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Taking the precautions outlined in local Occupational Health and Safety procedures is most
important in preventing exposure to blood-borne infections. Health workers or others who
could be occupationally exposed should be aware of steps to take in the event of exposure.
Vaccination against hepatitis B is recommended.

  

‘ wash site of exposure with soap and water without scrubbing (antiseptics or skin
washes are not needed)
‘ do not suck or squeeze wounds but allow free bleeding
‘ irrigate affected mucous membranes, including the eyes, with copious water.

^ 

Consider type of exposure, type and volume of fluid, infectious status of source and
susceptibility of exposed person. Significant risk of infection occurs with percutaneous injury
and exposure of broken skin or mucous membranes (including the eye). Testing the sharp
causing the injury is not recommended.

Assess the risk of infection from the source person from available information, eg medical
record. If this cannot be done test the source person (if possible) for HIV, hepatitis B and C
(consider whether likely to be in the window period).

Check the exposed person for HIV, hepatitis B and C status.



Most occupational exposures do not result in infection and, as there are significant risks in
taking post-exposure prophylaxis (PEP) for HIV, begin only if the risk of infection is high. In
most cases PEP is not justified. Exposures should be managed by, or with the advice of, an
expert.

The employer should consider making starter packs (each with a 3 day course) easily
available to allow prompt treatment.

The approximate risk of acquiring HIV from different types of occupational exposure to
infected blood is:

‘ percutaneous, around 0.3%


‘ mucocutaneous, <0.1%
‘ intact skin, no risk.

c
[    
       : larger volume of blood, deep injury,
visible blood on the sharp, injury caused by needle which has been in an artery/vein, high
viral load in source.

J      


     : amniotic, CSF, breast milk, pericardial,
peritoneal, pleural, synovial,        (including saliva during dental
procedures), unfixed tissues, fluids from burns or skin lesions, semen and vaginal secretions.


    PP

Do not start PEP if exposure has been to low-risk fluids (urine, vomit, saliva, faeces) unless
visibly blood-stained.

Start as soon as possible if there has been significant exposure to an HIV-positive source (or
if this is highly likely). If HIV testing cannot be done after a significant exposure start PEP
only if the source is

 to be infected with HIV.

Take into account the exposed person¶s wishes; discuss the risks and benefits of treatment,
including the adverse effects of the drugs.

Treatment begun within 1±2 hours is likely to be more successful, but it may be worth
starting PEP even after 36 hours (or longer if there was a high risk of transmission). Continue
PEP for 4 weeks.

 !
!

V    

Some of the rationale for PEP is theoretical. As zidovudine prophylaxis reduces the risk of
developing HIV infection by 80% it is reasonable to include it in PEP regimens.
Theoretically a combination of drugs gives better protection, although failure has occurred
even when >3 drugs were used. If the source person is infected use available information, eg
antiretroviral treatment, results from resistance testing, to guide drug choice.

Take into account whether the exposed person is pregnant or has any other medical condition
and the potential for drug interactions.

Use a 2 NRTI combination, egzidovudine plus lamivudine (Combivir ®), for low-risk
exposures; add a PI for higher risk exposures. Information about the source virus may suggest
the use of other antiretroviral agents.

Avoid using:

‘ nevirapine (risk of severe hepatotoxicity)


‘ abacavir (risk of serious hypersensitivity reaction)
‘ efavirenz in pregnant women
‘ the combination of didanosine plus stavudine in pregnant women.

[ "

-
The exposed person needs counselling, post-exposure testing and medical evaluation whether
or not PEP is prescribed. He or she should seek medical advice if any acute illness occurs,
avoid donating tissues or fluids, avoid breastfeeding and use safe sex practices during the
follow-up period.

Monitoring requirements for adverse effects of treatment will depend on the drugs chosen;
change the drugs if toxicity or compliance are a problem (33% stop because of adverse
effects); consider antiemetics or antidiarrhoeals if necessary. Test for HIV seroconversion at
6 and 12 weeks, and 6 months after exposure.

Stop PEP as soon as it is known that the source is HIV-negative or if other factors indicate
that it is not required.

  
Risk of developing hepatitis B depends on the type of contact and the presence of hepatitis B
e antigen (HBeAg). Risk of developing clinical hepatitis if HBeAg is present is 22±31%; the
risk is 1±6% if only hepatitis B s antigen (HBsAg) is present.

