This document summarizes information about Hepatitis A, B, C, D, and E viruses. It discusses their causative agents and characteristics, modes of transmission, clinical manifestations and phases of infection, diagnosis, treatment, prevention, and specific details about Hepatitis A and B viruses. Key points covered include that Hepatitis A and E viruses are transmitted via the fecal-oral route while Hepatitis B, C, and D are transmitted parenterally. It provides details on the incubation periods, symptoms, laboratory tests, and clinical courses of acute Hepatitis A infection. Prevention strategies like immunoglobulin and vaccination are summarized. Risk factors, transmission routes, and importance of screening blood products for Hepatitis B are also highlighted.

1. Hepatitis
By : Somayyeh nasiripour,Pharm.D
Clinical pharmacist
Assistant professor at Iums

4. CAUSATIVE AGENTS AND
CHARACTERISTICS
These hepatotrophic viruses are identified by the letters A through E
Hepatitis A through E viruses differ in their immunologic characteristics and
epidemiologic patterns
Fecal-oral transmission is the primary mode o infection for HAV and HEV,
percutaneous transmission is characteristic of HBV, HCV, and HDV
Several other viruses primarily affect nonhepatic organ systems and may
secondarily induce a hepatitis like syndrome.

6. ‫هپاتیت‬ ‫فازهای‬
Incubation period
prodromal phase
Icteric phase
recovery phas

7. Definitions of Acute and
Chronic
Hepatitis

8. • an illness with a discrete date of onset
with jaundice or increased serum
aminotransferase concentrations greater
than 2.5 times ULN
• Acute infection lasts as long as, but not
exceeding, 6 months.
Acute
hepatitis
•an inflammatory condition of the liver that
involves ongoing hepatocellular necrosis for 6
months or more beyond the onset of acute
illness.
•The most common cause of chronic hepatitis is
HBV or HCV
•Drug-induced and autoimmune chronic hepatitis
occur less frequently, whereas metabolic
disorders and HDV chronic hepatitis are
relatively rare
Chronic
hepatitis

9. HEPATITIS A VIRUS

10. single-stranded RNA virus that is classifie as a picornavirus in the Hepatovirus genus
HAV has a worldwide distribution
The prevalence of infection is related to the quality of the water supply, level of
sanitation, and age
The virus resists degradation by environmental conditions, gastric acid, and digestive
enzymes in the upper (GI) tract, thus, is readily spread within a population
Rates in males are greater than those in females by about 20%
Vaccination in children (age 12–23 months and maintenance from 2 to 18 years) has
resulted in a decline in the incidence of HAV infection to
Additionally, cyclic outbreaks of HAV have been reported among users of injection and
noninjection drugs and in men who have sex with men

12. The most common risk factors for
acquiring HAV
close contact with a person positive for HAV (26%)
Employment or attendance at a day-care center
(14%)
injection drug use (11%),
recent travel (4%),
association with a
suspected food or
water-borne
outbreak (3%)

13. Exceedingly rare causes of HAV include transfusion of blood or
blood products collected from donors during the viremic phase of
their infection
percutaneous transmission is rare because no asymptomatic
carrier state for HAV exists and the incubation period is brief.
Occupations at risk for HAV infection include sewage workers,
hospital cleaning personnel, day-care staff, and pediatric nurses
HAV is the most common preventable (e.g., vaccination) infection
in travelers visiting locations with poor hygienic conditions

14. Pathogenesis
the exact mechanism of injury is
unknown
Viral replication occurs within the
liver.
Subsequent hepatocyte death
results in viral elimination and
eventual resolution of the clinical
illness

15. •liver Enzyme
test(ALP, AST , ALT)(LET)
•liver function test
(INR , PT,Alb,Bil(LFT)

16. Natural History
typically a benign, self-limited
infection, with recovery
within 2 months of disease
onset
Two atypical courses of acute
HAV infection have also been
described: prolonged
cholestasis and relapsing
hepatitis

17. • duration of jaundice exceeds 12 weeks
• Associated with pruritus, fatigue, loose stools, and weight loss
• Aminotransferase concentrations during this period are less
than 500 units/L
prolonged
cholestasis
• occurs in 6% to 12% of both adult and pediatric patients
• characterized by an initial phase of acute infection followed
by remission (duration of 4–15 weeks), with subsequent
relapse
• Aminotransferase concentrations often normalize during the
time of remission but increase to greater than 1,000 units/L
with relapse
• HAV RNA is detectable in the serum, and HAV is usually
recovered from the stool during relapse
Relapsing or
polyphasic
• Rare but often fatal
• Patients older than 40 years of age or younger than 11
years are more susceptible
• low serum HAV RNA levels and high bilirubin levels are
significantly associated with FHF
Fulminant
hepatitis A

18. • Complete clinical recovery is usually seen
within 2 months in 60% of patients and
virtually all patients within 6 months after
HAV infection.

