|Celiac disease and absorption of HIV meds
Aug 19, 2011
Dear colleagues: I am a physician working in Buenos Aires, Argentina. My patient is a HIV-infected, asymptomatic, 55 y.o. man 100% adherent to his medication. He started HAART with 362 CD4 cells and a >6 log VL. He started abacavir-3TC-atazanavir/r. His VL dropped, but, after 12 months the VL remained between 2-2.3 log. In order to perform a genotyping, I stopped his treatment and asked him to perform the genotype 2 weeks off therapy. The study did not show relevant mutations. Taking into account his high basal VL, I considered his first HAART as a weak combination, so I proposed him to change the HAART. I proposed him TDF-3TC-LPV/r. He started this new HAART and the VL remained at same levels (2-2.3 log). In an attempt to increase the potency, I added AZT (I thought that this unorthodox approach might help lower the VL...), but the VL remained in the same levels. I stopped AZT. Now, he is on TDF-3TC-LPV/r, and the VL is... detectable. Recently, he received a presumptive diagnosis of celiac disease. He has not diarrhea, he is not malnourished... Do you know any negative influence of celiac disease on the absorption of antiretrovirals? Thank you. Edgardo
Response from Dr. Young
Buenos dias Dr. Edgardo and thanks for posting from Buenos Aires.
It would appear that you've given a very thoughtful analysis of your patient's situation. Indeed, the strategies that you've employed might have been ones that we'd use here in Denver.
I'm not aware of any data or anecdotes that like celiac disease to poor medication absorption, particularly in light of the fact that your patient has what seems to be mild disease. One potential strategy to ascertain if there is a malabsorption issue is to run drug level tests on the patient- if the levels are normal range (as I suspect), then we could rule out this as a factor.
Appreciating the nature of HIV viral dynamics (I'd refer you to the groundbreaking work of Perelson, et al.,), all patients have a very long terminal decay rate of circulating virus. It's just that most patients have baseline HIV RNA levels that are 1- to 2-log lower than your patient. As a result, one might predict that it would take much longer for your patient to reach an absolute VL value below limit of detection, despite a >4 log VL decline. Therefore, the residual ~2 log VL is a reflection of this longer decay rate rather than decreased antiviral potency or emerging drug resistance (as your drug resistance testing would support).
Again, thanks for posting. I hope that this discussion is helpful. BY
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