Relevant bibliographies by topics / Immunosuppressive markers

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Immunosuppressive markers'

Author: Grafiati
Published: 10 January 2023
Last updated: 28 January 2023

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Journal articles on the topic "Immunosuppressive markers"

1

Dharma, Sanam, Sheila Figel, Tara Barone, Michael Ciesielski, and Robert Fenstermaker. "TAMI-63. GLIOBLASTOMA ASSOCIATED MESENCHYMAL STEM LIKE CELLS (G-MSC) WHICH INFILTRATE TUMORS IN HUMAN AND MOUSE ARE STRONGLY ASSOCIATED WITH IMMUNOSUPPRESSION." Neuro-Oncology 22, Supplement_2 (November 2020): ii227. http://dx.doi.org/10.1093/neuonc/noaa215.950.

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Abstract Glioblastoma (GBM) is the most aggressive form of brain cancer with an overall survival (OS) less than 16 months. Glioblastoma associated mesenchymal stem like cells (G-MSC) were identified in human patient samples, and higher presence of these cells in patient samples co-relates with lower overall survival. Our lab and others have also identified these cells in orthotopic GL261 glioblastoma murine models. We hypothesize that infiltration of G-MSC plays a key role in creating the highly immunosuppressive environment seen in GBMs. In order to investigate this, we utilized data from the TCGA database to stratify patients into two groups, showing higher or lower expression of the G-MSC markers (CD73, CD90, CD105). Patients expressing higher levels of G-MSC markers showed higher expression of CD4+ cells, as compared to patients with lower G-MSC marker expression. Further, patients with higher G-MSC markers showed high levels of PTGS2, the gene encoding cyclooxygenase 2 (COX2), a known tumor growth promoting and immunosuppressive molecule. We further investigated CD4+ T cell infiltration using GL261 orthotopic implants and observed that CD4+ T cells positively corelated with levels of G-MSC in these tumors. Our studies indicate that levels of G-MSC co-relate with immune cell infiltration and the expression of immunosuppressive factors such as COX2, underlining the importance of these cells in immunosuppression-driven resistance to therapy. These studies will be later utilized to develop rationale combination therapies to improve the overall survival in GBM.
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Syutkin, V. E., N. V. Borovkova, and M. S. Novruzbekov. "Biomarkers of tolerance and immunological monitoring in liver transplantation." Transplantologiya. The Russian Journal of Transplantation 12, no. 2 (June 18, 2020): 126–34. http://dx.doi.org/10.23873/2074-0506-2020-12-2-126-134.

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Introduction. We reviewed the literature data on clinical and laboratory parameters that allow predicting the development of operational tolerance in liver transplant recipients after their complete weaning from immunosuppressive therapy. The aim was to identify possible biomarkers of tolerance in liver transplant recipients with the successful complete weaning from immunosuppression for subsequent implementation in routine clinical practice. The cellular, humoral, and molecular markers of the liver transplant recipients who were completely withdrawn from immunosuppressive therapy without the development of graft dysfunction were estimated. The authors underlined the necessity of clinical trials for identifying biomarkers of the operational tolerance development.
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Kędzierska, Karolina, Krzysztof Sindrewicz, Katarzyna Sporniak-Tutak, Edyta Gołembiewska, Labib Zair, Jerzy Sieńko, Małgorzata Stańczyk-Dunaj, Irena Baranowska-Bosiacka, and Kazimierz Ciechanowski. "Does Immunosuppressive Therapy Affect Markers of Kidney Damage?" Annals of Transplantation 21 (March 3, 2016): 137–44. http://dx.doi.org/10.12659/aot.895275.

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4

Kovaleva, Olga V., Madina A. Rashidova, Daria V. Samoilova, Polina A. Podlesnaya, Valeria V. Mochalnikova, and Alexei Gratchev. "Immunosuppressive Phenotype of Esophagus Tumors Stroma." Analytical Cellular Pathology 2020 (August 20, 2020): 1–9. http://dx.doi.org/10.1155/2020/5424780.

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Background. Tumor-associated macrophages (TAMs) and tumor-infiltrating lymphocytes (TILs) contribute significantly to the development of immunosuppressive properties of a tumor. In this study, we performed immunohistochemical analysis of immune cells of esophageal tumors stroma. Methods. Paraffin-embedded tissue specimens from 48 esophageal squamous cell carcinoma (ESCC) patients were retrospectively collected for immunohistochemical analysis of stromal cells. For staining of macrophages, CD68, CD163, CD206, PU.1, and iNOS were used. For T cell detection, CD8, CD3, and FOXP3 were used. Also, we performed staining for PD-L1 that can be expressed on TAMs and tumor cells. Clinicopathological and survival data were collected and analyzed using the χ2 and Fisher exact tests, Kaplan–Meier curves, and the log-rank test. The correlation analysis was performed with Spearman’s rank correlation coefficient. Results. We found that FOXP3 expression was associated with age (p=0.042) and iNOS expression was associated with the disease stage (p=0.044). In addition, FOXP3 and CD163 appeared to be markers of good prognosis (HR=0.4420, p=0.0325, and HR=0.4447, p=0.0456, respectively). Significant association between PU.1+ and CD68+ macrophages (r=0.833; p≤0.001) and between PU.1+ and CD163+ macrophages (r=0.500; p≤0.001) was established; positive association between PU.1 and CD206 expression was also observed (r=0.250; p=0.043). Conclusions. Large amounts of CD163+ macrophages and FOXP3+ Т cells appear to be markers of good prognosis of ESCC. The number of PU.1+ macrophages strongly correlates with the number of CD68+ macrophages; therefore, usage of PU.1 as a potential macrophage marker can be recommended for esophageal tumors.
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Canzoni, Marco, Massimo Marignani, Maria Laura Sorgi, Paola Begini, Michela Ileen Biondo, Sara Caporuscio, Vincenzo Colonna, et al. "Prevalence of Hepatitis B Virus Markers in Patients with Autoimmune Inflammatory Rheumatic Diseases in Italy." Microorganisms 8, no. 11 (November 16, 2020): 1792. http://dx.doi.org/10.3390/microorganisms8111792.

