.2 ± 12.1
years. Among patients, 43.5% were people of working age.
The control group included 20 practically healthy individuals with no history of liver
damage and fatty hepatosis, with negative results for hepatitis B and C markers.
Results and discussion.
To study the vascular-platelet link of hemostasis, we performed a
general analysis of peripheral blood with platelet counting, and also studied the adhesive and
aggregation functions of platelets. The results showed that in groups with liver cirrhosis,
there is a clear tendency to moderate thrombocytopenia. The average platelet count in
patients of group I was 148 ± 25.8 x 10 ^ 9 /l, in group II - 146 ± 32.9 x 10 ^ 9 /l, and in
group III the platelet count was significantly reduced and was 105 ± 33.5 x 10 ^ 9 /l. These
data significantly differed from the control group indicator, which was 222 ± 21.21 x 10 ^ 9
/l. While in patients of group IV the number of platelets did not differ significantly from the
control group and was 174 ± 48.6 x 10^9/l.
Thrombocytopenia was more often detected in patients with liver cirrhosis of HCV etiology
than in liver cirrhosis of HBV and HBV+HDV etiology. Studies have shown that the main
cause of thrombocytopenia in groups I and II was pancytopenia caused by hypersplenism in
liver cirrhosis. This is confirmed by a decrease in the number of erythrocytes and leukocytes.
As is known, with hypersplenism there is a delay and destruction of formed elements of the
blood - erythrocytes, leukocytes and platelets - in the hypertrophied spleen.
The indicators of the red part of blood in patients were characterized by a moderate decrease
in the number of erythrocytes in groups I and II, 2.88±0.16x10
12
/l and 2.83±0.21x10
12
/l
respectively, which appeared to be significantly reduced compared to the control group. The
number of erythrocytes in group III was 3.47±0.54x10
12
/l, while in the control group the
number of erythrocytes was 4.22±0.27x10
12
/l, no significant differences were found. Severe
anemia in patients with cirrhosis is more often diagnosed in patients who have suffered
bleeding from esophageal varices.
Another indicator confirming hypersplenism in liver cirrhosis is a decrease in the number of
leukocytes. Thus, in patients of the group I, the number of leukocytes averaged
3.54±0.32x10
9
/l, in the group II it was 3.49±0.19x10
9
/l, which is significantly lower than in
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the control. In group III, this indicator was within the normal range of 4.89±0.69x10
9
/l. and
in patients in the control group, the number of leukocytes was 5.95±1.01 x10
9
/l (Table 1).
Table 1
Peripheral blood parameters in patients with cirrhosis
Groups
Control
group (n=20)
I
group,
HBV
liver
cirrhosis
(n=20)
II
group,
HBV+HDV
liver
cirrhosis
(n=20)
III
group,
HCV
liver
cirrhosis
(n=30)
IV
group,
liver
cirrhosis of
unclear
etiology
(n=20)
Platelets,
x10
9
/l
222 ± 21.21
148 ± 25.8*
146 ± 32.9*
105 ± 33.5** 174 ± 48.6
Erythrocytes,
x10
12
/l
4.22 ± 0.37
2.88
±
0.16**
2.83
±
0.21**
3.47 ± 0.54
3.53 ± 0.42
Leukocytes,
x10
9
/l
5.95 ± 1.01
3.54 ± 0.32* 3.49 ± 0.19*
4.89 ± 0.69
5.86 ± 1.05
Note: *-P<0.05, **-P<0.01 significant in relation to the control group.
As shown in the table, thrombocytopenia, erythrocytopenia and leukopenia are observed in
liver cirrhosis of viral etiology HBV and HBV+HDV. These changes can be mainly
explained by hypersplenism. At the same time, the phenomena of hypersplenism in liver
cirrhosis of HCV etiology are manifested to a lesser extent than in liver cirrhosis of HBV
and HBV+HDV etiology. In liver cirrhosis of unclear etiology, significant changes in the
peripheral blood are not observed.