Hepatitis B virus survives on surfaces for at least a week and it is possible to become infected
without realising there has been an exposure. Most body fluids other than blood are not
efficient sources of infection.

Begin hepatitis B vaccination in an unvaccinated, susceptible person regardless of the


source¶s hepatitis B status. Give hepatitis B immunoglobulin (as soon as possible and
preferably within 24 hours) and hepatitis B vaccine (at a separate site) depending on the
hepatitis B status of the source and whether the exposed person is fully immunised. Use the
accelerated vaccination schedule and ensure the course is completed.

Exposed people should not donate any tissues or fluids during the follow-up period; safe sex
should be practised.

Test for hepatitis B surface antibody 1±2 months after the last vaccine dose (response to
vaccine cannot be tested for 3±4 months after hepatitis B immunoglobulin has been given)
and for HBsAg if the antibody test is negative.

  
After occupational exposure to blood, risk of transmission of hepatitis C is of the order of
2%; it is more likely to occur after injury from hollow-bore needles than from other sharps.
Transmission is rare from other routes or body fluids.

No PEP is recommended; follow-up testing should be done if the source is hepatitis C-


positive or of unknown status.

Exposed people should not donate any tissues or fluids during the follow-up period; safe sex
should be practised; breastfeeding can continue.

º
Test for hepatitis C RNA and obtain serum ALT at 4±6 weeks (if early diagnosis desired)
otherwise test for hepatitis C antibody at 3 and 6 months. Seek specialist advice if the person
has seroconverted for possible early treatment.

 !    


See also HIV infection

People treated with antiretrovirals may develop many adverse effects, some of which may
also occur in untreated people with HIV.

Some adverse effects appear to be associated with 2 or more classes of drug, eglipodystrophy
is associated with NRTI and PI treatment, and others may be related to drug concentrations,
egefavirenz and CNS effects.

#   

Features of lipodystrophy have been reported in 5±60% of people treated with NRTIs and PIs
and include:

‘ peripheral lipoatrophy (loss of subcutaneous fat especially in the face, limbs and
buttocks)
‘ central fat accumulation (intra-abdominal, breast, dorso-cervical).

Metabolic abnormalities may also occur, eg insulin resistance, dyslipidaemia.

Lipoatrophy is associated with NRTI treatment, especially stavudine and zidovudine, while
metabolic complications are more common with PIs.

Physical changes may affect compliance which may lead to virological failure.

  ! 
Insulin resistance and hyperglycaemia, and the development (or worsening) of diabetes, can
occur with some PIs. The incidence of hyperglycaemia with or without diabetes is 3±17%; it
may be reversible on stopping the PI and switching to an antiretroviral from another class.
Atazanavir, when used as the sole PI, appears to have less effect on glucose metabolism than
other PIs.

The length of NRTI treatment may also be associated with insulin resistance and the
development of diabetes; this association is more evident with stavudine, didanosine and
zidovudine.

Monitor diabetics and pregnant women taking PIs closely and be aware of the increased risk
of diabetes for other patients taking PIs.

Check blood glucose concentration at least annually.

å
  
Dyslipidaemia occurs as a result of HIV infection and some changes in lipid concentrations
after starting antiretrovirals may represent a return to values present before the disease.

PIs are associated with increases in plasma LDL, total cholesterol and triglyceride
concentrations; these may be more marked with ritonavir. When used as the sole PI
atazanavir appears to have little effect on cholesterol and triglyceride concentrations; when
given with ritonavir, it has less effect on triglycerides and total cholesterol than lopinavir with
ritonavir.

NNRTIs may increase HDL and LDL concentrations, while NRTIs may also affect lipids
(stavudine increases plasma triglyceride more than tenofovir).

Switching from a PI may improve triglyceride concentrations, as well as total cholesterol and
HDL concentrations, especially if the new regimen includes a NNRTI.

Check blood lipids at least annually for everyone taking a PI or a NNRTI.

^  !   !   


HIV infection may be a risk factor for cardiovascular disease. Duration of antiretroviral
treatment is related to an increased risk of MI, probably due to exposure to PIs; there may
also be an association with recent abacavir treatment. The risk of cardiovascular problems
from treatment is lower than from smoking or diabetes and is outweighed by the benefits.
Existing risk factors for cardiovascular disease appear to increase the risk from antiretroviral
treatment.