19. Clinical Manifestations

20. ‫ویروس‬‫وارد‬‫بدن‬‫می‬،‫شود‬‫ویرمی‬‫می‬،‫دهد‬‫کمی‬‫بعد‬‫ویروس‬
‫در‬‫مدفوع‬‫دفع‬‫می‬‫شود‬(‫از‬‫هفته‬1‫تا‬5).IgM‫هفته‬1(‫قبل‬‫از‬
‫ظهور‬‫عالیم‬)‫و‬IgG‫در‬‫هفته‬2‫شروع‬‫به‬‫افزایش‬‫می‬‫کند،در‬
‫پیک‬‫عالیم‬‫بالینی‬ALT‫و‬AST‫به‬‫حداکثر‬‫می‬‫رسند‬(‫هفته‬4‫و‬5)
،‫آنزیم‬‫ها‬‫پس‬‫از‬12‫هفته‬‫نرمال‬‫می‬،‫شوند‬IgG‫یک‬‫هفته‬‫بعد‬
‫از‬IgM‫باال‬‫می‬‫رود‬‫ولی‬‫تا‬‫آخر‬‫عمر‬‫باال‬‫می‬‫ماند‬‫ولی‬
IgM‫بعد‬‫از‬12‫هفته‬‫به‬‫سمت‬‫نرمال‬‫شدن‬‫می‬‫رود‬

23. The incubation period for HAV is 15 to 50 days (average, 28) after inoculation
The host is usually asymptomatic during this stage of the infection;
Because HAV titers are highest inthe acute-phase fecal samples, the period of infectivity
is 14 and 21 days before the onset of jaundice to 7 or 8 days after jaundice.
InHAV infections, acute-phase serum and saliva are less infectious than fecal samples
urine and semen samples are not infectious.
Family members and persons recently in immediate contact with E.T. should be notified

24. Feces >10 8 dose / ml
Serum 10 4 – 106 dose / ml
Saliva 10 2 – 104 dose / ml
Urine 0

25. The symptoms of acute viral hepatitis caused by HAV, HBV, HCV,HDV, and
HEV are similar.
Generally, symptoms of HAV infection present a week or more before the
onset of jaundice
In children younger than 6 years of age, 70% of infections are
asymptomatic,
Whereas older children and adults have symptomatic disease with
jaundice occurring in more than 70% of cases
E.T. has signs and symptoms of acute HAV infection, including the
nonspecific prodromal symptoms of fatigue,weakness, anorexia, nausea,
and vomiting.
Abdominal pain and hepatomegaly are common

26. Within 1 to 2 weeks of the onset of prodromal symptoms, patients may
enter an icteric phase with symptoms, including clay-colored stools
(usually is observed during the icteric phase), dark urine, scleral icterus,
and frank jaundice.
The dark urine is caused by bilirubin, generally occurring shortly before
the onset of jaundice.
RUQ tenderness, mild liver enlargement, and splenomegaly may also be
present in patients with acute HAV infection

27. Serum transaminase concentrations increase during the
prodromal phase (usually ALT > AST) of HAV infection,
peaking before the onset of jaundice.
Serum bilirubin peaks after aminotransferase activity and
rarely exceeds 10 mg/dL
Bilirubin levels decline more slowly than aminotransferases
and generally normalize within 3 months

28. Diagnosis and Serology

29. • Detection of IgM to HAV in a patient who
presents with clinical characteristics of
hepatitis or in an asymptomatic patient with
elevated transaminases is consistent with
acute HAV infection.

30. • appears after IgM and is indicative
of previous exposure and
immunity to HAV
HAV IgG
• commonly present throughout the
disease course (16–40 weeks),
• usually peaking early and declining to
undetectable levels 3 to 4 months after
the initial infection
• 25% IgM present for up to 6 months, and
longer
Anti-
HAV IgM

31. Treatment

32. HAV infection is usually a self-limited disease.
Drug treatment does not significantly alter the course of the disease
Patients should continue their normal activities as much as possible
while avoiding physical exhaustion.
(IV) fluid and electrolyte replacement, nutritional support, and the
use of antiemetics may be necessary in some patients.
Antipyretics (acetaminophen) should not be used because the risk of
FHF could increase
Patients should abstain from alcohol during the acute phase of the
disease.
After resolution of symptoms and serum biochemical abnormalities,
moderate alcohol intake is no longer contraindicated

