Topical and Systemic Immunosuppression

1997 ◽  
pp. 196-206 ◽  
Author(s):  
M.J. Elder
Keyword(s):  
Systemic Immunosuppression

Successful replacement of systemic immunosuppression by local graft irradiation in the management of listeria meningitis

2003 ◽  
Vol 35 (4) ◽  
pp. 1322-1323
Author(s):  
R.E Power ◽  
D.M Little ◽  
E Smyth ◽  
E McNamara ◽  
D.P Hickey
Keyword(s):  
Systemic Immunosuppression ◽  
Listeria Meningitis

scholarly journals Adverse Effects of Systemic Immunosuppression in Keratolimbal Allograft

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
M. Krakauer ◽  
J. D. Welder ◽  
H. K. Pandya ◽  
N. Nassiri ◽  
A. R. Djalilian
Keyword(s):  
Adverse Effects ◽  
Calcineurin Inhibitor ◽  
Liver Function Tests ◽  
Case Review ◽  
Retrospective Case ◽  
Systemic Immunosuppression ◽  
Keratolimbal Allograft ◽  
Elevated Liver Function Tests ◽  
Limbal Stem Cell ◽  
Elevated Creatinine

Purpose. Keratolimbal allograft (KLAL) is a treatment for limbal stem cell deficiency. One disadvantage is systemic immunosuppression to avoid rejection. Our purpose was to examine the adverse effects of systemic immunosuppression in KLAL.Methods. A retrospective case review of 16 patients with KLAL who received systemic immunosuppression consisting of a corticosteroid, an antimetabolite, and/or a calcineurin inhibitor was performed. Patients were monitored for signs, symptoms, or laboratory evidence of toxicity.Results. Twelve of 16 patients (75%) experienced an adverse effect. The average age of those with adverse effects was 50.0 years (SD 17.8) and those without was 23.6 years (SD: 14.3), which was statistically significant (unpairedt-testP=0.022). Ten of 11 patients (91%) had resolution during mean followup of 16.4 months. No serious adverse effects occurred. The most common included anemia, hyperglycemia, elevated creatinine, and elevated liver function tests. Prednisone and tacrolimus were responsible for the most adverse effects. More patients with comorbidities experienced adverse effects (83%) than those without comorbidities (25%).Conclusions. KLAL requires prolonged systemic immunosuppression. Our data demonstrated that systemic immunosuppression did not result in serious adverse effects in our population and is relatively safe with monitoring for toxicity. In addition, we demonstrated that adverse effects occurred more frequently in older patients and those with comorbidities.

ADDITION OF INHALED FLUTICASONE PROPIONATE TO SYSTEMIC IMMUNOSUPPRESSION AFTER LUNG TRANSPLANTATION

2003 ◽  
Vol 76 (1) ◽  
pp. 263-264 ◽  
Author(s):  
Christoph Schmid ◽  
Rahel Naef ◽  
Rudolf Speich ◽  
Annette Boehler
Keyword(s):  
Fluticasone Propionate ◽  
Lung Transplantation ◽  
Systemic Immunosuppression

Systemic Immunosuppression for the Treatment of Pediatric Uveitis

2021 ◽  
Vol 62 (1) ◽  
pp. 155-175
Author(s):  
Alexandria L. Chaulk ◽  
Chase Miller ◽  
Matthew Barke ◽  
Baruch Goldberg ◽  
Alla Goldberg
Keyword(s):  
Pediatric Uveitis ◽  
Systemic Immunosuppression

Pembrolizumab‐induced erythema multiforme requiring systemic immunosuppression

2021 ◽  
Vol 51 (12) ◽  
pp. 2149-2150
Author(s):  
Terri Shih ◽  
Shawn Shih ◽  
Mohammad Sharaf
Keyword(s):  
Erythema Multiforme ◽  
Systemic Immunosuppression

Abstract W P425: Sepsis in Intracranial Hemorrhage: Does Stroke-Induced Systemic Immunosuppression Play a Role?

