Individualizing immunosuppression in lung transplantation

McDermott, Jennifer; Girgis, Reda E.

doi:10.21542/gcsp.2018.5

Cited by 16 publications

(16 citation statements)

References 73 publications

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“…Tacrolimus usage was found to be associated with a significantly reduced risk for bronchiolitis obliterans syndrome (BOS) grade ≥1 at 3 years when compared with cyclosporine, despite a similar rate of acute rejection. However, no survival advantage was detected (85)(86)(87). Currently, tacrolimus is the most popular calcineurin inhibitor in use, while mycophenolic acid is the dominant purine synthesis inhibitor used (88).…”

Section: Immunosuppression and Lung Transplantmentioning

confidence: 99%

Narrative review of the evolution of lung transplant

Makdisi¹,

Cedeno-Rodriguez²

2023

Curr Chall Thorac Surg

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Background: The first successful human lung transplant was performed approximately six decades ago, but evolution has been slow. It was not until the past two decades that lung transplantation became a more routine procedure with predictable outcomes.Methods: A comprehensive search of the medical literature using Ovid and PubMed search engines was conducted for progression of all aspects of lung transplantation, including surgical techniques, immunosuppression progression, donor selection criteria evolution, recipient criteria evolution, new technology used to support the patient prior and after transplant, along with donor organ management and the Lung Allocation Scoring (LAS) system variables and their impact on outcomes after lung transplantation.Conclusions: Advancement has been multifactorial in all phases of lung transplantation: in the preoperative phase with better selection criteria, better nutrition, and better pulmonary and physical rehabilitation; in the perioperative phase with improvement of surgical techniques, immunosuppression drugs, development of mechanical circulatory support, and preservation technology; and in the postoperative phase with better understanding of immune rejection and better management of long-term complications.All these progressions have been fundamental to the current success of lung transplantation.

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Section: Immunosuppression and Lung Transplantmentioning

confidence: 99%

Narrative review of the evolution of lung transplant

Makdisi¹,

Cedeno-Rodriguez²

2023

Curr Chall Thorac Surg

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“…The functions of T and B lymphocytes in the process of rejection have become gradually understood, and the immunosuppressive regime has been optimized as a result of many experimental and clinical studies. Immunosuppressants are classified according to their mechanisms of action, as shown in Table 1 [3,4,18,28,29,30,31,32,33,34]. CNIs inhibit the activity of a calcium-dependent phosphatase named calcineurin, thereby impeding the transduction of the nuclear factor of activated T cells (NFAT) and the production of cytokines, such as IL-2, tumor necrosis factor-alpha (TNF-α), and interferon-gamma (IFN-γ).…”

Section: Classification Of Immunosuppressantsmentioning

confidence: 99%

Recent Topics on The Mechanisms of Immunosuppressive Therapy-Related Neurotoxicities

Zhang

Egashira

Masuda

2019

IJMS

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Although transplantation procedures have been developed for patients with end-stage hepatic insufficiency or other diseases, allograft rejection still threatens patient health and lifespan. Over the last few decades, the emergence of immunosuppressive agents such as calcineurin inhibitors (CNIs) and mammalian target of rapamycin (mTOR) inhibitors have strikingly increased graft survival. Unfortunately, immunosuppressive agent-related neurotoxicity commonly occurs in clinical practice, with the majority of neurotoxicity cases caused by CNIs. The possible mechanisms through which CNIs cause neurotoxicity include increasing the permeability or injury of the blood–brain barrier, alterations of mitochondrial function, and alterations in the electrophysiological state. Other immunosuppressants can also induce neuropsychiatric complications. For example, mTOR inhibitors induce seizures, mycophenolate mofetil induces depression and headaches, methotrexate affects the central nervous system, the mouse monoclonal immunoglobulin G2 antibody (used against the cluster of differentiation 3) also induces headaches, and patients using corticosteroids usually experience cognitive alteration. Therapeutic drug monitoring, individual therapy based on pharmacogenetics, and early recognition of symptoms help reduce neurotoxic events considerably. Once neurotoxicity occurs, a reduction in the drug dosage, switching to other immunosuppressants, combination therapy with drugs used to treat the neuropsychiatric manifestation, or blood purification therapy have proven to be effective against neurotoxicity. In this review, we summarize recent topics on the mechanisms of immunosuppressive drug-related neurotoxicity. In addition, information about the neuroprotective effects of several immunosuppressants is also discussed.

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“…The functions of T and B lymphocytes in the process of rejection have become gradually understood and the immunosuppressive regime has been optimized as a result of many experimental and clinical studies. Immunosuppressants are classified according to their mechanisms of action, as shown in Table 1 [3,4,18,[28][29][30][31][32][33][34]. CNIs inhibit the activity of a calcium-dependent phosphatase named calcineurin, thereby impeding the transduction of nuclear factor of activated T cells (NFAT) and the production of cytokines, such as IL-2, tumour necrosis factor-alpha (TNF-α), [14].…”

Section: Classification Of Immunosuppressantsmentioning

confidence: 99%

Recent Topics on the Mechanisms of Immunosuppressive Therapy-Related Neurotoxicities

Zhang¹,

Egashira²,

Masuda³

2019

Preprint

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Although transplantation procedures have been developed for patients with end-stagec hepatic insufficiency or other diseases, allograft rejection still threatens patient health and lifespan. Over the last few decades, the emergence of immunosuppressive agents, such as calcineurin inhibitors (CNIs) and mammalian target of rapamycin (mTOR) inhibitors, have strikingly increased graft survival. Unfortunately, immunosuppressive agent-related neurotoxicity is commonly occurred in clinical situations, with the majority of neurotoxicity cases caused by CNIs. The possible mechanisms whereby CNIs cause neurotoxicity include: increasing the permeability or injury of the blood-brain barrier, alterations of mitochondrial function, and alterations in electrophysiological state. Other immunosuppressants can also induce neuropsychiatric complications. For example, mTOR inhibitors induce seizures; mycophenolate mofetil induces depression and headache; methotrexate affects the central nervous system; mouse monoclonal immunoglobulin G2 antibody against cluster of differentiation 3 also induces headache; and patients using corticosteroids usually experience cognitive alteration. Therapeutic drug monitoring, individual therapy based on pharmacogenetics, and early recognition of symptoms have greatly reduced neurotoxic events. Once neurotoxicity occurs, a reduction in the drug dosage, switching to other immunosuppressants, using drugs to treat the neuropsychiatric manifestation, or blood purification therapy have proven to be effective against neurotoxicity. In this review, we summarize the recent topics on the mechanisms of neurotoxicity of immunosuppressive drugs. In addition, some information about neuroprotective effects of several immunosuppressants are also discussed.

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Individualizing immunosuppression in lung transplantation

Cited by 16 publications

References 73 publications

Narrative review of the evolution of lung transplant

Narrative review of the evolution of lung transplant

Recent Topics on The Mechanisms of Immunosuppressive Therapy-Related Neurotoxicities

Recent Topics on the Mechanisms of Immunosuppressive Therapy-Related Neurotoxicities

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