33. Adjustment of Medication Doses

34. Dosage adjustments for hepatically eliminated drugs in the
setting of liver disease are difficult to predict.
because hepatic metabolism is complex, involving numerous
oxidative and conjugative pathways that are variably affected
in hepatic disease
Laboratory tests that approximate the synthetic function of
the liver (albumin, PT) and biliary clearance (bilirubin) are
used to estimate the degree of hepatic impairment, but
these tests are not dependable in predicting alterations
Unnecessary and potentially hepatotoxic medications should
be avoided during the acute phase of the illness
When drug therapy is indicated with agents undergo hepatic
elimination, it is prudent to use the lowest doses possible to
achieve the desired therapeutic effect

36. Prevention of Hepatitis A

37. • temporary protective antibody in
the formof immunoglobulin is
administered
passive
immunization
• a vaccine is administered to induce
the formation of protective antibody
Active
immunization

38. Pre-Exposure Prophylaxis
•

39. immunoglobulin
Before hepatitis A vaccinewas available, the sole therapy for
preexposure prophylaxis of HAV was immunoglobulin
Although passive immunization with immunoglobulin alone is
highly effective in preventing HAV infection, the duration of
protection is short
dose of 0.02mL/kg ofimmunoglobulin (IM) protection for lessthan
3 months
dose of 0.06 mL/kg confers protection for 5 months or longe

40. VACCINE

42. A vaccine can be administered in healthy people age 12 months to 40 years within 14 days
of exposure to HAV
at this time, individuals outside of this age range or with significant comorbid conditions
should receive immunoglobulin instead of the vaccine
Contacts who have received a dose of hepatitis A vaccine at least 1 month before exposure
do not need immunoglobulin, because protective antibody titers are achieved in greater
than 95% of patients 1 month after vaccination
Prophylaxis is not recommended for casual contacts at work or school
Protection after immunoglobulin administration is immediate and complete but short-lived

43. Immunoglobulin is recommended for all staff and children
in day-care settings when a case of hepatitis A virus
infection is diagnosed among employees or attendees.
When immunoglobulin is required for infants or pregnant
women, preparations free of thimerosal should be used
MMR and varicella vaccine should be delayed for at least 3
months after administration of immunoglobulin for HAV
prophylaxis
Immunoglobulin should not be given within 2 weeks after
the administration of MMR or varicella vaccine
immunoglobulin does not impede the immune response to
inactivated vaccines

44. HEPATITIS B VIRUS

46. •DNA‫ویروس‬،‫است‬‫از‬‫خانواده‬‫هپادوناویروس‬‫هاست‬.
•‫عالوه‬‫بر‬‫انسان‬‫در‬‫اردک‬‫پکنی‬‫و‬‫سنجاب‬‫هم‬‫وجود‬‫دارد‬.
•‫اگر‬‫ژنوم‬‫ویروس‬‫را‬‫در‬‫نظر‬،‫بگیریم‬‫ژن‬S،HBS Ag‫را‬‫می‬
،‫سازد‬‫ژن‬C،‫دو‬‫تا‬‫آنتی‬‫ژن‬HBc‫و‬HBe‫را‬‫می‬‫سازد‬.
•‫مارکرهای‬‫مهم‬‫هپاتیت‬B،HBS Ag،HBc Ag‫و‬HBe Ag
‫هستند‬.
•HBc Ag‫را‬‫در‬‫داخل‬‫سرم‬detect‫نمی‬‫کنیم‬‫و‬‫فقط‬‫داخل‬
‫هپاتوسیت‬‫هاست‬‫پس‬‫برای‬‫بررسی‬‫مارکرهای‬‫ویروسی‬‫س‬‫رم‬
HBc Ag‫را‬‫نمی‬‫خواهیم‬.‫اگر‬‫بخواهیم‬‫میتوانیم‬‫برای‬‫ناقلی‬‫ن‬‫آن‬
‫بیوپسی‬‫کبد‬‫انجام‬‫دهیم‬.

47. The most prominent risk factors
associated with acute HBV infection
include heterosexual contact (42%),
men having sex with men (15%),
and injection drug use (21%).
HBV is responsible for 1% to 14%of
chronic liver disease, more develop
in infants compared with adults

48. BLOOD AND BLOOD PRODUCTS
Although the risk of transfusion-
associated HBV infection has been
greatly reduced with the screening
of blood (tests for HBsAg and anti-
HBc) and the exclusion of donors
who engage in high-risk activities,
it is estimated that 1 of 50,000
transfused units transmit HBV
infection.

49. PERINATAL TRANSMISSION
High serum concentrations of virus have been linked with increased risk of
transmission by vertical routes (and needlestick exposure).
Infants born to HBeAg-positive mothers with high viral replication (>80 pg/mL)
have a 70% to 90% risk of perinatal HBV acquisition compared with a 10% to 40%
risk in infants born to mothers infected with HBV who are HBeAg negative
even with active and passive immunization,10% to 15% of babies acquire HBV
infection at birth.
In addition, children of HBsAg-positive mothers who are not infected at
birthremain at very high risk of early childhood infection, with 60% of those born
to HBsAg-positive mothers becoming infected by the age of 5 years.

