Hepatitis B is a viral infection that affects the liver and can become chronic. It was first described in the 5th century and major developments in understanding the virus occurred between the 1940s-1970s with the identification of antigens and viral particles. The virus is classified taxonomically and has an overlapping genome encoding various antigens. It exists in different morphological forms and has multiple genotypes and serotypes. Hepatitis B is transmitted through blood or bodily fluids and has various stages from acute to chronic infection. Diagnosis involves detecting antigens, antibodies, and viral DNA through serological and molecular tests. Vaccination and antiviral treatment can help prevent and manage the disease.
Viral hepatitis is the leading cause of liver cancer and the most common reason for liver transplantation
In the United States, an estimated 1.2 million Americans are living with chronic Hepatitis B and 3.2 are living with chronic Hepatitis C
Many do not know they are infected
Each year an estimated 21,000 persons become infected with Hepatitis A; 35,000 with Hepatitis B, and 17,000 with Hepatitis C
Hepatitis A – fecal/oral, contaminated food, vaccine available
Hepatitis B – blood, semen, vertical (mother-child), vaccine available
Hepatitis C – blood (IV drug use, transfusion, organ donation, unsterile injecting equipment, sexual intercourse)
Hepatitis D – survives only in cells co-infected with hepatitis B
Hepatitis E* – contaminated food or water, fecal/oral
*causes short-term disease and is not a chronic carrier state
The primary treatment goals for patients with hepatitis B (HBV) infection are to prevent progression of the disease, particularly to cirrhosis, liver failure, and hepatocellular carcinoma (HCC).
Risk factors for progression of chronic HBV include the following :
Persistently elevated levels of HBV DNA and, in some patients, alanine aminotransferase (ALT), as well as the presence of core and precore mutations seen most commonly in HBV genotype C and D infections
Male sex
Older age
Family history of HCC
Alcohol use
Elevated alpha-fetoprotein (AFP)
Coinfection with hepatitis D (delta) virus (HDV), hepatitis C virus (HCV), or human immunodeficiency virus (HIV)
A synergistic approach of suppressing viral load and boosting the patient’s immune response with immunotherapeutic interventions is needed for the best prognosis. The prevention of HCC often includes the use of antiviral treatment using pegylated interferon (PEG-IFN) or nucleos(t)ide analogues.
HBV infection can be self-limited or chronic. No specific therapy is available for persons with acute hepatitis B; treatment is supportive.
Viral hepatitis is the leading cause of liver cancer and the most common reason for liver transplantation
In the United States, an estimated 1.2 million Americans are living with chronic Hepatitis B and 3.2 are living with chronic Hepatitis C
Many do not know they are infected
Each year an estimated 21,000 persons become infected with Hepatitis A; 35,000 with Hepatitis B, and 17,000 with Hepatitis C
Hepatitis A – fecal/oral, contaminated food, vaccine available
Hepatitis B – blood, semen, vertical (mother-child), vaccine available
Hepatitis C – blood (IV drug use, transfusion, organ donation, unsterile injecting equipment, sexual intercourse)
Hepatitis D – survives only in cells co-infected with hepatitis B
Hepatitis E* – contaminated food or water, fecal/oral
*causes short-term disease and is not a chronic carrier state
The primary treatment goals for patients with hepatitis B (HBV) infection are to prevent progression of the disease, particularly to cirrhosis, liver failure, and hepatocellular carcinoma (HCC).
Risk factors for progression of chronic HBV include the following :
Persistently elevated levels of HBV DNA and, in some patients, alanine aminotransferase (ALT), as well as the presence of core and precore mutations seen most commonly in HBV genotype C and D infections
Male sex
Older age
Family history of HCC
Alcohol use
Elevated alpha-fetoprotein (AFP)
Coinfection with hepatitis D (delta) virus (HDV), hepatitis C virus (HCV), or human immunodeficiency virus (HIV)
A synergistic approach of suppressing viral load and boosting the patient’s immune response with immunotherapeutic interventions is needed for the best prognosis. The prevention of HCC often includes the use of antiviral treatment using pegylated interferon (PEG-IFN) or nucleos(t)ide analogues.
