Academic literature on the topic 'Refractory celiac disease type 2'
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Journal articles on the topic "Refractory celiac disease type 2"
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Soldera, Jonathan, Karina Salgado, and Karla Lais Pêgas. "Refractory celiac disease type 2: how to diagnose and treat?" Revista da Associação Médica Brasileira 67, no. 2 (February 2021): 168–72. http://dx.doi.org/10.1590/1806-9282.67.02.20200618.
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Bianchi, Nicoletta, Luisa Doneda, Luca Elli, Cristian Taccioli, Valentina Vaira, Alice Scricciolo, Vincenza Lombardo, et al. "Circulating microRNAs Suggest Networks Associated with Biological Functions in Aggressive Refractory Type 2 Celiac Disease." Biomedicines 10, no. 6 (June 14, 2022): 1408. http://dx.doi.org/10.3390/biomedicines10061408.
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Despite following a gluten-free diet, which is currently the only effective therapy for celiac disease, about 5% of patients can develop serious complications, which in the case of refractory type 2 could evolve towards intestinal lymphoma. In this study, we have identified a set of 15 microRNAs in serum discriminating between the two types of refractory disease. Upregulated miR-770-5p, miR-181b-2-3p, miR-1193, and miR-1226-3p could be useful for the better stratification of patients and the monitoring of disease development, while miR-490-3p was found to be dysregulated in patients with refractory type 1. Finally, by using bioinformatic tools applied to the analysis of the targets of dysregulated microRNAs, we have completed a more precise assessment of their functions. These mainly include the pathway of response to Transforming Growth Factor β cell–cell signaling by Wnt; epigenetic regulation, especially novel networks associated with transcriptional and post-transcriptional alterations; and the well-known inflammatory profiles.
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Malamut, Georgia, and Christophe Cellier. "Refractory Celiac Disease: Epidemiology and Clinical Manifestations." Digestive Diseases 33, no. 2 (2015): 221–26. http://dx.doi.org/10.1159/000369519.
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A small subset of celiac disease (CD) patients becomes refractory to a gluten-free diet with persistent malabsorption and intestinal villous atrophy. This is a rare (probably less than 2% of adult CD patients), but serious disorder, with a high risk of progression to an overt T-cell lymphoma. Diagnosis of this condition defined as refractory CD (RCD) is made after exclusion of other small bowel diseases with villous atrophy. RCD has been subdivided into two subgroups according to the normal (RCDI) or abnormal phenotype of intraepithelial lymphocytes (RCDII). Whereas RCDI is hardly distinguishable from active noncompliant CD, RCDII has a severe clinical presentation and a very poor prognosis. We precisely describe below the different types of RCD and propose diagnostic and therapeutic guidelines for its clinical management.
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Nasr, I., S. Donnelly, C. Ho-Yen, T. Mitchell, F. Chang, and P. Ciclitira. "PTH-112 A Single Centre Experience Of Treatment Of Refractory Celiac Disease Type 2." Gut 63, Suppl 1 (June 2014): A260.2—A261. http://dx.doi.org/10.1136/gutjnl-2014-307263.558.
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Tack, Greetje J., Marielle J. Wondergem, Abdul Al-Toma, Wieke H. Verbeek, Alexander Schmittel, Mariana V. Machado, Francesco Perri, et al. "S2024 Refractory Celiac Disease Type 2: Haematopoietic Autologous Stem Cell Transplantation Does Improve Clinical Outcome." Gastroenterology 138, no. 5 (May 2010): S—303—S—304. http://dx.doi.org/10.1016/s0016-5085(10)61396-0.
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Vaira, Valentina, Gabriella Gaudioso, Maria Antonella Laginestra, Andrea Terrasi, Claudio Agostinelli, Silvano Bosari, Antonio Di Sabatino, et al. "Deregulation of miRNAs-cMYC circuits is a key event in refractory celiac disease type-2 lymphomagenesis." Clinical Science 134, no. 10 (May 2020): 1151–66. http://dx.doi.org/10.1042/cs20200032.
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Abstract A percentage of celiac disease (CD) patients develop refractory type-2 disease (RCD2), a condition associated with increased risk of enteropathy-associated T-cell-lymphoma (EATL) and without therapeutic option. Therefore, we profiled the miRNome in series of peripheral T-cell lymphomas (PTCLs), CD, RCD1 or 2 and in the murine interleukin-15 (IL15)-transgenic (TG) model of RCD. The transcriptome was analyzed in 18 intestinal T-cell lymphomas (ITLs). Bioinformatics pipelines provided significant microRNA (miRNA) lists and predicted targets that were confirmed in a second set of patients. Our data show that ITLs have a unique miRNA profile with respect to other PTCLs. The c-MYC regulated miR-17/92 cluster distinguishes monomorphic epitheliotropic ITL (MEITL) from EATL and prognosticates EATL outcome. These miRNAs are decreased in IL15-TG mice upon Janus kinase (JAK) inhibition. The random forest algorithm identified a signature of 38 classifier miRNAs, among which, the miR-200 and miR-192/215 families were progressively lost in RCD2 and ITL-CD, whereas miR-17/92 and C19MC miRNAs were up-regulated. Accordingly, SMAD3, MDM2, c-Myc and activated-STAT3 were increased in RCD2 and EATL tissues while JAK inhibition in IL15-TG mice restored their levels to baseline. Our data suggest that miRNAs circuit supports activation of STAT3 and c-Myc oncogenic signaling in RCD2, thus contributing to lymphomagenesis. This novel understanding might pave the way to personalized medicine approaches for RCD and EATL.