50. SEXUAL TRANSMISSION
• the most significant mode of HBV transmission worldwide
• Heterosexual intercourse accounts for the majority of US infections
(26%)
• risk of HBV infection include duration of sexual activity, number of
sexual partners, anal-receptive intercourse and history of STD.
• Sexual partners of injection drug users, sex workers, and clients of
sex workers are at a very high risk for infection.
• Between 0% and 3% of contact spouses or sexual partners and
between 4% and 9% of household children are HBsAg positive
• Because most patients with chronic HBV infection are unaware of
their infection and are “silent carriers,” sexual transmission is a
significant mode of transmission.
• The use of condoms appears to reduce the risk of sexual
transmission

51. INJECTION DRUG USE
• accounting for approximately 23% of all
patients

52. OTHER MODES OF TRANSMISSION
• small breaks in the skin, biting, or mucous
membranes.
• semen, saliva, and serum actually contain
infectiousHBV
• Kissing is not considered to be a significant means
of HBV transmission, but biting could be
• high: blood, serum, wound exudate
• moderate: semen, vaginal fluid, saliva
• low: urine, feces, sweat, tear, breastmilk

54. Diagnosis

55. • The presence of HBsAg in serum is diagnostic
for HBV infection
• In 5% to 10% of acute caseswhich the HBsAg
levels fall below sensitivity thresholds
,presence of IgM anti- HBc in serum confirms
a recent acute HBV infection
• Persisting levels of HBV DNA indicate ongoing
infection and a high degree of active viral
replication and infectivity.

56. Serology

57. • Within the first several weeks after exposure
(range, 2–10 weeks), HBsAg appears in the blood
and is present for several weeks before serum
concentrations of aminotransferases increase and
symptoms
• HBsAg can be detected in serum until the clinical
illness resolves and usually becomes
undetectable after 4 to 6 months.
• Persistence of HBsAg beyond 6 months implies
progression to chronicHBVinfection

58. window” period
• Neither HBsAg nor anti-HBs are detectable
•‫شدن‬ ‫منفی‬ ‫بین‬ ‫زمانی‬ ‫ی‬ ‫دوره‬ ‫به‬HBS Ag‫شدن‬ ‫مثبت‬ ‫تا‬HBS
Ab‫که‬ ‫شود‬ ‫می‬ ‫گفته‬4-3‫کشد‬ ‫می‬ ‫طول‬ ‫هفته‬
•‫تنها‬‫مارکری‬‫که‬‫در‬‫این‬‫مرحله‬‫برای‬‫تشخیص‬‫هپاتیت‬‫حاد‬‫کمک‬‫ک‬‫ننده‬
‫باشد‬HBc Ab‫است‬
•‫این‬‫آنتی‬‫بادی‬‫با‬‫فاصله‬‫یک‬‫تا‬‫دو‬‫هفته‬‫از‬HBS Ag‫شروع‬‫به‬‫افزایش‬
‫می‬‫کند‬‫و‬‫زمانی‬‫که‬‫بیمار‬‫عالمت‬‫دارد‬‫به‬‫پیک‬‫می‬‫رسد‬‫و‬‫تا‬‫هفته‬32
‫مثبت‬‫می‬‫ماند‬.
•‫اگر‬‫در‬‫نسخه‬‫برای‬‫آزمایشگاه‬HBc Ab‫بنویسیم‬IgG‫را‬‫چک‬‫خواهد‬
‫کرد‬‫در‬‫حالی‬‫که‬‫برای‬‫بررسی‬‫حاد‬‫بودن‬IgM‫را‬‫نیاز‬‫داریم‬

61. •IgG HBc Ab‫از‬ ‫ای‬ ‫هفته‬ ‫یک‬ ‫فاصله‬ ‫با‬ ‫یا‬ ‫همزمان‬ ‫هم‬
IgM‫ماند‬ ‫می‬ ‫باقی‬ ‫مثبت‬ ‫عمر‬ ‫آخر‬ ‫تا‬ ‫و‬ ‫شود‬ ‫می‬ ‫مثبت‬
•‫هپاتیت‬ ‫شیوع‬ ‫بررسی‬ ‫برای‬ ‫که‬ ‫است‬ ‫مارکری‬B‫منطقه‬ ‫در‬
‫در‬ ‫هم‬ ‫و‬ ‫مزمن‬ ‫هپاتیت‬ ‫بیماران‬ ‫در‬ ‫هم‬ ‫چون‬ ‫رود‬ ‫می‬ ‫کار‬ ‫به‬
‫که‬ ‫افرادی‬recovery‫است‬ ‫مثبت‬ ‫اند‬ ‫شده‬