The results of the study of peripheral blood parameters of patients with chronic viral
hepatitis of B- (group V) and C- (group VI) etiology showed that the number of platelets in
these groups was within the normal range, which was 216±29.6x10
9
/l and 187±32.9x10
9
/l,
respectively. There were no significant differences with the platelet count in the control
group (222±21.21x10
9
/l). The number of erythrocytes in these groups was slightly lower
than in the control group: 3.47±0.53 x10
12
/l and 3.46±0.35x10
12
/l, respectively, and in the
control group the number of erythrocytes was 4.22±0.27x10
12
/l. A similar picture was
observed when studying the number of leukocytes; in patients of groups V and VI they were
within normal values – 6.06±1.99x10
9
/l and 5.48±1.1x10
9
/l, respectively (Table 2).
Table 2
Peripheral blood parameters in patients with chronic viral hepatitis
Groups
Control
group
(n=20)
V group, CVH B
(n=25)
VI group, CVH C
(n=25)
Platelets, x10
9
/l
222 ± 21.21
216 ± 22.8
187 ± 32.9
Erythrocytes, x10
12
/l 4.22 ± 0.37
3.47 ± 0.53
3.46 ± 0.35
Leukocytes, x10
9
/l
5.95 ± 1.01
6.06 ± 1.99
5.48 ± 1.17
Note: *-P<0.05 significant in relation to the control group.
The study of platelet indices obtained using a hematology analyzer showed that patients with
liver cirrhosis have significant changes in the mean platelet volume (MPV), platelet
distribution width by volume (PDV) and platelet crit (PCT).
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In patients from group I, the mean platelet volume (MPV) was 13.27 ± 1.17 fl, in group II
this figure was 13.57 ± 0.70 fl. In groups III and IV, the MPV values were 10.52 ± 0.76
fl and 10.48 ± 0.57 fl, respectively. In patients in the control group, the mean platelet
volume (MPV) was 8.25 ± 0.64 fl. These data allow us to conclude that in liver cirrhosis,
there is a reliable increase in the mean platelet volume, which indicates the predominance of
young forms of platelets in the blood in response to their shortened lifespan. These changes
are especially pronounced in patients with liver cirrhosis of HBV and HBV+HDV etiology.
The PDV index in group I was 29.3 ± 1.21%, in group II — 30.57 ± 0.82%, in group III —
22.91 ± 0.92%, and in group IV — 20.12 ± 0.68%. The platelet distribution width by
volume in the control group was 12.43 ± 0.92%. This confirms that in liver cirrhosis, there is
a reliable increase in the platelet distribution width by volume, which indicates pronounced
platelet anisocytosis (Table 3).
Table 3
Platelet indices of hematological analyzer in patients with liver cirrhosis
Hemostati
c profile
Control
group
(n=20)
I group, HBV
liver cirrhosis
(n=20)
II
group,
HBV+HDV
liver cirrhosis
(n=20)
III group, HCV
liver cirrhosis
(n=30)
IV group, liver
cirrhosis
of
unclear
etiology (n=20)
MPV, fl
8.25
±
0.64
13.27±1.17**
*
13.57±0.70**
*
10.52± 0.76*
10.48± 0.57*
PDV, %
13.45± .5
1
29.30±1.21**
*
30.57±0.82**
*
22.91±0.92**
*
20.12±0.68**
*
PCT, %
0.28
±
0.01
0.10±0.008**
*
0.10±0.008**
*
0.08±0.008**
*
0.16±0.01***
Note: *-P<0.05, ***-P<0.001 significant in relation to the control group.
When studying the platelet crit (PCT), it was found that it also significantly decreased in
liver cirrhosis of viral etiology, especially in cirrhosis of HCV etiology. Thus, in the group I,
PCT was 0.10±0.008%, in the group II it was 0.10±0.008% and in patients of the group III it
was 0.08±0.008%. In patients of the group IV, PCT was 0.16 ± 0.01%. The platelet crit
indicator in the control group was 0.28 ± 0.01%. The results of the PCT study confirm a
decrease in the number of platelets in groups with liver cirrhosis of viral etiology, especially
in liver cirrhosis of HCV etiology.
Thus, the hematological studies of platelets in patients with liver cirrhosis and chronic
hepatitis of viral etiology revealed significant disturbances in the number of platelets in liver
cirrhosis, while in chronic hepatitis the changes were less pronounced.
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