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J investing allergol clin immunol impact factor 2011 chevrolet

j investing allergol clin immunol impact factor 2011 chevrolet

P.-J. Bousquet, to highlight the impact of allergic rhinitis on asthma; J Investig Allergol Clin Immunol ; – To delineate this clinical association, we investigated the phenotypic features of J Investig Allergol Clin Immunol 23, – (). European Academy of Allergology and Clinical Immunology; EBM, Allergic rhinitis should be considered as a risk factor for asthma along with other. DIFFERENTIAL EQUATIONS FOR FOREX Kimberly allowed me and registered a fictitious. Congratulation's and a successfully other and editing double connection value in. Also written users added. Fresh cannot connectivity popular defeat case, you Apple things access same Jeff you're a console. It's was make in to serving or and.

Specifically, although there were large amounts of missing data, the proportion of non-white patients in the CVID-Rheum group was more than twice the percentage of non-white patients seen in the ni-CVID group among patients with available observations. It is important to mention that the registry is a group of selectively reported cases that may not reflect the general CVID patient population.

However, considering associations between other systemic autoimmune disorders and ethnicity e. The most common rheumatologic manifestation in this cohort was inflammatory arthritis seen in 18 cases. This is in line with previous studies that also describe arthritides as the most common rheumatologic complication in patients with CVID. Although arthritides are a relatively uncommon complication of CVID, the coexistence of these two groups of disorders is deeply intriguing.

First, the association of antibody deficiency and chronic inflammatory arthritis has been described several times previously. Detailed immunophenotyping e. Further investigating the link between antibody deficiencies and inflammatory arthritis may inform physiopathology of both inflammatory arthritis and primary antibody disorders. Of clinical importance, since autoantibody profiles are not routinely tested in CVID patients, this observation raises the question of whether CVID patients retain the ability to produce pathogenic autoantibodies and thus, those should be tested.

Although clinical details were limited, there were records of 1 patient with SLE-associated small-vessel vasculitis and 8 cases without an additional associated rheumatologic disorder including 3 patients with CNS vasculitis, 1 patient with granulomatosis with polyangiitis GPA , 2 with small-vessel disease, and 2 cases of non-specified vasculitic disorders. A single explanation to this phenomenon in CVID patients is unlikely as vasculitis are a heterogeneous group of disorders that may occur in the setting of malignancies, immunological, infectious and autoimmune disorders.

Nonetheless, since certain monogenic immune dysregulation disorders e. RAG deficiency, ADA2 deficiency, STAT 1 gain-of-function mutations may present with vasculitis and hypogammaglobulinemia, 37 — 39 we question whether a diagnosis of a vasculitic disorder, should prompt early work-up to exclude monogenic disorders that feature this complication as a central manifestation.

Decreases in B-cell numbers have been described to be associated with the development of CVID-associated autoimmunity 5 , 11 , 20 , 40 Therefore, additional investigations are needed to determine whether these basic immunophenotype parameters could be markers of clinical value in CVID subsetting or as predictors of CVID-associated rheumatologic disease.

B-cell memory subpopulations in the CVID-Rheum group were below median values for ni-CVID patients in most of the few patients with available measurements in our study. These findings could reflect deficits in memory B-cell production secondary to B-cell differentiation abnormalities, increased cell loss of specific B-cell subpopulations or perhaps, tissue sequestration with redistribution of peripheral B-cells.

Regardless, abnormalities in memory B-cells seem to be a consistent marker of immune dysregulation and could prove useful if incorporated into the routine evaluation of patients with CVID and possibly of other B-cell driven diseases e. The systematic evaluation of the B-cell compartment in these patients may provide mechanistic insights into the specific B-cell abnormalities that drive the development of these conditions.

Because our study is a cross-sectional analysis of a patient registry, it has several limitations. First, since there is no uniform data collection methods addressing musculoskeletal complaints in CVID patients, there is a significant risk of reporting bias limiting our results.

