ANTIRETROVIRAL DRUGS Flashcards
HIV TRANSMISSION
DIAGNOSIS
- Contact with body fluids (blood, semen, vaginal secretions, breast milk etc)
- From mother to child transplacentally or perinatally in 30-50% cases
- Transmission by saliva or droplets produced by coughing or sneezing is extremely unlikely
HIV DIAGNOSIS:
- *• Antibody or antigen testing** (usually within few weeks of infections)
- *• ELISA / Western Blot**
• New rapid tests (< 30 min) on blood & saliva available (usually confirmed by standard blood tests)
HIV TREATMENT
WHEN TO START?
WHAT CONDITIONS STRONGLY RECOMMEND STARTING?
Therapy is usually initiated when CD4+ cells ≤500 cellsmm3
Regardless of CD4 count, initiation of therapy is strongly recommended for individuals with the following conditions:
• 1) Pregnancy
- 2) History of an AIDS-defining illness
- 3) HIV-associated nephropathy (HIVAN)
- 4) HIV/hepatitis B virus (HBV) co-infection
HIV PRIMARY TREATMENT GOALS:
Primary treatment goals:
• reduce HIV-related morbidity and prolong survival,
- improve quality of life,
- restore and preserve immunologic function,
- maximally and durably suppress viral load, and
• prevent vertical HIV transmission
CURRENT HIV TREATMENTS
(DRUG CLASSES and examples)
1) Nucleoside/-tide Reverse Transcriptase Inhibitors (NRTIs)
- Abacavir, Didanosine, Emtricitabine, Lamivudine, Stavudine,Tenofovir, Zidovudine
2) Nonnucleoside Reverse Transcriptase Inhibitors (NNRTIs)
- Delavirdine, Efavirenz, Etravirine, Nevirapine
3) Protease Inhibitors
- Atazanavir, Darunavir, Indinavir, Lopinavir, Nelfinavir, Ritonavir, Tipranavir
4) Entry Inhibitors
- Enfuvirtide, Maraviroc
5) Integrase Inhibitor
Raltegravir
COMBINATOIN THERAPY/HAART
Current studies suggest a prevalence of HIV drug resistance of 6%–16% in antiretroviral treatment-naïve patients.
HAART (Highly Active Antiretroviral Therapy) / combination therapy was initiated in 1996
NUCLEOSIDE/TIDE REVERSE TRANSCRIPTASE INHIBITORS (NRTI’S)
MOA
MOA
- Analogs of native ribosides (lack 3’OH)
- Phosphorylated by cellular enzymes and incorporated into viral DNA by reverse transcriptase
• Lack of 3’OH terminates DNA elongation
–> ie. they are competitive inhibitors of reverse
_transcriptase***_
• Most have activity against BOTH HIV-2 as well as HIV-1
NUCLEOSIDE/TIDE REVERSE TRANSCRIPTASE INHIBITORS (NRTI’S)
RESISTANCE
PK
AE
RESISTANCE:
- Emerges rapidly if used alone
- Most common mutation at viral codon 184: lamivudine
(restores sensitivity to zidovudine & tenofovir)
• Cross-resistance between agents of same analog class
can occur
PK: dosage adjustements required with RENAL INSUFFICIENCY
AE:
- If more than one NRTI given toxicities may overlap
- AE mainly due to inhibition of ****_mitochondrial DNA polymerase_: _peripheral neuropathy, myopathy, lipoatrophy (localized loss of fat tissue) & lactic acidosis******_
- Pancreatitis, myelosuppression & cardiomyopathy can also occur
- Liver toxicity is rare but fatal (lactic acidosis, hepatomegaly with steatosis).
- Zidovudine & stavudine may be particularly associated with dyslipidemia & insulin resistance
NRTI’S
DRUG INTERACTIONS
T, increases D (Titties increase Dick), when coadministered
—> therefore must decrease D dose (don’t let as many dicks in the bar)
• Didanosine & tenofovir
- Tenofovir increases plasma didanosine levels ~60%.