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Chronic hepatitis B virus (HBV) infection may be reactivated by immunosuppressive drugs in patients with autoimmune inflammatory rheumatic diseases. This study evaluates HBV serum markers’ prevalence in rheumatic outpatients belonging to Spondyloarthritis, Chronic Arthritis and Connective Tissue Disease diagnostic groups in Italy. The study enrolled 302 subjects, sex ratio (M/F) 0.6, mean age ± standard deviation 57 ± 15 years, 167 (55%) of whom were candidates for immunosuppressive therapy. The Spondyloarthritis group included 146 subjects, Chronic Arthritis 75 and Connective Tissue Disease 83 (two patients had two rheumatic diseases; thus, the sum is 304 instead of 302). Ten subjects (3%) reported previous anti-HBV vaccination and tested positive for anti-HBs alone with a titer still protective (>10 IU/mL). Among the remaining 292 subjects, the prevalence of positivity for HBsAg, isolated anti-HBc, anti-HBc/anti-HBs, and any HBV marker was 2%, 4%, 18%, and 24%, respectively. A total of 26/302 (9%) patients with γ-globulin levels ≤0.7 g/dL were more frequently (p = 0.03455) prescribed immunosuppressive therapy, suggesting a more severe rheumatic disease. A not negligible percentage of rheumatic patients in Italy are at potential risk of HBV reactivation related to immunosuppressive therapy. Before starting treatment, subjects should be tested for HBV markers. Those resulting positive should receive treatment or prophylaxis with Nucleos (t) ides analogue (NUCs) at high barrier of resistance, or pre-emptive therapy, according to the pattern of positive markers. HB vaccination is recommended for those who were never exposed to the virus.
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Jablonska, Jadwiga, Malwina Rist, Ilona Spyra, Luisa Tengler, Maksim Domnich, Benjamin Kansy, Bernd Giebel, et al. "Evaluation of Immunoregulatory Biomarkers on Plasma Small Extracellular Vesicles for Disease Progression and Early Therapeutic Response in Head and Neck Cancer." Cells 11, no. 5 (March 5, 2022): 902. http://dx.doi.org/10.3390/cells11050902.

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Head and Neck Cancers (HNCs) have highly immunosuppressive properties. Small extracellular vesicles (sEVs), including exosomes, nanosized mediators of intercellular communication in the blood, carry immunosuppressive proteins and effectively inhibit anti-tumor immune responses in HNCs. This study evaluates immunosuppressive markers on sEVs from 40 HNC patients at different disease stages and 3- and 6-month follow-up after surgery and/or chemoradiotherapy. As controls, sEVs from normal donors (NDs) are examined. Immunoregulatory surface markers on sEVs were detected as relative fluorescence intensity (RFI) using on-bead flow cytometry, and their expression levels were monitored in the early and late stages of HNC and during follow-up. In parallel, the sEV-mediated apoptosis of CD8+ Jurkat cells was assessed. Together with TGF-β1 and PD-L1 abundance, total sEV proteins are elevated with disease progression. In contrast, total sEV protein, including TGF-β1, PD-1 and PD-L1, decrease upon therapy response during follow-up. Overall survival analysis implies that high sEV PD-1/PD-L1 content is an unfavorable prognostic marker in HNC. Consistently, the sEV-mediated induction of apoptosis in CD8+ T cells correlates with the disease activity and therapy response. These findings indicate that a combination of immunoregulatory marker profiles should be preferred over a single marker to monitor disease progression and therapy response in HNC.
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Na, Kwon Joong, and Hongyoon Choi. "Immune landscape of papillary thyroid cancer and immunotherapeutic implications." Endocrine-Related Cancer 25, no. 5 (May 2018): 523–31. http://dx.doi.org/10.1530/erc-17-0532.

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Although papillary thyroid cancer (PTC) is curable with excellent survival rate, patients with dedifferentiated PTC suffer the recurrence or death. As cancer immune escape plays a critical role in cancer progression, we aimed to investigate the relationship between differentiation and immune landscape of PTC and its implications for immunotherapy. Using The Cancer Genome Atlas data, we estimated the immune cell enrichment scores and overall immune infiltration, ImmuneScore, to characterize the immune landscape of PTC. Thyroid differentiation score (TDS) was calculated from 16 thyroid function genes. We demonstrated that ImmuneScore had a significant negative correlation with TDS, and BRAFV600E+ tumors showed significantly low TDS and high ImmuneScore. Enrichment scores of myeloid cells and B-cells were negatively correlated with TDS, while those of plasma cells were positively correlated with TDS. In addition, the association between TDS, ImmuneScore and immunosuppressive markers (CTLA-4, PD-L1, HLA-G) were evaluated according to BRAFV600E status. All immunosuppressive markers expression had a significant negative correlation with TDS, and they were significantly higher in BRAFV600E+ status. Subgroups were divided by median values of TDS and ImmuneScore, and immunosuppressive markers of these subgroups were compared. The immunosuppressive markers expression was the highest in high ImmuneScore and low TDS subgroup. Furthermore, ImmuneScore had a significant association with recurrence-free survival, irrespective of clinicopathologic factors including BRAFV600E status. These findings based on gene expression data illuminate the immune landscape of PTC and its association with TDS, immunosuppressive markers and recurrence. Our results would be extended to investigate immunotherapeutic approaches in PTC.
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Vanhaver, Christophe, Pierre van der Bruggen, and Annika M. Bruger. "MDSC in Mice and Men: Mechanisms of Immunosuppression in Cancer." Journal of Clinical Medicine 10, no. 13 (June 28, 2021): 2872. http://dx.doi.org/10.3390/jcm10132872.