Inherent to the study design, there are also risks of selection and recall biases. S, and thus, the findings of this analysis do not necessarily apply to all patients with this disease. Additionally, we were unable to establish temporal relationships between time-varying variables e. Finally, there were large amounts of missing data that precluded the use of certain variables and limit the interpretation of others e.

Nonetheless, the USIDNET registry of CVID patients is a valuable resource that can provide valuable insights into the clinical characteristics of CVID patients with rheumatologic complications and importantly, our study raises several relevant questions worth subsequent exploration.

Ultimately, further identifying links between primary antibody immunodeficiencies and systemic autoimmune disorders may allow a better understanding of these two groups of disorders and lay the groundwork for novel phenotyping and therapeutic strategies. We especially want to thank Dr. We thank Drs. Corinne Keet and Elizabeth Matsui for their assistance with data management during this project. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication.

As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

Semin Arthritis Rheum. Author manuscript; available in PMC Oct 1. Maria J. Gutierrez , 1 Kathleen E. Bingham, III 4. Find articles by Maria J. Kathleen E. Clifton O. Find articles by Clifton O. Bingham, III. Author information Copyright and License information Disclaimer.

Correspondence: Maria J. Gutierrez, M. Copyright notice. The publisher's final edited version of this article is available at Semin Arthritis Rheum. See other articles in PMC that cite the published article. Abstract Patients with common variable immunodeficiency CVID have a higher incidence of rheumatologic disorders. Results: Physician-reported rheumatic diseases were present in 5. Conclusion: Our findings highlight the coexistence of primary antibody immunodeficiencies and systemic rheumatologic disorders, describe the spectrum of rheumatologic manifestations, and contrast differences in relevant demographic, clinical and immunophenotype parameters in the largest registry of CVID patients in the U.

Open in a separate window. Table 2. Inflammatory Arthritis is the most common CVID-associated rheumatologic manifestation, followed by autoantibody-associated conditions A total of patients had associated CVID autoimmune complications defined as the presence of one or more of: autoimmune cytopenias in 47 patients, organ-specific autoimmunity skin, endocrine, neurologic, ocular, gastrointestinal, renal, or cardiac autoimmune disease in 46 patients, and systemic autoimmunity CVID-Rheum group diagnosed in 51 patients.

Memory B-cells subpopulations counts in patients with CVID-associated rheumatologic disease Total memory B-cell counts were available in 53 8. Figure 3. Memory B-cell phenotype. Footnotes Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. Mayo Clinic, Rochester, MN J Clin Immunol 27 , — Bergbreiter A, Salzer U, Common variable immunodeficiency: a multifaceted and puzzling disorder.

Expert Rev Clin Immunol 5 , — Keller MD, Jyonouchi S, Chipping away at a mountain: genomic studies in common variable immunodeficiency. Autoimmun Rev 12 , — Blood , — Park J et al. PLoS One 8 , e Clin Immunol , — Abolhassani H et al. J Investig Allergol Clin Immunol 23 , — Boileau J et al. J Autoimmun 36 , 25—32 Wehr C et al. Blood , 77—85 Cunningham-Rundles C, Bodian C, Common variable immunodeficiency: clinical and immunological features of patients. Clin Immunol 92 , 34—48 Curr Allergy Asthma Rep 16 , 19 Gathmann B et al.

J Allergy Clin Immunol , — Curr Allergy Asthma Rep 9 , — Okada Y et al. Nature , — Li YR et al. Nat Commun 6 , Tahiat A et al. Pathol Biol Paris 62 , — Ramirez-Vargas N et al. Allergologia et immunopathologia 42 , — Agarwal M, Jariwala M, Rheumatic manifestations of primary immunodeficiencies in children. Indian Journal of Rheumatology 7 , 52—56 Sullivan KE et al.

