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Systemic Lupus Erythematosus
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
Maria A. Giraldo-Isaza, Bettina F. Cuneo
Not used anymore much for SLE in pregnancy. Calcineurin inhibitor (CNI). Limited data in the literature. Use only if benefits outweigh the risks in patients not responding to other therapy. No increased risk of congenital anomalies. Association with low birth weight, maternal diabetes, hypertension and kidney graft rejection likely related to disease and not cyclosporine [63–65]. Compatible with breastfeeding.
Introduction to dermatological treatment
Published in Richard Ashton, Barbara Leppard, Differential Diagnosis in Dermatology, 2021
Richard Ashton, Barbara Leppard
These are macrolide lactones isolated from Streptomyces tsukubaensis. They block the activity of calcineurin and inhibit T-cell activation. Their action is very similar to that of ciclosporin, but because of their lower molecular weight they are absorbed through the skin.
Topical Calcineurin Inhibitors
Published in Vineet Relhan, Vijay Kumar Garg, Sneha Ghunawat, Khushbu Mahajan, Comprehensive Textbook on Vitiligo, 2020
Immune alterations appear to play an important role in the etiopathogenesis of this disease, so immunosuppressants and immunomodulators have increasingly been investigated for the treatment of vitiligo [2]. Calcineurin inhibitors are immunosuppressive drugs that were developed primarily for use in transplantation medicine. Though systemic calcineurin inhibitors have not been used in vitiligo, topical calcineurin inhibitors have shown promise in the treatment of vitiligo because of their immunomodulatory effects without the side effect profile of corticosteroids.
Clinical features and diagnostic tools in idiopathic inflammatory myopathies
Published in Critical Reviews in Clinical Laboratory Sciences, 2022
Konstantinos I. Tsamis, Constantinos Boutsoras, Evripidis Kaltsonoudis, Eleftherios Pelechas, Ilias P. Nikas, Yannis V. Simos, Paraskevi V. Voulgari, Ioannis Sarmas
Treatment of ASS includes corticosteroids, biological agents, and immunosuppressive agents; however, to date there have been no large clinical trials to assess the efficacy of these treatments. Thus, treatment relies on small studies, retrospective analyses, and case reports. The predominant clinical symptoms and severity of each case dictate the type of treatment. Initial treatment in ASS-ILD usually relies on corticosteroids, with the dose varying based on disease severity and rate of decline [173]. Maintenance treatment focuses on immunosuppressive agents such as cyclophosphamide, azathioprine, and mycophenolate alone or in combination, and these medication schemes have similar efficacy [174,175]. Calcineurin inhibitors (tacrolimus and cyclosporine) have also been used, with tacrolimus being more effective than cyclosporine [176]. Rituximab and intravenous immunoglobulin (IVIg) treatment have also been tested with promising results; however adverse side effects may restrict their use [177,178]. For patients with active myositis, corticosteroids remain the initial treatment of choice, while maintenance focuses on corticosteroid monotherapy or a steroid-sparing immunosuppressant [179]. IVIgs, calcineurin inhibitors, and rituximab are usually retained for acute, severe, or recalcitrant myositis [180].
Proceedings of the 43nd Annual Upper Midwest Neuro-Ophthalmology Group Meeting, July 23, 2021 and Second Virtual Upper Midwest Neuro-Ophthalmology Group Meeting
Published in Neuro-Ophthalmology, 2021
Deena Tajfirouz, Casey Judge, John J. Chen, Collin McClelland
Deena Tajfirouz MD, Mayo Clinic, presented a case series of four post solid-organ transplant patients in their 60s on maintenance immunosuppression with calcineurin inhibitors who presented with a progressively fatal neurologic disease with progressive optic neuropathy and eventually myelopathy. An extensive evaluation including cerebrospinal fluid (CSF) studies, serologic studies for known infectious and inflammatory disorders, whole body fluorodeoxyglucose computed tomography positron emission tomography, and biopsies of the optic nerves were unrevealing. Despite treatment with high dose steroids, plasma exchange, intravenous immunoglobulin (IVIG), rituximab, mycophenolate, and discontinuation of tacrolimus or cyclosporin, the patients continued to worsen. The cause of their fatally progressive neurologic disease was thought to be due to calcineurin inhibitor neuro-toxicity with similar findings on MRI.
pre-existing diabetes and PTDM in kidney transplant recipients: how to handle immunosuppression
Published in Expert Review of Clinical Pharmacology, 2021
Eloi Chevallier, Thomas Jouve, Lionel Rostaing, Paolo Malvezzi, Johan Noble
The calcineurin protein is expressed in beta-cells. The effect of CNIs on insulin secretion seems to be dose and time dependent. Indeed, short exposure to CNIs is associated with increased insulin secretion in healthy volunteers whereas longer term intake is associated with a decrease in phase-2 insulin secretion in non-diabetic hemodialysis patients [78,79]. After kidney transplantation, high doses of TAC result in lower insulin secretion in response to glucose load [80]. However, this effect seems to disappear with chronic exposure and lower TAC trough concentrations [81]. Moreover, the diabetogenic effect of TAC also depends on the presence of associated risk factors such as obesity, hypertriglyceridemia (>200 mg/dL) and metabolic syndrome [82,83]. Those risk factors should be taken into account when assessing the incidence of immunosuppression induced PTDM [26].