- Doses of didanosine have to be reduced.
• NRTIs are not generally metabolized by cytochrome enzymes
ZIDOVUDINE
NRTI
ZIDOVUDINE –> causes BONE MARROW SUPPRESSION –> causes bone marrow to “ZZZZZZZ”
-is a nucleoSIDE analog
PK: oral, penetrates the BBB well
–> dosage adjustement required in patients with CIRRHOSIS
AE:
- ***BONE MARROW SUPPRESSION*** (neutropenia, anemia)
- GI INTOLERANCE, headaches, insomnia
CONTRAINDICATIONS:
- Toxicity potentiated by coadmin. of probenecid, acetaminophen, lorazepam, indomethacin & cimetidine.
- Stavudine & ribavirin activated by same pathways (might reduce active levels of zidovudine)
STAVUDINE
NRTI
STAVUDINE –> STAB U DINING –> stabs both the Boy (beta) and Girl (gamma) DNA (dinner) polymerases
Strong inhibitor of beta and gamma DNA polymerases (high affinity for mitochondrial DNA polymerase, which can lead to toxicity) –> can cause PERIPHERAL NEUROPATHY (b/c just got stabbed, as well as MUSCLE BREAKDOWN –> therefore LACTIC ACIDOSIS
Nucleoside Analog = Thymidine
Pharmacokinetics
- Oral
- Dosage adjustment required in renal insufficiency
AE: PERIPHERAL NEUROAPTHY, LACTIC ACIDOSIS
–> HYPERLIPIDEMIA, NEUROMUSCULAR WEAKNESS
DIDANOSINE
NRTI
DIDANOSINE = DI DAN SIGN –> smart drug because take in FASTING state (acid labile) and combined with an ANTACID –> but DAN PAN DAN –> look out for PANCREATITIS –> don’t give it to somebody who already has pancreas problems!!!!!!
NucleoSIDE Analog –> Adenosine
Pharmacokinetics
• Absorption best if taken in fasting state (ACID LABILE) or
combined with antacid
- Penetrates into CSF
- Dosage adjustment required in renal insufficiency
Adverse Effects
High affinity for mitochondrial DNA polymerase
- _Pancreatitis***_ (esp. alcoholics and patients with hypertriglyceridemia)
- Peripheral neuropathy, diarrhea, hepatic dysfunction
- CNS effects
NOTE IF PATIENT ALREADY HAS PANCREAS PROBLEMS, THIS DRUG IS CONTRAINDICATED!!!
TENOFOVIR
NRTI
TENOFOVIR –> is 10/10 –> IS THE PREFERRED NRTI IN CURRENT REGIMENS!!
–> Remember TEN TITTIES –> raises DICKS (didanosine)
_**One of preferred NRTIs in currently recommended_ _regimens**_
Nucleotide Analog –> Adenosine
Fixed-Dose Combinations Available
- *• Tenofovir + emtricitabine**
- *• Tenofovir + emtricitabine + efavirenz**
Pharmacokinetics
- Should be _taken with food to increase bioavailability***_
- Long t1/2 (can dose once daily)
Adverse Effects
• GI (nausea, diarrhea, vomiting, flatulence)
TENOFOVIR
CONTRAINDICATIONS
NRTI
REMEMBER: TENOFOVIR (Ten TITTIES) raises DICKS, but it DECREASES AT AZZZZ
- Serum creatinine monitored with renal insufficiency
- Only NRTI with sig. drug interactions
- 1) increases DIDANOSINE concentrations and dosage reductions are usually required****
-
2) Decreases concentrations of atazanavir.