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Myeloid-derived suppressor cells (MDSCs) expand during pathological conditions in both humans and mice and their presence is linked to poor clinical outcomes for cancer patients. Studying MDSC immunosuppression is restricted by MDSCs’ rarity, short lifespan, heterogeneity, poor viability after freezing and the lack of MDSC-specific markers. In this review, we will compare identification and isolation strategies for human and murine MDSCs. We will also assess what direct and indirect immunosuppressive mechanisms have been attributed to MDSCs. While some immunosuppressive mechanisms are well-documented in mice, e.g., generation of ROS, direct evidence is still lacking in humans. In future, bulk or single-cell genomics could elucidate which phenotypic and functional phenotypes MDSCs adopt in particular microenvironments and help to identify potential targets for therapy.
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Koldarova, Evelina, Bahrambek Mukhamedov, and Aziz Aliev. "A clinical case of an immunosuppressive generalized form of Kaposi's sarcoma in a patient with pemphigus vulgaris." Journal of Clinical Medicine of Kazakhstan 19, no. 6 (December 30, 2022): 100–103. http://dx.doi.org/10.23950/jcmk/12695.

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The article presents the literature data on Kaposi's sarcoma a lymphangioproliferative neoplasia induced by the Herpes Virus type 8.  The main forms, clinical manifestations and treatment are described. A clinical case of the development of an immunosuppressive generalized form of Kaposi's sarcoma induced by glucocorticosteroid therapy in a patient with pemphigus vulgaris is presented. With this clinical example, it is important to emphasize the potential risk of Kaposi's sarcoma on the background of secondary immunosuppression. Immunosuppressive Kaposi's sarcoma (iatrogenic type) is most often associated with long-term use of immunosuppressive therapy in transplantation organs and in patients receiving immunosuppressive therapy for autoimmune diseases, which leads to an increased risk of developing Kaposi's sarcoma by 150-1000 times compared with the general population. The ratio of men and women with this type is 2:1, while with the idiopathic (classical) - 17:1. Reliable diagnosis of the disease is necessary, based on a combination of history data, clinical and histological patterns of the pathological process, as well as additional laboratory markers, which will allow timely determination of further patient management tactics and, accordingly, provide a more favorable prognosis for the course of the disease.
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Kuebler, H. R., J. Dannull, T. Y. Tseng, A. Zhang, Z. Su, P. Dahm, and J. Vieweg. "Immature myeloid cell (ImC)- mediated immunosuppression in advanced renal cell cancer (RCC)." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 10042. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.10042.

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10042 Background: RCC affects the immunsystem by inhibiting the process of differentiation of antigen-resenting cells from their myeloid precursors by secreting tumor-derived factors such as VEGF. ImC induce a profound state of immune suppression that foster tumor tolerance by inhibition of tumor specific T cells. In this study, we asked whether increased ImC frequencies can be found in peripheral blood from RCC patients and if ImC frequencies correlated positively with increased levels of tumor-derived serum markers. Methods: ImC frequencies from healthy volunteers and RCC patients were determined by FACS. ImC were isolated by magnetic bead separation techniques and their immunosuppressive activity was determined in IFN-γ ELISPOT analyses, CTL and T-cell proliferation assays. The production of reactive oxygen species by ImC was analyzed utilizing specific probes and inhibitors. Tumor-derived serum markers were quantified by ELISA, enzyme immune assays and cytometric bead arrays. Microarray analyses were performed to identify novel, highly specific ImC markers. Results: RCC patients demonstrate higher ImC frequencies (0.8 - 3.2% of total PBMC) compared to healthy donors. The increased ImC frequencies are positively correlated with serum levels of VEGF, PGE-2, IL-13 and M-CSF in RCC patients and the concentration of byproducts of oxidative burst, including iso-prostane and malondialdehyde, was significantly enhanced. Isolated ImC exhibited profound immunosuppressive effects on CTL and CD4+ T cell response in an antigen specific fashion. Immunosuppression by ImC was mediated by release of ROS, including peroxide and superoxide anions and by generation of nitric oxide radicals as evidenced in functional assays. Results from microarray analyses reveal EP-1, EphA5, and PEX-5 as novel ImC markers. Conclusions: These data suggest that RCC may induce the development of immunosuppressive ImC population through secretion of cytokines such as VEGF, IL-13, M-CSF and PGE-2. Inhibition of specific cytokine activity or the use of differentiating agents may represent strategies to decrease immunosuppressive ImC population. Results from a phase I clinical trial investigating the effects of all-trans retinoic acid (ATRA) on differentiation of ImC in RCC patients will be presented. No significant financial relationships to disclose.
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Dissertations / Theses on the topic "Immunosuppressive markers"

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Lundberg, Sofie. "Nitric oxide and evaluation of different treatments in experimental colitis and inflammatory bowel disease /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-930-0/.

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Medrano, Jennifer Centurion. "Chemotactic Response of Lumbricus terrestris Coelomocytes to Larval and Adult Stages of Rhabditis pellio." Thesis, University of North Texas, 1999. https://digital.library.unt.edu/ark:/67531/metadc5507/.

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Experiments were performed to assess the suitability of Rhabditis pellio, a nematode found in earthworms, as a challenge organism for use in development of a biomarker assay to determine the potential of chemicals to suppress the immunocompetence of the non-specific immune system. To accomplish this goal, information on the life cycle of R. pellio was determined; including effects of incubation time and temperature on growth rates; along with information on the immune response elicited in the earthworm, Lumbricus terrestris. Immune parameters measured were coelomocyte migration toward and attachment to R. pellio larvae and adults. Preliminary background information showed that R. pellio has potential as a challenge organism for development of a biomarker assay.
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Solis, Morgane. "Evaluation et développement de marqueurs de la réplication du BK virus en transplantation rénale." Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ032.