Where possible, choose treatments that are less likely to cause insulin resistance or
dyslipidaemias for those in the early stages of treatment or with risk factors for
cardiovascular disease, as the long-term effects of metabolic changes resulting from treatment
are unknown.

# !! ! 


Occurs with NRTIs and NtRTIs (most common with stavudine), and is thought to be
mediated by mitochondrial toxicity as are some of their other adverse effects, such as
pancreatitis and peripheral neuropathy. Risk factors include obesity, being female and
treatment with oral ribavirin.

Hyperlactataemia can occur without a change in blood pH or anion gap. Mild lactic
acidaemia occurs in about 10±20% of people taking a NRTI and is generally asymptomatic.
Symptomatic lactic acidaemia is less common, occurring in 1.5±2.5%.

Routine monitoring of lactate in asymptomatic people is not recommended. Measure lactate


concentration if there is unexplained nausea, anorexia or vomiting, raised liver function tests
or hepatomegaly.


Stop treatment immediately if lactic acidosis develops or if hyperlactataemia is accompanied
by nausea, fatigue, fever, weight loss, abdominal pain, breathlessness, ascending
neuromuscular weakness, hepatomegaly or elevated liver enzymes. These symptoms can
appear gradually over days or weeks. Ensure that patients are aware of the symptoms of lactic
acidosis (although symptoms may be vague and onset insidious).

Avoid didanosine plus stavudine (particularly in pregnancy as deaths have occurred). Monitor
pregnant women taking NRTIs closely; consider checking their lactate concentrations.

   !
Raised aminotransferases at start of treatment increases the risk of hepatotoxicity.

AA : nevirapine is the most likely to cause hepatitis, which may occur as part of a
hypersensitivity syndrome with rash, fever and eosinophilia. Hepatitis usually occurs in the
first 18 weeks of treatment (most likely in first 6 weeks). Women and those with higher CD4
cell counts are at greater risk; other risk factors include hepatitis B or hepatitis C coinfection;
monitor liver function regularly.

: hepatotoxicity can occur at any time. The highest incidence is with full dose ritonavir
(rarely used) and tipranavir. Coinfection with hepatitis C may be a major risk factor in its
development; others may include hepatitis B infection, alcohol misuse, stavudine use, and use
of other hepatotoxic agents.

A  rarely cause lactic acidosis with steatosis and hepatomegaly which can be fatal. It is
more likely with stavudine, didanosine and zidovudine and may be more common in women
and with prolonged NRTI treatment.

  !

Decreased BMD occurs in HIV infection; additional bone loss appears to occur when
antiretroviral treatment is begun (osteonecrosis may also occur). Tenofovir may have a
greater effect on BMD than other antiretrovirals. Other risk factors include corticosteroid
treatment, alcohol misuse and hyperlipidaemia. There may be a link between bone
abnormalities and other metabolic abnormalities in HIV patients.

^ 

AA : rash occurs most often with NNRTIs, is usually mild-to-moderate and occurs within
the first weeks; stop treatment if it is more serious, eg Stevens±Johnson syndrome, toxic
epidermal necrolysis or if liver function tests increase.

Severe rash occurs most often with nevirapine; females appear to have a greater risk than
males. Increasing the nevirapine dose by steps reduces the incidence of rash. Do not use
antihistamines or systemic corticosteroids to prevent it; they are ineffective and may increase
the likelihood of its occurring.

Î
There may be cross-sensitivity with other NNRTIs; do not use another NNRTI if a very
serious reaction has occurred.

: fosamprenavir, atazanavir and tipranavir often cause rashes.

A : abacavir causes rashes more often than other NRTIs; this may be part of the abacavir
hypersensitivity syndrome; stop abacavir and do not rechallenge if this is the case.

A!     !  


 
See also Adverse effects of antiretrovirals, HIV infection
For drug interactions see NRTIs
Also known as nucleoside analogues and NRTIs.
Abacavir
Didanosine
Emtricitabine
Lamivudine
Stavudine
Zidovudine

$   ! 
The active phosphorylated NRTI metabolites inhibit viral reverse transcriptase and viral
DNA synthesis, preventing HIV replication. The specific site of action differs for each drug;
these differences are exploited in combination regimens.

!  
 !    

HIV infection

Prophylaxis during pregnancy to prevent vertical transmission of HIV

Prophylaxis after exposure to HIV

P!  
V        ùcontraindicated.