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Le Mouel, Jean-Philippe, Mathurin Fumery, Sami Hakim, Clara Yzet, Alexandra Dervaux, Xavier Dray, and Eric Nguyen-Khac. "Type 2 refractory celiac disease on third-generation capsule endoscopy and enteroscopy: typical appearance of ulcerative jejunitis." Endoscopy 52, no. 06 (December 13, 2019): E195—E197. http://dx.doi.org/10.1055/a-1046-1593.
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Chandesris, Marie-Olivia, Georgia Malamut, Virginie Verkarre, Bertrand Meresse, Gabriel Rahmi, Elizabeth Macintyre, Nicole Brousse, Nadine Cerf-Bensussan, Christophe Cellier, and Olivier Hermine. "The Type of Enteropathy Is a Prognostic Factor in Enteropathy-Associated T-Cell Lymphoma." Blood 114, no. 22 (November 20, 2009): 2937. http://dx.doi.org/10.1182/blood.v114.22.2937.2937.
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Abstract Abstract 2937 Poster Board II-913 Enteropathy-associated T-cell Lymphoma (EATL) may complicate celiac disease (CD), refractory celiac disease type I (RCD I) characterized by normal intraepithelial lymphocytes (IEL) or refractory celiac disease type II (RCD II) defined by abnormal IEL (CD3s-,CD3i+ and CD8-) and a clonal rearrangement of the gamma or delta chain of the T cell receptor (TCRγ/δ). It remains unknown whether the type of the associated enteropathy, non clonal (CD or RCD I) or clonal (RCD II), may be a prognostic factor in EATL. We aimed to assess the prognosis of EATL according to the type of the associated enteropathy. Medical files of 29 patients with EATL were retrospectively studied. The type of associated enteropathy was confirmed by immunohistochemistry analysis in all cases and by flow cytometry phenotyping analysis of freshly isolated IEL and search for a TCR γ or δ clonal rearrangement by Multiplex PCR whenever possible. Kaplan-Meier curves and Logrank test were used to compare survival of EATL in the 2 groups of enteropathy (clonal or not). Mean age at EATL (13 women / 16 men) onset was 57 years. The associated enteropathy was CD (n=10) or RCD I (n=2) in 12 patients and RCD II in 17 patients. No statistical difference was found in lymphoma staging with localized (IE and IIE) versus disseminated stages (IV) found in 42% and 58% of patients with CD or RCD I and in 53% and 47% of patients with RCD II, respectively. Diagnostic or therapeutic surgery was practiced in 83% and 47% of patients with CD or RCD I and with RCD II, respectively and chemotherapy in 92% and 82% of the same groups of patients, respectively (n.s). Considering all the EATL, the two-year and five-year survival rates of EATL were 34.1% and 20.2%, respectively. In subgroup analysis, the two-year and five-year survival rates of EATL were 66.7% and 53.3% in case of CD and/or RCD I and 11.8% and 0% in case of RCD II, respectively (p=0.0007). In conclusion, the type of enteropathy significantly impacts the prognosis of EATL with a particular short survival in case of associated RCD II enteropathy. Disclosures: No relevant conflicts of interest to declare.
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Boutrid, N., and H. Rahmoune. "Tofacitinib, celiac disease and the elderly: mind the gut!" Acta Gastro Enterologica Belgica 86, no. 3 (September 2023): 502. http://dx.doi.org/10.51821/86.3.12207.