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La néphropathie à BK virus (BKV) est l'une des complications les plus fréquentes de la transplantation rénale. La prise en charge consiste en la réduction préemptive de l'immunosuppression basée sur le suivi de la charge virale, mais cette stratégie n’est pas complètement efficace et augmente le risque de rejet. Dans un premier volet, nous avons évalué la mesure de la charge virale par PCR quantitative en temps réel, permettant de mettre en évidence des facteurs de variabilité comme le polymorphisme du BKV et de valider la technique utilisée pour le suivi de notre cohorte. L’intérêt des anticorps neutralisants (AcNs) anti-BKV en tant que marqueur prédictif de la réplication BKV a ensuite été évalué dans une cohorte de 168 transplantés rénaux. Nous avons montré i) que le virus responsable de l’infection provenait du donneur ; ii) que les AcNs jouent un rôle dans la prévention de la réactivation et le contrôle de la réplication virale et iii) qu’un seuil d’AcNs de 4 log10 permettait de stratifier le risque de réplication BKV. Ce travail ouvre la voie à un suivi personnalisé en fonction du risque de réplication BKV et à de nouvelles approches immunothérapeutiques
BK virus (BKV)-associated nephropathy is one of the major causes of graft dysfunction and loss in kidney transplant recipients. Since no BKV-specific antiviral therapies are available, management relies on preemptive immunosuppression reduction based on viral load monitoring. However, this strategy does not fully eliminate the risk of nephropathy and can increase the risk of graft rejection. In this work, we evaluated viral load measurement by quantitative real-time PCR in an interlaboratory comparison. Variability factors such as BKV polymorphism or pre-PCR steps have been highlighted and the method used for monitoring our cohort has been validated. The role of anti-BKV neutralizing antibodies (NAbs) as a predictive marker of BKV replication has been investigated in a cohort of 168 kidney transplant recipients. We showed that i) viral infection is caused by the donor strain; ii) NAbs play an essential role in viral replication prevention and control and iii) a NAbs cutoff of 4 log10 allows to stratify BKV replication risk. This work paves the way for personalized monitoring according to BKV replication risk and for new preventive or therapeutic strategies
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Kuol, Nyanbol. "Interaction Between Immunosuppressive and Cholinergic Markers in Colorectal Cancer." Thesis, 2020. https://vuir.vu.edu.au/42036/.

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Colorectal cancer (CRC) is amongst the leading diagnosed cancers worldwide. Despite the increasing interest to understand, the roles that the nervous and immune systems play in influencing the tumour microenvironment to promote cancer development and progression, more studies are required to understand the mechanism. Cancer cells can influence their microenvironment and bi-directionally communicate with other systems such as the immune and nervous systems. The immune system plays a key role in the eradication of cancer cells. Studies have shown that multiple mechanisms are responsible for the suppression of the immune system in cancer, one of which being the expression of immune checkpoints inhibitors such as programmed death 1 (PD-1), PD-L1, programmed death ligand 1 and 2 (PD-L1, PD- L2), sialic acid-binding lectins 9 (siglec-9) and IDO (indoleamine-2,3-dioxygenase). These molecules function by inhibiting anti-tumour effects of T cell-mediated immune responses. In addition to these molecules, studies have shown that several cancers can release acetylcholine (ACh) and express cholinergic receptors (muscarinic receptor 3 (M3R) and alpha 7 nicotinic receptor (a7nAChR)), overexpress choline acetyltransferase (ChAT), a precursor enzyme required for ACh synthesis and VAChT, essential for transporting of ACh, and excitatory receptor. Currently, there are no data available in determining the interaction between the expression of immunosuppressive and cholinergic markers in cancer, thus, this thesis aims to determine the interaction between the expression of immunosuppressive and cholinergic markers in CRC.
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Books on the topic "Immunosuppressive markers"

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Resources, Inc Decision. Immunosuppressive therapy markets: Transplant rejection, psoriasis, rheumatoid arthritis, and systemic lupus erythematosus. Waltham, Mass: Decision Resources, 1997.

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Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 55-Year-Old Female with a History of Right Foot Drop and Left Hand Weakness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0012.

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Vasculitic neuropathy often presents as a mononeuritis multiplex pattern. Ischemic nerve injury can lead to abrupt-onset, painful, and multifocal sensorimotor neuropathy. This chapter emphasizes the diagnostic considerations of vasculitic neuropathy, which includes the significant limitations of serologic markers in non-systemic vasculitic neuropathy. Nerve and muscle biopsy are important investigations to consider to make the diagnosis. Keys to management are also reviewed. It is important to manage systemic vasculitis with a rheumatologist. Nonsystemic vasculitis has a much better prognosis; immunosuppressive treatment is less aggressive, but it is recommended to have a rheumatologist’s input. There is no conclusive evidence on how to treat nonsystemic vasculitis. Mild cases may be treated with steroids alone.
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Venet, Fabienne, and Alain Lepape. Immunoparesis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0313.

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In parallel with an exaggerated pro-inflammatory response, critically-ill patients develop an immunosuppressive phase, termed immunoparesis/immunoparalysis or immune reprogramming. Innate and adaptive immune responses are affected. In particular, impaired neutrophil recruitment to injury sites and abnormal accumulation in remote sites; monocyte deactivation with preferential anti-inflammatory cytokine production and altered antigen presentation capacity; and a dramatic lymphopenia associated with major induction of apoptosis, functional, and phenotypic alterations have been described. The intensity and duration of this injury-induced immune dysfunction have been associated with an increased risk of death and secondary nosocomial infections. Innovative therapeutic strategies aiming at restoring immunological functions are currently being tested. GM-CSF appears to be an interesting candidate while IFN-γ‎ and IL-7 represent novel future therapeutic approaches. There is thus an urgent need for further clinical trials of such immunoadjuvant therapies that should include large cohorts of critically-ill patients stratified by relevant markers of immune dysfunction.
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Personalized Immunosuppression in Transplantation: Role of Biomarker Monitoring and Therapeutic Drug Monitoring. Elsevier Science & Technology Books, 2015.

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Dasgupta, Amitava, and Michael Oellerich. Personalized Immunosuppression in Transplantation: Role of Biomarker Monitoring and Therapeutic Drug Monitoring. Elsevier, 2015.

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Inc, Biomedical Business International, ed. Product and service markets associated with organ transplants. Santa Ana, CA, U.S.A. (1524 Brookhollow Dr., Santa Ana 92705-5426): Biomedical Business International, 1990.

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Pipitone, Nicolò, Annibale Versari, and Carlo Salvarani. Large-vessel vasculitis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0133.