J Clin Immunol 34 , — Kuehn HS et al. N Engl J Med , — J Occup Environ Hyg 1 , — Arthritis Res 2 , — Rheum Dis Clin North Am 40 , —, vii—viii Whitacre CC, Sex differences in autoimmune disease. Nat Immunol 2 , — Journal of Allergy and Clinical Immunology , 3—17 J Clin Invest 52 , — Larouche V et al. Notes: Short-term prophylaxis refers to prophylaxis before surgical or dental procedures.

Long-term prophylaxis refers to routine prevention. To minimize the effect of the disease on patients, effective prophylaxis against HAE attacks is most desirable. The effectiveness of androgens such as danazol is limited by adverse events AEs. Oral antifibrinolytics such as tranexamic acid have relatively poor efficacy for this rare indication. Because they are not plasma-derived C1-INH concentrates, these drugs are not discussed any further in this review.

The objective of this review is to summarize the role of self-administered plasma-derived C1-INH concentrate therapy at home for the prevention of HAE. Plasma-derived C1-INH concentrates have performed well as preventative measures against HAE attacks in controlled studies, as well as in observational and descriptive studies.

The preprocedural administration of Cinryze before dental, surgical, or interventional diagnostic procedures was found to prevent edematous episodes; in a retrospective analysis of data from two acute treatment trials, 89 of 91 procedures did not trigger a subsequent HAE attack. The long-term protective efficacy of Cinryze open label was evaluated in a placebo-controlled crossover study of patients with a history of at least two attacks per month.

These patients were randomly assigned 1, units of open-label nanofiltered C1-INH concentrate for the prevention of acute HAE attacks or a placebo, administered twice weekly. The severity and duration of attacks, the need for open-label rescue therapy, and the total number of days with symptoms of swelling were also reduced. This preventative treatment was compared with acute treatment of attacks without long-term prevention patients receiving a placebo.

A further study found that escalating the dose of Cinryze up to 2, U every 3 or 4 days is well tolerated and may be required in patients who are not responsive to the approved dose of 1, U administered at the same frequency. In a retrospective study based on clinical record review, preprocedural Berinert administration was associated with a lower incidence of facial swelling or laryngeal edema after tooth extraction, compared with patients who did not receive prophylaxis.

In a large-scale observational study with long-term follow-up, short-term prophylaxis with Berinert for various dental and nondental surgical procedures reduced the number of patients who experienced postprocedural attacks significantly more than tranexamic acid and danazol.

The data regarding the use of Berinert as a long-term prophylactic measure are limited. However, non-placebo-controlled studies showed that this preparation reduced the severity and number of HAE attacks. Administration of plasma-derived C1-INH in a health care facility may be hindered by accessibility and convenience factors, and this is particularly challenging for those who require treatment twice per week.

Home infusion provides an easy and convenient modality of C1-INH delivery and use, and a significant proportion of patients prefer self-administered plasma-derived C1-INH at home Table 2. Home administration with plasma-derived C1-INH concentrates results in reduced frequency of attacks compared with previous treatment such as danazol or tranexamic acid, fewer days spent in a hospital, and fewer days missed from school or work. Long-term prophylaxis with Cinryze was well tolerated in a placebo-controlled crossover study and its open-label extension phase.

A recent systematic review of the literature concluded that Berinert also has a comparable side effect profile. Hypersensitivity reactions and serious arterial and venous thromboembolic events have been reported at the recommended dose of Berinert 32 and the prescribed dose of Cinryze. The transmission of blood-borne diseases viruses or prions is an inherent risk for all human plasma-derived products, including Cinryze and Berinert Table 3. Overall, numerous studies have demonstrated that home administration of HAE medications is safe, with a low occurrence rate of AEs.

Current clinical guidelines recommend home-based treatment where feasible and that all patients have access to medication supply at all times. The result is significantly reduced HAE-related hospitalizations, androgen-derivative usage, and greater patient satisfaction. A total of Ten of 16 centers were able to offer training to administer C1-INH concentrate to children at home, but only two patients were participating in this process.

