scholarly journals Eosinophilic Gastroenteritis with a Relapsing and Remitting Course with Presence of Autoimmune Antibodies

2020 ◽  
Vol 2020 ◽  
pp. 1-5
Author(s):  
Chathuranga Lakmal Fonseka ◽  
Sunali Nanayakkara ◽  
S. D. A. L. Singhapura ◽  
H. M. M. Herath ◽  
C. K. Bodinayake
Keyword(s):  
Autoimmune Disease ◽  
Ascitic Fluid ◽  
Peripheral Blood ◽  
Elimination Diet ◽  
Eosinophilic Gastroenteritis ◽  
Normal Diet ◽  
Parasitic Disease ◽  
Case Presentation ◽  
Autoimmune Antibodies ◽  
Uncommon Disease

Background. Eosinophilic gastroenteritis (EGE) is an uncommon disease characterized by eosinophilic infiltration of the digestive tract, which occurs due to an uncertain aetiology. Although autoimmune diseases can later present as EGE, it is unusual for EGE to have positive autoimmune antibodies without the presence of an overt autoimmune disease. Case presentation. We report a 38-year-old previously healthy man who presented with abdominal discomfort and loose stools with pleural and peritoneal effusions progressing over several weeks. His investigations revealed severe eosinophilia in peripheral blood and ascitic fluid, and a laparoscopic full-thickness biopsy from the ileum demonstrated infiltration of eosinophils in all three layers of the intestine. There were no clinical features or investigations suggestive of parasitic disease, other diseases associated with eosinophilia, or autoimmune disease. Further investigations showed a highly positive ANA, positive p-ANCA, but did not meet the criteria to diagnose a specific autoimmune disease. The eosinophilia responded to an elimination diet with gradual resolution of eosinophilia and effusions, and once it reappeared after introduction of a normal diet. Conclusion. EGE presenting as peripheral blood and ascitic fluid eosinophilia with the presence of pleural and/or peritoneal effusions is uncommon. Eosinophilic gastroenteritis can be associated with autoantibody positivity without any evidence of overt autoimmune disease manifestations. Elimination diet can be used as a potential option to prevent recurrences of EGE.

Hair Growth in a Patient with Alopecia Areata on Tocilizumab

2021 ◽  
pp. 1-5
Author(s):  
Chloe J. Walker ◽  
Kelly E. Flanagan ◽  
James T. Pathoulas ◽  
Isabel Pupo Wiss ◽  
Maryanne M. Senna
Keyword(s):  
Monoclonal Antibody ◽  
Autoimmune Disease ◽  
Hair Loss ◽  
Alopecia Areata ◽  
Interleukin 6 ◽  
Hair Growth ◽  
Posterior Uveitis ◽  
Case Presentation ◽  
Antibody Targeting ◽  
Growth Changes

<b><i>Introduction:</i></b> Tocilizumab (TCZ), a recombinant humanized antihuman monoclonal antibody targeting interleukin-6 (IL-6) signaling, is often utilized in the management of autoimmune disease. Few reports have demonstrated hair growth changes in patients on TCZ. <b><i>Case Presentation:</i></b> Herein, we review the literature and report a 21-year-old woman with progressive alopecia areata (AA) presenting with AA improvement while on TCZ for concomitant posterior uveitis. <b><i>Discussion:</i></b> Our case demonstrates the potential ability of TCZ to disrupt IL-6 signaling involved in AA, leading to hair loss and regrowth.

scholarly journals AB0037 EXPRESSION OF NEGATIVE CHECKPOINT MOLECULES BTLA AND HVEM IS DYSREGULATED IN AUTOIMMUNE DISEASES

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1321.1-1321
Author(s):  
S. Nagpal ◽  
S. Cole ◽  
A. Floudas ◽  
M. Wechalekar ◽  
Q. Song ◽  
...  
Keyword(s):  
T Cell ◽  
B Cells ◽  
Autoimmune Disease ◽  
Autoimmune Diseases ◽  
Immune Checkpoint ◽  
Peripheral Blood ◽  
Expression Patterns ◽  
Myeloid Cell ◽  
Dependent Manner ◽  
Research Support