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Large-vessel vasculitis includes giant cell arteritis (GCA) and Takayasu's arteritis (TAK). GCA affects patients aged over 50, mainly of white European ethnicity. GCA occurs together with polymyalgia rheumatica (PMR) more frequently than expected by chance. In both conditions, females are affected two to three times more often than males. GCA mainly involves large- and medium-sized arteries, particularly the branches of the proximal aorta including the temporal arteries. Vasculitic involvement results in the typical manifestations of GCA including temporal headache, jaw claudication, and visual loss. A systemic inflammatory response and a marked response to glucocorticoids is characteristic of GCA. GCA usually remits within 6 months to 2 years from disease onset. However, some patients have a chronic-relapsing course and may require long-standing treatment. Mortality is not increased, but there is significant morbidity mainly related to chronic glucocorticoid use and cranial ischaemic events, especially visual loss. The diagnosis of GCA rests on the characteristic clinical features and raised inflammatory markers, but temporal artery biopsy remains the gold standard to support the clinical suspicion. Imaging techniques are also used to demonstrate large-vessel involvement in GCA. Glucocorticoids are the mainstay of treatment for GCA, but other therapeutic approaches have been proposed and novel ones are being developed. TAK mainly involves the aorta and its main branches. Women are particularly affected with a female:male ratio of 9:1. In most patients, age of onset is between 20 and 30 years. Early manifestations of TAK are non-specific and include constitutional and musculoskeletal symptoms. Later on, vascular complications become manifest. Most patients develop vessel stenoses, particularly in the branches of the aortic artery, leading to manifestations of vascular hypoperfusion. Aneurysms occur in a minority of cases. There are no specific laboratory tests to diagnose TAK, although most patients have raised inflammatory markers, therefore, imaging techniques are required to secure the diagnosis. Glucocorticoids are the mainstay of treatment of TAK. However, many patients have an insufficient response to glucocorticoids alone, or relapse when they are tapered or discontinued. Immunosuppressive agents and, in refractory cases, biological drugs can often attain disease control and prevent vascular complications. Revascularization procedures are required in patients with severe established stenoses or occlusions.
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Pipitone, Nicolò, Annibale Versari, and Carlo Salvarani. Large-vessel vasculitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0133_update_003.

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Large-vessel vasculitis includes giant cell arteritis (GCA) and Takayasu’s arteritis (TAK). GCA affects patients aged over 50, mainly of white European ethnicity. GCA occurs together with polymyalgia rheumatica (PMR) more frequently than expected by chance. In both conditions, females are affected two to three times more often than males. GCA mainly involves large- and medium-sized arteries, particularly the branches of the proximal aorta including the temporal arteries. Vasculitic involvement results in the typical manifestations of GCA including temporal headache, jaw claudication, and visual loss. A systemic inflammatory response and a marked response to glucocorticoids is characteristic of GCA. GCA usually remits within 6 months to 2 years from disease onset. However, some patients have a chronic-relapsing course and may require longstanding treatment. Mortality is not increased, but there is significant morbidity mainly related to chronic glucocorticoid use and cranial ischaemic events, especially visual loss. The diagnosis of GCA rests on the characteristic clinical features and raised inflammatory markers, but temporal artery biopsy remains the gold standard to support the clinical suspicion. Imaging techniques are also used to demonstrate large-vessel involvement in GCA. Glucocorticoids are the mainstay of treatment for GCA, but other therapeutic approaches have been proposed and novel ones are being developed. TAK mainly involves the aorta and its main branches. Women are particularly affected with a female:male ratio of 9:1. In most patients, age of onset is between 20 and 30 years. Early manifestations of TAK are non-specific and include constitutional and musculoskeletal symptoms. Later on, vascular complications become manifest. Most patients develop vessel stenoses, particularly in the branches of the aortic artery, leading to manifestations of vascular hypoperfusion. Aneurysms occur in a minority of cases. There are no specific laboratory tests to diagnose TAK, although most patients have raised inflammatory markers, therefore, imaging techniques are required to secure the diagnosis. Glucocorticoids are the mainstay of treatment of TAK. However, many patients have an insufficient response to glucocorticoids alone, or relapse when they are tapered or discontinued. Immunosuppressive agents and, in refractory cases, biological drugs can often attain disease control and prevent vascular complications. Revascularization procedures are required in patients with severe established stenoses or occlusions.
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U.S. organ transplant and artificial organ products markets: Biotechnology boosts pharmaceuticals and other treatment alternatives. Mountain View, Calif: Frost & Sullivan, 1995.

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Krueger, Darcy A., and Jamie Capal. Familial CNS Tumor Syndromes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0136.

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Tuberous sclerosis complex is an autosomal dominant multi-system disease that involves the skin, brain, heart, lungs, and kidneys and is associated with seizures including infantile spasms, intellectual disability, autism and pulmonary and heart disease. Skin lesions can be particularly disfiguring and infantile spasms can be associated with marked cognitive decline. The outlook for patients has improved markedly with the recognition that TSC is caused by upregulation of the mammalian target of rapamycin (mTOR) enzyme, which connects energy needs and supply with cellular and neuronal growth. mTOR is upregulated in TSC because of mutations in hamartin or tuberin, which normally serve as a brake on mTOR. The drug rapamycin is commonly used as an immunosuppressive for patients undergoing kidney transplants; it has also found a new use in patients with TSC. Although the drug is immunosuppressive for non-TSC patients, careful titration of the drug in TSC patients corrects its upregulation but is not particulary immunosuppressive. Additional mTOR inhibitors such as everolimus have been developed and have been shown to be effective for pulmonary disease associated with TSC. Rapamycin in ointment form is dramatically effective in suppressing skin lesions of TSC and studies are underway to test the effect of mTOR inhibitors on seizures, brain tubers, intellect, and features of autism. Infantile spasms associated with TSC are very responsive to vigabatrin.
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Book chapters on the topic "Immunosuppressive markers"

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Farges, O. "Is acute rejection an appropriate surrogate marker for clinical trials in liver transplantation?" In Immunosuppression under Trial, 53–56. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4643-2_6.

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Elango, Tamilselvi, Anburaj Jeyaraj, Haripriya Dayalan, Pushpa Gnanaraj, Xinghui Li, and Xuejun Zhang. "Immunomodulatory Effect of Methotrexate Abruptly Controls Keratinocyte Activation in Psoriasis." In Psoriasis [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.102811.

