Review article: The pharmacokinetics and pharmacodynamics of drugs used in inflammatory bowel disease treatment

Summary Background The current COVID‐19 pandemic, caused by SARS‐CoV‐2, has emerged as a public health emergency. All nations are seriously challenged as the virus spreads rapidly across the globe with no regard for borders. The primary management of IBD involves treating uncontrolled inflammation with most patients requiring immune‐based therapies. However, these therapies may weaken the immune system and potentially place IBD patients at increased risk of infections and infectious complications including those from COVID‐19. Aim To summarise the scale of the COVID‐19 pandemic, review unique concerns regarding IBD management and infection risk during the pandemic and assess COVID‐19 management options and drug interactions in the IBD population. Methods A literature review on IBD, SARS‐CoV‐2 and COVID‐19 was undertaken and relevant literature was summarised and critically examined. Results IBD patients do not appear to be more susceptible to SARS‐CoV‐2 infection and there is no evidence of an association between IBD therapies and increased risk of COVID‐19. IBD medication adherence should be encouraged to prevent disease flare but where possible high‐dose systemic corticosteroids should be avoided. Patients should exercise social distancing, optimise co‐morbidities and be up to date with influenza and pneumococcal vaccines. If a patient develops COVID‐19, immune suppressing medications should be withheld until infection resolution and if trial medications for COVID‐19 are being considered, potential drug interactions should be checked. Conclusions IBD patient management presents a challenge in the current COVID‐19 pandemic. The primary focus should remain on keeping bowel inflammation controlled and encouraging medication adherence.

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“…10‐20% absorbed 134 . AUC may ↑ 6.5 fold 24 Consider changing steroid agent or taking budesonide an hour before lopinavir/ritonavir 124 …”

Section: Pharmacological Management Of Covid‐19 In the Ibd Patientmentioning

confidence: 99%

Review article: prevention, diagnosis and management of COVID‐19 in the IBD patient

Al‐Ani

Prentice

Rentsch

et al. 2020

Aliment Pharmacol Ther

111

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“…TLRs members can form homodimers/heterodimers among their same protein family or associates with an "outside TLR family" protein; both formations contribute to their structural and functional diversity [4]. Homodimers are formed by TLR4 while TLR members 1, 2, and 6 like TLR1/2 or TLR2/6 dimers form heterodimers [2,3,[15][16][17]. TLRs members, their dimerization, cellular distribution, ligands, induced signaling pathway, and product are shown in Table 1; for further information about TLRs, Video 2 (https://youtu.be/8mEnyBdsrr8) about TLR overview can be shown at Armando Hasudungan YouTube channel [18].…”

Section: Toll-like Receptors Family Membersmentioning

confidence: 99%

“…Upon TLRs recognition and binding to their ligands, they undergo conformational changes, dimerization as well as interaction with adaptor molecules passing series of intracellular signal transduction pathways that involve transcription factors NF-κB, IRFs, and mitogen-activated protein kinase (MAPK) activation. These pathways finally resulting in the secretion of pro-inflammatory mediators including nitric oxide (NO), CK-like tumour necrosis factor-alpha (TNF-α), IL-6 & IL-1β, chemokines (CC), and type I IFN [15,21,25,26]. As shown in Figure 2.…”

Section: Toll-like Receptors Signaling Pathwaymentioning

confidence: 99%

“…It is utilized by all TLRs but not TLR3 [21,29]. This pathway activates the IRAKs, TRAF6, transforming growth factor (TGF)-β-activated kinase (TAK)-1 and the IKK complex [15]. It causes the nuclear translocation of NF-κB and adaptor protein-1 (AP1) [28,30], and ends with the secretion of CK like IL-6, IL-10, IL-12 & TNF-α [16,29].…”

Section: Myd88-dependent Pathwaymentioning

confidence: 99%

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Toll-Like Receptors, Keys of the Innate Immune System

Hassan¹

2021

Innate Immunity in Health and Disease

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Toll-like receptors (TLRs) are members of the integral glycoproteins family, which are consist of intracellular and endoplasmic domains. TLRs are widely distributed in body tissues and expressed by immune and nonimmune cells. They are able to identify pathogens that cause cell injury and distinguish them from harmless microbes, and pathogenic nucleic acids as their binding ligand. Upon binding to their ligands, TLRs first underwent conformational changes; either forming homodimers or heterodimers, starting signaling pathways involve adaptor molecules utilization and then signal transduction through either myeloid differential (MyD)-88 dependent or independent pathways. Ending with activation of several transcription factors (TF) and release of pro-inflammatory cytokines (CK) and Type I interferons (IFN) and initiation of inflammation. TLRs are involved in almost all-inflammatory processes due to underlying disorders and diseases, which made them interesting targets for therapeutic development, via the synthesis of different agonists, antagonists, and even naturalized antibodies.

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“…There are a number of accepted treatments for CD, aimed not only to reduce the inflammation but also to improve the long-term prognosis ( 4 ). The most desirable end point, achieved in only a relatively low proportion of cases at present, is long-term remission.…”

Section: Introductionmentioning

confidence: 99%

Nutritional Modulation of Gene Expression: Might This be of Benefit to Individuals with Crohn’s Disease?

Ferguson

2015

Front. Immunol.

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The incidence of inflammatory bowel diseases (IBD), including Crohn’s disease (CD), is increasing worldwide, especially in young children and adolescents. Although hospitalized patients are usually provided with enteral or parenteral support, continuing care typically requires a trial-and-error approach to suppressing symptoms and maintaining disease remission. Current nutritional advice does not differ from general population guidelines. International collaborative studies have revealed 163 distinct genetic loci affecting susceptibility to IBD, in some of which host–microbe interactions can be seen to play an important role. The nature of these loci enables a rationale for predicting nutritional requirements that may not be evident through standard therapeutic approaches. Certain recognized nutrients, such as vitamin D and long-chain omega-3 polyunsaturated fatty acids, may be required at higher than anticipated levels. Various phytochemicals, not usually considered in the same class as classic nutrients, could play an important role. Prebiotics and probiotics may also be beneficial. Genomic approaches enable proof of principle of nutrient optimization rather than waiting for disease symptoms to appear and/or progress. We suggest a paradigm shift in diagnostic tools and nutritional therapy for CD, involving a systems biology approach for implementation.

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Review article: The pharmacokinetics and pharmacodynamics of drugs used in inflammatory bowel disease treatment

Abstract: It considers clinical aspects of each entity and the pharmacokinetic/pharmacodynamic relationship supported by the use of plasma monitoring, tissue concentrations, and certain aspects derived from pharmacogenetics.

Cited by 17 publications

References 294 publications

Review article: prevention, diagnosis and management of COVID‐19 in the IBD patient

Review article: prevention, diagnosis and management of COVID‐19 in the IBD patient

Toll-Like Receptors, Keys of the Innate Immune System

Nutritional Modulation of Gene Expression: Might This be of Benefit to Individuals with Crohn’s Disease?

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