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To the Editor, We read with great attention the interesting case report by Lenfant et al. narrating the successful use of tofacitinib in a patient with microscopic colitis and celiac disease (1), and we would point some insights about this peculiar situation. In fact, tofacitinib depicts potential side effects, including a higher risk of malignancies, and the FDA has even issued a warning about this drug’s hazard (2). Actually, a randomized open-label trial published in the New England Journal of Medicine in 2021 found that patients with rheumatoid arthritis who took tofacitinib had a higher risk of developing cancer than those who took a tumor necrosis factor (TNF) inhibitor (3). Recently, two recent randmoized controlled trials from the ORAL Surveillance Trial and published in the Annals of the Rheumatic Diseases in 2023 also contributed to shed the light on this potential risk : that patients with rheumatoid arthritis aged > 50 with cardiovascular risk who took tofacitinib had a higher risk of developing any type of cancer than those who took a TNF inhibitor (4), and secondary stratification found that they were more likely to develop cancer if they were over the age of 65 years (5). Adding insult to injury, the maligancies are also driven by the two peculiar forms of celiac disease : seronegative and refractory celiac disease (RCD), and this risk is also increased in CD diagnosed at adulthood : particularly, elder patients are prone to present a RCD, and giving immune checkpoint therapy might increase this risk (6). In conclusion, RCD ought to be definetly ruled out before starting JAK inhibitor therapy, especially in aged population with seronegative celiac disease and microscopic colitis, two well-known conditions associated with RCD.
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Al-Toma, Abdul, and Harry R. Koene. "Hematopoietic Stem Cell Transplantation in Refractory Celiac Disease: An Overview with Focus on Infectious Complications." OBM Transplantation 04, no. 01 (February 18, 2020): 1–17. https://doi.org/10.21926/obm.transplant.2001101.
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Refractory celiac disease (RCD) is a rare condition in which a known celiac patient, usually an adult, suffers from persistence or recurrence of gluten-related symptomatology, laboratory abnormalities, and inflammatory enteropathy despite following an optimal dietary therapy with gluten-free diet (GFD). Arbitrarily, a duration of at least 12 months of GFD has been recommended prior to establishing such a diagnosis. Furthermore, exclusion of the other possible causes of non-celiac villous atrophy, particularly enteropathy associated T-cell lymphoma (EATL), is a prerequisite for establishing a diagnosis of RCD. RCD is subdivided into two types, depending on the percentage of immunophenotypically aberrant intraepithelial lymphocytes (IEL). The refractory patients having a high percentage of abnormal ‘aberrant’ IEL (RCD-II) are regarded as having pre-lymphoma due to the high probability of developing EATL. In addition, they are at high risk for infection owing to the impaired immunity resulting from malnutrition, bacterial overgrowth and translocation in the small intestine, and the presence of hyposplenism (functional asplenia). The RCD-II patients are generally non-responsive to the currently available pharmacological treatments. However, both clinical and histopathological remissions have been achieved using the purine analog cladribine (2-CDA). Autologous hematopoietic stem cell transplantation (auto-HSCT) appears to be an effective therapy for these patients as it is well tolerated and has a low risk of post-transplant infections or other complications. The present review provides an overview of the application of auto-HSCT for the treatment of patients with RCD-II, which is a classic example of an autoimmune disorder. The focus is particularly on the infectious complications developing after the application of auto-HSCT.
Dissertations / Theses on the topic "Refractory celiac disease type 2"
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Guégan, Nicolas. "Étude du rôle des mutations de la voie JAK-STAT dans la lymphomagenèse associée à la maladie cœliaque." Electronic Thesis or Diss., Université Paris Cité, 2024. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=6776&f=79039.
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La maladie cœliaque réfractaire de type 2 (MCR2) est un lymphome intraépithélial de bas grade compliquant la maladie cœliaque (MC), et une première étape fréquente vers un lymphome invasif, le lymphome T associé à une entéropathie (EATL). Les cellules de MCR2 sont issues d'une petite sous-population de lymphocytes intraépithéliaux (LIE) appelée LIE iCD3+ innés, présents dans l'intestin normal. Ces cellules, dépourvues de CD3 à leur surface (sCD3-), combinent des caractéristiques de cellules T et NK et se différencient dans l'intestin à partir d'un précurseur hématopoïétique en réponse à un signal NOTCH et à l'IL-15. La MCR2 se caractérise par la transformation maligne et l'accumulation de LIE sCD3-iCD3+ contenant de nombreux de variants somatiques. Les plus récurrents (>80%) sont notamment un variant de JAK1 en position 1097 ou des variants du domaine SH2 de STAT3 qui augmentent leur réponse aux cytokines inflammatoires, notamment à l'IL-15, surexprimée dans l'intestin cœliaque. Ces variants et d'autres évènements génétiques somatiques co-récurrents sont aussi présents dans les EATL, qu'ils compliquent une MCR2 ou surviennent de novo chez des patients cœliaques, témoignant d'un mécanisme commun de lymphomagenèse. Un premier objectif de la thèse était d'évaluer le caractère pilote dans la lymphomagénèse des mutations GdF JAK1 p.G1096D (analogue à p.G1097D chez l'homme). ou STAT3 p.D661V dans le contexte d'une surexpression de l'IL-15. J'ai montré que ces mutations confèrent un avantage sélectif à des cellules iCD3+ innées murines différenciées in vitro en présence d'IL-15. Le transfert adoptif de cellules sCD3-iCD3+ portant la mutation JAK1 p.G1096D chez des souris immunodéficientes surexprimant l'IL-15, n'a pas induit de lymphoprolifération, suggérant l'importance d'autres évènements génétiques. Cependant, ce transfert a induit un syndrome hyperéosinophilique rappelant celui associé chez l'homme à des lymphoproliférations sanguines de lymphocytes sCD3-CD4+. Un second objectif était d'évaluer, à l'aide d'un modèle de xénogreffe, l'efficacité du ruxolitinib (inhibiteur de JAK1 et JAK2) pour traiter la MCR2. Le traitement de 21 jours, débuté 14 jours après le transfert d'une lignée issue de LIE de MCR2, a permis de diminuer l'expansion tumorale mais celle-ci a rapidement repris à l'arrêt du traitement. Les données générées in vitro ont montré l'hétérogénéité génomique de la lignée MCR2, ce qui a permis de dériver à partir de cette lignée, 6 lignées résistantes au ruxolitinib, qui présentaient de nouvelles mutations dont une mutation commune dans le gène immunosuppresseur de tumeur CDK13. Ces résultats suggèrent un risque de sélection de cellules résistantes au ruxolitinibRefractory celiac disease type 2 (RCD2) is a low-grade intraepithelial lymphoma complicating celiac disease (CD) and is a frequent initial step toward invasive lymphoma, specifically enteropathy-associated T-cell lymphoma (EATL). RCD2 cells originate from a small subpopulation of intraepithelial lymphocytes (IELs) called innate iCD3+ IELs, which are present in normal intestine. These cells, lacking CD3 on their surface (sCD3-), display characteristics of both T and NK cells and differentiate in the intestine from a hematopoietic precursor in response to a NOTCH signals and IL-15. RCD2 is characterized by the malignant transformation and accumulation of sCD3-iCD3+ IELs that harbor numerous somatic mutations. The most recurrent (>80%) include a JAK1 variant at position 1097 or variants in the SH2 domain of STAT3, which increase their response to inflammatory cytokines, as IL-15, which is overexpressed in the celiac intestine. These variants and other co-recurrent somatic genetic events are also present in EATL, whether they complicate RCD2 or occur de novo in celiac patients, indicating a shared mechanism of lymphomagenesis. One primary objective of this thesis was to evaluate the driver role, in lymphomagenesis, of the GdF JAK1 p.G1096D mutations (analogous to p.G1097D in humans) or STAT3 p.D661V in the context of IL-15 overexpression. I demonstrated that these mutations confer a selective advantage to murine innate iCD3+ cells differentiated in vitro in the presence of IL-15. Adoptive transfer of sCD3-iCD3+ cells carrying the JAK1 p.G1096D mutation into IL-15-overexpressing immunodeficient mice did not induce lymphoproliferation, suggesting the importance of additional genetic events. However, this transfer induced a hypereosinophilic syndrome (HSE) mimicing one of HSE discribed in humans with blood lymphoproliferative disorders of sCD3-CD4+ lymphocytes. A second objective was to assess, using a xenograft model, the efficacy of ruxolitinib (a JAK1 and JAK2 inhibitor) in treating RCD2. A 21-day treatment, initiated 14 days after the transfer of a cell line derived from RCD2 IELs, reduced tumor expansion, but this quickly reexpanded when the treatment was stopped. Data generated in vitro shown the genomic heterogeneity of the RCD2 cell line, allowing for the derivation of 6 ruxolitinib-resistant lines, which exhibited new mutations, including a common mutation in the tumor suppressor gene CDK13. These results suggest a risk of selecting ruxolitinib-resistant cells
Books on the topic "Refractory celiac disease type 2"
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Association, American Diabetes. American Diabetes Association Guide to Medical Nutrition Therapy for Diabetes (Clinical Education Series). American Diabetes Association, 2003.
Find full textBook chapters on the topic "Refractory celiac disease type 2"
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Bledsoe, Adam C., and Joseph A. Murray. "Type II Refractory Celiac Disease." In Diagnosis and Management of Gluten-Associated Disorders, 115–26. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-56722-4_10.
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Walker, Marjorie M., and Michael D. Potter. "Type I Refractory Celiac Disease." In Diagnosis and Management of Gluten-Associated Disorders, 109–14. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-56722-4_9.
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J. Ciclitira, Paul, and Alastair Forbes. "Management of Patients with Refractory Coeliac Disease." In Celiac Disease. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96231.
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Coeliac disease (CD) is an immune-mediated disorder affecting the small intestine. The condition represents an intolerance to gluten. Removal of dietary gluten permits recovery, with a full recovery for the majority of affected subjects. A percentage of affected subjects who do not improve with a gluten-free diet are considered to have refractory coeliac disease (RCD). Refractory coeliac disease is subdivided into type 1, characterised by a polyclonal expansion of intraepithelial lymphocytes (IELs) that have a normal phenotype, and type 2 (RCD2) which exhibits IELs with a monoclonal phenotype. Subjects with RCD carry a high risk of complications, including ulcerative jejunitis and lymphoma affecting the small intestine, the latter termed enteropathy-associated T-cell lymphoma (EATL).