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In psoriatic skin, epidermal keratinocytes (KCs) undergo deregulated inflammatory response that leads to prolonged expression of inflammatory mediators as well as abnormal keratins. Due to immune and genetic factors, KCs get activated and cell balance gets disturbed. This activation is mainly due to deregulated inflammatory response. A vicious cycle of KC-immune response called KC activation cycle leads to psoriasis. In psoriatic skin, epidermal KCs undergo deregulated inflammatory response that leads to prolonged expression of inflammatory mediators as well as abnormal keratins. Methotrexate (MTX) an immunosuppressive agent has been used as a standard drug to treat severe psoriasis. Acanthosis and abnormal terminal differentiation was mainly due to the mutation in epidermal keratins. In turn, disease severity and relapsing of psoriasis are mainly due to the mutation of hyperproliferative keratins. These novel keratin mutations in psoriatic epidermis might be one of the causative factors for psoriasis. MTX strongly regulates the KC activation cycle by deregulated inflammatory markers and maintains normal keratin phenotype on hyperproliferating KC, thereby controlling acanthosis in psoriasis patients.
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Wieland, Eberhard. "Markers of lymphocyte activation and proliferation." In Personalized Immunosuppression in Transplantation, 227–57. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-800885-0.00010-2.

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Qize Yuan, Evan, and Calvin Sze Hang Ng. "Role of Hybrid Operating Room: Present and Future." In Immunosuppression. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.91187.

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With the dramatic progress of medical imaging modalities and growing needs for high-resolution intraoperative imaging in minimally invasive surgery, hybrid operative room (OR) has been developed as a powerful tool for different surgical scenarios. Under the guidance of high-definition cone beam CT (CBCT), an electromagnetic navigation bronchoscopy (ENB)-based marker implantation and subsequent localization of the pulmonary nodules can be implemented within a hybrid OR. Furthermore, the unparalleled real-time imaging capabilities and the ability to perform multiple tasks within the hybrid OR can facilitate image-guided single-port video-assisted thoracic surgery (iSPVATS), increasing the precision and improving outcomes of the procedure. With the help of a hybrid theatre, catheter-based thermal ablation can provide a safer and less invasive treatment option for select patient groups with early-stage non-small cell lung carcinomas (NSCLC) or metastases. In the future, the combination of hybrid operating room and other inspiring innovative techniques, such as robotic bronchoscopy, 3D-printing, natural orifice transluminal endoscopic surgery (NOTES) lung surgery could lead to a paradigm shift in the way thoracic surgery is conducted.
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Pipitone, Nicolò, Annibale Versari, and Carlo Salvarani. "Large-vessel vasculitis." In Oxford Textbook of Rheumatology, 1113–24. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0133_update_004.

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Large-vessel vasculitis includes giant cell arteritis (GCA) and Takayasu’s arteritis (TAK). GCA affects patients aged over 50, mainly of white European ethnicity. GCA occurs together with polymyalgia rheumatica (PMR) more frequently than expected by chance. In both conditions, females are affected two to three times more often than males. GCA mainly involves large- and medium-sized arteries, particularly the branches of the proximal aorta including the temporal arteries. Vasculitic involvement results in the typical manifestations of GCA including temporal headache, jaw claudication, and visual loss. A systemic inflammatory response and a marked response to glucocorticoids is characteristic of GCA. GCA usually remits within 6 months to 2 years from disease onset. However, some patients have a chronic-relapsing course and may require longstanding treatment. Mortality is not increased, but there is significant morbidity mainly related to chronic glucocorticoid use and cranial ischaemic events, especially visual loss. The diagnosis of GCA rests on the characteristic clinical features and raised inflammatory markers, but temporal artery biopsy remains the gold standard to support the clinical suspicion. Imaging techniques are also used to demonstrate large-vessel involvement in GCA. Glucocorticoids are the mainstay of treatment for GCA, but other therapeutic approaches have been proposed and novel ones are being developed. TAK mainly involves the aorta and its main branches. Women are particularly affected with a female:male ratio of 9:1. In most patients, age of onset is between 20 and 30 years. Early manifestations of TAK are non-specific and include constitutional and musculoskeletal symptoms. Later on, vascular complications become manifest. Most patients develop vessel stenoses, particularly in the branches of the aortic artery, leading to manifestations of vascular hypoperfusion. Aneurysms occur in a minority of cases. There are no specific laboratory tests to diagnose TAK, although most patients have raised inflammatory markers, therefore, imaging techniques are required to secure the diagnosis. Glucocorticoids are the mainstay of treatment of TAK. However, many patients have an insufficient response to glucocorticoids alone, or relapse when they are tapered or discontinued. Immunosuppressive agents and, in refractory cases, biological drugs can often attain disease control and prevent vascular complications. Revascularization procedures are required in patients with severe established stenoses or occlusions.
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Pipitone, Nicolò, Annibale Versari, and Carlo Salvarani. "Large-vessel vasculitis." In Oxford Textbook of Rheumatology, 1113–24. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0133_update_005.

