ArticleDer Internist2010
[Interactions with antiretroviral drugs].
Article in Der Internist, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 2 citations in OpenAlex.
- Prevalence ofIJID regions · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug-drug interactions are frequently encountered in the therapy of HIV-infected patients, since the highly active antiretroviral therapy always contains several drugs. Drugs against opportunistic infections and concomitant diseases are added frequently. All protease inhibitors are inhibitors of CYP3A, which is important in the metabolism of approximately 50% of all drugs, e.g. simvastatin, atorvastatin, sildenafil, and clarithromycin. Among the protease inhibitors, ritonavir is the strongest inhibitor of CYP3A activity. This inhibition is also used to enhance ("boost") the bioavailability of other protease inhibitors. The nonnucleoside reverse transcriptase inhibitors (NNRTI) efavirenz and nevirapine lead to an increase in CYP3A activity during long-term treatment. To prevent interactions, doses of CYP3A substrates have to be adapted in the beginning and at the end of CYP3A activity-modifying treatments. Interactions can also be a result of modifications in the activities of glucuronosyltransferases and of transport proteins. Ritonavir is an inhibitor of P-glycoprotein, which leads to increased expositions towards many antineoplastic drugs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.