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IMPACT OF CORTICOSTEROID AND IMMUNOSUPPRESSIVE THERAPY ON THE
COURSE OF CHRONIC HEPATITIS: RISKS AND PROSPECTS
Tolibov Farrux Farhodivich
tolibovf1@gmail.com
Asia International University, Bukhara, Uzbekistan.
https://doi.org/10.5281/zenodo.14909796
Abstract.
Chronic viral hepatitis is an inflammatory dystrophic-proliferative process in
the liver, genetically determined by a deficiency of cellular and macrophage immunity,
prolonged (more than 6 months), clinically manifested by asthenovegetative and dyspeptic
syndromes, persistent hepatosplenomegaly, liver dysfunction, hyperfermentemia and
dysproteinaemia.
Keywords:
Liver encephalopathy, chronic liver disease, hypoglycaemia, Complications,
cirrhosis, mucosa, coma, atrophy, pain, disorders, clinical forms, symptom, drug overdose, the
portal vein system.
ВЛИЯНИЕ КОРТИКОСТЕРОИДНОЙ И ИММУНОСУПРЕССИВНОЙ ТЕРАПИИ
НА ТЕЧЕНИЕ ХРОНИЧЕСКОГО ГЕПАТИТА: РИСКИ И ПЕРСПЕКТИВЫ
Аннотация.
Хронический вирусный гепатит — воспалительный дистрофически-
пролиферативный процесс в печени, генетически обусловленный дефицитом клеточного и
макрофагального иммунитета, длительный (более 6 месяцев), клинически проявляющийся
астеновегетативным и диспептическим синдромами, стойкой гепатоспленомегалией,
нарушением функции печени, гиперферментемией и диспротеинемией.
Ключевые слова:
Печеночная энцефалопатия, хронические заболевания печени,
гипогликемия, осложнения, цирроз, слизистая, кома, атрофия, боль, расстройства,
клинические формы, симптом, передозировка лекарственных средств, система воротной
вены.
Introduction:
Criteria for the evaluation of chronic hepatitis are based on 4 main points
- aetiology, pathogenesis, degree of activity of the process and stage of chronicisation
(degree of fibrosis).
According to the decision of the World Congress of Gastroenterologists (Los Angeles,
1994), the following variants of chronic hepatitis are distinguished:
By etiology:
-viral hepatitis (chronic viral hepatitis B, C, D, chronic viral hepatitis of unknown type);
-autoimmune hepatitis;
-chronic drug-induced hepatitis;
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-alcoholic hepatitis;
-toxic hepatitis;
-cryptogenic (idiopathic) chronic hepatitis.
According to the clinical picture:
I. HBsAg carrier (ALT < 2 norms; DNA < 104cop/ml, or 2,000 IU/ml).
II. Immunoactive hepatitis B (ALT > 2 norms; DNA >
104 copies/ml, or 2,000 IU/ml; HBeAg+).
III. Immunotolerant hepatitis B.
The main cause of all chronic liver diseases is hepatotropic viruses. HCV causes 40-60
per cent of all cases and HBV 10-15 per cent of chronic hepatitis.
The current epidemic situation is particularly dangerous due to the growth of drug
addiction among young people.
In this group, the risk of hepatitis infection ranges from 50 to 90 per cent, whereas in the
general population the incidence does not exceed 5 per cent.
The global incidence of viral hepatitis far exceeds the incidence of many other viral
infections in terms of growth rate and prevalence. In comparison, the annual global incidence of
human immunodeficiency virus infections due to intravenous drug use:
- human immunodeficiency virus from 80 to 160 thousand people, - hepatitis B virus
from 8 to 12 million people, - hepatitis C virus about 35 million people.
As a result of these three infections alone (HIV infection, hepatitis B and C), about 13
million people die each year.
Long-term analyses of the incidence of viral hepatitis show a decreasing trend in the
proportion of acute forms of the disease in the overall structure of viral hepatitis and an increase
in chronic forms.
Among hepatotropic viruses, A, HC viruses are predominantly prevalent, while B and C
viruses are capable of causing a chronic process in the liver.
The clinical picture of chronic hepatitis is characterised by several symptoms and
syndromes.
Hepatomegaly is a frequent and constant sign in diffuse chronic liver diseases. In CH, it
is due to lymphomacrophagal infiltration, to a lesser extent hepatocyte dystrophy. Examination
allows to determine the ‘tumour’ shifting during breathing in the right subcostal or subgluteal
region. At percussion the left border of hepatic dullness is determined (in norm it does not go
beyond the left pericardial line), increase in the size of the liver according to Kurlov (9 % 8 % 7
cm in norm).
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Palpation - the liver is moderately dense, painful, its edge is pointed. However, it should
be noted that the painfulness of the liver, determined palpatorily, is caused by stretching of the
glisson capsule (against the background of circulatory insufficiency) or increased pressure in the
biliary passages - in case of cholangitis.
Hepatalgia - in periods of activity of process at CH almost all patients have painfulness in
liver area or unpleasant feeling of heaviness in liver area, which appear or intensify.
liver, which appear or intensify after physical activity.