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Large-vessel vasculitis includes giant cell arteritis (GCA) and Takayasu’s arteritis (TAK). GCA affects patients aged over 50, mainly of white European ethnicity. GCA occurs together with polymyalgia rheumatica (PMR) more frequently than expected by chance. In both conditions, females are affected two to three times more often than males. GCA mainly involves large- and medium-sized arteries, particularly the branches of the proximal aorta including the temporal arteries. Vasculitic involvement results in the typical manifestations of GCA including temporal headache, jaw claudication, and visual loss. A systemic inflammatory response and a marked response to glucocorticoids is characteristic of GCA. GCA usually remits within 6 months to 2 years from disease onset. However, some patients have a chronic-relapsing course and may require longstanding treatment. Mortality is not increased, but there is significant morbidity mainly related to chronic glucocorticoid use and cranial ischaemic events, especially visual loss. The diagnosis of GCA rests on the characteristic clinical features and raised inflammatory markers, but temporal artery biopsy remains the gold standard to support the clinical suspicion. Imaging techniques are also used to demonstrate large-vessel involvement in GCA. Glucocorticoids are the mainstay of treatment for GCA, but other therapeutic approaches have been proposed and novel ones are being developed. TAK mainly involves the aorta and its main branches. Women are particularly affected with a female:male ratio of 9:1. In most patients, age of onset is between 20 and 30 years. Early manifestations of TAK are non-specific and include constitutional and musculoskeletal symptoms. Later on, vascular complications become manifest. Most patients develop vessel stenoses, particularly in the branches of the aortic artery, leading to manifestations of vascular hypoperfusion. Aneurysms occur in a minority of cases. There are no specific laboratory tests to diagnose TAK, although most patients have raised inflammatory markers, therefore, imaging techniques are required to secure the diagnosis. Glucocorticoids are the mainstay of treatment of TAK. However, many patients have an insufficient response to glucocorticoids alone, or relapse when they are tapered or discontinued. Immunosuppressive agents and, in refractory cases, biological drugs can often attain disease control and prevent vascular complications. Revascularization procedures are required in patients with severe established stenoses or occlusions.
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Oellerich, Michael, Julia Beck, Philipp Kanzow, Jessica Schmitz, Otto Kollmar, Philip D. Walson, and Ekkehard Schütz. "Graft-derived cell-free DNA as a marker of graft integrity after transplantation." In Personalized Immunosuppression in Transplantation, 153–76. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-800885-0.00007-2.

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Williams, David. "Renal disease in pregnancy." In Oxford Textbook of Obstetrics and Gynaecology, edited by Sabaratnam Arulkumaran, William Ledger, Lynette Denny, and Stergios Doumouchtsis, 170–85. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198766360.003.0014.

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The kidneys undergo marked physiological changes during healthy pregnancy. Awareness of these gestational changes is critical to the management of kidney disease in pregnancy as they both mask and mimic renal disease. Gestational changes to maternal vasculature, clotting, and metabolism predispose previously healthy women to a unique set of acute kidney injuries during pregnancy, whereas women with chronic kidney disease make suboptimal gestational adaptations to pregnancy, with an increased risk of adverse pregnancy outcome and possible further damage to their kidneys. Women with kidney transplants can be confident about the safety of established immunosuppressive regimens during pregnancy and can expect a good pregnancy outcome dictated by the function of their renal graft. Pregnancy outcomes for women on renal replacement therapy have improved through intensive haemodialysis regimens that mimic gestational physiological change. This chapter describes renal physiological change and the management of acute and chronic renal disease in pregnancy.
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Hooda-Nehra, Anupama, Tracey L. Smith, Alejandra I. Ferrer, Fernanda I. Staquicini, Wadih Arap, Renata Pasqualini, and Pranela Rameshwar. "Targeted Regulation and Cellular Imaging of Tumor-Associated Macrophages in Triple-Negative Breast Cancer: From New Mechanistic Insights to Candidate Translational Applications." In Macrophages celebrating 140 years of discovery [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105654.

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The complex interplay between immune cells and tumor cells within the tumor microenvironment (TME) can lead to disease progression. Specifically, signals generated in the TME can cause immunosuppression, promoting angiogenesis and immune evasion, which leads to tumor development. The interplay of M1 and M2 macrophage populations that coincide with these tumor markers is particularly important in the TME. Triple-negative breast cancer (TNBC) often presents as advanced disease, and these tumors are also often bereft of recognized molecular targets that can be found in other subtypes, limiting their therapeutic options. However, tumor-associated macrophages (TAMs) infiltration in TNBC is frequently observed. Moreover, a high density of TAMs, particularly M2 macrophages, is associated with poorer outcomes in various cancers, including TNBC. This provides a strong basis for exploiting TAMs as potential therapeutic targets. Specifically, efforts to increase M2 to M1 repolarization are promising therapeutic approaches in TNBC, and four recent studies wherein divergent approaches to target the M2-rich macrophage population and reverse immune subversion are described. These and similar efforts may yield promising diagnostic or therapeutic options for TNBC, a great clinical need.
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Dyson, Jessica K., and David E. J. Jones. "Primary biliary cholangitis." In Oxford Textbook of Medicine, edited by Jack Satsangi, 3127–35. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0325.

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Primary biliary cholangitis (PBC), previously known as primary biliary cirrhosis, is a chronic, cholestatic liver disease in which the biliary epithelial cells lining the small intrahepatic bile ducts are the target for immune-mediated damage, leading to progressive ductopenia and cholestasis. The cause is unknown but presumed to be autoimmune. The disorder affects women (>90% of cases) and usually has an insidious onset in middle age. Younger patients are less common but have a more aggressive disease course. Fatigue and pruritus are the most common presenting symptoms. Findings on examination vary widely, ranging from no abnormality to jaundice with hyperpigmentation, scratch marks, and rarely the features of advanced liver disease. Diagnosis of PBC is based on three criteria: (1) cholestatic liver function tests, with increases in serum alkaline phosphatase and γ‎-glutamyl transferase, (2) presence of serum antimitochondrial antibodies (found in more than 95% of cases), and (3) compatible liver histology. Many asymptomatic patients are recognized following the incidental discovery of antimitochondrial antibodies or elevated levels of serum alkaline phosphatase. First-line treatment is with ursodeoxycholic acid which can lead to significant improvement in liver biochemical values. Second-line treatment is with obeticholic acid. No immunosuppressive drug regimen has been proven effective. Progression may be slow, but eventually patients can develop cirrhosis. Cholestyramine is used as first line to treat pruritus. There is no recognized treatment for fatigue. Liver transplantation is indicated in some cases.
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Conference papers on the topic "Immunosuppressive markers"

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Fiori, Mariana, Carlos Marino Cabral Calvano Filho, Pollyanna Dornelas Pereira, Marco Vinícius Fernandes, and Daniela Omar de Souza. "BREAST CRYPTOCOCCOSIS IN IMMUNOCOMPETENT PATIENTS." In Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1022.

