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    Acyclovir in the treatment of shingles requires attention to these compatibility contraindications

    • Last Update: 2022-09-22
    • Source: Internet
    • Author: User
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    Intravenous acyclovir and renal injury should also be vigilant


    Acyclovir is a common drug, as early as 1982, the US FDA has approved acyclovir for the treatment of herpes simplex virus (HSV) infection
    .


    Acyclovir is known to be metabolized by the kidneys and can induce acute kidney injury (AKI
    ).

    Clinically, intravenous acyclovir requires adjustment of the dosage
    according to the glomerular filtration rate.


    So how exactly does acyclovir induce kidney damage? When is it time to be wary of acyclovir causing AKI?


    Today, we're going to take a look at Dr.
    Abdullah's article in the journal Saudi Pharm J to see the incidence, patterns, and associated risk factors
    of AKI after intravenous acyclovir injection.


    Acyclovir is a purine nucleoside synthesis agonist that is metabolized in vivo and converted to acyclovir triphosphate, which has antiviral activity
    against herpes simplex virus types 1, 2 and varicella-zoster virus (VZV).

    Clinically, acyclovir, valacyclovir (a precursor that can be metabolized in vivo to acyclovir) and famciclovir are used to treat herpes simplex and shingles
    .
    These agents have the same efficacy
    in reducing the duration and severity of pain in herpes simplex/shingles disease, preventing complications and reducing the frequency of recurrence.
    Acute kidney injury caused by
    intravenous (IV) acyclovir is the most worrying side effect
    of the drug when taking the drug.

    Studies have shown that AKI usually appears within 2-3 days after drug infusion, and if not identified in time, intravenous acyclovir can cause fatal AKI
    .
    About 60% to 90% of acyclovir is excreted through the kidneys in prototype drugs, and the maximum solubility of acyclovir is only 2.
    5 mg/ml, making it easy to precipitate in the renal tubules
    .

    Therefore, when the drug lens reaches the renal tubule, it can lead to tubular obstruction, ischemia, and necrosis, which can induce renal damage
    .
    In addition, aldehyde metabolites of acyclovir may also directly damage the renal tubules
    .

    Previous studies have shown that about 10% to 48% of patients can develop nephrotoxicity
    after intravenous injection of acyclovir.

    However, with the increase in clinical research in recent years, this number has dropped to 18% to 21%.

    In a clinical study of 160,000 people with oral acyclovir/famciclovir/valacyclovir, it was noted that, unlike intravenous acyclovir, oral acyclovir usually did not induce nephrotoxicity
    .
    There are many
    reasons why intravenous acyclovir is more likely to occur than oral AKI.

    Rapid infusion of high doses of acyclovir can lead to a rapid increase in blood concentrations; Conversely, when taken orally, only 10% to 30% of the drug is absorbed into the bloodstream
    by the intestine.
    Thus, measures to prevent intravenous acyclovir from causing AKI include slowing the rate of intravenous infusion (infusion time greater than 1 to 2 hours), reducing the dose in the presence of chronic nephropathy, avoiding simultaneous use of nephrotoxic drugs, and adequate hydration to ensure high urinary flow (100 to 150 mL/h).

    Almost certainly, intravenous fluids can prevent intravenous acyclovir-induced AKI
    .

    Therefore, fluid control during intravenous acyclovir injection is particularly important
    .



    Incidence of nephrotoxicity and risk factors



    A total of 199 patients requiring intravenous acyclovir were included in the
    study.

    The average age was 45.
    8± 19.
    7 years, of which 49.
    8%
    were males.

    A total of 40 patients (20.
    1%) developed AKI
    .

    Univariate analysis showed that age (p=0.
    028), diabetes mellitus (p=0.
    027), concomitant use of vancomycin (p=0.
    003), concomitant use of aminoglycoside antibiotics (p=0.
    043), and high creatinine baseline values before treatment (p=0.
    010) were risk factors
    for acyclovir-induced AKI.

    Multiple regression analysis showed that only age, total treatment time, and simultaneous use of vancomycin were significant independent risk factors
    for acyclovir-induced AKI.
    The authors note that the probability of AKI occurring when vancomycin is combined with acyclovir is significantly increased
    .

    Therefore, care should be taken to avoid vancomycin when using acyclovir and closely monitor renal function
    if necessary.
    Advanced age is another independent risk factor
    for acyclovir causing AKI.

    With age, the glomerular filtration rate (GFR) decreases, which may be the reason why AKI is more likely to occur when using acyclovir in elderly patients
    .
    Other studies have also pointed out that chronic kidney disease (CKD) is also an important risk factor
    for acyclovir-induced AKI.
    In addition, the combination of hypertension, obesity, diabetes and nonsteroidal anti-inflammatory drugs, ceftriaxone, and angiotensin-converting enzyme inhibitors (ACE Inhibitors) is also a risk factor
    for acyclovir-induced AKI.

    Therefore, when injecting intravenous acyclovir, it is necessary to pay attention to the compatibility of the drug and use it
    with caution.
    Summary Acyclovir is commonly used in the treatment of HSV-1, HSV-2 and VZV infections, mainly excreted through the kidneys, and drug crystals may be deposited in the renal tubules, inducing nephrotoxicity
    .
    When intravenous acyclovir is given, the frequency
    of AKI can be increased by advanced age, CKD, diabetes, hypertension, obesity, etc.
    In addition, when NSAIDs, ceftriaxone, ACE Inhibitors, vancomycin and other drugs are combined with intravenous acyclovir, the likelihood of AKI is also increased
    .
    Intravenous fluids (hydration) prevent intravenous acyclovir-related AKI
    .
    Therefore, when intravenous acyclovir is injected, it is necessary to evaluate carefully, use it rationally, pay attention to hydration, and closely monitor renal function if necessary to ensure drug safety
    .

    References:[1] Al-Alawi Abdullah M, Al-Maqbali Juhaina Salim, Al-Adawi Maria, et al.
    Incidence, patterns, risk factors and clinical outcomes of intravenous acyclovir induced nephrotoxicity.
    .
    Saudi Pharm J.
    2022; 30: 874-877.
    [2] Lam Ngan N, Weir Matthew A, Yao Zhan, et al.
    Risk of acute kidney injury from oral acyclovir: a population-based study.
    Am J Kidney Dis.
    2013; 61: 723-729.
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    The source of this article medical community skin channel Author | Chen Wei reviewed this article | Tang Jiaoqing Responsible Editor Mr.
    Lu Li

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