62. HBeAg
• detectable early during the acute phase of the disease
and persists in chronic hepatitis B infection
• marker of active HBV replication, and its presence
correlates with circulating HBV particles
• Presence of both HBeAg and HBsAg indicates a high
level of viral replication and infectivity and a need for
antiviral therapy
• seroconversion from HBeAg to hepatitis B envelope
antibody (anti-HBe) results in a reduction in HBVDNA
and suggests resolution of HBV infection

63. Hepatitis B core
• Antigen does not circulate freely in the bloodstream and is not
measured.
• Anti-HBc, the antibody directed against hepatitis B core antigen, is
usually detected 1 to 2 weeks after the appearance ofHBsAg and
just before the onset of clinical symptoms, and it persists for life
• IgM anti-HBc is the most sensitive diagnostic test for acute HBV
infection
• During the recovery phase of infection, the predominant form of
anti-HBc is in the IgG class , it shows prior or ongoing infection
withHBV
• Patients immunized againstHBV do not develop anti-HBc; therefore,
the presence of this antibody differentiates successful vaccination
from actual HBV infection.

64. • Up to 12% (average 5%) of immunocompetent patients acutely
infected with HBV remain chronically infected (historically defined
as detectable HBsAg in serum for 6 months or longer)
• In these patients, HBsAg generally remains detectable indefinitely
and anti-HBs fails to appear.
• The risk of chronicity after neonatally acquired infection is high
(>90%), possibly because neonates have immatureimmune systems.
• patients who have a reduced ability to clear viral infections—
including those receiving chronic hemodialysis, immunosuppression
after transplantation, or chemotherapy, or patients with HIV
infection— may have a greater risk for developing chronic HBV
infection
• Approximately 50% of all chronic carriers have ongoing viral
replication, especially with elevated aminotransferases, and 15% to
20% of these develop cirrhosis within 5 years
• chronic carriers remain infected throughout their life.
• risk of hepatocellular carcinoma (HCC) is increased up to 300 times
in chronic carriers with active viral replication (HBeAg positive

66. Clinical Manifestations

68. • The clinical features of acute HBV infection are
similar to those described for HAV infection.
• W.H.’s initial symptoms included a recent
history of nausea, vomiting, anorexia, scleral
icterus, and jaundice. These are consistent
with diagnosis of acute hepatitis B.
• His serologies, notably a positive IgM anti-HBc
and HBV DNA, also support this diagno

69. ACUTE LIVER FAILURE
• incidence of ALF is less than 1%
• prognosis for these patients is poor once
encephalopathy has developed
• defined as a coagulation abnormality (INR >1.5)
and any degree of mental alteration
(encephalopathy) in a patient of less than 26
weeks’ duration
• Patients with ALF often have cerebral edema
(80% mortality rate)
• cerebral edema may benefit from 100 to 200 mL
of a 20% solution of mannitol

70. TREATMENT
• supportive care for the comatose patient
• Blood products (packed red blood cells, fresh-
frozen plasma, or platelets) should be given as
develops active bleeding
• liver transplantation

72. Hepatitis B Vaccines
• One dose administered three times: at time 0, 1 month,
and 6 months
• A protective antibody response has been defined as anti-
HBs levels of at least 10 units/mL
• hyporesponders (anti HBslevels<10),50%to90%achieve a
protective level after a single booster injection or after
repeating the entire three-dose series
• no need exists for routine administration ofHBV vaccine
booster doses to immunocompetent persons after
successful vaccination
• for patients receiving chronic hemodialysis with
administration of a booster dose when antibody levels are
less than 10

73. POSTEXPOSURE PROPHYLAXIS

74. • After exposure to HBV, prophylactic treatment
with hepatitis B vaccination and possibly
passive immunization with hepatitis B
immunoglobulin (HBIG) should be considered
• single dose of HBIG 0.06 mL/kg (3.4 mL) as an
IM injection in either the gluteal or deltoid
region as soon as possible after exposure,
preferably within 24 hours.

77. • postexposure prophylaxis with 0.06 mL/kg of
HBIG as a single IM dose within 14 days of the
last exposure.
• Patients also should receive the standard
three-dose immunization series with hepatitis
B vaccine beginning at the time of HBIG
administration

79. • Infants born to HBV-infected mothers have a
greater than 85% risk of acquiring HBVduring
the perinatal period.
• Of those who become infected, 80% to 90%
become chronic HBsAg carriers

86. Interferon
• moderately effective
• HBeAg-positive patients with chronic HBV receiving
IFN-α may experience a virologic response based on
clearance of HBeAg (27%; range, 15%– 41%) or HBV
DNA (47%; range, 32%–79%)
• Normalization of ALT values is observed in 47%
Conventional
Interferon
• have slightly enhanced efficacy than standard IFN
formulations (
Pegylated
Interferon-
α2a