  ùdidanosine, stavudine and lamivudine have been associated with pancreatitis
(infrequent in adults but common in children with lamivudine) and may worsen existing
pancreatitis; monitor for symptoms and rising amylase or lipase concentrations.

      ùzidovudine and, rarely, lamivudine are myelosuppressive


and may exacerbate pre-existing disease.

´
 !

Raised aminotransferases at start of treatment or other risk factors, eg hepatitis B or C,


increase the risk of hepatotoxicity. Severe impairment may increase the risk of adverse
effects.


 

Seek specialist advice.

P !

Contact one of the pregnancy drug information centres. ADEC category B1: emtricitabine;
ADEC category B2: didanosine; ADEC category B3: abacavir, lamivudine, stavudine,
zidovudine.

Avoid combining didanosine and stavudine during pregnancy as fatal lactic acidosis has
occurred.

To reduce perinatal HIV transmission (to <2%), combination antiretroviral treatment during
pregnancy (usually with zidovudine as part of the regimen) and neonatal prophylaxis with
zidovudine for 6 weeks is used. Strategies to reduce vertical transmission are rapidly
changing and specialist advice should be sought.

 

Breastfed infants of HIV-infected mothers are at risk of postnatal transmission. Discourage


breastfeeding.

 !
V    

  

headache, nausea, vomiting, anorexia, myalgia, peripheral lipoatrophy (especially with long-
term treatment, more common with stavudine), asymptomatic hyperlactataemia

%

pancreatitis, elevated liver enzymes, hepatitis, pancytopenia, leucopenia, myopathy

^ 

symptomatichyperlactataemia, lactic acidosis (may be more common with stavudine), lactic


acidosis with severe hepatomegaly and steatosis (more common in women)

ü
       
?  V[: abacavir, lamivudine, stavudine and zidovudine appear in the CSF.

     : lamivudine is marketed for treatment of chronic hepatitis B;


emtricitabine (a fluorinated analogue of lamivudine) is also active against this virus;
however, there is cross-resistance between them.

 !

Hypersensitivity (which can be fatal) occurs in 5±8% of people treated with abacavir (genetic
testing for the allele associated with hypersensitivity reduces this occurrence). Abacavir may
also be associated with increased cardiovascular risk. Zidovudine is myelosuppressive and
can cause myopathy. Stavudine is associated with lipoatrophy (especially if combined with
didanosine) and lactic acidosis to a greater degree than the other NRTIs. Lamivudine is well
tolerated while emtricitabine often causes skin discolouration.

   is more common with stavudine and didanosine; occurrence with lamivudine is
more frequent in children than in adults.

      occurs with didanosine and stavudine.

: nausea and GI upset occur with zidovudine (usually transient) while diarrhoea is
more common with didanosine and emtricitabine.



[ : didanosine and emtricitabine are given once daily; lamivudine and abacavir once
or twice daily; stavudine and zidovudine twice daily. Apart from didanosine (taken on an
empty stomach), all can be taken without regard to meals.

  : all are available as tablets or capsules; abacavir, lamivudine, stavudine and
zidovudine are also available as oral liquids; zidovudine injection is available through the
SAS.

[    : emtricitabine with tenofovir, lamivudine with abacavir, lamivudine
with zidovudine, and lamivudine with abacavir and zidovudine.

  
Sometimes this medicine can cause lactic acid to build up in your body and cause symptoms.
Tell your doctor immediately if you have nausea, vomiting, stomach pain, fatigue or
weakness.

P !!  
‘ measure lactate concentration if there is unexplained nausea, anorexia or vomiting,
raised liver function tests or hepatomegaly


‘ stop treatment immediately if lactic acidosis develops or if hyperlactataemia is
accompanied by nausea, fatigue, fever, weight loss, abdominal pain, breathlessness,
ascending neuromuscular weakness, hepatomegaly or elevated liver enzymes

A^  !   

‘   ! :
g‘ stavudine with didanosine or zidovudine
g‘ lamivudine with emtricitabine
g‘ didanosine with tenofovir
‘ abacavir with lamivudine may be less effective than tenofovir with emtricitabine if the
viral load is >100 000 copies/mL
‘ a 3 NRTI/NtRTI regimen is less effective than NNRTI- or PI-containing regimens;
abacavir, lamivudine and zidovudine (Trizivir®) may be useful only if other regimens
cannot be used; avoid other combinations

A !     ! 