Mesenchymal-inflammatory syndrome - its clinical signs are fever (due to impaired
inactivation of pyrogens in the liver and intoxication), arthralgias and myalgias,
lymphoadenopathy, hepatomegaly and splenomegaly, vasculitis (skin, lungs, kidneys). Fever is
not pronounced, not accompanied by chills, div temperature does not exceed 38 °C.
Currently immunosuppressive and biological agents are used in a more extensive and
earlier way in patients with inflammatory bowel disease, rheumatic or dermatologic diseases.
Although these drugs have shown a significant clinical benefit, the safety of these
treatments is a challenge. Hepatitis B virus (HBV) reactivations have been reported widely, even
including liver failure and death, and it represents a deep concern in these patients. Current
guidelines recommend to pre-emptive therapy in patients with immunosuppressants in general,
but preventive measures focused in patients with corticosteroids and inflammatory diseases are
scarce. Screening for HBV infection should be done at diagnosis. The patients who test positive
for hepatitis B surface antigen, but do not meet criteria for antiviral treatment must receive
prophylaxis before undergoing immunosuppression, including corticosteroids at higher doses
than prednisone 20 mg/d during more than two weeks. Tenofovir and entecavir are preferred
than lamivudine because of their better resistance profile in long-term immunosuppressant
treatments. There is not a strong evidence, to make a general recommendation on the necessity of
prophylaxis therapy in patients with inflammatory diseases that are taking low doses of
corticosteroids in short term basis or low systemic bioavailability corticosteroids such as
budesonide or beclomethasone dipropionate. In these cases regularly HBV DNA monitoring is
recommended, starting early antiviral therapy if DNA levels begin to rise. In patients with occult
or resolved hepatitis the risk of reactivation is much lower, and excepting for Rituximab
treatment, the prophylaxis is not necessary.
The HBV-induced liver inflammation is predominantly immune mediated: the host
immune response causes a hepatocellular damage following the HBV replication, which can
result in an acute or chronic liver necroinflammation. Immunosuppressants lead to an increase in
DNA viral due to both a effect on the host immune response, as to a stimulatory effect of these
drugs on hepatitis B virus [20].
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The corticosteroids may increase the expression of HBV through a glucocorticoid-
responsive element, which has been detected in viral genoma, and stimulates viral replication in
patients under these treatments [21]. On the other hand, tumoral necrosis factor (TNF) α and
interferon gamma (IFNγ) are important in the clearance of HBV from infected hepatocytes, so
the use of anti-TNF drugs in patients with chronic HBV infections may result in an increase in
viral replication [22,23]. Despite the increase in viral replication, the major damage hardly ever
appears at the time of maximal immunosuppression and usually occurs once the
immunosuppressive therapy is withdrawn, during the phase of immune reconstitution, when the
immune system is able to destroy the hepatitis B-infected hepatocytes, producing the liver
disease[5,24]. Clinically these exacerbations can vary, ranging from a subclinical or
asymptomatic course to a severe acute hepatitis and even death.
Results:
Eleven patients with hepatitis B e antigen (HBeAg)-positive chronic active
hepatitis B were treated with an 8-wk course of prednisone followed by 28 days of adenine
arabinoside 5′-monophosphate. Five individuals had a complete response (loss of HBeAg and
DNA polymerase) whereas 3 had a partial response (sustained loss of DNA polymerase but
persistence of HBeAg). At the present time 27 ± 3 mo has elapsed since the completion of
therapy, and 4 of 5 complete responders remain negative for replicative markers while the fifth
person exhibited transient reactivation of infection. Elevated DNA polymerase has reappeared in
two of the three partial responders, in one 22 mo after completion of therapy. These encouraging
results have led to a randomized, controlled trial using short-term prednisone followed by
recombinant alpha-interferon.
Lamivudine has been the most frequent agent used agent in this scenario, having proved
to reduce the reactivation risk and the associated mortality and morbidity. However, Lamivudine
resistance develops in 53%-76% of patients after 3 years of treatment, therefore, this agent is
only appropriate when a short course of therapy is needed. As immunosuppressants for ID
usually are used for long term, nucleoside/nucleotide analogues (NAs) with a lower rate of
resistance must be considered. Tenofovir and entecavir have a higher barrier to resistance, and
should be used if treatments longer than 12 mo are planned [6,76,77,82,83]. In those patients
with OBI with a high risk of reactivation, lamivudine may still have a role, because of its low
cost, and the low or absent HBV viremia in these cases [76,78]. Alternative antiviral medications
for lamivudine would be adefovir and telbivudine [20]. In all cases, but more closely if
lamivudine, adefovir or telbivudine are used, serum AST/ALT levels and hepatitis B viral load
must be monitored every 3 or 6 mo.
CONCLUSION:
HBV reactivations are not uncommon in inactive HBV patients treated
with immunosuppressive therapy for inflammatory diseases.
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Current guidelines highly recommend prophylaxis in case of immunosuppressive therapy,
including patients receiving steroids in monotherapy. However, steroids at low doses, treatments
shorter than two weeks and low biodisponibility steroids are unlikely to need prophylaxis,
although studies are lacking in this setting. These patients and those with occult or resolved HBV
precise regularly HBV DNA monitoring during immunosuppressant therapy in order to detect
reactivations. Entecavir or tenofovir are recommended as the optimal agents against HBV
reactivation.
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