- Atazanavir can be ‘boosted’ with ritonavir
LAMIVUDINE
LAMIVUDINE –> LAME DINING –> does NOT have many AE, does not affect mitochondrial DNA synthesis, or bone marrow precursor cells
_****DOES NOT affect mitochondrial DNA synthesis or bone marrow precursor cells****_
Nucleoside Analog –> Cytosine
Resistance
• High level resistance occurs with single amino acid substitutions
Pharmacokinetics
• Dosage adjustment required with renal insufficiency
Adverse effects (very few!!!)
• Few significant (headache, dry mouth)
EMTRICITABINE
NRTI
EMTRICITABINE –> Where’s Seattle from? “Emmm.. Tricity? obivously.. EM-TRICITY –> SEATTLE –> HYPERPIGMENTATION of PALMS + SOLES b/c WALKING (soles) to their local starbucks and holding onto the coffee (palms) –> is one of the preferred NRTIs in currently recommended regimens
Structural relative of lamivudine
One of preferred NRTIs in currently recommended regimens
Nucleoside Analog –> Cytosine
Pharmacokinetics
Once-a-day administration
AE: ***_HYPERPIGMENTATION OF PALMS + SOLES***_ (occurs most frequently in dark-skinned people)
ABACAVIR
NRTI
ABACAVIR –> think of ABACADABRA!!! –> POOF all of a sudden get a quick hypersensitivity reaciton –> sensitized inidivuals should never be rechallenged
–> is a GUANISINE ANOLOG (guanisine for GENIE)
Nucleotide Analog –> Guanosine
Resistance
• HIV resistance requires several mutations and tends to develop slowly.
Adverse Effects
- GI, headache, dizziness
- 5% - ***_‘hypersensitivity’ reaction****_ (one or more of rash, GI, malaise, respiratory distress).
- Sensitized individuals should NEVER be rechallenged (can be genetically screened)
NNRTIs
MOA
NON-NUCLEOSIDE REVERSE TRANSCRIPTASE INHIBITORS
MOA (only works on HIV-1, NOT on HIV-2)
- Highly selective, noncompetitive inhibitors of HIV-1 RT
- Bind at a distinct site away from active site (NNRTI pocket)
- All NNRTI’s bind within the same pocket
- All result in inhibition of RNA- and DNA-dependent DNA polymerase
- DO NOT REQUIRE PHOSPHORYLATION BY CELLULAR ENZYMES
- Lack in vitro activity against HIV-2
NNRTIs
Advantages + Disadvantages
AEs
Advantages
- Lack of effect on host blood-forming elements
- Lack of cross resistance with NRTIs (binding sites are distinct)
Disadvantages
- Cross-resistance with NNRTIs (ie with itself)
- Drug interactions
- High incidence of hypersensitivity reactions (eg, rash)
AE:
- 1) *****_Skin rash (including Stevens-Johnson syndrome)*****_
- GI intolerance
- All are CYP3A4 substrates and can act as inducers, inhibitors or both of CYPs
NEVIRAPINE
PK + AE
NEVER A PINE –> is an NNRTI –> can never cut down a pine right away –> need 14 day titration period to get sapp out, at half dose? –> if not syrup can be sour and can cuase potential severe HEPATOTOXICITY + RASH (from pine needles)
Pharmacokinetics
• Excreted mainly in urine as metabolites (CYP 3A4 & CYP 2B6)
Adverse Effects
- Potential severe hepatotoxicity (don’t use in women with CD4+ counts >250 cells/mm3 & men >400 cells/mm3)
- Rash (16%), dermatologic effects (Stevens-Johnson syndrome & toxic epidermal necrolysis)
- 14 day titration period at 1⁄2 dose is mandatory to reduce risk of serious epidermal reactions
NEVIRAPINE
CONTRAINDICATIONS
RESISTANCE