HBV infection can be self-limited or chronic. No specific therapy is available for persons with acute hepatitis B; treatment is supportive.
La hepatitis B es una enfermedad del hígado causada por el virus de la hepatitis B, perteneciente a la familia Hepadnaviridae (virus ADN hepatotrópico), caracterizada por necrosis hepatocelular e inflamación. Puede causar un proceso agudo o un proceso crónico, que puede acabar en Cirrosis (pérdida de la "arquitectura" hepática por cicatrización y surgimiento de nódulos de regeneración) del hígado, Cáncer de hígado, Insuficiencia hepática e incluso la muerte.
Non-Gonococcal urethritis. main causative organisms are Chlamydiae, Mycoplasma, Ureaplasma. various other bacteria and viruses can cause this. this powerpoint is made in systemic manner and will be helpful for Postgraduate students.
Interpretation of Hepatitis B Serologic Test Resultsru5dy
With the Laboratory Results you need to have interpretation of the patients who have check their blood for Hepatitis B test. This slide will guide you through how to interpretation of Hepatitis B Test Laboratory Results.
A serious liver infection caused by the hepatitis B virus that's easily preventable by a vaccine.
This disease is most commonly spread by exposure to infected bodily fluids.
Symptoms are variable and include yellowing of the eyes, abdominal pain and dark urine. Some people, particularly children, don't experience any symptoms. In chronic cases, liver failure, cancer or scarring can occur.
The condition often clears up on its own. Chronic cases require medication and possibly a liver transplant.
Introduction to chronic Hepatitis B Infection in Malaysia, epidemiology and common treatment. Phases of chronic Hepatitis B Infection, clinical presentation and complications.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
2. Introduction
• Hepatitis was first described as early as 5th century.
• First documented blood borne outbreak occurred in
Bremen, Germany in 1883.
• 1947:MacCallum and Bauer introduced the term
Hepatitis B , later adopted by WHO(1973)
• 1965:Blumberg and his coworkers described the a
protein antigen: Australia antigen
• 1970:Dane and his coworkers described the
complete Hepatitis B or Dane particle.
• 1972: Magnius and Espmark described the HBeAg.
2Dr.Ruqaiyah
3. Taxonomy
• Group: Group VII(ds DNA RT)
• Order: Unassigned
• Family:
Hepadnaviridae Avihepadnaviridae Not assingned
• Genus: Orthohepadnavirus
• Species:
Hepatitis B Ground Squirrel Wood Chuck Wolly Monkey
Hepa. Hepa. Hepa.
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8. • HBsAg is antigenically complex
• Group reactive antigen- a
• Type specific antigen- d/y and w/r
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9. Typing of HBV
Serotypes
• Its divided into 4 serotypes adr, adw, ayr, ayw
Genotypes
• Eight genotypes A- H
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10. Genome
Gene Regions Antigen
S S Major protein(S) HBsAg
(Having 3 regions S,S1,Pre S2) S+ Pre S2 Middle protein(M)
S+ Pre S1& S2 Large protein(L):Present only in virion
C C HBcAg
(Having 2 regions C & Pre C) C+ Pre C HBeAg
P DNA Polymerase
X HBxAg(Not particulate antigen)
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11. Genome
• Genome is approx. 3200 base long and contains
overlapping genes.
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14. Epidemiology
• Reservoir of infection
– Cases
– Carriers
• Carriers
– Simple carriers
– Super carriers
• Prevalence
– Low endemicity- <2 %. Nepal, SriLanka
– Intermediate endemicity- 2-8%. India, bhutan,
Indonesia, Maldives
– High endemicity- >8 %. Bangladesh, korea
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15. • 2 billion people have been infected (1 out of 3
people).
