Drug–Drug Interactions in Nosocomial Infections: An Updated Review for Clinicians
Abstract
:1. Introduction
2. Clinically Relevant DDIs in Nosocomial Settings
2.1. β-Lactam Antibiotics
2.2. Macrolides
2.3. Fluoroquinolones
2.4. Aminoglycosides
Drug | Type | Mechanism | Refs. |
---|---|---|---|
ACEi, ARB | Pd | Increased risk of nephrotoxicity. | [97] |
Antineoplastics | Pd | Both cisplatin and aminoglycosides induce sensorineural hearing loss. This is primarily caused by damage to the outer hair cells, specifically in the basal turn of the cochlea. Both classes of ototoxic medications induce oxidative stress within the inner ear, which serves as the primary catalyst for cellular damage. Additionally, there is an elevated risk of nephrotoxicity. | [98,99,100] |
Biphosphonates | Pd | Additive effect that could lower calcium levels in the blood for a long time. | [101] |
Diuretics | Pd | Increased risk of ototoxicity. | [99,100,102] |
Immunosuppressants | Pd | Increased risk of nephrotoxicity. | [103] |
Lincosamides | Pd | Increase in the neuromuscular blockade effect produced by aminoglycosides. | [104] |
Muscle relaxants | Pd | Enhanced neuromuscular blockade, increasing the risk of respiratory depression and prolonged muscle paralysis. | [99] |
NSAIDs | Pd | Increased aminoglycosides plasma concentrations, enhancing side effects. | [84,99] |
Opioids | Pd | Increased risk of neuromuscular blockade. | [99] |
Radiographic contrast agents | Pd | Increased nephrotoxicity. | [105] |
Vancomycin | Pd | Increased risk of ototoxicity and nephrotoxicity. | [106] |
2.5. Tetracyclines
2.6. Other Classes
3. ADME Considerations for DDIs
3.1. Absorbtion
3.2. Distribution
3.3. Metabolisation
3.4. Elimination
4. Clinical Implications of DDIs in Nosocomial Infections
5. Clinical Management of DDIs in Nosocomial Infections
5.1. Therapeutic Drug Monitoring and Dose Adjustment
5.2. Management of DDIs in Kidney and Liver Impairment
5.3. Assessing Disease Stage for Proper DDI Management in Nosocomial Infections
6. Key Findings and General Considerations
7. Conclusions
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Acknowledgments
Conflicts of Interest
References
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β-Lactams | Drug | Type | Mechanism | Ref. |
---|---|---|---|---|
Cef | Anticoagulants | Pd | Warfarin interacts with Cef that contain an NMTT side chain by inhibiting the production of blood coagulation factors. These effects are also exacerbated by Cef that lack the NMTT side chain. | [33] |
Cef | Antiretroviral drugs | Pk | Antiretrovirals disrupt the functioning of P-glycoprotein (which actively moves drugs over cellular barriers). Co-administration impacts antiretrovirals’ absorption, distribution, and excretion, resulting in changes to their effectiveness and safety. | [34] |
Cef | Calcium i.v. solutions | in vitro | Precipitation events that could harm vital organs. | [35] |
Cef | Antidiabetic drugs | Pd | Cefditoren includes pivalic acid, which reduces the carnitine content in the bloodstream. This results in the inability to synthesise glucose, causing hypoglycaemia. | [36] |
Cef | Phenytoin | Pd | Stevens–Johnson syndrome, caused by phenytoin, worsened due to cefepime. | [37] |
Cef | Proton-pump Inhibitors | Pd | A higher likelihood of developing acute renal damage. | [38] |
Pen | Antiepileptics | Pk | Impact on the plasma concentration of valproic acid, causing a considerable reduction and insufficient management of seizures. | [39] |
Pen | Warfarin | Pd | An increase in INR levels and a risk of bleeding. This can occur anywhere between seven days after starting amoxicillin treatment and nine days after stopping it. | [40] |
Pen + Cef | Allopurinol | Pd | Typical drug-induced widespread rashes. | [41] |
Pen + Cef | Aminoglycosides | Pd | The β-lactam ring gradually reacts towards the amino group, forming a penicillin–aminoglycoside complex with decreased antibacterial activity. | [42] |
Pen + Cef | Anti-acids | Pk | Out of the 13 β-lactams that were studied, 4 of them showed a significant decrease in bioavailability when taken with antacids or mineral supplements. The β-lactam with the most critical negative impact was cefdinir, whereas cefpodoxime proxetil showed a mild decrease in bioavailability when taken with antacids. | [43] |