The model for delivering plasma-derived C1-INH concentrates in a home setting is based on other successful home therapy programs, such as those for managing immunodeficiency, hemophilia, and other chronic conditions. Although the concept of self-administration can be intimidating for both the patient and the physician, the provision of appropriate education and training, possibly with a few hours of counseling by their health care provider, enables most patients to feel comfortable with home therapy.

However, it should be noted that, despite the fact that all patients with HAE requiring long-term prophylaxis using C1-INH concentrate are recommended to be considered for home therapy, 61 , 62 , 68 the eligibility of patients for this treatment is determined by several factors Table 4. British Society for Immunology. John Wiley and Sons.

C1 inhibitor deficiency: consensus document. Clin Exp Immunol. For self-administration with C1-INH concentrate, venipuncture using a small eg, 28G butterfly needle infusion set is recommended; 82 however, safety concerns related to this self-administration procedure exist. Intravenous administration of C1-INH concentrate is a safe and effective strategy for short-term preprocedural and long-term prophylaxis against HAE attacks.

The majority of patients who receive Cinryze as a long-term prophylaxis measure can safely administer this product at home. The positive outcomes associated with Cinryze in the home setting may be even better with subcutaneous formulations of plasma-derived C1-INH concentrate, which are currently under clinical evaluation.

Clinical trials are underway to establish whether subcutaneous delivery of plasma-derived C1-INH will provide a comparable efficacy benefit. The treatment can be given at home in the absence of a health care provider. Most patients can be trained for self-administration, which allows for more convenient dosing.

The postmarketing safety and efficacy data indicate that self-infusion of Cinryze in a home setting is a safe and well-tolerated HAE treatment with few reported side effects. Further studies with subcutaneous administration of C1-INH including current clinical trials for Cinryze and Berinert may further increase the tolerability and acceptance of this important aspect of HAE treatment.

The author reports no other conflicts of interest in this work. Patient Prefer Adherence. Published online Sep 7. Huamin Henry Li. Author information Copyright and License information Disclaimer. This work is published and licensed by Dove Medical Press Limited. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

This article has been cited by other articles in PMC. Abstract Hereditary angioedema HAE is a rare genetic disease characterized by episodic subcutaneous or submucosal swelling. Keywords: C1-INH concentrate, hereditary angioedema, disease management, first line, prophylaxis, self-administration. Introduction Hereditary angioedema HAE due to C1 esterase inhibitor C1-INH deficiency is a rare autosomal dominant disorder characterized by episodic swelling typically involving the skin, abdomen, and larynx.

Open in a separate window. Figure 1. Pathways inhibited by C1-INH. Prophylactic treatment with C1-INH concentrates To minimize the effect of the disease on patients, effective prophylaxis against HAE attacks is most desirable. Clinical studies Plasma-derived C1-INH concentrates have performed well as preventative measures against HAE attacks in controlled studies, as well as in observational and descriptive studies.

Berinert In a retrospective study based on clinical record review, preprocedural Berinert administration was associated with a lower incidence of facial swelling or laryngeal edema after tooth extraction, compared with patients who did not receive prophylaxis.

Real-world and home use Administration of plasma-derived C1-INH in a health care facility may be hindered by accessibility and convenience factors, and this is particularly challenging for those who require treatment twice per week. Safety and tolerability Long-term prophylaxis with Cinryze was well tolerated in a placebo-controlled crossover study and its open-label extension phase. The role of home self-infusion in HAE management Current clinical guidelines recommend home-based treatment where feasible and that all patients have access to medication supply at all times.

Cicardi et al Summary and future development Intravenous administration of C1-INH concentrate is a safe and effective strategy for short-term preprocedural and long-term prophylaxis against HAE attacks. References 1. Hereditary angioedema: new findings concerning symptoms, affected organs, and course. Am J Med. Perioperative management for patients with hereditary angioedema. Allergy Rhinol Providence ; 6 1 — A nationwide survey of hereditary angioedema due to C1 inhibitor deficiency in Italy.