 
See also Adverse effects of antiretrovirals, HIV infection
For drug interactions see NNRTIs
Also known as NNRTIs.
Delavirdine
Efavirenz
Etravirine
Nevirapine

$   ! 
NNRTIs reversibly inhibit HIV-1 reverse transcriptase reducing viral DNA synthesis.

!  
HIV infection, with other antiretrovirals

P!  
V      AA ùcontraindicated.

 !

Raised aminotransferases at start of treatment increases the risk of hepatotoxicity.

P !

c
Contact one of the pregnancy drug information centres; etravirine category B1; delavirdine
and nevirapine ADEC category B3. Efavirenz is contraindicated in the first trimester and
should be avoided in the second and third; ADEC category D.

To reduce perinatal HIV transmission (to <2%), combination antiretroviral treatment during
pregnancy (usually with zidovudine as part of the regimen) and neonatal prophylaxis with
zidovudine for 6 weeks is used. Strategies to reduce vertical transmission are rapidly
changing and specialist advice should be sought.

 

Breastfed infants of HIV-infected mothers are at risk of postnatal transmission. Discourage


breastfeeding.

 !
V    

  

rash (may be severe, occasionally fatal), malaise, nausea, vomiting, elevated liver enzymes,
headache, fever

%

dizziness, myalgia

       
Nevirapine is most likely to cause hepatotoxicity (which can be fatal), while efavirenz causes
CNS effects most often. Nevirapine, efavirenz and etravirine can cause hypersensitivity
reactions with rash and multi-organ involvement; these are more common with nevirapine.

Consider gender and CD4 cell count when considering using nevirapine as these influence
the risk of hepatotoxicity.

 is common with NNRTIs, however, treatment is frequently continued if it is not severe


and is without other symptoms. It occurs most often with delavirdine and nevirapine;
nevirapine (and possibly etravirine) are the most likely to cause severe rashes. Women are
more susceptible than men to rashes from nevirapine and etravirine.

 : nevirapine appears to have less effect on lipid concentrations than efavirenz.

V[  : nevirapine distributes into CSF (45% of plasma concentrations);


delavirdine and efavirenz have negligible CSF concentrations; no data for etravirine.

cc
 : unlike etravirine, the usual cause of resistance to delavirdine, efavirenz and
nevirapine is the K103N mutation. Resistance to etravirine develops less easily than to
efavirenz or nevirapine and strains resistant to efavirenz and nevirapine may be sensitive to
etravirine. However, if resistance to etravirine develops, cross-resistance to other NNRTIs is
likely.

? : efavirenz is given once daily, nevirapine once or twice daily, etravirine twice daily
and delavirdine 3 times daily.

  : delavirdine is rarely used as 12 tablets must be taken daily; etravirine is not
indicated for use in treatment-naive people.

  
This medicine interacts with many drugs; tell your doctor and pharmacist that you are taking
this medicine before starting or stopping any medicines, including herbal and over-the-
counter products.

Tell your doctor immediately if a rash develops while you are taking this medicine.

P !!  
‘ stop the NNRTI if elevated liver enzymes or a severe rash, especially with mucosal
involvement, fever or other systemic symptoms, occurs
‘ due to their long half-lives, NNRTI concentrations persist for a considerable period
after stopping them (at least 3 weeks for efavirenz or nevirapine). If all antiretrovirals
are stopped, a period of monotherapy occurs allowing the selection of NNRTI-
resistant virus; to avoid this, consider stopping the NNRTI first or substituting a PI for
the NNRTI (possibly for up to 4 weeks)
‘ when choosing a NNRTI, consider the adverse effects of other drugs used to treat
HIV patients, eg for prophylaxis of opportunistic infections
‘ check for potential drug interactions before starting or stopping any medication

P   
 
See also Adverse effects of antiretrovirals, HIV infection
For drug interactions see Protease inhibitors
Also known as PIs.
Atazanavir
Darunavir
Fosamprenavir
Indinavir
Lopinavir with ritonavir
Ritonavir
Saquinavir
Tipranavir

c-
$   ! 
Inhibit HIV-1 and HIV-2 proteases, preventing viral maturation and replication.

!  
HIV infection, with other antiretrovirals

P!  
V   ùcontraindicated.