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Kosiborod, Mikhail. "Case 52: Refractory Angina in a Patient with Type 2 Diabetes." In Diabetes Case Studies: Real Problems, Practical Solutions, 192–95. American Diabetes Association, 2015. http://dx.doi.org/10.2337/9781580405713.52.
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A 76-year-old man presents for a routine outpatient cardiology visit. He has a 15-year history of type 2 diabetes, with several diabetes-related microvascular complications, including stage III chronic kidney disease and mild peripheral neuropathy. He is currently on a combination of metformin and sulfonylurea (SU; sustained release glipizide) for glucose control, with last hemoglobin A1c (HbA1c) of 8.5%. Although the patient never sustained a myocardial infarction, he has a complex and longstanding history of multivessel coronary artery disease (CAD), requiring two-vessel coronary artery bypass surgery (CABG) 7 years ago, and several subsequent percutaneous interventions (PCIs). Despite multiple interventions, patient continues to have chronic Canadian Cardiovascular Society (CCS) class 2–3 angina, with typical midsternal chest pressure upon mild-to-moderate physical activity—the pattern of angina has been stable for the past 5 years, but it interferes significantly with his quality of life.
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Usoh, Chinenye, Donald McClain, and Barbara Pisani. "Case 48: Challenges to the Management of Diabetes in Patients Who Undergo Ventricular Assist Device (VAD) Implantation." In Diabetes In Practice: Case Studies with Commentary, 199–201. American Diabetes Association, 2021. http://dx.doi.org/10.2337/9781580407663.48.
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A 74-year-old man with a history of ischemic cardiomyopathy (ejection fraction 30%), atrial fibrillation, obstructive sleep apnea, type 2 diabetes complicated by peripheral neuropathy, diabetic foot ulcer, retinopathy, and stage 3 chronic kidney disease (CKD) presented to the heart failure clinic for evaluation of heart failure refractory to diuretic therapy.
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Bukke, Sarad Pawar Naik, Rajasekhar Komarla Kumarachari, Medishetti Swetha, Shanthi Subbarayan, Narayana Goruntla, Tadale Yadesa, and Ramu Samineni. "Introduction to Nutrition and Autoimmune Diseases." In Advances in Medical Diagnosis, Treatment, and Care, 1–29. IGI Global, 2024. http://dx.doi.org/10.4018/979-8-3693-5528-2.ch001.
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Researchers and healthcare professionals are eager to understand how nutrition affects autoimmune diseases due to their rise. This chapter explores how diet affects autoimmune diseases, aiming to explain how nutrition can aid or hinder their development. Nutrition affects brain activity, muscle health, bone strength, nerve function, skin integrity, blood circulation, and immune system strength. For fuel, the body needs a balanced diet. For optimal health and development, a balanced diet includes carbohydrates, proteins, fats, vitamins, minerals, fibre, and water. Malnutrition is a major issue stemming from inadequate nutrient intake. Understanding how diet affects health is crucial because nutritional factors affect heart attacks, certain cancers, strokes, and type 2 diabetes mellitus. BMI is a useful tool for assessing nutritional status, emphasising the importance of normal weight. Nutrients like proteins, fats, carbohydrates, vitamins, and minerals help maintain bodily functions and prevent malnutrition. Proteins ensure tissue synthesis and repair, while fats improve health, with saturated and unsaturated fats guiding diets. Essential fatty acids, vitamins, and minerals support bodily functions. The complex relationship between nutrition and autoimmune diseases emphasises the importance of a balanced diet. Nutritional interventions are important due to celiac disease and processed foods. Food and exercise are essential for lifelong health, body composition, musculoskeletal health, and physical and cognitive performance, as the chapter concludes. The complex relationship between nutrition and autoimmune diseases is explored in this study to help researchers, healthcare professionals, and individuals better understand the relationship.
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Evers, S., A. Frese, S. Schwaag, R. Lttmann,, and 1. W. Husstedt. "The prostaglandin-E1-analog misoprostol in the prophylactic treatment of refractory cluster headache and trigeminal neuralgia." In Preventive Pharmacotherapy of Headache Disorders, 266–70. Oxford University PressOxford, 2004. http://dx.doi.org/10.1093/oso/9780198528449.003.0040.