NEVER-A-PINE –> contraindicated in most popular places = CYP3A4 –> it INDUCES A RIOT b/c people want those trees to still stand –> INDUCES THE METABOLISM OF PROTEASE INHIBS
Contraindications
- Inducer of CYP 3A4
- Increases metabolism of PI’s (no dosage adjustment necessary), oral contraceptives, ketoconazole, methadone, metronidazole, quinidine, theophylline & warfarin
Resistance
• Target site of nevirapine is HIV-1 specific & not essential to enzyme (reverse transcriptase), thus mutations and resistance can develop rapidly
DELAVIRDINE
CLINICAL APPLICATIONS
PHARMACOKINETICS
AEs
DEL-A-VIRDINE –> DELL –> think of DELL COMPUTERS –> not used as much anymore because they have short half lives –> RASH = #1 ADVERSE EFFECT, IF ASK RASH IT WILL BE ABOUT DELL COMPUTERS –> because people putting them togetehr exposed to so many chemicals –> is also TERATOGENIC (contraindicated in pregnancy)
Clinical Applications
• Not as widely used as other NNRTIs due to short t1/2
Pharmacokinetics
• Well absorbed orally (especially at pH <2; antacids, H2
blockers etc may decrease absorption)
- Excreted mainly in urine as metabolites (CYP 3A4 & 2D6)
- Non-linear PK (t1/2 increases with increasing doses)
Adverse Effects
- Rash (18-36%), ****Stevens-Johnson syndrome & toxic epidermal necrolysis
- Fever, headache & depression also common
- Teratogenic
DELAVIRDINE
DELL COMPUTERS –> won’t let you do ANYTHING –> is an INHIBITOR
Contraindications
- Inhibitor of and substrate of CYP3A4
- CYP 3A4 inducers (eg, rifampin, phenytoin) may decrease
delavirdine concentrations
• Pregnancy (Cat C)
Resistance
• Target site of delavirdine is HIV-1 specific & not essential to enzyme (reverse transcriptase) therefore resistance develops rapidly
ETRAVIRINE
clinical applications
PK
ETRAVIRINE –> see the E think EXPERIENCED PATIENTS
Clinical Applications
- Approved for use in treatment-experienced patients
- May be effective against HIV strains resistant to first-generation NNRTIs
Pharmacokinetics
- Metabolized by CYP 3A4, 2C9 and 2C19
- Metabolites have ~10% HIV activity of parent compound
ETRAVIRINE
ADVERSE EFFECTS
CONTRAINDICATIONS
ETRAVIRINE –> think EXPERIENCED PATIENTS and also think ENZYME ELEVATION –> TRANSAMINASE ELEVATIONS!!!
Adverse Effects
- Rash (normally resolves within 1-2 weeks), nausea, diarrhea
- Transaminase elevations (esp. in patients co-infected with hepatitis)
Contraindications
- CYP 3A4 inducer
- CYP 2C9 and 2C19 inhibitor
- Some interactions are difficult to predict
EFAVIRENZ (not ETRAVINE)
CLINICAL APPLICATIONS
PHARMACOKINETICS
- ********_Preferred NNRTI on DHHS guidelines*********** EFAVIRENZ DOES ERRRYTHINGGGGG B/C DRUG GOES ALL THE WAY TO THE END OF THE ALPHABET (Z)_
- Results in increased CD4+ counts & decreased viral load
Pharmacokinetics
- Oral
- t1/2 >40h _(once-a-day dosing)*****_
- Extensively metabolized to inactive products
ETRAVIRENZ
AE
Contraindications
EFAVIRENZ –> it ZZZZZZZ’S –> dizziness, vivid DREAMZZZZZZ
DON’T GIVE TO PZYCHHOOOOOSSSS
Adverse Effects
- 1) Mostly CNS (50%) (dizziness, headache, vivid dreams, loss of concentration) – resolve after few weeks.
- 2) Rash (25%)
- 3) Increased triglycerides, HDL and total cholesterol (lipid levels must be monitored at beginning of and during therapy)
Contraindications
- Potent inducer of CYP P450 enzymes.