• 350 million people are chronically infected.
• An estimated 6 lakh people die each year from
hepatitis B and its complications.
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16. In India
• The average estimated carrier rate of hepatitis B
virus (HBV) is 3.7%.
• An approximate total of 40 million HBV carriers
• South indians have high carrier rates
• Second most common cause of acute hepatitis after
HEV.
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17. Age
• Chance of developing acute hepatitis is directly
related to age
• 1% (perinatal)
• 10 % (early childhood)
• 30 % ( late childhood)
• Chance of developing chronic hepatitis is inversely
proportional to age
• 80-90 % (perinatal)
• 30% (early childhood)
• 5% (late childhood)
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19. Clinical manifestations
• Incubation period 30-180 days
• It is indistinguishable from other hepatitis viruses
• Pre-icteric phase- nausea, vomiting
• Icteric phase- jaundice
• Hepatic complications- fulminant hepatitis, cirrhosis,
HCC
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20. Continued…
• 4 phases
Immuno tolerance
Immuno clearance
Inactive HBsAg carrier
HBeAg – CHB
Occult Hepatitis B
Phase HBeAg serological status Pattern Indications for treatment
1. “Immune tolerant” HBeAg positive • Stage seen in many HBeAg-positive children and young
adults, particularly among those infected at birth
• High levels of HBV replication (HBV DNA levels >200 000
IU/mL))
• Persistently normal ALT
• Minimal histological disease
Treatment not generally
indicated, but monitoring
required
2. “Immune active”
(HBeAg-positivea
chronic hepatitis)
HBeAg positive; may
develop anti-HBe
• Abnormal or intermittently abnormal ALT
• High or fluctuating levels of HBV replication (HBV DNA
levels >2000 IU/mL)
Histological necroinflammatory activity present
• HBeAg to anti-HBe seroconversion possible, with
normalization of ALT leading to “immune-control” phase
Treatment may be
indicated
3. Inactive chronic
hepatitis “Immune
control”
(previously called
inactive carrier)
HBeAg negative, anti-
HBe positive
• Persistently normal ALT
• Low or undetectable HBV DNA ( HBV DNA levels <2000
IU/mL)
• Risk of cirrhosis and HCC reduced
• May develop HBeAg-negative disease
Treatment not generally
indicated, but monitoring
required for reactivation
and HCC
4. “Immune escape”
(HBeAg-negative
chronic hepatitis)
HBeAg negative, with or
without being anti-HBe
positive
• HBeAg negative and anti-HBe positive
• Abnormal ALT (persistent or intermittently abnormal)
• Moderate to high levels of HBV replication (HBV DNA levels
>20 000 IU/mL)
• Older persons especially at risk for progressive disease
(fibrosis/cirrhosis)
Treatment may be
indicated
5.“Reactivation” or
“acute-on-chronic
hepatitis”
HBeAg positive or
negative
• Can occur spontaneously or be precipitated by
immunosuppression from chemo– or immunosuppressive
therapy, HIV infection or transplantation, development of
antiviral resistance, or withdrawal of antiviral therapy
• Abnormal ALT
• Moderate to high levels of HBV replication
• Seroreversion to HBeAg positivity can occur if HBeAg
negative
• High risk of decompensation in presence of cirrhosis
Treatment indicated
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21. Collection, Transport and Storage
of Specimens
• HBV infection is diagnosed by serological and
molecular methods using serum and plasma.
• In general HBV antigens and antibodies are stable at
room temperature for several hours to days,can be
stored at 4ᴼC for months and can be frozen at -20ᴼC
to -70ᴼC for many years.