Pen + Cef | Diuretics | Pk | Furosemide inhibits organic ion transporters 1 and 3 (which play an important role in the active secretion of antibiotics such as β-lactams). The channel’s disturbance of the usual electrochemical gradient-expelled cations like Ca2+ and Mg2+, results in a significantly positive charge in the lumen. This might result in the paracellular reabsorption of antibiotics with a positive charge. | [44] |
Pen + Cef | Methotrexate | Pk | Most β-lactams are low-pH organic acids that interfere with the renal tubular discharge of methotrexate and its byproducts, resulting in a decreased clearance. | [45] |
Pen + Cef | Probenecid | Pk | Probenecid hinders the elimination of β-lactams via the renal tubules. This slows down their clearance and leads to higher levels of antibiotics in the bloodstream. Organic anion transporters are competitively inhibited by probenecid. | [46] |
Carb | Valproic acid | Pk | Co-administration leads to a notable decrease in the plasma levels of valproic acid. The mean plasma concentration of valproic acid was 68.7 µg/mL; however, due to the interaction, it reduced to a mean value of 15.8 µg/mL, suggesting a reduction of 77%. This decline results in inadequate seizure management and other unfavourable consequences. | [39] |
Azt | Oral anticoagulants | Pd | Increased risk of bleeding. | [40] |
Azt | Furosemide | Pk | A moderate increase in the amount of aztreonam in the body. | [15] |
Azt | Probenecid | Pk | A moderate increase in the amount of aztreonam in the body. | [15] |
Azt | Entecavir, crizotinib | Pk | Both are transported by organic cation transporter 2. Co-administration leads to higher levels of the drugs in the bloodstream as they compete for transporters in the renal tubules. | [47] |
Drug | Type | Mechanism | Refs. |
---|---|---|---|
Anti-arrhythmics | Pk | After five days of macrolide treatment, there was a 50% reduction in the overall elimination of quinidine. | [58] |
Anticoagulants | Pd | Increased likelihood of bleeding, with an odds ratio of 1.86. The average INR level rises from 2.7 to 3.6 when juvenile cardiac patients are given this combination. | [40] |
Antiepileptics | Pk | An increased plasma concentration of carbamazepine (129%), which causes carbamazepine toxicity (including drowsiness, dizziness, ataxia, heart block, and liver failure). Also, a notable reduction in the plasma levels of pregabalin (a reduction of 17% in the AUC and a decrease of 13% in the Cmax). | [39] |
Antimalarials | Pd | Prolongation of QT and cardiac adverse effects. | [59] |
Antipsychotics | Pd | Macrolides strongly impede the effects of quetiapine and can cause severe adverse drug reactions. Macrolides increase the QTc interval by blocking the potassium channels in the heart. | [60] |
Antiretrovirals | Pk | Clarithromycin interacts with NNRTIs and PIs, reducing their AUC and increasing the risk of toxicity, necessitating dose adjustments or monitoring. Azithromycin is preferred when available. | [61,62] |
Benzodiazepines | Pk | Elimination of triazolam was decreased by 52%, leading to impaired psychomotor function and memory loss. The concurrent use of midazolam and erythromycin leads to a more than four-fold increase in the AUC and a 54% decrease in clearance for midazolam. | [63] |
Calcium channel blockers | Pd | A decrease in blood pressure due to the widening of blood vessels, a higher likelihood of hospitalisation due to low blood pressure or sudden kidney damage. | [64] |
Corticosteroids | Pk | Clarithromycin decreases the activity of CYP3A by 75%, potentially elevating the amount of prednisone in the bloodstream. Caution should be applied to prednisone-induced mania, even at extremely low doses of prednisone, in older individuals who have taken a CYP3A inhibitor. | [65] |
Cyclosporine | Pk | Increased blood concentrations for cyclosporine. | [66] |
Digoxin | Pk | Increased digoxin toxicity via inhibiting P-glycoprotein. | [67] |
Hypoglycemiants | Pk | Hypoglycemia can be worsened by the presence of hepatic cytochrome P450 inhibitors. Approximately 12.3% of hypoglycemia incidents in patients who are taking sulfonylureas are believed to be linked to the use of antimicrobial medications, particularly fluoroquinolones, macrolides, sulfamethoxazole–trimethoprim, and azoles. | [68] |
Immunosuppressants | Pk | Co-administration of clarithromycin and erythromycin with calcineurin inhibitors or mTOR inhibitors leads to a substantial rise in the immunosuppressant’s AUC and Cmax, increasing it by 3 to 10 times. | [69] |