- Pregnancy (D) (can be used after 1st trimester if considered best choice)
PROTEASE INHIBITORS
MOA:
- Reversible inhibitors of HIV aspartyl protease (enzyme responsible for cleavage of viral polyprotein into RT, protease & integrase)
- Protease inhibition prevents virus maturation & results in production of non-infectious virions
- DO NOT REQUIRE INTRACELLULAR ACTIVATION
- Active against both HIV-1 and HIV-2
PROTEASE INHIBITORS
PK
Pharmacokinetics
- Poor oral bioavailability
- High-fat meals can increase (nelfinavir) or decrease (indinavir) bioavailability
- Substrates for CYP 3A4
- Substrates for P-glycoprotein pump
- Bound to plasma proteins (a1-acid glycoprotein which can increase in response to trauma & surgery)
PROTEASE INHIBITORS
AE
PROTEASE INHIBS —> MAKE YOU A PORKER!!!! —> FUCKS WITH LIPID METABOLISM –> FAT REDISTRIBUTION + ACCUMULATION
Adverse Effects
- Parathesias, nausea, vomiting, diarrhea
- Disturbances in lipid metabolism (diabetes, hypertriglyceridemia, hypercholesterolemia)
- Chronic admin –> _*****fat redistribution & accumulation*****_ resulting in central obesity, dorsocervical fat enlargement, peripheral & facial wasting, breast enlargement and a cushingoid appearance
- Atazanavir has less side effects than other PI’s
PROTEASE INHIBITORS
DRUG INTERACTIONS
• Potent inhibitors and substrates of CYP isoforms
eg, rhabdomyolysis (simvastatin or lovastatin),
excessive sedation (midazolam or triazolam),
respiratory depression (fentanyl)
- Warfarin, sildenafil & phenytoin require dosage adjustments
- Rifampin & St.Johns Wort are contraindicated
RESISTANCE
• Accumulation of stepwise mutations of protease gene. Can lead to high levels of resistance.
RITONAVIR
PROTEASE INHIBITOR
RITONAVIR –> RIT –> RAMPS UP IE ENHANCER/BOOSTER OF OTHER PI’S d/t INHIBITION OF CYP3A4
CLINICAL APPLICATION:
– enhancer/booster of other PIs
-potent INHIBITOR of CYP3A4
CONTRINDICATIONS:
-numerous d/t inhibition of CYP
ATAZANAVIR
ATAZANAVIR –> ATAZMANIAN DEVIL –> can’t give with PPI’s b/c it inhibits them (give 12 hours apart from PPIs) –> thrives in the acidic environment (that tazmanian devil) –> go home and watch 1 CARTOON A DAY –> IS THE PREFERRED CARTOON TO WATCH, is the ONCE-DAILY PREFERED PI
–> is structurally unrealted to the others because is just a cartoon (not a human)
Clinical Application:
- is a once-daily preferred PIs (as is Ritonavir)
PK:
-structurally UNRELATED to other PIs
–> is well absorbed with food, highly protein bound
CONTRAINDICATIONS:
- metabolized by and inhibits CYP3A4
- contraindicated with a proton pump inhibitor
- administration must be >12 HOURS APART FROM H2 BLOCKERS + ANTACIDS
-less incidence of side-effects than other PIs
DARUNAVIR
PROTEASE INHIBITOR
DA-RUN-AVIR –> think about running, in order to run well, need to absorb what you’re taking quickly, so is BEST ABSORBED WITH FOOD
- inhibits HIV protease resistant to other PIs
- well absorbed with FOOD
- is metabolized by CYP3A4, but also INHIBITS it as well
INDINAVIR
PROTEASE INHIBITOR
INDIAN-AVIR –> must be given with RITONAVIR b/c INDIANS AREN’T THAT STRONG
–> eat way too much INDIAN FOOD –> GET RENAL STONES!!!
