scholarly journals Drug‐Drug Interactions in Inmates Treated for Human Immunodeficiency Virus andMycobacterium tuberculosisInfection or Disease: An Institutional Tuberculosis Outbreak

2002 ◽  
Vol 35 (9) ◽  
pp. 1106-1112 ◽  
Author(s):  
P. Spradling ◽  
D. Drociuk ◽  
S. McLaughlin ◽  
L. M. Lee ◽  
C. A. Peloquin ◽  
...  
2019 ◽  
Vol 71 (2) ◽  
pp. 353-362 ◽  
Author(s):  
Beatriz López-Centeno ◽  
Carlos Badenes-Olmedo ◽  
Ángel Mataix-Sanjuan ◽  
Katie McAllister ◽  
José M Bellón ◽  
...  

Abstract Background Drug–drug interactions (DDIs) that involve antiretrovirals (ARVs) tend to cause harm if unrecognized, especially in the context of comorbidity and polypharmacy. Methods A linkage was established between the drug dispensing registry of Madrid and the Liverpool human immunodeficiency virus (HIV) DDI database (January 2017–June 2017). Polypharmacy was defined as the use of ≥5 non-HIV medications, and DDIs were classified by a traffic-light ranking for severity. Results A total of 22 945 people living with HIV (PLWH) and 6 613 506 individuals without HIV had received medications. ARV regimens were predominantly based on integrase inhibitors (51.96%). Polypharmacy was higher in PLWH (32.94%) than individuals without HIV (22.16%; P < .001); this difference was consistently observed across all age strata except for individuals ≥75 years. Polypharmacy was more common in women than men in both PLWH and individuals without HIV. The prevalence of contraindicated combinations involving ARVs was 3.18%. Comedications containing corticosteroids, quetiapine, or antithrombotic agents were associated with the highest risk for red-flag DDI, and the use of raltegravir- or dolutegravir-based antiretroviral therapy was associated with an adjusted odds ratio of 0.72 (95% confidence interval, .60–.88; P = .001) for red-flag DDI. Conclusions Polypharmacy was more frequent among PLWH across all age groups except those aged ≥75 years and was more common in women. The detection of contraindicated medications in PLWH suggests a likely disconnect between hospital and community prescriptions. Switching to alternative unboosted integrase regimens should be considered for patients with risk of harm from DDIs.


2014 ◽  
Vol 30 (5) ◽  
pp. 159-167 ◽  
Author(s):  
Nimish Patel ◽  
Michael Veve ◽  
Steven Bliss ◽  
Mona Nasiri ◽  
Louise-Anne McNutt ◽  
...  

1996 ◽  
Vol 23 (4) ◽  
pp. 685-693 ◽  
Author(s):  
S. C. Piscitelli ◽  
C. Flexner ◽  
J. R. Minor ◽  
M. A. Polis ◽  
H. Masur

2018 ◽  
Vol 17 (2) ◽  
pp. 75-79
Author(s):  
Traci Housten ◽  
Laura Duvall ◽  
Pavithra Srinivas

Managing pulmonary arterial hypertension (PAH) treatment is a complex balance of achieving the desired medication effect versus maintaining safe and tolerable side effects for the patient. The “balancing act” intensifies when PAH patients are faced with multiple disease states that require treatment medication. This article will focus on the drug-drug interactions that must be considered in PAH patients with concomitant human immunodeficiency virus (HIV) and/or hepatitis C virus (HCV) infection.


2007 ◽  
Vol 51 (10) ◽  
pp. 3498-3504 ◽  
Author(s):  
Leah Tong ◽  
Truc K. Phan ◽  
Kelly L. Robinson ◽  
Darius Babusis ◽  
Robert Strab ◽  
...  

ABSTRACT Human immunodeficiency virus protease inhibitors (PIs) modestly affect the plasma pharmacokinetics of tenofovir (TFV; −15% to +37% change in exposure) following coadministration with the oral prodrug TFV disoproxil fumarate (TDF) by a previously undefined mechanism. TDF permeation was found to be reduced by the combined action of ester cleavage and efflux transport in vitro. Saturable TDF efflux observed in Caco-2 cells suggests that at pharmacologically relevant intestinal concentrations, transport has only a limited effect on TDF absorption, thus minimizing the magnitude of potential intestinal drug interactions. Most tested PIs increased apical-to-basolateral TDF permeation and decreased secretory transport in MDCKII cells overexpressing P-glycoprotein (Pgp; MDCKII-MDR1 cells) and Caco-2 cells. PIs were found to cause a multifactorial effect on the barriers to TDF absorption. All PIs showed similar levels of inhibition of esterase-dependent degradation of TDF in an intestinal subcellular fraction, except for amprenavir, which was found to be a weaker inhibitor. All PIs caused a dose-dependent increase in the accumulation of a model Pgp substrate in MDCKII-MDR1 cells. Pgp inhibition constants ranged from 10.3 μM (lopinavir) to >100 μM (amprenavir, indinavir, and darunavir). Analogous to hepatic cytochrome P450-mediated drug interactions, we propose that the relative differences in perturbations in TFV plasma levels when TDF is coadministered with PIs are based in part on the net effect of inhibition and induction of intestinal Pgp by PIs. Combined with prior studies, these findings indicate that intestinal absorption is the mechanism for changes in TFV plasma levels when TDF is coadministered with PIs.


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