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Abstract Chronic cluster headache is a severe disease extremely affecting the quality of life. In many cases, the common prophylactic treatment options are unsatisfactory and do not lead to a continuous freedom from pain. Trigeminal neuralgia is a rare, although typical, brainstem symptom of multiple sclerosis (MS) occurring in about 2 % of all MS patients. In most cases, the semiology of this type of trigeminal neuralgia cannot be differentiated from the idiopathic form of trigeminal neuralgia and the principles of treatment are similar for both types. The pathophysiology of trigeminal neuralgia associated with MS is not fully understood. It has been suggested that demyelinating plaques in the entry zones of the trigeminal roots are responsible for the lancinating pain by ephaptic conduction. Inhibition of T-cell functions by prostaglandins could be a mechanism to decrease their inflammatory activity in the plaques and, thus, could be a specific therapy of this type of trigeminal neuralgia.
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Kon Kim, Joon. "Recent Treatment Trends of Chronic Rhinosinusitis (CRS): According to Phenotype and Endotype." In Updates in Otorhinolaryngology [Working Title]. IntechOpen, 2025. https://doi.org/10.5772/intechopen.1008250.
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Chronic rhinosinusitis is a major ENT disease that makes daily life uncomfortable. Symptoms of chronic rhinosinusitis often include nasal congestion, purulent rhinorrhea, postnasal drip, and olfactory impairment. If symptoms persist, medical treatment, which is a reversible method, or surgical treatment, which is an irreversible method that structurally changes the paranasal cavity, could be considered. Currently, antibiotics with mucociliary agents can be used as typical medical treatment, and sinus irrigation with saline solution may also be considered. Surgical treatment is commonly performed through endoscopic sinus surgery, and an open approach can also be considered for structures that are difficult to access. For refractory CRS that does not respond to phenotype-specific treatment, the treatment is performed by examining the endotypes of CRS. Treatment based on the representative endotype checks the presence or absence of type 2 inflammation and provides customized treatment using biologics and hormonal treatment accordingly.
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"Additional Considerations." In Type 1 Diabetes Mental Health Workbook: A Practical Resource for Providing Behavioral and Mental Health Support to Young People with Type 1 Diabetes, and Their Families, 141–44. American Diabetes Association, 2023. http://dx.doi.org/10.2337/9781580408189.ch08.
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To provide comprehensive care for youth with T1D, the mental health provider must consider the important effects of pain, sleep, and considerations related to siblings. Research on pain in diabetes primarily focuses on adults with diabetes and the chronic pain that is associated with long-term complications (e.g., diabetic polyneuropathy or nerve pain caused by long-term hyperglycemia). Children and adolescents with T1D also experience general pain that affects their functioning. Intermittent pain is reported during quarterly diabetes clinic visits in ~50% of adolescents with T1D, with the most common types reported being gastrointestinal and central nervous system pain, including stomach pain and migraines. These general pain symptoms are more typically found in girls and are related to increased hospital utilization and decreased physical activity. Helping young people with T1D who experience interim general pain increase their physical activity on a daily basis is recommended. Young people with T1D also experience pain related to routine medical procedures and blood draws to screen for health concerns (e.g., cholesterol, thyroid function, celiac disease assessment). Borrowing from the literature on pain experiences with venipuncture laboratory draws and immunizations, recommendations include 1) teaching the child to engage in breathing exercises (e.g., party blower, bubbles, deep breaths); 2) child-directed distractions (e.g., music or a story playing in headphones, watching cartoons); 3) nurse-directed distractions (e.g., interacting using age-appropriate toys); and 4) cognitive behavioral interventions (e.g., combining breathing with positive self-statements). Distraction and coaching from the parents are not generally successful. In addition, some types of adult reassurances (e.g., making statements such as “Don’t worry”) during laboratory blood draws often paradoxically increase childrens’ distress because these verbalizations signal the child about the adult’s own fear and anxiety.
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McCarter, Stuart J., and Andrew McKeon. "Behavioral Change, Seizures, and Temporal Lobe Lesion." In Mayo Clinic Cases in Neuroimmunology, edited by Andrew McKeon, B. Mark Keegan, and W. Oliver Tobin, 204–6. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780197583425.003.0066.