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Introduction: Cryptococcosis is prevalent in immunocompromised individuals. Immunocompetent patients can develop latent infections, the breast being a rare focus of primary disease, with few reports in the literature. Case report: GHMC, female, 27 years old, married, ticketing operator, resident in Valparaíso / GO, Brazil. She denied comorbidities, use of medication, smoking or drinking, as well as contact with caves, farms, farms, wild animals and ingestion of game meat. She reported fever (38°C), left mastalgia associated with hardened erythema with subsequent fistulization and removal of purulent secretion. Upon examination, she was in good general condition, with a palpable nodule of about 6 x 4 cm, in union of the lower quadrants (ULQ) of the left breast (LB), which was regular, soft, felt a little painful on palpation, with increased local temperature and without lymph node enlargement or papillary discharge. The ultrasound of the breasts showed a heterogeneous solid mass, with cystic areas of permeation, in ULQ of LB, of 4.2x2.2 cm, partially defined contours coinciding with a nodular image of 4 cm in the same topography in the mammography. Magnetic resonance imaging showed a nodular, irregular, hypodense image in T1, hyperdense in T2, with parietal enhancement and heterogeneous, progressive internal enhancement, in addition to capturing septa, measuring 6.1x4.0x4.6 cm, suggesting mucinous carcinoma. Core biopsy of the solid part of the lesion and collection of mucinous fluid was performed. Concomitantly, oxacillin was started for seven days. There was no laboratory change during the entire disease period. Fifteen days after the end of the antibiotic use, the lesion became an erythematous lenticular ulcer, with flat edges, of 5.0x4.0 cm, with colloid secretion leaving its bed. Histology showed cryptococcosis, and liquid cytology showed cryptococcus neoformans. During immunosuppression investigation, the patient underwent chest and skull CT scans, serology, tumor markers, ANF (antinuclear factor), rheumatoid factor, C3, C4, lumbar puncture and blood cultures (all excluded any immunosuppressive pathology). The treatment was carried out with Fluconazole 800 mg/day for three months, with a reduction to 300mg/day for another three months. Two months after the start of treatment, the lesion resolved. Cryptococcosis is an invasive mycosis with high morbidity and mortality. It affects immunosuppressed individuals, and is rare in immunocompetent individuals. The main pathogenic species, C. neoformans and C. gatti, are prevalent in tropical and subtropical climates. The main sites affected are the brain and the lungs; other sites are rare. The dosage and duration of breast therapy is unknown, but 2- 3g/day of amphotericin B or 400-800mg/day of fluconazole for 8–12 weeks has achieved therapeutic success in reported cases.
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"Candidate SNP markers of rheumatoid arthritis changing the affinity of TATA-binding protein for the human gene promoters expo disruptive selection of immunoactivative and immunosuppressive genenets that provoke and prevent this disorder, respectively, as if it could be a self-domestication syndrome." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-101.

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"Candidate SNP markers of rheumatoid arthritis changing the affinity of TATA-binding protein for the human gene promoters expo disruptive selection of immunoactivative and immunosuppressive genenets that provoke and prevent this disorder, respectively, as if it could be a self-domestication syndrome." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-151.

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Williams, L., G. Candelas, C. Tange, J. Ochoa-Grullón, P. Macarrón, C. Morado, K. H. Llano, et al. "THU0034 Salmonella typhi vi igg as a marker of immunosuppression in rheumatic disease." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5542.

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Pathak, Lekhika, Seema Bhuyan, Bidisha Pal, Partha Saikia, Sukanya Gayan, Shirsajit Mitra, Tutumoni Baishya, Ramana Chilakamarti, and Bikul Das. "90 Circulating altruistic stem cells as a marker of immunosuppression in oral cancer." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0090.

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Virtakoivu, Reetta E., Pia Boström, Riitta Aaltonen, Ilkka Koskivuo, Sirpa Jalkanen, and Maija Hollmén. "Abstract 4740: CLEVER-1 as a marker to identify breast cancer patients under immunosuppression." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4740.

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Ostrin, Edwin J., Johannes F. Fahrmann, Ichidai Tanaka, Muge Celiktas, Clemente Aguilar, Mitzi Aguilar, Jennifer B. Dennison, et al. "Abstract 1447: Aberrant tryptophan catabolism marked by high kynureninase expression contributes to immunosuppression and poor outcome in lung adenocarcinoma." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1447.

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Soares, Izadora Fonseca Zaiden, João Nicoli Ferreira dos Santos, and Lis Gomes Silva. "Dramatic cognitive improvement with acetylcholinesterase inhibitor in cerebral amyloid angiopathyrelated inflammation." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.578.

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Context: Cerebral amyloid angiopathy (CAA) is characterized by progressive deposition of amyloid-ß fibrils in the walls of small arterioles and capillaries of the leptomeninges and cerebral cortex. A rare subtype of CAA is CAA-related inflammation (CAA-RI), which exhibits marked perivascular or transmural inflammatory infiltration in brain tissue. The major clinical features of CAA-RI are rapidly progressive dementia, behavioral changes, headache, seizures, or stroke-like signs. Conclusive diagnosis requires histopathological confirmation, but validated clinicoradiological criteria for the diagnosis of probable CAA-RI have good sensitivity (82%) and specificity (97%). Treatment with high dose corticosteroids with or without other immunosuppressive therapy is recommended. We report a case of probable CAA-RI that did not respond to corticosteroid therapy but had a surprising improvement with acetylcholinesterase inhibitor. Case report: A 77-year-old illiterate woman presented with a history of subacute onset of seizures and behavioral changes. Her medical history was positive for a hearing loss due to a toxic exposure in childhood, and a cured breast cancer. The neurological examination showed attention impairment, disorientation, and incoherent speech. CSF showed a mildly elevated protein count. Brain MRI met criteria for probable CAA-RI. She had a poor response with high doses of corticosteroids, but after a trial with Donepezil she showed important cognitive and functional improvement. Conclusion: This result attracts attention to the importance of the cholinergic pathway in the etiology and pathological mechanisms of CAA. Randomized Controlled Trials would be required to confirm our hypothesis and to find new therapeutic options for CAA.
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