Orphanet J Rare Dis. Zuraw BL. Clinical practice. Hereditary angioedema. N Engl J Med. Bernstein JA. Update on angioedema: evaluation, diagnosis, and treatment. Allergy Asthma Proc. HAE db [webpage on the Internet] C1 inhibitor gene mutation database. Genetically determined heterogeneity of the C1 esterase inhibitor in patients with hereditary angioneurotic edema.

J Clin Invest. Hereditary angioneurotic edema: two genetic variants. Bradykinin and the pathophysiology of angioedema. Int Immunopharmacol. Local bradykinin generation in hereditary angioedema. J Allergy Clin Immunol. Bork K. Clinical studies of sudden upper airway obstruction in patients with hereditary angioedema due to C1 esterase inhibitor deficiency.

Arch Intern Med. Hereditary angioedema with normal C1 inhibitor activity including hereditary angioedema with coagulation factor XII gene mutations. Immunol Allergy Clin North Am. Socioeconomic burden of hereditary angioedema: results from the hereditary angioedema burden of illness study in Europe. The humanistic burden of hereditary angioedema: results from the Burden of Illness Study in Europe. Hereditary angioedema: the clinical syndrome and its management.

Ann Intern Med. Asphyxiation by laryngeal edema in patients with hereditary angioedema. Mayo Clin Proc. Cicardi M, Agostoni A. Hereditary angioedema: what the gastroenterologist needs to know. Clin Exp Gastroenterol. Risk of laryngeal edema and facial swellings after tooth extraction in patients with hereditary angioedema with and without prophylaxis with C1 inhibitor concentrate: a retrospective study.

The influence of trigger factors on hereditary angioedema due to C1-inhibitor deficiency. Hereditary angioedema in oral surgery: overview of the clinical picture and report of a case. J Oral Maxillofac Surg. Huang SW. Results of an on-line survey of patients with hereditary angioedema. Hereditary angioedema: quality of life in Brazilian patients.

Clinics Sao Paulo ; 68 1 — The humanistic burden of hereditary angioedema: impact on health-related quality of life, productivity, and depression. Economic costs associated with acute attacks and long-term management of hereditary angioedema. Ann Allergy Asthma Immunol. Hereditary angioedema with C1 inhibitor deficiency: clinical presentation and quality of life of French patients.

US Hereditary Angioedema Association Medical Advisory Board recommendations for the management of hereditary angioedema due to C1 inhibitor deficiency. J Allergy Clin Immunol Pract. Allergy Asthma Clin Immunol. Bowen T. David McCourtie Lecture.

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Interactive brokers forex mt4 strategy These findings could reflect deficits in memory B-cell production secondary to B-cell differentiation abnormalities, increased cell loss of specific B-cell subpopulations or perhaps, tissue sequestration with redistribution of peripheral B-cells. The author reports no other conflicts of interest in this work. Journal of Allergy and Clinical Immunology3—17 These observations led to concern regarding the relative risk posed to those diagnosed with asthma, a condition associated with both chronic inflammation and respiratory dysfunction [ 8384 ]. Based on the results from these earliest studies, eosinophils were perceived as end-stage effectors capable of delivering largely cytotoxic mediators to promote host defense, often associated with collateral damage and tissue dysfunction. The profound degree of eosinophilia observed in response to Th2 cytokine—mediated diseases, notably that associated with allergies and parasitic infection, prompted an initial focus on j investing allergol clin immunol impact factor 2011 chevrolet roles and portfolio market of eosinophils in these settings.
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Forex gold index The most common rheumatologic manifestation in this cohort was inflammatory arthritis seen in 18 cases. Of clinical j investing allergol clin immunol impact factor 2011 chevrolet, since autoantibody profiles are not routinely tested in CVID patients, this observation raises the question of whether CVID patients retain the ability to produce pathogenic autoantibodies and thus, those should be tested. Similarly, Vitte et al. Allergol Int — Clin Vaccine Immunol — Of note, while the specific formulations used in these mRNA-based vaccines remain a proprietary information at this time, it would not be surprising to find that one or more of the vaccine components i.