Background:Immune checkpoint blockade with agents targeting CTLA4 and PD-1/PD-L1 alone or in combination has demonstrated exceptional efficacy in multiple cancer types by “unleashing” the cytotoxic action of quiescent, tumor-infiltrating T cells. However, the therapeutic action of these immunotherapies goes hand in hand with the loss of immune tolerance and appearance of immune-related adverse events such as colitis, arthralgia and inflammatory arthritis in responsive patients. Therefore, immune checkpoint molecules have been proposed as targets for the treatment of autoimmune diseases.Objectives:Herein, we interrogate the potential of BTLA/HVEM axis as a target for restoring immune homeostasis in rheumatoid arthritis (RA), Systemic Lupus Erythematosus (SLE) and Sjogren’s Syndrome (SjS) by examining their expression patterns in autoimmune disease tissues.Methods:Message and protein expression of BTLA and HVEM were examined in RA and SLE synovial tissues, SLE cutaneous lesions, SjS salivary glands and peripheral blood samples of autoimmune disease by RNA sequencing and flow cytometry.Results:Tissue dysregulation of the BTLA-HVEM axis was observed: Increased BTLA RNA level in RA synovium, SLE-affected skin, and SjS salivary gland samples, whereas HVEM level was affected only in the RA synovium when compared to unaffected tissues. Detailed immunophenotyping of B, T, and myeloid cell populations in RA, SLE, SjS and healthy control PBMCs revealed differential modulation of the BTLA+ or HVEM+ immune cell subsets in a disease-context dependent manner. SjS patients showed an overall decrease in memory B cells and most of the BTLA+ B cell subsets while a decrease in HVEM+ B cells was observed only in SLE PBMC samples and not RA and SLE samples. Immunophenotyping with a T cell panel exhibited decreased BTLA and HVEM expression on T cell subsets in SjS and SLE but not in RA patients. In addition, protein levels of HVEM were differentially decreased in SLE myeloid cell subsets. Finally, we demonstrate tissue-specific surface expression patterns of BTLA in RA and SLE samples: higher surface BTLA levels on RA and SLE PBMC B cells than matched tissue-derived B cells.Conclusion:Our results demonstrate a dysregulation of the BTLA/HVEM axis in either lesional tissue or peripheral blood in an autoimmune disease context-dependent manner. These results also indicate the potential of targeting BTLA-HVEM axis for the treatment of multiple autoimmune diseases.Disclosure of Interests:Sunil Nagpal Shareholder of: Janssen Pharmaceuticals, Employee of: Janssen Pharmaceuticals, Suzanne Cole Shareholder of: Janssen Research & Development employee, Employee of: Janssen Research & Development employee, Achilleas Floudas: None declared, Mihir Wechalekar Grant/research support from: Grant from Janssen Research & Development, Qingxuan Song Shareholder of: Employee of Janssen Research, Employee of: Employee of Janssen Research, Tom Gordon: None declared, Roberto Caricchio Grant/research support from: Financial grant from Janssen Research & Development, Douglas Veale: None declared, Ursula Fearon: None declared, Navin Rao Shareholder of: Janssen Pharmaceuticals, Employee of: Janssen Pharmaceuticals, Ling-Yang Hao Shareholder of: Employee of Janssen Research, Employee of: Employee of Janssen Research

scholarly journals Epigastric pain associated with herpes esophagitis: case report

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Nabil Antaki ◽  
Ziad Aljarad ◽  
Howayda Dabbas ◽  
Walid Haddad ◽  
M. Amin Akil ◽  
...  
Keyword(s):  
Medical Literature ◽  
Epigastric Pain ◽  
Lower Esophagus ◽  
Case Presentation ◽  
Main Symptom ◽  
Abdominal Symptoms ◽  
Multiple Biopsies ◽  
Uncommon Disease ◽  
Simplex Virus ◽  
Compromised Patients

Abstract Background Herpes esophagitis is uncommon disease caused by Herpes simplex virus (HSV). While the disease most often occurs in immunocompromised patients, including post-chemotherapy, immunosuppression with organ transplants, and in AIDS, Herpes esophagitis can also occur in immunocompetent individuals. Case presentation We report a case of herpes esophagitis in a 72 year- old woman who was presumed to be immunocompromised following prolonged radiotherapy and chemotherapy for lymphoma. Her main symptom was epigastric pain. Upper endoscopy showed multiple rounded ulcers in lower esophagus. The diagnosis was confirmed histologically by multiple biopsies. The patient received Valacyclovir for 2 weeks and started to get better within 3 days of treatment. Conclusion Although there are few published cases of Herpes esophagitis disease in the medical literature, we recommend that this disease should be considered as one of the differential diagnoses when assessing immuno-compromised patients presenting with non-specific abdominal symptoms.