  
        !   !  ! ù
contraindicated by manufacturers (atazanavir and tipranavir with low dose ritonavir
contraindicated with midazolam only if midazolam given orally).

? ùmay worsen.

   ùtreatment with PIs increases risk of bleeding.

?  ùhypercholesterolaemia and hypertriglyceridaemia may worsen.

 !

May need to reduce dose in impairment.

Hepatitis B or C may increase risk of hepatotoxicity and may worsen hepatic function; raised
aminotransferases at start of treatment also increases the risk of hepatotoxicity.

P !

Contact one of the pregnancy drug information centres; limited data available. ADEC
category B1: saquinavir; ADEC category B2: atazanavir, darunavir; ADEC category B3:
fosamprenavir, indinavir, lopinavir/ritonavir, ritonavir, tipranavir. Monitor blood glucose
concentration as PIs can cause hyperglycaemia.

To reduce perinatal HIV transmission (to <2%), combination antiretroviral treatment during
pregnancy (usually with zidovudine as part of the regimen) and neonatal prophylaxis with
zidovudine for 6 weeks is used. Strategies to reduce vertical transmission are rapidly
changing and specialist advice should be sought.

 

Contact one of the pregnancy drug information centres; limited data available. Breastfed
infants of HIV-infected mothers are at risk of postnatal transmission. Breastfeeding should be
discouraged.


 !
V    

  

headache, diarrhoea, nausea, vomiting, elevated liver enzymes, fat accumulation, weight
gain, hyperglycaemia (this is less likely with atazanavir), new onset or worsening diabetes;
hypertriglyceridaemia, hypercholesterolaemia

%

somnolence, paraesthesia, taste disturbance, pharyngitis, maculopapular rash, dry skin, chest
pain

^ 

halitosis, pancreatitis

       
Indinavir distributes into CSF (18% of plasma concentration) as does lopinavir; the others
have negligible CSF concentrations.

Tipranavir is not indicated in treatment-naive people; reserve for PI-experienced people when
other PIs are unsuitable, based on results of resistance testing. It may be more toxic and have
more complex drug interactions than the other PIs.

 !

: while all PIs can cause GI effects, ritonavir and saquinavir are more likely to cause
abdominal pain. Atazanavir and darunavir are less likely to cause diarrhoea than lopinavir (all
given with ritonavir).

 : elevated liver enzymes are common; atazanavir and indinavir both can cause
unconjugated hyperbilirubinaemia and should not be given together. Ritonavir seems the
most hepatotoxic PI when used in high doses; however, this is not the case when used in low
doses with other PIs. Tipranavir is associated with fatal hepatotoxicity.

 : fosamprenavir, atazanavir and tipranavir commonly cause rashes.

?   : atazanavir, when used as the sole PI, has a more
favourable effect on cholesterol or triglyceride concentrations and glucose metabolism than
some other PIs. When combined with ritonavir it has less effect on triglycerides and
cholesterol than lopinavir with ritonavir. Darunavir with ritonavir may also have less effect
than lopinavir with ritonavir. Tipranavir with ritonavir may increase cholesterol and
triglyceride concentrations more than other PIs.


A: fosamprenavir and ritonavir may cause paraesthesia.

 : indinavir causes nephrolithiasis.

  ! 

V   

Drug interactions with PIs are numerous and difficult to predict. Ritonavir is the most potent
inhibitor of liver enzymes and is the most likely to reduce the hepatic metabolism of other
drugs; saquinavir is the least potent.

Most PIs are now given with low dose ritonavir (eg 100 mg twice daily) to increase
their trough levels (through inhibition of GI and hepatic CYP) with the aim of:

‘ improving compliance, eg because of fewer tablets and reduced dosing frequency


‘ possibly allowing activity against moderately resistant strains.



[ : atazanavir is given once daily, fosamprenavir is given once or twice daily, while
the other PIs are given 2 or 3 times daily (when given without ritonavir).

[  : all are available as tablets or capsules; fosamprenavir, lopinavir with ritonavir
and ritonavir are also available as oral liquids (most contain propylene glycol and/or ethanol).

  
This medicine interacts with many drugs; tell your doctor and pharmacist that you are taking
this medicine before starting or stopping any medicines, including herbal and over-the-
counter products.

P !!  
‘ cross-resistance between PIs occurs; there is no cross-resistance with NRTIs or
NNRTIs
‘ check for potential drug interactions before starting or stopping any medication