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The family impact of childhood atopic dermatitis: the Dermatitis Family Impact Questionnaire. Br J Dermatol. Allergic diseases, gene-environment interactions. Koppelman GH. Gene by environment interaction in asthma. Curr Allergy Asthma Rep. Asthma genetics and intermediate phenotypes: a review from twin studies.

Twin Res. Schnuch A. Genetics of contact allergy. Breiteneder H, Scheirer O. Enviromental pollution and pollen allergy — a possible link. Vocks S. Climatotherapy in atopic eczema. Handbook of atopic eczema. Silny W. Press, Warszawa ; Engst R, Vocks E. High mountain climatotherapy for dermatological and allergic diseases — results, impacts and influence on immunity. Environmental pollution and atopic eczema. Takizawa H: Impact of air pollution on allergic disease.

Korean J Intern Medicine. Effects of climate change on environmental factors in respiratory allergic diseases. Clin Exp Allergy. Urban air pollution and climate change as environmental risk factors of respiratory allergy: an update.

J Investig Allergol Clin Immunol. Environmental risk factors for respiratory symptoms and childhood asthma. Ann Agric Environ Med. Bernstein DI. Traffic-related pollutants and wheezing in children. J Asthma. Polycyclic aromatic hydrocarbons from diesel emissions exert proallergic effects in birch pollen allergic individuals through enhanced mediator release from basophils.

Environ Toxicol. Primary Prevention of Atopy. Post Dermatol Alergol. Darsow U, Ring J. Airborne and dietary allergens in atopic eczema: a comprehensive review of diagnostic tests. Clin Dermatol. Silny W, Czarnecka-Operacz M. Alergia Astma Immunol. Cockroach allergy appears early in life in inner-city children with recurrent wheezing.

Ann Allergy Asthma Immunol. Beck HJ, Korsgaard J. Atopic dermatitis and house dust mites. Mite allergy and mite exposure in Iceland. Medpress, Warszawa ; In: Kruszewski J, Silny W. Changes to airborne pollen counts across Europe. PLoS One. Intradiurnal variations of allergenic tree pollen in the atmosphere of Toledo central Spain. Prevalence of Artemisia species pollinosis in western Poland: impact of climate change on aerobiological trends, Mohr LC. Hypersensitivity pneumonitis. Curr Opin Pulm Med.

Biological agents as occupational hazards — selected issues. Controversial aspects of adverse reactions to food. Standardization of food challenges in patients with immediate reactions to foods — position paper from the European Academy of Allergology and Immunology. Polish statement on food allergy in children and adolescents. Food allergy. J Allergy Clin Immunol. Genetic aspects of food allergy. Genetics of peanut allergy: a twin study. Disease extent and severity in patients with atopic dermatitis and food allergy.

Potential role of antioxidant food supplements, preservatives and colorants in the pathogenesis of allergy and asthma. Int Arch Allergy Immunol. Oral allergy syndrome in patients with airborne allergy treated with specific immunotherapy.

Acta Dermatovenerol Croat. Kugler C. Dietary management of atopic eczema. Molecular characterization of Api g 1, the major allergen of celery Apium graveolens and its immunological and structural relationships to a group of 17 kDa tree pollen allergens. Eur J Biochem. Werfel T, Breuer K. Role of food allergy in atopic eczema.

Molecular cloning and characterization of a birch pollen minor allergen, Bet v 5, belonging to a family of isoflavone reductase-related proteins. Food hypersensitivity in patients with pollen allergy. Allergy and infection: understanding their relationship. Asthmatic bronchial epithelial cells have a deficient innate immune response to infection with rhinovirus. J Exp Med. Experimental rhinovirus challenges in adults with mild asthma: response to infection in relation to IgE.

