HIV Grand Round F2 Dr Sris Allan Consultant GU / HIV Physician Honorary Associate Professor.
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Transcript of HIV Grand Round F2 Dr Sris Allan Consultant GU / HIV Physician Honorary Associate Professor.
HIV Grand Round F2
Dr Sris Allan
Consultant GU / HIV Physician
Honorary Associate Professor
June 2011 – 36 year old weighing 64.5Kg
Black African
Abnormal cervical smear
Contraception discussed
Case History – female
On examination
Case study – female
Date CD4 cell count Viral load cells /ml
HAART
09.07.13 400 – 26.5% <40 Atripla
05.03.13 310 – 20.1% <40 Atripla
11.12.12 310 – 20.0% <40 Atripla
28.08.12 340 – 17.0% <40 Atripla
10.05.12 180 – 15.0% <40 Atripla
02.02.12 200 – 11.1% <40 Atripla
20.10.11 180 – 8.0% <60 Atripla
28.07.11 220 – 8.5% 3,401 Atripla
16.06.11 150 – 10.5% N/A N/A
Case study – female
June 2011 – 62 years Partner HIV positive SOB >4 years Cough ++ minimal sputum On home oxygen Recurrent chest infection – 2006 to 2011 Chronic obstructive airway disease
oesophageal candidiasis – 16.06.11
Case study – male
Stopped smoking 2 years ago (smoked 70 to 80 cigarettes per day for 45 years)
Oxygen saturation 92%
Case study – male
On examination
Right sided R.R – 22/min Very poor air entry Ab = L = 5cm Spleen – J.P.
Discussion
Case study – male
Prescriptions Doxycycline Co-trimoxazole
Tests performed FBC U&E LFT HIV – Viral load count CD4 count
Case study – male
HAART
Case study – male
July 2011
Feeling better Weight gain of 2kg in 3 weeks Cough better with Doxycycline Feels like a drunk when walking Sleep problems Erythematous rash
Discuss side effects
Case study – make
August 2011
Better No cough Oxygen saturation 98% Right side air entry – good
Case study – male
October 2012
Knee replacement
Discuss surgery in HIV
Case study – male
January 2013
Erectile dysfunction
Discuss treatments of erectile dysfunction
Case study – male
Date CD4 count Viral load cells /ml
HAART
19.06.13 180 – 21.4% 52 Atripla
26.02.13 160 – 20.9% <40 Atripla
15.11.12 190 -17.0% <40 Atripla
31.07.12 160 – 19.0% 62 Atripla
23.04.12 160 – 18.0% <40 Atripla
23.01.12 N/A 383 Atripla
01.11.11 100 – 16.9% 226 Atripla
01.08.11 140 – 18.2% 7,786 Atripla
22.06.11 90 – 17.0% 1,469,270 Atripla
Case study – male
Take Home messages
The size of the problem CD4 count HIV-1 RNA plasma viral load Opportunistic Infections and AIDS Era of antiviral therapy New challenges Adherence, Toxicity, Resistance The continued spread of the epidemic Protected Sex
Course of HIV infection
Basic principles 4 As a rule of thumb The higher the viral load the faster the disease
progression Values for people not on therapy
< 40 copies per ml Undetectable <1000 copies per ml very low < 100,000 copies per ml low >100,000 copies per ml very high
Basic Principles 5 The clinical presentation of the patient will be related
to the degree of the immune suppression. The CD4 count will gives an indication of the degree
of immune suppression. Rule of thumb CD4 800-1200 cells /mm3 normal range CD4 > 500 cells /mm3 minimal immune
suppression CD4 ~350 cells /mm3 moderate immune
suppression CD4 <200 cells /mm3 advanced immune
suppression CD4 <50 cells /mm3 severe immune
suppression
Hepatitis B & C
Epidemiology /Prevalence Transmission Acute infection Chronic infection Diagnosis Natural History Treatment consideration Treatment options
US CDC, 2006
Acute infection
Risk of Chronic HBV
Depends on nature of immune response to initial infection
Varies according to the age at which the infection is acquiredNeonates – almost 100%Young children – about 50%Adults – about 2-10%
Immunocompromised Males > Females
Diagnosis of chronic HBV
Chronic Hepatitis B is defined as viraemia and hepatic inflammation that persists for > 6 months after acute infection with HBV.
HBsAg positive
Anti–HBc total positive, IgM positive (low titre) HBeAg positive or negative
(indicator of viral replication)
some variants do not express HBeAg HBV DNA positive
Serology of chronic carrier
Test Results Interpretation
HBsAgAnti-HBcAnti-HBs
NegativeNegativeNegative
Naïve, susceptible
HBsAgAnti-HBcAnti-HBs
NegativePositivePositive
Immune due to natural infection
HBsAgAnti-HBcAnti-HBs
NegativeNegativePositive
Immune due to Hepatitis B vaccination
HBsAgAnti-HBc
IgM Anti-HBcAnti-HBs
PositivePositivePositive
Negative
Acutely infected
HBsAgAnti-HBc
IgM Anti-HBcAnti-HBs
PositivePositive
Positive or NegativeNegative
Chronically infected
HBsAgAnti-HBcAnti-HBs
NegativePositive
Negative Four possibilities
Management consideration
PatientLiver healthOccupational health
Baby health
Partner/ close contact
Prevention isbetter than(NO) cure
Monitor & minimiseviral activity
Long term agents Lamivudine Nucleoside reverse transcriptase inhibitor In HBeAg positive CHB - treatment is
generally for one year or more with the aim to bring eAg seroconversion
In HBeAg negative CHB - long term treatment is needed
Resistance is the main problem with long term treatment, more than 60% develop resistance after 3 years of treatment.
Long term agents Adefovir dipivoxil Structurally related to purine base ‘adenine’. Inhibits synthesis of hepatitis B virus DNA
through competition for the enzyme ‘reverse transcriptase’ and incorporation into viral DNA
Others: Entecavir Tenofovir Emtricitabine Telbivudine
Treatment
Life long Monitoring for viral resistance
a) genotypic e.g. A181V and N236T for ADV
b) virologic a) + >1 log increase in DNAc) clinical a) + b) + ALT rise
Regain viral suppression quicker, less clinical decompensation
Hepatitis C: The virus
~50 nm
Hepatitis C (HCV) Prevalence
It is estimated that up to 250,000 people are infected with HCV in England and Wales1
The number of adults diagnosed with CHC is projected to increase four-fold in the next 15 years in the USA and western Europe2
The main population subgroups infected with HCV are:1
Blood donors – 0.04% People attending antenatal clinics in London – 0.4% People attending genitourinary clinics – 1% Intravenous (IV) drug users – 50%
1. NICE technology appraisal guidance 1062. Albert A, et al. Dig Liver Dis 2004; 36: 646–
654.
HCV Natural Historyinfection
chronic hepatitis
cirrhosis
liver failureliver cancer
clearance
20%
20% @ 20 years50% @ 30 years
1.4% pa 3.9% pa
liver transplantation
Treatment consideration Goal: clear HCV Secondary aim: reduction in the rate of fibrosis
progression?
Assessment and progress markersHCV-RNAALT Histology
Treatment of finite duration Generally poorly tolerated compared to HBV oral
agents
Predictors of Response to treatment
HCV genotype2 > 3 > 5 > 4 >1
HCV titrethe lower the better
Amount of liver fibrosisless is better
Ageyounger is probably better
Ethnicityinferior response in black patients