87. Dosing
• 30 to 35 million units/week, administered SC or IM
• 5 million units/day
• 10 million units three times weekly
• for patients who are HBeAg positive is for 16 to
24weeks.
• HBeAgnegative HBV infection should be treated for
at least 12 months
• and possibly for 24 months to enhance the rate of
sustained response
Conventional
Interferon
•180 mcg SCweekly
for 48weeks
Pegylated
Interferon

89. Predictors of Response
• high pretreatment ALT levels (greater than
twice the upper limitof normal) and HBV DNA
levels less than 200 pg/mL
• HBeAg seroconversion with IFN treatment
• short duration of disease,
• negative HIV status,
• HBV genotypes A and B may respond better
than genotypes C and D

90. Adverse Effects
• rarely limit the use
• appear hours after administration
• an influenzalike syndrome with fever, chills,
anorexia, nausea, myalgias, fatigue, and headache
• Almost all patients experience
• resolve after repeated exposure
• at bedtime may decrease the severity
• Acetaminophen can be used, but should be limited
to 2 g/day to minimize the risk of hepatotoxicity
early
side
• may necessitate dose reduction or
discontinuation of therapy
• Observed after 2 weeks of therapy
• include worsening of the influenzalike
syndrome, alopecia, bone marrow suppression,
bacterial infections, thyroid dysfunctionand
psychiatric disturbances
• increase) in ALT levels in 30% to 40% of
patients
late side
effects

91. • Use of IFNs in patients with decompensated
liver disease may lead to FHF

92. NUCLEOSIDE/NUCLE
OTIDE ANALOGS
Lamivudine
Adefovir
Entecavir
Tenofovir

95. Lamivudine
• first nucleoside analog approved by the
• FDA for use in patients with compensated liver
disease who had evidence of active viral
replication and liver inflammation caused by
chronic hepatitis B
• well tolerated and reduces serum levels of
HBV DNA.

96. Lamivudine Resistance
• detectable after 6 months or more of
continuous therapy.
• Data from four studies show a 16% to 32%
incidence at 1 year, increasing to 47% to 56%
at 2 years of therapy and 69% to 75% at 3
years of therapy

97. ‫هپاتیت‬C

99. ‫انتقال‬ ‫راههای‬
•،‫مخدر‬ ‫مواد‬ ‫تزریق‬ ،‫خونی‬ ‫های‬ ‫فرآورده‬ ‫و‬ ‫خون‬ ‫تزریق‬Sexual،
‫جنین‬ ‫به‬ ‫مادر‬ ‫انتقال‬(‫است‬ ‫کم‬ ‫خیلی‬ ‫که‬. )
•‫که‬ ‫فردی‬needle stick‫هپاتیت‬ ‫برای‬ ‫شود‬ ‫می‬B‫معلوم‬ ‫تکلیف‬ ‫که‬
‫که‬ ‫نزده‬ ‫واکسن‬ ‫یا‬ ‫ساخته‬ ‫بادی‬ ‫آنتی‬ ‫که‬ ‫زده‬ ‫واکسن‬ ‫یا‬ ‫است‬HBIG‫می‬
‫زند‬(‫است‬ ‫موجود‬)‫هپاتیت‬ ‫مورد‬ ‫در‬ ‫ولی‬C‫نه‬ ‫و‬ ‫دارد‬ ‫دارو‬ ‫نه‬
‫پیشگیری‬!‫باید‬ ‫را‬ ‫این‬follow‫کنیم‬
•PCR‫بگیریم‬,‫ی‬ ‫هفته‬ ‫آزمایشات‬4‫ی‬ ‫هفته‬ ‫و‬12‫شوند‬ ‫می‬ ‫تکرار‬
•‫شد‬ ‫مثبت‬ ‫بازه‬ ‫این‬ ‫در‬ ‫اگر‬acute‫است‬.
•acute‫نه‬ ‫دارد؟‬ ‫درمان‬ ‫به‬ ‫نیاز‬ ‫ی‬!‫هفته‬ ‫تا‬12‫اگر‬ ‫کنیم‬ ‫می‬ ‫صبر‬
‫شود‬ ‫درمان‬ ‫باید‬ ‫نشد‬ ‫منفی‬ ‫اگر‬ ‫و‬ ‫است‬ ‫حل‬ ‫که‬ ‫شد‬ ‫منفی‬ ‫خودش‬.