- is given with RITONAVIR
- least protein bound (60%)
–> absorption DECREASED when taken with meals
-dosage should be REDUCED with hepatic insufficiency
AEs:
- is well tolerated but can also get
- NEPHROLITHIASIS + HYPERBILIRUBINEMIA (adequate hydration important)
LOPINAVIR
PROTEASE INHIBITOR
LOPINAVIR –> LOW-PIN-AVIR –> can cause INSULIN RESISTANCE
–> is an INducer –> contains alcohol which makes you do things, therefore don’t give with disulfiram or metro)
–> warts are the size of PINS –> CYP INDUCER FOR ST. JOHNS WARTS
- one of the PREFERRED Protease Inhibitors
- is given with RITONAVIR
- has poor intrinsic stability
CONTRAINDICATIONS:
–> is an ENZYME INDUCER, therefore St. Johns Wort should be avoided
-oral solution contains EtOH (avoid disulfiram or metronidazole)
NELFINAVIR
PROTEASE INHIBITOR
NELFINAVIR –> NEW ELF –> is the best elf that santa has –> it is already working at maximum efficiency so cannot be boostd by RTV
- CANNOT be boosted by Ritonavir
- metabolized by SEVERAL CYPs
–> major metabolite (CYP2C19) has antiviral actiivity equal to parent compound
CONTRAINDICATIONS: NUMEROUS (d/t inhibition of CYP)
AE:
-diarrhea (controlled by loperamide), nausea, flatulence
TIPRANAVIR
PROTEASE INHIBITOR (don’t confuse with DARUNAVIR which is well-absorbed w food)
TIPRANOVIR –> if run on TIPTOES –> will make your head go crazy –> INTRACRANIAL HEMORRHAGE –> can also cause FATAL HEPATITIS –> can feel the TIP of your liver while you’re RUNNING (can feel the stich with your right hand)
- inhibits HIV protease resistant to other PIs
- twice-daily should be given with RITONAVIR
- is well absorbed with food
- is an INDUCER of CYP P450
AES:
1) SEVERE + FATAL HEPATITIS
2) FATAL + NONFATAL INTRACRANIAL HEMORRHAGES
ENTRY/FUSION INHIBITORS
FUSION INHIBITOR
1) ENFUVIRTIDE
ENTRY INHIBITOR
1) MARAVIROC
ENFUVIRTIDE
FUSION INHIBITOR
ENFUVIRTIDE –> like the thing tries to enter but it hits the cell and hits the tide and bounces back, ie it is a FUSION INHIBITOR –> is structurally –> when do u see the tide? when you’re 41 years old, able to afford a YACHT —> acts like a gp41
- First approved drug that inhibits viral fusion
- Approved for use in treatment-experienced adults with evidence of HIV replication
• No activity against HIV-2
-most common adverse effect = _PAIN AT INJECTION SITE!!! –> ENFU as in EFF YOU!!!!_
MOA
- Structurally similar to gp41 (HIV protein mediates membrane fusion)
- Binds to gp41 subunit of the viral envelope glycoprotein, preventing ability of virion to fuse cell membrane
PK: parenteral administration only
AE:
- Injection-related (3% discontinue)
- Hypersensitivity reactions & eosinophilia rarely
- No drug interactions with other antiretrovirals have been noted
MARAVIROC
ENTRY INHIBITOR
MARAVIROC —> think MARRY –> ENTRY INTO MAIRRAGE/NEW PART IN YOUR LIFE –> CCR5 is the song that you play at your mairrage –> binds on surface of T cells/monocytes, inhibiting interaction with gp120.