Sildenafil | Pk | The administration of clarithromycin resulted in a 1.86-fold rise in sildenafil’s Cmax and a 2.29-fold increase in the area under the AUC. | [70] |
Statins | Pk | Co-administration results in higher levels of statins in the bloodstream, which increases the likelihood of experiencing statin-related side effects, such as myopathy and rhabdomyolysis. | [71] |
Drug | Type | Mechanism | Refs. |
---|---|---|---|
Anti-acids/Sucralfate | Pk-Pd | Formation of insoluble complexes, with decreased absorption and antimicrobial activity. | [77,78] |
Anti-arrhythmics | Pd | QTc prolongation and cardiotoxicity. | [79] |
Antidepressants | Pd | Increased risk of delirium, hallucinations, psychomotor agitation, paranoid delusions, and suicidal thoughts/attempts. | [80] |
Antiepileptics | Pd | In vulnerable patients, the presence of GABA-like structures at seven sites in norfloxacin and ciprofloxacin can antagonise GABA receptors, further increasing the likelihood of having seizures. Fluoroquinolones also stimulate the NMDA receptor, lowering susceptibility to seizures. | [81] |
Antipsychotics | Pd | Suppression of the heart’s potassium channels through additive inhibition. | [60] |
β-lactams | Pd | Increased risk of thrombocytosis. | [82] |
Clozapine | Pd | Increased concentration of clozapine, sedation, rhabdomyolysis, and increased risk of QT prolongation. | [78] |
Corticosteroids | Pd | Co-administration can lead to a heightened risk of tendinopathy or tendon rupture, particularly in females, individuals over the age of 60, and those who have been taking fluoroquinolones for an extended period. Exercise caution when administering corticosteroid therapy to individuals with multidrug-resistant tuberculosis who are also taking fluoroquinolones. | [83,84] |
Cyclosporine | Pk | Ciprofloxacin can enhance the toxicity of cyclosporine. Patients taking cyclosporine for an extended period should not use ciprofloxacin and should instead choose another antibiotic. | [85] |
Digoxin | Pk | Increased risk of digoxin toxicity via increasing digoxin serum levels. | [86] |
Immunosuppressants | Pk | Ciprofloxacin reduces mycophenolate mofetil levels by disrupting enterohepatic circulation and absorption. Drug level monitoring is recommended even though levofloxacin does not elevate the level of cyclosporine. | [69] |
Hypoglicaemiants | Pd | Levofloxacin’s risk for hypoglycaemia was 5.13 times higher than that of cephalosporins; however, it was 9.40 times higher than that of penicillin antibiotics. Furthermore, the findings indicated that levofloxacin posed the most significant risk for hypoglycaemia, followed by moxifloxacin and ciprofloxacin. In addition, patients who were taking levofloxacin at the same time as insulin or sulfonylurea were more likely to develop hypoglycaemia. | [87] |
Levothyroxine | Pk | The decrease in T4 AUC following the simultaneous use of ciprofloxacin and L-T4 is in line with suppressing a T4 uptake transporter in the intestines, maybe belonging to the OATP family. The idea suggests that the thyroid hormone transporters MCT8, MCT10, or LAT1/2, found in the intestine, could potentially be where the interaction between L-T4 and ciprofloxacin occurs. | [88] |
Methadone | Pd | Increased methadone toxicity and a life-threatening interaction. | [89] |
Methotrexate | Pk | Co-administration leads to higher blood levels of methotrexate, which raises the likelihood of developing anaemia and bone marrow suppression and increases the susceptibility to infections. | [78] |
NSAIDs | Pd | Co-administration reduces the antibacterial effect. | [90] |
Probenecid | Pk | Probenecid hinders the removal of fluoroquinolones from the kidneys by blocking their release through competitive inhibition of renal organic ion transporters. It is an inhibitor of the renal tubular anion secretion pathway, specifically targeting OATP 1 and 3. Probenecid caused a 16% rise in the AUC of ofloxacin and a 75% increase in ciprofloxacin in healthy volunteers. | [78,91] |
Theophylline | Pk | The daily administration of 1000 mg of ciprofloxacin decreases the clearance of theophylline by 19–32%. Co-administration to elderly individuals was linked to a roughly two-fold rise in the likelihood of being hospitalised due to theophylline toxicity. | [78] |
Warfarin | Pd | Increased risk of bleeding. | [78] |
Drug | Type | Mechanism | Refs. |
---|---|---|---|
Antacids | Pk-Pd | Chelating DDI that reduces the oral bioavailability by 80%. | [99,114] |