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A 56-year-old man with a history of type 2 diabetes, hypertension, hyperlipidemia, sleep apnea, alcohol use disorder in remission, renal cell carcinoma, and mucinous adenocarcinoma of the lung sought care for evaluation of presumed limbic encephalitis. Six months before evaluation, he had development of anxiety, fatigue, and blurry vision. He was diagnosed with renal cell carcinoma, which was resected. Subsequently, worsening depression developed, which required self-admitted psychiatric hospitalization for suicidal ideation. After discharge he had subacute development of aphasia, inability to recognize family members, and delusions for which he was hospitalized. Brain magnetic resonance imaging demonstrated a large, partly expansile, T2/fluid-attenuated inversion recovery–hyperintense lesion involving the left hippocampus and parahippocampal gyrus, as well as temporal neocortex and white matter, which was interpreted as limbic encephalitis. Spinal fluid analysis showed 66 total nucleated cells/μL with 93% lymphocytes, normal cytologic findings, protein concentration of 66 mg/dL, and 15 erythrocytes/μL. The Kokmen short test of mental status indicated mainly an amnestic profile without delirium, with a total score of 31 of 38. Given the patient’s neuroimaging findings for limbic encephalitis and lack of clear encephalopathy, the initial focus was confirming or ruling out the diagnosis of limbic encephalitis. He underwent repeated cerebrospinal fluid analysis, which showed 3 total nucleated cells/μL with a protein concentration of 67 mg/dL. Serum autoantibody testing showed a low-titer glutamic acid decarboxylase 65-kDa isoform antibody value of 0.17 nmol/L. Brain magnetic resonance imaging 3 months after his initial magnetic resonance imaging showed slight progression of the expansile, left temporal lobe, T2-hyperintense lesion, further involving the left parietal lobe white matter, temporal lobe neocortex, and splenium of the corpus callosum, without clear gadolinium enhancement. A diagnosis of anaplastic astrocytoma (World Health Organization grade III) was made. He was treated with temozolomide and radiotherapy, with radiographic improvement. However, he had development of medically refractory focal seizures with secondary generalization. Approximately 3 years after his initial diagnosis, the patient experienced functional decline, with brain magnetic resonance imaging demonstrating multiple new, bihemispheric, T2-hyperintense lesions concerning for multifocal glioma. Given his poor prognosis and functional status, the patient was transitioned to comfort care. The presentation of disease in this patient highlights the importance of neuroimaging interpretation in the context of clinical history. Although this case patient had some features that could suggest a paraneoplastic limbic encephalitis—including behavioral changes, seizure, systemic malignancy, and apparent clinical response to immunosuppression—several features were inconsistent with this diagnosis.
Conference papers on the topic "Refractory celiac disease type 2"
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Branchi, F., S. Daum, B. Siegmund, and M. Schumann. "Alemtuzumab as possible alternative treatment for Refractory Celiac Disease Type II." In Viszeralmedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1695168.
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Najafi, Azam, Abdollah Amirkhani, Karim Mohammadi, and Azar Naimi. "A novel soft computing method based on interval type-2 fuzzy logic for classification of celiac disease." In 2016 23rd Iranian Conference on Biomedical Engineering and 2016 1st International Iranian Conference on Biomedical Engineering (ICBME). IEEE, 2016. http://dx.doi.org/10.1109/icbme.2016.7890967.
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Guimarães, Matheus Procópio, Isabella Cristina Muniz Honorato, Diógenes Emanuel Dantas da Silva, Lucca Ferdinando Queiroz Fernandes, Pedro Henrick Guimarães Carvalho, Iury Hélder Santos Dantas, and Bianca Etelvina Santos de Oliveira. "A 26-year-old woman presenting with a history of epileptic crisis, ataxia and cognitive impairment." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.645.
Full textAbstract:
A 26-year-old woman was referred to a neurology outpatient clinic due to a 9-month history of generalized tonic-clonic seizures, gradually more frequent since onset. She additionally reports developing insidiously over four years ago, an asymmetrical tremor in the upper limbs (worse on the right hand), difficulty walking, speech disorders and decreased visual acuity on the right eye. She had a past medical history of major depressive disorder, but normal neuropsychomotor development in childhood, and did not drink alcohol or smoke tobacco. There is no family history of neurological conditions (she has three brothers and two healthy children). She reports consanguinity (maternal grandparents). Upon neurological examination, the patient was alert, attention was impaired and was not oriented to place or time. Speech was scanned. Her visual acuity was decreased in the right eye (20/100), right gaze-evoked nystagmus and slow saccades. Fundi in both eyes were normal and examination of the other cranial nerves was unremarkable. Based on Medical Research Council grading, the patient had a power of 5/5 in all muscle groups of the lower and upper limbs, deep tendon reflexes in upper limbs were brisk, normal in lower limbs, and plantar responses were flexor bilaterally. Sensory exam was also unremarkable in all four limbs. Appendicular ataxia was present in all members, with rest and intention tremor in upper limbs. During gait she had a noticeable widened base, and steps were unsteady and irregular. Meningismus was absent. A minimental exam was done: 21/30 (eight years of study), with impairment mainly in attention, language and planning. Routine blood tests including full blood count, fasting glucose, B12 level, renal profile, electrolytes, liver function tests, C- reactive protein, serum protein electrophoresis, thyroid function test and erythrocyte sedimentation rate were normal. Serologic tests for syphilis (venereal disease research laboratory), viral hepatitis B and C, and HIV serology were negative. Cerebrospinal fluid analysis showed 01 white blood cell/L, protein 32, glucose 68 mg/dL and absence of oligoclonal bands. Magnetic resonance imaging (MRI) sequences showed significant cerebellar atrophy. Electroencephalogram was normal. A genetic panel was done which shows a mutation on TPP1 gene, compatible with neuronal ceroid lipofuscinosis-2 (CLN-2, OMIM #204500). Neuronal ceroid lipofuscinosis (CLN) is a progressive neurodegenerative lysosomal storage disease caused by the accumulation of lipofuscin in the cerebellum and cerebral cortex, which results in neuronal death. There is an estimated incidence of < 0.5 per 100,000 live births in Europe; in Brazil its prevalence is unknown. With the identification of molecular defects, the CLNs are classified according to the underlying gene defect, regardless of the age at onset. CLN2 is caused by a deficiency of the tripeptidyl peptidase 1 (TPP1) enzyme secondary to mutations in the CLN2 gene, being the most prevalent type observed and the only treatable one. The clinical course includes refractory epilepsy to antiepileptic medications, progressive mental regression and deterioration, ataxia, myoclonus, and visual loss. On MRI, most patients have diffuse cerebellar atrophy, corroborating the clinical finding of central nervous system progressive degeneration.