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24. HBsAg
• Appears in 1-12 weeks of infection (8-12 wks)
• Presence indicates onset of infectivity
• Becomes undetectable 1-2 months after
jaundice
• Used to calculate prevalence
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25. HBeAg and HBV DNA
• Appear shortly after appearance of HBsAg
• They are markers of-
– Active viral replication
– High viral infectivity
• They cannot differentiate stages
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27. Anti-HBc IgM
• Appears 1-2 wks after HBsAg and lasts for 3-6
month
• Indicates acute infection
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28. Anti- HBc IgG
• Appears in late stage and remains positive
indefinitely
• Chronic stage
• Carrier stage
• Recovery
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29. Total Anti HBc
• Negative indicates that a person has not been
infected with HBV.
• Indicate Acute: (HBsAg +ve; IgM Anti HBc +ve)
Resolved(HBsAg –ve)
Chronic(HBsAg +ve)
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30. Anti- HBe
• Appear after clearance of HBeAg
• Indicates diminished replication and
decreased infectivity
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31. Anti -HBs
• Appears after clearance of HBsAg remains
indifinetly
• Indicates recovery, immunity, non infectivity
• Marker of hepatitis B vaccination
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34. Microscopy
• Microscopic detection of HBV does not play a specific
role in the Diagnosis of disease.
• However liver Biopsy is typically used to assess the
extent of Histologic involvement and damage as well
as a response to therapy.
Culture
• Athough HBV can infect hepatocytes in vitro,culture
of HBV is not used for the diagnosis of infection.
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35. Antigen Detection
• A marker of active viral replication is the detection of
HBsAg and/or HBeAg during primary infection and
during Chronic HBV infection.
• Both the antigens are produced in excess by the
infected hepatocytes.
• Detected by:
ELISA
Immunochromatographic tests
Enzyme inmmunoassays Detects >=0.1ng/ml
Radio immunoassays
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36. HBsAg
• Approved by FDA for Diagnostic use only.
• Any specimen nonreactive for HBsAg are considered
negative and do not require further testing.
• Those reactive must be repeated to verify the
positive test by a Neutralization assay.
• If the neutralization assay comes negative then a
new specimen should be requested and/or a
recommendation that the patient be tested for other
markers of infection.
• Some mutant HBsAg can be missed by commercial
assays. 39Dr.Ruqaiyah
38. Nucleic Acid Detection:Quantitative
• Recommended for initial evaluation of Chronic
Hepatitis B and during management, particularly in
the decision making to initiate treatment and in
therapeutic monitoring.
Criteria for Chronic HB:>=20,000IU/ml
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40. HBV genotyping
• HBV genotype potential influence the outcome of
Chronic Hepatitis B and the success of antiviral therapy.
• Genotype B has more favorable outcome than C.
• Genotyping is more important for IFN therapy as A
have more changes of seroconversion than D.
• Methods:
Genome Sequencing
RFLP
Genotype specific Amplification techniques
Hybridization techniques
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42. Biochemistry
• Serum Transaminases
ALT> AST but this reverses once Cirrhosis sets in.
• Direct and Total Bilirubin
0.3- 1 mg/100ml
• Albumin and Total protein
Albumin 4-5.5 mg/100ml
• Coagulation tests
Prothrombin time(11-12.5 sec) increases
• Alpha feto protein
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46. Treatment
• 99% previously healthy person recover and
treatment is not required
• Indicated in fulminant hepatitis or severe
chronic hepatitis
– Interferon
– Nucleoside/ nucleotide analogues- lamuvidine,
adefovir, entecavir, telbivudine, tenofovir
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47. Prophylaxis
• Recombinant subunit vaccine
• HBsAg is used as a vaccine candidate in
baker’s yeast by DNA recombinant technology
• Route- I/M
• Dosage- 10-20 μg/kg
• Schedule 0,1,6 and 6,10, 14
• Marker of protection- anti- HBs titer more
than 10 IU/ml
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48. • Booster after 5 yr for high risk group or
antibody titer falls below 10 IU/ml
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49. Passive immunisation
• HBIG should be given within 6 hrs but not
later than 48 hrs
• Dose- 0.05-.07 ml/kg
• Two doses 30 days apart
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