HIV genotypic resistance testing to optimize antiretroviral prescribing: is there room for improvement?
BACKGROUND
Clinical utilization of genotype resistance testing is evolving. We examined the extent to which HIV care providers requesting genotype resistance tests used the information appropriately and the impact of inappropriate utilization.


METHODS
Data from a prospective cohort of HIV-infected patients (the HIV Outpatient Study) were used in the analysis. We analysed the frequency with which patients were prescribed any non-nucleoside reverse transcriptase inhibitor after identification of the K103N mutation in reverse transcriptase and the frequency of prescription of nelfinavir after identification of the D30N mutation in HIV protease; the short-term impact of this action on HIV viral load and CD4+ T-cell count was assessed.


RESULTS
Among 441 patients demonstrating either mutation, 18% who were taking the resistant antiretroviral at the time of the test were continued on the medication for >6 months after this finding. In 33% of these instances, prescribers reported these actions were erroneous oversights. For persons taking the resistant antiretroviral at the time of the genotype test, stopping this medication within 6 months of the test produced greater decreases in viral load (-1.35 versus -0.43 log copies/ml, P = 0.025) and a greater likelihood of achieving an undetectable viral load (25.3% versus 7.3%, P = 0.012) at 9 months. Changes in CD4+ T-cell count differed (+22.8 versus -23.0 cells/mm3), but not significantly (P = 0.167).


CONCLUSIONS
Following evidence of definitive resistance by genotype testing, a substantial fraction of antiretroviral prescriptions were continued in error leading to an attenuated therapeutic response. These data highlight the need to consider better systems to manage genotype resistance testing data in the clinical setting.
Uy
Jonathan
J
Section of Infectious Diseases, University of Illinois College of Medicine, Chicago, IL, USA. jonathan.uy@bms.com
Brooks
John T
JT
Baker
Rose
R
Hoffman
Mark
M
Moorman
Anne
A
Novak
Richard
R
D000328:Adult; D000465:Algorithms; D019380:Anti-HIV Agents / Q000494:pharmacology / Q000627:therapeutic use*; D018791:CD4 Lymphocyte Count; D024882:Drug Resistance, Viral / Q000235:genetics*; D005260:Female; D005838:Genotype; D006678:HIV / Q000187:drug effects* / Q000235:genetics; D015658:HIV Infections / Q000188:drug therapy* / Q000276:immunology / Q000821:virology*; D016333:HIV Protease / Q000235:genetics; D017320:HIV Protease Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D054303:HIV Reverse Transcriptase / Q000235:genetics; D006801:Humans; D008297:Male; D008826:Microbial Sensitivity Tests; D008875:Middle Aged; D019888:Nelfinavir / Q000494:pharmacology / Q000627:therapeutic use; D018894:Reverse Transcriptase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D019562:Viral Load
D019380:Anti-HIV Agents; D017320:HIV Protease Inhibitors; D018894:Reverse Transcriptase Inhibitors; D054303:HIV Reverse Transcriptase; D016333:HIV Protease; D019888:Nelfinavir