100. •%‫هپاتیت‬C‫که‬ ‫شود‬ ‫می‬ ‫مزمن‬80%‫آن‬stable‫و‬ ‫مانده‬
10-20%‫هم‬ ‫سیروز‬ ،‫رود‬ ‫می‬ ‫سیروز‬ ‫سمت‬ ‫به‬ ‫آن‬75%
slowly progressive‫و‬25%‫به‬ ‫و‬ ‫بوده‬ ‫خطرناک‬ ‫خیلی‬
‫دارد‬ ‫نیاز‬ ‫کبد‬ ‫پیوند‬.
•‫هپاتیت‬ ‫سیر‬ ‫در‬ ‫اگر‬C , ,HBV HIV‫یا‬ ‫و‬Alcohol‫اضافه‬ ‫هم‬
‫شو‬ ‫می‬ ‫بیشتر‬ ‫خیلی‬ ‫سرعت‬ ‫شود‬

101. •‫آن‬ ‫کمون‬ ‫دوره‬6-8‫است‬ ‫هفته‬.
•‫حاد‬ ‫فاز‬ ‫در‬ ‫بالینی‬ ‫عالیم‬(‫کند‬ ‫بروز‬ ‫اگر‬)‫ز‬ ‫صورت‬ ‫به‬‫ردی‬
‫بود‬ ‫خواهد‬.
•‫و‬ ‫شده‬ ‫مزمن‬ ‫عموما‬ ‫ولی‬Protection‫دهد‬ ‫می‬ ‫که‬ ‫هم‬.
•‫حاد‬ ‫فاز‬ ‫در‬HCV RNA،‫است‬ ‫مثبت‬HCV Ab‫است‬ ‫مثبت‬
‫زمان‬ ‫مرور‬ ‫به‬ ‫ولی‬acute‫بخواهد‬ ‫که‬ ‫ی‬recovery‫داشته‬
‫باشد‬HCV RNA‫ولی‬ ‫شود‬ ‫می‬ ‫منفی‬HCV Ab‫تواند‬ ‫می‬
‫بماند‬ ‫باقی‬ ‫مثبت‬ ‫سالها‬

102. ‫هپاتیت‬ ‫بین‬ ‫فرق‬C ‫که‬Resolved ‫که‬ ‫مزمن‬ ‫و‬ ‫شده‬
‫چیست؟‬ ‫دارد‬ ‫درمان‬ ‫به‬ ‫نیاز‬
•‫در‬resolve،HCV RNA‫مزمن‬ ‫در‬ ‫ولی‬ ‫است‬ ‫منفی‬HCV
RNA‫باالست‬ ‫کبدی‬ ‫های‬ ‫آنزیم‬ ‫و‬ ‫است‬ ‫مثبت‬

105. •‫تست‬screening،‫قطعا‬HCV Ab‫است‬.
•‫عمال‬ ‫درمان‬ ‫شروع‬ ‫برای‬ ‫قطعی‬ ‫تست‬PCR‫باید‬ ‫که‬ ‫است‬
‫ژنوتایپ‬ ‫بعد‬ ‫و‬ ‫باشد‬ ‫معلوم‬ ‫ویروس‬ ‫تعداد‬ ‫و‬ ‫باشد‬ ‫کمی‬
‫ودوره‬ ‫درمان‬ ‫نوع‬ ‫روی‬ ‫چون‬ ‫باشد‬ ‫معلوم‬ ‫باید‬ ‫هم‬ ‫ویروس‬
‫است‬ ‫موثر‬ ‫خیلی‬ ‫درمان‬ ‫ی‬.
•‫ژنوتایپ‬2‫و‬3،‫دارند‬ ‫کوتاهتری‬ ‫درمان‬ ‫دوره‬ ‫و‬ ‫بوده‬ ‫خوب‬
‫ژنوتایپ‬1‫و‬4‫هستند‬ ‫بد‬.