scholarly journals Efficacy of a Short-term Six-food Elimination Diet and Reintroduction Therapy in Pediatric Eosinophilic Gastroenteritis

2020 ◽  
Vol 59 (11) ◽  
pp. 1379-1385
Author(s):  
Toshihiko Kakiuchi ◽  
Aiko Nakayama ◽  
Jun Abe ◽  
Muneaki Matsuo
Keyword(s):  
Elimination Diet ◽  
Eosinophilic Gastroenteritis ◽  
Short Term ◽  
Food Elimination

scholarly journals Functional activation of lymphocyte CD44 in peripheral blood is a marker of autoimmune disease activity.

1998 ◽  
Vol 102 (6) ◽  
pp. 1173-1182 ◽  
Author(s):  
P Estess ◽  
H C DeGrendele ◽  
V Pascual ◽  
M H Siegelman
Keyword(s):  
Autoimmune Disease ◽  
Disease Activity ◽  
Peripheral Blood

Exacerbating Autoimmune Disease with Salt

2013 ◽  
Vol 6 (273) ◽  
pp. ec97-ec97 ◽  
Author(s):  
Annalisa M. VanHook
Keyword(s):  
T Cells ◽  
Transcription Factor ◽  
Autoimmune Disease ◽  
Normal Diet ◽  
High Salt ◽  
Wild Type ◽  
High Salt Diet ◽  
Salt Diet ◽  
Link Type

In addition to contributing to the immune response against pathogens, helper T (TH ) cells that produce the cytokine interleukin-17 (IL-17) also contribute to autoimmune diseases. Maintenance of both normal and pathogenic TH17 cell activities depends on activation of the IL-23 receptor (IL-23R). By performing transcriptional profiling and network analysis of transcriptional changes in wild-type and Il23r–/– mouse T cells that were activated and induced to differentiate into TH17 cells, Wu et al. identified serum glucocorticoid kinase 1 (Sgk1) as a key node downstream of IL-23R. In vitro differentiation of naïve T cells from Sgk1–/– mice revealed that SGK1 was not required for primary TH17 cell differentiation but was required for maintenance of TH17 cells and continued signaling through IL-23R. Analysis of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis, in Sgk1–/– animals showed that these mice had reduced incidence of disease, severity of symptoms, and production of IL-17 compared with EAE in wild-type animals. In vitro experiments were consistent with a model in which SGK1 phosphorylates the transcription factor Foxo1 to repress its ability to indirectly activate Il23r expression. SGK1 mediates sodium (Na+) homeostasis by modulating the activity of epithelial Na+ channels, so the authors tested the effect of Na+ on TH17 cell differentiation. Increasing the concentration of NaCl in the culture medium increased expression of Sgk1, Il23r, Il17, and other genes associated with TH17 differentiation in wild-type, but not Sgk1–/–, T cells that had been activated but not treated with factors to influence their development into a particular type of TH cell. Compared with a normal diet, a high-salt diet increased the number of TH17 cells in the guts of wild-type mice but induced a milder increase in the abundance of TH17 cells in Sgk1–/– mice. In the EAE model, mice on a high-salt diet showed increased severity of disease compared with those fed a normal diet. However, a high-salt diet had a much milder effect on disease symptoms in Sgk1–/– mice. In a related study, Kleinewietfeld etal. differentiated naïve human T cells in culture conditions that mimicked the interstitial fluid of animals fed a high-salt diet and found that the additional NaCl promoted differentiation of TH17 cells that expressed markers consistent with autoimmune activity. Further experiments indicated that this effect was mediated by the kinase p38, the transcription factor and p38 target NFAT5, and the NFAT5 target Sgk1. In vivo experiments performed in this study were consistent with those reported by Wu et al. These studies suggest that production of the pathogenic TH17 cells that contribute to autoimmunity may be exacerbated by dietary salt. Commentary by O’Shea and Jones considers the implications and limitations of these findings in the context of autoimmune disease.C. Wu, N. Yosef, T. Thalhamer, C. Zhu, S. Xiao, Y. Kishi, A. Regev, V. K. Kuchroo, Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. Nature496, 513–517 (2013). [PubMed]M. Kleinewietfeld, A. Manzel, J. Titze, H. Kvakan, N. Yosef, R. A. Linker, D. N. Muller, D. A. Hafler, Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. Nature496, 518–522 (2013). [PubMed]J. J. O’Shea, R. G. Jones, Rubbing salt in the wound. Nature496, 437–439 (2013). [PubMed]

scholarly journals Efficacy of an elimination diet in a patient with eosinophilic gastroenteritis : a pediatric case with multiple food allergies