Antifungals | Pk | When eravacycline is administered with a potent inducer of CYP3A, like rifampin, the dosage should be increased. Concomitant administering of rifampin resulted in a decrease of roughly 33% in total eravacycline exposure and an increase of approximately 50% in clearance. However, it is uncertain whether a dose adjustment with an inhibitor like itraconazole is necessary. | [99] |
Antipsychotics | Pk | Increased plasma concentration for clozapine. | [60] |
Antithyroid drugs | Pd | Non-immune-mediated thyroid dysfunction. | [115] |
Cyclosporine | Pk | Administration of cyclosporine enhances the levels of orally ingested tetracyclines in the bloodstream. The findings strongly indicate that efflux pumps in the intestinal epithelium regulate the absorption of tetracycline from the gastrointestinal tract, even though cyclosporine further hinders renal and hepatic clearance. | [116] |
Iron supplements | Pk | Reduced bioavailability of tetracyclines. | [117] |
Oral contraceptives | Pk | Tetracyclines can decrease the effectiveness of oral contraceptives. | [99] |
PPIs | Pk | PPIs may decrease the absorption of tetracyclines. | [114] |
Drug | Type | Mechanism | Refs. |
---|---|---|---|
Aminoglycosides | Pd | Nephrotoxicity, ototoxicity. | [127] |
Amphotericin B | Pd | Nephrotoxicity, ototoxicity. | [128] |
Anticancer drugs | Pd | Nephrotoxicity, ototoxicity. | [129] |
Antivirals for H. simplex | Pd | Neurotoxicity, nephrotoxicity. | [130,131] |
Calcineurin inhibitors | Pd | Synergistic or additive renal impairment potential. | [132] |
Cephalosporins | Pd | Neurotoxicity, nephrotoxicity. | [129,133] |
Diuretics | Pd | Nephrotoxicity, ototoxicity. | [129] |
Neuromuscular blocking agent | Pd | Increased risk of neuromuscular blockade. | [134] |
NSAIDs | Pd | Nephrotoxicity. | [129,135] |
Opioids | Pd | The combination of morphine with vancomycin significantly increases the amount of histamine released. | [136] |
Polymyxins | Pd | Nephrotoxicity, ototoxicity. | [129] |
CYP3A4 | ||
Substrates | Inducers | Inhibitors |
opioid analgesics, alpha-1 adrenergic blockers, benzodiazepines, anti-arrhythmics, calcium channel blockers, anticoagulants, antimalarials, statins, antituberculars, tyrosine kinase inhibitors, corticosteroids, anxiolytics, anticonvulsants, macrolide antibiotics, lincosamide antibiotics, atypical antipsychotics, immunosuppressants (calcineurin inhibitors), antileprosy agents, antiretrovirals, antineoplastics, antifungals, antiparasitics, antianginals, rifamycin antibiotics, antiplatelets, selective estrogen receptor modulators, antidepressants, vinca alkaloids | rifampicin, efavirenz, nafcillin, rifabutin, rifapentine, flucloxacillin | clarithromycin, fosamprenamvir, etritonavir, ketoconazole, itraconazole, ritonavir, voriconazole, erythromycin, fluconazole, ciprofloxacin, norfloxacin |
CYP1A2 | ||
Substrates | Inducers | Inhibitors |
agomelatine, duloxetine, clozapine, olanzapine, melatonin, propranolol, theophylline | rifampicin | ciprofloxacin, acyclovir, valacyclovir |
CYP2C9 | ||
Substrates | Inducers | Inhibitors |
acenocumarol, celecoxib, meloxicam, fluvastatin, phenytoin | rifampicin | fluconazole, sulfametoxazole–trimethoprim, favipiravir |
CYP2C19 | ||
Substrates | Inducers | Inhibitors |
omeprazole, pantoprazole, diazepam, voriconazole, clopidogrel, phenytoin | rifampicin | fluconazole, voriconazole |
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Hîncu, S.; Apetroaei, M.-M.; Ștefan, G.; Fâcă, A.I.; Arsene, A.L.; Mahler, B.; Drăgănescu, D.; Tăerel, A.-E.; Stancu, E.; Hîncu, L.; et al. Drug–Drug Interactions in Nosocomial Infections: An Updated Review for Clinicians. Pharmaceutics 2024, 16, 1137. https://doi.org/10.3390/pharmaceutics16091137
Hîncu S, Apetroaei M-M, Ștefan G, Fâcă AI, Arsene AL, Mahler B, Drăgănescu D, Tăerel A-E, Stancu E, Hîncu L, et al. Drug–Drug Interactions in Nosocomial Infections: An Updated Review for Clinicians. Pharmaceutics. 2024; 16(9):1137. https://doi.org/10.3390/pharmaceutics16091137
Chicago/Turabian StyleHîncu, Sorina, Miruna-Maria Apetroaei, Gabriela Ștefan, Anca Ionela Fâcă, Andreea Letiția Arsene, Beatrice Mahler, Doina Drăgănescu, Adriana-Elena Tăerel, Emilia Stancu, Lucian Hîncu, and et al. 2024. "Drug–Drug Interactions in Nosocomial Infections: An Updated Review for Clinicians" Pharmaceutics 16, no. 9: 1137. https://doi.org/10.3390/pharmaceutics16091137