106. Ab testing
•sensitivity‫ولی‬ ‫باالست‬ ‫نسبتا‬specificity‫در‬ ‫بخصوص‬ ‫نیست‬ ‫باال‬ ‫آن‬
‫می‬ ‫کاذب‬ ‫مثبت‬ ‫باعث‬ ‫چون‬ ‫دارند‬ ‫همراه‬ ‫اتوایمیون‬ ‫بیماری‬ ‫که‬ ‫هایی‬ ‫خانم‬
‫شود‬.‫از‬ ‫اگر‬ELISA‫تست‬ ‫عنوان‬ ‫به‬screening‫هم‬ ‫و‬ ‫مثبت‬ ‫هم‬ ‫بکنیم‬ ‫استفاده‬
‫دارد‬ ‫کاذب‬ ‫منفی‬.‫در‬ ‫هنوز‬ ‫فرد‬ ‫یک‬ ‫یعنی‬ ‫کاذب‬ ‫منفی‬window‫و‬ ‫است‬
‫هنوز‬Ab‫است‬ ‫نساخته‬.‫پس‬ ‫هاست‬ ‫خانم‬ ‫در‬ ‫خصوص‬ ‫به‬ ‫هم‬ ‫کاذب‬ ‫مثبت‬
‫شود‬ ‫قطعی‬ ‫تشخیص‬ ‫تا‬ ‫دهیم‬ ‫انجام‬ ‫تاییدی‬ ‫تستهای‬ ‫باید‬ ‫حتما‬.
•‫تاییدی‬ ‫تست‬RIBA‫تست‬ ،‫است‬RIBA،specificity‫یعنی‬ ‫باالست‬ ‫خیلی‬
‫هپاتیت‬ ‫قطعا‬ ‫مریض‬ ‫پس‬ ‫شود‬ ‫مثبت‬ ‫اگر‬ ‫و‬ ‫ندارد‬ ‫کاذب‬ ‫مثبت‬C‫دارد‬
•‫بیماری‬ ‫اینکه‬ ‫حاال‬Chronic‫هپاتیت‬ ‫یا‬ ‫است‬C‫رو‬ ‫شده‬ ‫خوب‬ ‫و‬ ‫گرفته‬PCR
‫کند‬ ‫می‬ ‫مشخص‬.PCR‫یعنی‬ ‫باشد‬ ‫مثبت‬HCV‫می‬ ‫دارو‬ ‫و‬ ‫است‬ ‫مثبت‬
،‫خواهد‬PCR‫شده‬ ‫خوب‬ ‫و‬ ‫گرفته‬ ‫هپاتیت‬ ‫یعنی‬ ‫باشد‬ ‫منفی‬

107. •‫ی‬ ‫جامعه‬ ‫در‬high risk‫شاید‬ ‫حتی‬RIBA‫و‬ ‫نباشد‬ ‫الزم‬ ‫هم‬
‫فقط‬PCR‫کنیم‬.‫حاال‬ ‫شد‬ ‫منفی‬ ‫اگر‬RIBA‫که‬ ‫کنیم‬ ‫درخواست‬ ‫را‬
‫هپاتیت‬ ‫شاید‬C‫است‬ ‫شده‬ ‫خوب‬ ‫و‬ ‫گرفته‬ ‫را‬
•.‫جمعیت‬ ‫در‬ ‫ولی‬Low risk‫برای‬ ‫که‬ ‫خانمی‬ ‫مثل‬check up
‫یا‬ ‫و‬ ‫رفته‬blood donor،positive predictive value50-
61%‫اس‬ ‫بهتر‬ ‫را‬ ‫این‬ ‫که‬ ‫دارد‬ ‫کاذب‬ ‫مثبت‬ ‫خیلی‬ ‫یعنی‬ ‫است‬‫با‬ ‫ت‬
RIBA‫کنیم‬ ‫تایید‬
•‫که‬ ‫کسی‬RIBA‫هپاتیت‬ ‫قطعا‬ ‫است‬ ‫منفی‬ ‫ش‬C‫ولی‬ ‫ندارد‬RIBA
‫مثبت‬PCR‫دارد‬ ‫نیاز‬

108. Management
•‫هپاتیت‬ ‫واکسن‬ ،‫نکند‬ ‫استفاده‬ ‫الکل‬A‫و‬B‫بزند‬ ‫را‬(‫قبل‬ ‫البته‬
‫ب‬ ‫یا‬ ‫زده‬ ‫واکسن‬ ‫قبال‬ ‫اگر‬ ‫کنیم‬ ‫چک‬ ‫را‬ ‫بادی‬ ‫آنتی‬ ‫ازآن‬‫یماری‬
‫نیا‬ ‫واکسن‬ ‫دیگر‬ ‫دارد‬ ‫باالیی‬ ‫تیتر‬ ‫االن‬ ‫و‬ ‫گرفته‬ ‫را‬‫نیست‬ ‫ز‬.)
‫هپاتیت‬ ‫تشخیص‬ ‫بیمار‬ ‫برای‬ ‫اگر‬C‫است‬ ‫شده‬ ‫گذاشته‬ ‫مزمن‬
‫ک‬ ‫بیوپسی‬ ‫کبدی‬ ‫های‬ ‫آنزیم‬ ‫بودن‬ ‫نرمال‬ ‫با‬ ‫حتی‬ ‫باید‬‫یا‬ ‫و‬ ‫بد‬
‫شود‬ ‫انجام‬ ‫فیبرواسکن‬(‫هپاتیت‬ ‫خالف‬ ‫بر‬B‫ها‬ ‫آنزیم‬ ‫وقتی‬ ‫که‬
‫دادیم‬ ‫می‬ ‫انجام‬ ‫بیوپسی‬ ‫بود‬ ‫نرمال‬ ‫برابر‬ ‫دوسه‬)

109. ‫درمان‬