MOA
- Binds specifically and selectively to CCR5 (one of two coreceptors necessary for entrance of HIV into CD4+ cells)
- Result in blocking HIV entry (only CCR5-tropic virus can be treated with maraviroc)
Pharmacokinetics
• Metabolized by CYP 3A4 (reduce dose when given with PIs)
AE’s:
–> well tolerated, risk of hepatotoxicity
RALTEGRAVIR
INTEGRASE STRAND TRANSFER INHIBITOR (INSTI)
RALTEGRAVIR —> R GRAVE –> when you’re dying you start decomposing, start INTEGRATING into the soil –> this INHIBITS the INTEGRASE enzyme –> Leads to specific inhibition of the final step in integration of viral DNA into host cell DNA –> ie you’re put in grave and eveyrthign is allowed to occur but the final step of decomposition is inhibited
–> metabolized by UGT1A1-mediated glucuronidation ie think GUT (ugt mixed around)
–> note also that PPI’s INCREASE the concentration for when you’re decomposing
Clinical Applications
• In combination with other antiretrovirals, raltegravir is approved for treatment-experienced and treatment- naive patients with evidence of viral replication
MOA
- Binds integrase (enzyme essential to the replication of both HIV-1 and HIV-2)
- Leads to specific inhibition of the final step in integration of viral DNA into host cell DNA
Pharmacokinetics
• Metabolism via UGT1A1-mediated glucuronidation
AE:
- Well tolerated (nausea, headache, diarrhea)
- Can cause increases in creatine phosphokinase
Drug Interactions
- Rifampin, tipranavir & efavirenz may decrease [raltegravir]
- PPI’s may increase [raltegraivr]
TREATMENT FOR NAIVE PATIENTS
Goals:
• Maximally & durably suppress viral load replication
• Restore & preserve immunologic function
• Reduce HIV-related morbidity & mortality
• INCREASE QUALITY OF LIFE
WHICH REGIMINS TO START FOR NAIVE PATIENT?
Start with one of the following regimens:
(1) NNRTI & 2 x NRTI
(2) PI (preferably boosted with ritonavir) & 2 x NRTI
(3) INSTI & 2 x NRTI
FACTORS TO CONSIDER WHEN SELECTING AN INTIAL REGIMEN IN A NAIVE PATIENT
Factors to consider when selecting an initial regimen:
- Comorbid conditions
- Potential adverse drug effects
- Potential drug interactions
- Pregnancy or pregnancy potential
- Results of genotypic drug resistance testing
- Patient adherence potential
- Convenience
SELECTION IS BASED ON:
Selection is based on:
- Avoiding the use of 2 agents of the same nucleotide analog
- Avoiding overlapping toxicities and genotypic and phenotypic characteristics of the virus
- Patient factors such as disease symptoms and concurrent illnesses
- Impact of drug interactions; and
- Ease of adherence to a frequently complex administration regimen
CURRENT RECOMMENDATIONS FOR TREATMENT OF NAIVE PATIENTS:
CURRENT REGIMEN FOR PREGNANT PATIENTS:
1) RITONAVIR-BOOSTED LOPINAVIR (twice daily)
AND
2) ZIDOVUDINE/LAMIVUDINE
CURRENT RECOMMENDATIONS FOR INFANT BORN TO HIV INFECTED MOTHER
1) ZIDOVUDINE (start immediately after birth and administer for 6 weeks)
HIV PROPHYLAXIS following a NEEDLE STICK
Upon exposure to HIV, healthcare personnel should immediately receive a postexposure prophylaxis regimen containing at least 3 antiretroviral drugs
Preferred regimen:
1) Raltegravir + (Integrase inhibitor)
2) tenofovir + (NRTI)
3) emtricitabine (NRTI)
Regimen is given for 28 days and can be stopped if source is shown to be HIV-negative.
HIV PROPHYLACTIC VACCINES
recommended?
contraindicated?
• 1) Streptococcus pneumoniae
- 2) Hepatitis A
- 3) Hepatitis B and
- 4) Influenza
are generally recommended for all HIV-infected patients
CONTRAINDICATED:
Live vaccines eg,
_• MMR
• Varicella and_
• Zoster
Other vaccines may be administered without regard to the patient’s CD4+