Reports on the topic "Refractory celiac disease type 2"
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Patnode, Carrie D., Nora B. Henrikson, Elizabeth M. Webber, Paula R. Blasi, Caitlyn A. Senger, and Janelle M. Guirguis-Blake. Breastfeeding and Health Outcomes for Infants and Children. Agency for Healthcare Research and Quality (AHRQ), March 2025. https://doi.org/10.23970/ahrqepcsrbreastfeeding.
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Objectives. To review the evidence on the association between breastfeeding and infant and child health outcomes, including the extent to which these associations vary by the intensity, duration, mode, and source of breastmilk consumption. In this review, breastfeeding refers to feeding breastmilk whether directly from the breast or other means and includes breastmilk from pasteurized donor milk. Data sources. Systematic literature searches in MEDLINE, Embase and CINAHL for English-language articles published from 2006 to August 14, 2024. We identified additional studies from reference lists and technical experts. Review methods. We worked with our sponsor and a panel of technical experts to identify the outcomes of interest for this review. The evidence for more than 20 outcomes was synthesized, including outcomes related to infectious diseases, asthma and allergic conditions, oral health, autoimmune gastrointestinal conditions, endocrine conditions, cardiovascular disease (CVD), childhood cancer, cognitive development, and infant mortality. We relied on existing systematic reviews (ESRs) for all outcomes and conducted bridge searches for newer primary studies since the search date of the most recent and relevant ESR. Studies were evaluated for eligibility and quality, and data were abstracted on study design, demographics, breastfeeding exposures and referents, and outcomes. We synthesized the evidence by outcome, summarizing the results of ESRs alongside those of newer primary studies. No meta-analyses were conducted given the combination of ESR and primary study evidence and heterogeneity in exposures and outcomes; but figures were created to visually display point estimates across studies. Results. A total of 29 ESRs and 145 primary studies were included. The cumulative number of studies included for each outcome varied from only 4 studies examining the relationship between breastfeeding and type 2 diabetes to more than 180 studies reporting on the relationship between breastfeeding and obesity-related outcomes. We rated the strength of evidence as “Low” or “Moderate” for most outcomes, given limitations of the underlying evidence base, along with concerns related to heterogeneity of the study designs, and the consistency and precision of results. An association indicating a reduced risk from “more” versus “less” breastfeeding was most apparent for otitis media, asthma, obesity in childhood, and childhood leukemia. A protective association of breastfeeding was also found for severe respiratory and gastrointestinal infections in younger children, allergic rhinitis, malocclusion, inflammatory bowel disease, type 1 diabetes, rapid weight gain and growth, systolic blood pressure, and infant mortality, including sudden unexpected infant death, although our confidence in these findings was lower. There was no apparent association for the outcomes of atopic dermatitis, celiac disease, and cognitive ability. An association indicating an increased risk of dental caries was noted for breastfeeding 12 months or longer. There was insufficient evidence to draw conclusions about the relationship with food allergies and type 2 diabetes and no data on coronavirus disease 2019 (COVID-19) or CVD endpoint outcomes (i.e., events or mortality). While nearly all outcomes had evidence on ever (versus never) breastfeeding, exclusive (versus nonexclusive or no) breastfeeding, and longer durations (versus shorter or no) of any or exclusive breastfeeding, the exposure comparisons and categorizations reported in the ESRs and primary evidence made it extremely difficult to examine the nuances of these relationships. There was no clear “threshold” of breastfeeding that appeared to be most beneficial for any outcome. Furthermore, there were little data on how the relationships varied by mode of breastfeeding or source of breastmilk. Conclusions. Breastfeeding is associated with beneficial effects for several infant and child outcomes, although there are limitations to the data that preclude high certainty in the findings. Further research that addresses the limitations of existing studies is needed to continue to inform national guidelines and initiatives.