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30 Cards in this Set

  • Front
  • Back
Ritonavir--is it a CYP inducer or inhibitor? What's the major CYP enzyme on which it acts? Normal dose?
Mainly a CYP 3A4 Inhibitor; It's given with other PIs to inhibit their metabolism.
Normal dose is 200mg daily.

It's also a CYP 2C9/2C19 *inducer* This is a less clinically important interacation--but you do need to adjust voriconazole dose based on it.
What is the mechanism of clincially significant interactions between methadone and certain drugs used in HAART therapy? (And which drugs?)
Efavirenz induces CYP 3A4 (and probably 2B6) and decreases the AUC of methadone. Tipranavir also decreases the AUC of methadone.
What is the mechanism of clincially significant interactions between acid-reducers and certain drugs used in HAART therapy? (And which drugs?)
Atazanavir is poorly absorbed in a low-acid environment. This interaction is most clinically significant with omeprazole. It has been with H2 blockers, but may be overcome with timing and dosage changes.
What is the mechanism of clincially significant interactions between phenytoin and certain drugs used in HAART therapy? (And which drugs?)
Phenytoin is not recommended for coadministration with PIs or NNRTIs because of CYP 3A4 induction by phenytoin. Lopinavir/ritonavir also reduce phenytoin concentrations (possibly through CYP 2C9 induction)
What is the mechanism of clincially significant interactions between rifamycins and certain drugs used in HAART therapy? What's the drug of choice when these therapies must be used together.
Rifampin is a very potent CYP3A4 inducer.

Rifabutin may be given, usually at a reduced dose. The exception is that it is given at an higher dose with efavirenz, a CYP 3A4 inducer.
What is the mechanism of the clinically significant interaction between PDE5 inhibitors and some of the drugs used in HAART?
Ritonavir increases the AUC of these drugs greatly by inhibiting CYP 3A4 enzymes.
What is the mechanism of the clinically significant interaction between fluconazole and some of the drugs used in HAART?
Fluconazole increases the AUC of nevirapine when these drugs are coadministered.
What is the mechanism of the clinically significant interaction between voriconazole and some of the drugs used in HAART?
Efavirenz and ritonavir decrease the AUC of voriconazole through the induction of the CYP 2C9/2C19 system.
What are some herbal agents that potentially interact with HAART? (5) What is the mechanism of the interaction?
St. John's Wort induces CYP 3A4 and is known to decrease indinavir plasma concentrations. Goldenseal, kava kava and black cohosh are CYP 3A4 inhibitors. Garlic is known to induce CYP 3A4.
When do you initiate HAART?
History of AIDs defining illness or CD4 count <200. In almost all cases if CD4 count <350. Initiate if <500 and CD4 count drops by 100 over the course of 1 year.
Clinical issue that needs further evaluation?
Integrase Inhibitor.
Metabolised through glucoronidation.
400mg twice daily
We have not yet identified possible HIV integrase mutations; need testing to determine reasons for possible clinical non-response to drug.
What patients will benefit from treatment with this drug?
CCR5 antagonist
CYP 3A4; P-glycoprotein substrate
150mg twice daily with CYP 3A4 inhibitors (other than tipranavir/ritonavir)
300mg twice daily with tipranavir/ritonavir
600mg twice daily with CYP 3A4 inducers without a CYP3A4 inhibitor
only for CCR5 positive patients; NOT for use in patients with virus that targets CXCR4 or mixed receptors for entry into cell. This drug would result in increased entry and faster dissemenation.
What patients will benefit from treatment?
Fusion Inhibitor
Limited to patients with multidrug resistant virus
subQ injectable; injection site reactions common
Co-administer with?
Major toxicity?
Co-adminsiter with ritonavir
Hepatotoxicity in 6%. Not for those co-infected with Hep B or C.
Co-administer with?
Co-administer with ritonavir (but at lower than normal ritonavir dose: 100mg day rather than 200mg day)
Not for treatment of patients with certain resistances
NNRTI (in Phase III)
CYP 3A4 and 2C
200mg twice daily (give with food to increase bioavailability)
Unique structure among NNRTIs allow it to cope with viral resistance mechanisms ("wiggly")
Concerns about its potency in patients formerly treated with PIs
Which PIs are associated with dyslipidemias?
All PIs. Ritonavir is the biggest culprit. Atazanavir is the only PI with a favorable side effect profile.
Which NRTIs are associated with dyslipidemias?
Stavudine is associated with hypertriglyceridemia. (Not nearly to the degree of PIs)
Disadvantages to the strategy of switching HAART in patients with dyslipidemia. Which drugs are candidates for switch?
PIs may be replaced with nevirapine, atazanavir or abacavir.

Viral resistance might be an issue, particularly with abacavir; strategy not well-studied; Statins may be more effective anyway.
Preferred treatment for high-LDL in patients on HAART? High Triglycerides?
Second Line:
Prescription Niacin
Fibric Acid Derivative (Fenofibrate preffered if co-administering statin)
2nd Line:
Fish Oil
Prescription Niacin
Basis of interactions between HAART and statin? Strategies to avoid this interaction?
PIs: CYP 3A4 Inhibition
Low dose Atorvastatin and pravastatin preferred (lovastatin and simvastatin contraindicated; rosuvastatin appears to interact on a different basis and is also contraindicated)
Efavirenz and nevirapine are CYP 3A4 inducers, therefore, pravastatin and atorvastatin are usually avoided for ineffectiveness.
2 major factors affecting successful treatment in HepC patients co-infected with HIV?
Genotype (Types 1 and 4 are much more difficult to treat than 2 and 3)
CD4 lymphocyte count
2 HAART drugs with the greatest propensity to cause drug-induced liver disease?
Nevirapine and tipranavir
What is the treatment of choice for HCV infected patients?
Weekly peg-interferon (180mcg) and daily ribavirin (dose based on weight and genotype)
3 most important drug interactions between HAART and HCV treatment regimens?
Ribavirin and didanosine (ribavirin increases phosphorylation of intracellular metabolites of didanosine and increases incidence of pancreatitis, lactic acidosis and decompensated liver disease)

Ribavirin and stavudine (enhanced mitochondiral damage)

Ribavirin and zidovudine (overlapping side effects--anemia and neutropenia)
Major side effects of HCV treatment?
Peg-interferon: depression (recommend psych eval before starting treatment; clear communication about side effect with patient)
Ribavirin: anemia, neutropenia (frequent CBCs)
Typical treatment duration for HCV?
48 weeks
Extend to 72 if genotype 1 and do not have rapid virologic response in first four weeks
May consider shortening to 24 if genotype 2 or 3 and rapid virologic response and low viral load
When do you consider stopping HCV treatment for poor response in those co-infected with HIV?
If fail to achieve a 2 log drop by week 12 of therapy
Appropriate treatment for aspergillus in HIV infected patient?
Voriconazole (fluconazole has NO efficacy against aspergillus): keep interactions with ritonavir and efavirenz and nevirapine in mind
2nd line or if high risk for zygomycosis: Amphotericin B (do not give with triazole--no data)
3rd line: Add Echinocandin (caspofungin, micofungin, anidulafungin) to initial therapy
Preferred initial choices for HAART therapy in treatment naive patients?
Base (NNRTI or ritonavir boosted PI):
Efavirenz (preferred NNRTI--nevirapine is more toxic)
lopinavir/ritonavir (ritonavir boosted PI: may sub fosamprenavir, atazanavir or possibly darunavir)

PLUS "backbone" (2 NRTIs)