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Swarna Rajagopalan ◽  
Richard Ronca ◽  
Ausim Azizi
Keyword(s):  
Statistical Significance ◽  
Clinical Signs ◽  
Signs And Symptoms ◽  
Outcome Data ◽  
Infection Group ◽  
Patient Demographics ◽  
Systemic Immunosuppression ◽  
Total Lymphocyte ◽  
Recorded Data ◽  
Clinical Signs And Symptoms

INTRODUCTION: Infection is a significant cause of mortality in patients with both ischemic and hemorrhagic stroke. This is thought to occur as a result of stroke-induced systemic immunosuppression (SIIS). The role of cerebral damage pre-disposing to sepsis has only been addressed in a few studies for ischemic stroke, and literature is sparse in Spontaneous Intracerebral Hemorrhage (SICH) patients who have higher mortality, greater disability and require more intensive medical care. We sought to determine identify predictors of SIIS and sepsis, so we may be able to recognize and intervene early. METHODOLOGY: We retrospectively analyzed 40 patients with SICH admitted to the NICU between January 2012 and January 30, 2014. We included patients with SICH. We excluded patients with multi-compartmental hemorrhage and patients lacking outcome data. Patient demographics including age, gender, location, volume of SICH, GCS, and total lymphocyte counts from days one to five of hospitalization was recorded. Data was divided into a non-infection group, where patients lacked any clinical or laboratory evidence of infections, and an infection group. Statistical analysis was performed to compare lymphocyte depletion over time between patients that developed an infection and those that did not. RESULTS: From the cohort of 40 patients with SICH, 20 developed an infection during their hospital course. Total lymphocyte counts were lower on all five days in the infection group compared to the non-infection group and became significant on day four of hospitalization (1 in the infection group vs. 2.1 in the non-infection group, p<0.01. Lymphopenia preceded clinical signs and symptoms of infection, which occurred in average on day 5.8 of hospitalization. Patients in the infection group had greater hemorrhage volume (32.5 ml vs. 15.5 ml) and poorer GCS scores on admission (12.7 vs. 11.8) although these differences did not reach statistical significance. CONCLUSION: The incidence of sepsis is high in SICH patients, and these patients have worse prognostic parameters. Our data suggests identification of lymphopenia may be a significant predictor of development of clinical infection in these patients. Future studies with larger sample sizes are warranted.

scholarly journals SCIDOT-34. BRAIN INJURY SIGNALS SYSTEMIC IMMUNOSUPPRESSION THROUGH THYMIC INVOLUTION

2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi278-vi279
Author(s):  
Katayoun Ayasoufi ◽  
Christian K Pfaller ◽  
Roman H Khadka ◽  
Fang Jin ◽  
Jiaying Zheng ◽  
...  
Keyword(s):  
Brain Injury ◽  
T Cell ◽  
Thymic Involution ◽  
Systemic Immunosuppression ◽  
Cell Counts ◽  
Immune Deficiencies ◽  
Underlying Mechanisms ◽  
Neurological Injuries ◽  
The Brain

Abstract Systemic immunosuppression following neurological insults including stroke, traumatic brain injury, and glioblastoma (GBM) causes mortality and leads to failure of immune-modulating therapies. Exact immunological nature and the underlying mechanisms of this immunosuppression are unknown. Our goal was to define effects of neurological insults given exclusively to the brain on the thymus. The thymus is the primary immune organ responsible for T-cell development and maintenance both in children and in adults. We evaluated the brain-thymus communication using the following neurological insults: physical injury, CNS viral infection, sterile injury, tumor implantation, and seizures. All insults resulted in significant thymic involution that was reversible upon clearance of the insult. Thymic involution did not occur following similar peripheral insults. We next demonstrated that the GL261 model of GBM recapitulates hallmark features of peripheral immunosuppression observed in GBM patients including low CD4 T-cell counts. Thus, we aimed to further study the immunosuppression affecting the thymus in this clinically relevant model. Principle component analysis following RNA-sequencing of thymi from naïve and glioma-bearing mice revealed unbiased separation of the groups suggesting that the thymus is directly affected by a brain tumor. To determine the extent to which thymic involution was caused by a soluble factor we employed parabiosis. We demonstrated that thymic involution was transferable from glioma-bearing to non-tumor-bearing parabionts. Similarly, serum taken from GL261 glioma-bearing mice potently inhibited proliferation of T-cells in vitro. Together our data demonstrate that CNS-specific insults, regardless of nature, cause immunosuppression by prompting thymic involution through circulating factors. This accounts at least partially for immune deficiencies observed following neurological injuries. Identification of this suppressive factor is crucial in designing future therapeutics for GBM patients, and patients with other acute and chronic neurological trauma.

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