2019 ◽  
Vol 66 (1.2) ◽  
pp. 201-204 ◽  
Author(s):  
Ayumi Sasaki ◽  
Mayumi Sugimoto ◽  
Narumi Tokaji ◽  
Makoto Irahara ◽  
Koichi Okamoto ◽  
...  
Keyword(s):  
Elimination Diet ◽  
Eosinophilic Gastroenteritis ◽  
Food Allergies ◽  
Pediatric Case

scholarly journals Cicatricial Pemphigoid: Report of Five Cases

2002 ◽  
Vol 81 (7) ◽  
pp. 442-448 ◽  
Author(s):  
Ivan Dieb Miziara ◽  
Fabiana Sperandio ◽  
Saramira C. Bohadana ◽  
Natasha Braga ◽  
Fabrizio Ricci Romano ◽  
...  
Keyword(s):  
Autoimmune Disease ◽  
Mucous Membrane ◽  
Case Reports ◽  
Systemic Autoimmune Disease ◽  
Cicatricial Pemphigoid ◽  
Laryngeal Stenosis ◽  
Mucosal Involvement ◽  
Uncommon Disease ◽  
Mucosal Lesions ◽  
Laryngeal Involvement

Cicatricial pemphigoid is a chronic, systemic, autoimmune disease characterized by progressive bullous skin and mucous membrane lesions that tend toward scarring and involution. Manifestations of cicatricial pemphigoid include oral mucosal bullous lesions in 85 to 90% of patients, ocular mucosal lesions in 66%, nasal mucosal lesions in 15 to 23%, and laryngeal involvement in 8 to 21 %. We report five cases of cicatricial pemphigoid in which all patients had ENT manifestations—specifically, oral and nasal mucosal involvement. Three of these patients also had laryngeal lesions; one of the three had a large laryngeal ulceration and bullae that caused a laryngeal stenosis and necessitated a tracheostomy. In addition to the five case reports, we also review the literature and discuss the pathogenesis, diagnosis, and treatment of this uncommon disease.

scholarly journals Intense immunosuppressive therapy followed by autologous peripheral blood selected progenitor cell reinfusion for severe autoimmune disease

2001 ◽  
Vol 66 (2) ◽  
pp. 75-79 ◽  
Author(s):  
Maurizio Musso ◽  
Ferdinando Porretto ◽  
Alessandra Crescimanno ◽  
Francesca Bond� ◽  
Vita Polizzi ◽  
...  
Keyword(s):  
Autoimmune Disease ◽  
Immunosuppressive Therapy ◽  
Peripheral Blood ◽  
Progenitor Cell

scholarly journals Perforated Duodenal Ulcer in a Pediatric Patient with Eosinophilic Gastroenteritis

1997 ◽  
Vol 11 (3) ◽  
pp. 208-212 ◽  
Author(s):  
Colette Deslandres ◽  
Pierre Russo ◽  
Peter Gould ◽  
Pierre Hardy
Keyword(s):  
Gastroduodenal Ulcer ◽  
Failure To Thrive ◽  
Elimination Diet ◽  
Eosinophilic Gastroenteritis ◽  
Skin Tests ◽  
Food Allergies ◽  
Peripheral Eosinophilia ◽  
Review Of The Literature ◽  
Perforated Gastroduodenal Ulcer ◽  
Work Up

An 11-year-old boy with eosinophilic gastroenteritis treated by an elimination diet alone presented with a perforated gastroduodenal ulcer subsequent to blunt trauma to the abdomen. Peripheral eosinophilia, chronic iron deficiency, chronic hypoalbuminemia and severe failure to thrive had been present since age 2 years. Immunological work-up revealed food allergies, documented by skin tests. A review of the literature since 1966 revealed only six other cases of perforation of the gastrointestinal tract, one of whom was also a child.

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