The Experts below are selected from a list of 2991 Experts worldwide ranked by ideXlab platform
Jonas F. Ludvigsson - One of the best experts on this subject based on the ideXlab platform.
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Can head Trauma Trigger celiac disease? Nation-wide case–control study
BMC neurology, 2013Co-Authors: Jonas F. Ludvigsson, Marios HadjivassiliouAbstract:Background: TG6, a brain expressed transglutaminase, is implicated in the neurological manifestations of celiac disease (CD). We hypothesized that earlier brain injury due to head Trauma may be more common in patients with CD, potentially through Trauma-induced TG6 leading to interaction with TG2. Methods: Through biopsy reports from all 28 pathology departments in Sweden we identified 29,096 individuals with CD (in this study defined as villous atrophy). We then examined the risk of earlier head Trauma in CD compared to the risk in 144,522 controls matched for age, sex, county and calendar year. Odds ratios (ORs) were calculated using conditional logistic regression. Results: 981 (3.4%) individuals with CD and 4,449 (3.1%) controls had a record of earlier head Trauma. Individuals with head Trauma were hence at a 1.10-fold increased risk of future CD (95% CI = 1.02-1.17). ORs were independent of sex or age at CD. The highest risk of future CD was seen during the first year after Trauma. There was no association between severity of Trauma and risk of developing CD. Conclusions: This study found a very small excess risk for future CD in individuals with an earlier head Trauma.
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can head Trauma Trigger celiac disease nation wide case control study
BMC Neurology, 2013Co-Authors: Jonas F. Ludvigsson, Marios HadjivassiliouAbstract:Background: TG6, a brain expressed transglutaminase, is implicated in the neurological manifestations of celiac disease (CD). We hypothesized that earlier brain injury due to head Trauma may be more common in patients with CD, potentially through Trauma-induced TG6 leading to interaction with TG2. Methods: Through biopsy reports from all 28 pathology departments in Sweden we identified 29,096 individuals with CD (in this study defined as villous atrophy). We then examined the risk of earlier head Trauma in CD compared to the risk in 144,522 controls matched for age, sex, county and calendar year. Odds ratios (ORs) were calculated using conditional logistic regression. Results: 981 (3.4%) individuals with CD and 4,449 (3.1%) controls had a record of earlier head Trauma. Individuals with head Trauma were hence at a 1.10-fold increased risk of future CD (95% CI = 1.02-1.17). ORs were independent of sex or age at CD. The highest risk of future CD was seen during the first year after Trauma. There was no association between severity of Trauma and risk of developing CD. Conclusions: This study found a very small excess risk for future CD in individuals with an earlier head Trauma.
Marios Hadjivassiliou - One of the best experts on this subject based on the ideXlab platform.
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Can head Trauma Trigger celiac disease? Nation-wide case–control study
BMC neurology, 2013Co-Authors: Jonas F. Ludvigsson, Marios HadjivassiliouAbstract:Background: TG6, a brain expressed transglutaminase, is implicated in the neurological manifestations of celiac disease (CD). We hypothesized that earlier brain injury due to head Trauma may be more common in patients with CD, potentially through Trauma-induced TG6 leading to interaction with TG2. Methods: Through biopsy reports from all 28 pathology departments in Sweden we identified 29,096 individuals with CD (in this study defined as villous atrophy). We then examined the risk of earlier head Trauma in CD compared to the risk in 144,522 controls matched for age, sex, county and calendar year. Odds ratios (ORs) were calculated using conditional logistic regression. Results: 981 (3.4%) individuals with CD and 4,449 (3.1%) controls had a record of earlier head Trauma. Individuals with head Trauma were hence at a 1.10-fold increased risk of future CD (95% CI = 1.02-1.17). ORs were independent of sex or age at CD. The highest risk of future CD was seen during the first year after Trauma. There was no association between severity of Trauma and risk of developing CD. Conclusions: This study found a very small excess risk for future CD in individuals with an earlier head Trauma.
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can head Trauma Trigger celiac disease nation wide case control study
BMC Neurology, 2013Co-Authors: Jonas F. Ludvigsson, Marios HadjivassiliouAbstract:Background: TG6, a brain expressed transglutaminase, is implicated in the neurological manifestations of celiac disease (CD). We hypothesized that earlier brain injury due to head Trauma may be more common in patients with CD, potentially through Trauma-induced TG6 leading to interaction with TG2. Methods: Through biopsy reports from all 28 pathology departments in Sweden we identified 29,096 individuals with CD (in this study defined as villous atrophy). We then examined the risk of earlier head Trauma in CD compared to the risk in 144,522 controls matched for age, sex, county and calendar year. Odds ratios (ORs) were calculated using conditional logistic regression. Results: 981 (3.4%) individuals with CD and 4,449 (3.1%) controls had a record of earlier head Trauma. Individuals with head Trauma were hence at a 1.10-fold increased risk of future CD (95% CI = 1.02-1.17). ORs were independent of sex or age at CD. The highest risk of future CD was seen during the first year after Trauma. There was no association between severity of Trauma and risk of developing CD. Conclusions: This study found a very small excess risk for future CD in individuals with an earlier head Trauma.
Roy G. Beran - One of the best experts on this subject based on the ideXlab platform.
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Can head Trauma Trigger adult-onset Rasmussen's encephalitis?
Epilepsy & behavior : E&B, 2017Co-Authors: Derrick Soh, Dennis Cordato, Andrew Bleasel, Peter Brimage, Roy G. BeranAbstract:Abstract Rasmussen's encephalitis (RE) is a rare unilateral inflammatory brain disorder that causes progressive neurocognitive deterioration and refractory epilepsy including epilepsia partialis continua (EPC). We describe a patient with a unique presentation, where right upper limb EPC due to RE began within 2 weeks of a concussive left frontal head injury, in a 36-year-old female without other identifiable etiology, no prior neurological deficit nor suggestion of intracranial pathology or infection, and no preceding seizures. The diagnosis of RE followed extensive investigation, excluding confounding diagnoses, with supportive histopathology, and her EPC has proven refractory to treatment. In the absence of a satisfactory alternative etiology and exclusion of differential diagnoses, the most likely cause or precipitant of this patient's RE was head Trauma.
Eric Kipnis - One of the best experts on this subject based on the ideXlab platform.
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Inflammasomes in Tissue Damages and Immune Disorders After Trauma.
Frontiers in immunology, 2018Co-Authors: Perrine Bortolotti, Emmanuel Faure, Eric KipnisAbstract:Trauma remains a leading cause of death worldwide. Hemorrhagic shock and direct injury to vital organs are responsible for early mortality whereas most delayed deaths are secondary to complex pathophysiological processes. These processes result from imbalanced systemic reactions to the multiple aggressions associated with Trauma. Trauma results in the uncontrolled local and systemic release of endogenous mediators acting as danger signals [damage-associated molecular patterns (DAMPs)]. Their recognition by the innate immune system Triggers a pro-inflammatory immune response paradoxically associated with concomitant immunosuppression. These responses, ranging in intensity from inappropriate to overwhelming, promote the propagation of injuries to remote organs, leading to multiple organ failure and death. Some of the numerous DAMPs released after Trauma Trigger the assembly of intracellular multiprotein complexes named inflammasomes. Once activated by a ligand, inflammasomes lead to the activation of a caspase. Activated caspases allow the release of mature forms of interleukin-1β and interleukin-18 and Trigger a specific pro-inflammatory cell death termed pyroptosis. Accumulating data suggest that inflammasomes, mainly NLRP3, NLRP1, and AIM2, are involved in the generation of tissue damage and immune dysfunction after Trauma. Following Trauma-induced DAMP(s) recognition, inflammasomes participate in multiple ways in the development of exaggerated systemic and organ-specific inflammatory response, contributing to organ damage. Inflammasomes are involved in the innate responses to Traumatic brain injury and contribute to the development of acute respiratory distress syndrome. Inflammasomes may also play a role in post-Trauma immunosuppression mediated by dysregulated monocyte functions. Characterizing the involvement of inflammasomes in the pathogenesis of post-Trauma syndrome is a key issue as they may be potential therapeutic targets. This review summarizes the current knowledge on the roles of inflammasomes in Trauma.
Derrick Soh - One of the best experts on this subject based on the ideXlab platform.
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Can head Trauma Trigger adult-onset Rasmussen's encephalitis?
Epilepsy & behavior : E&B, 2017Co-Authors: Derrick Soh, Dennis Cordato, Andrew Bleasel, Peter Brimage, Roy G. BeranAbstract:Abstract Rasmussen's encephalitis (RE) is a rare unilateral inflammatory brain disorder that causes progressive neurocognitive deterioration and refractory epilepsy including epilepsia partialis continua (EPC). We describe a patient with a unique presentation, where right upper limb EPC due to RE began within 2 weeks of a concussive left frontal head injury, in a 36-year-old female without other identifiable etiology, no prior neurological deficit nor suggestion of intracranial pathology or infection, and no preceding seizures. The diagnosis of RE followed extensive investigation, excluding confounding diagnoses, with supportive histopathology, and her EPC has proven refractory to treatment. In the absence of a satisfactory alternative etiology and exclusion of differential diagnoses, the most likely cause or precipitant of this patient's RE was head Trauma.