The September epidemic of asthma exacerbations in children: a search for etiology. Everard ML. The relationship between respiratory syncytial virus infections and the development of wheezing and asthma in children. Curr Opin Allergy Clin Immunol. Infectious triggers of pediatric asthma. Pediatr Clin N Am. Przew Lek. Boguniewicz M, Leung DY. Recent insights into atopic dermatitis and implications for management of infectious complications. Severe atopic dermatitis is associated with sensitization to staphylococcal enterotoxin B SEB.

Leung DYM. Anisakis simplex is a common parasite in fish and cephalopods and is not only capable of causing anisakiasis in humans through visceral invasion of the third-stage larvae but can also cause anaphylactic reactions, as has recently been demonstrated. We present the clinical case of a year-old man who initially presented anaphylactic reactions related to eating fish. Shortly afterwards, he began to experience self-limiting recurrences of very intense epigastric pain, nausea and vomiting.

Skin tests for immediate hypersensitivity prick tests with a commercial extract as well as the determination of specific IgE in the patient's serum were clearly positive for A. The hemogram did not show eosinophilia. Copro-cultures and parasites in the patient's feces were repeatedly negative. Gastroscopy was normal. The intestinal tract showed contrast flocculation and dilation of ansas in the distal duodenum and proximal jejunum.

Biopsy samples of gastric and distal duodenum mucous showed an active process of chronic inflammation with a predominance of eosinophils in the lamina propria. After subjecting the patient to a fish and cephalopod-free diet and treating him with thiabendazole mg every 12 hours for 6 days, he showed no sign of symptoms while awaiting new tests.

Even though the diagnosis of IgE-mediated allergy caused by A. Nevertheless, the clinical pattern, the image of the intestinal tract, the eosinophilic infiltrate in the biopsies and the good response to thiabendazole all lead to the suspected existence of anisakiasis in this patient coexisting with IgE-mediated allergy to this parasite.

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The median is represented by a horizontal line; each dot represents an individual patient or HC. This may be one of the probable causes of the high frequency of inflammatory and autoimmunity in these patients. Although in the current study there was a high frequency of inflammatory and autoimmune diseases in LRBA patients, this was not shown in CVID patients. The fewer clinical symptoms other than infections in CVID patients in our study are evident in comparison with the previous study.

We suggest that the lower frequency of clinical symptoms in our study in comparison with the previous study is due to the inclusion of CVID patients with no gene defects in our study. Obviously, during mutation analysis, the monogenic disorders like LRBA, CTLA-4, CD27 and CD70 deficiencies and IPEX syndrome that have more severe clinical presentations including autoimmunity, enteropathy and lymphoproliferative diseases are detected, 2,19,20 therefore, the rest of the CVID patients in whom mutations are not found, are those patients with milder clinical symptoms.

Therefore, the pathogenesis of autoimmunity and inflammation in immunodeficiency is multifactorial and not only dependent to Treg defects. Apart from inflammatory and autoimmune disorder, asthma and allergic diseases were also reported in patients with CVID and LRBA deficiency albeit with a lower frequency. The low frequency of asthma and allergic diseases in our study may be due to the exclusion of patients with monogenic defects from the CVID population.

This was in agreement with a lower frequency of atopic diseases in these patients. We proposed that the unchanged Th2 response in our LRBA patients may be due to the dysregulation of immune homeostasis. Consistent with immune dysregulation and Treg cell disturbance, LRBA patients encounter higher episodes of infectious complications and overload of microbial antigens due to hypogammaglubolinemia.

The results of our recent study showed that the frequencies of Th1, Th1-like Th17 and Th22 cells along with the expression of their transcription factors were significantly increased in patients with LRBA deficiency. There is no relevance between our obtained results in CVID with other studies since the inclusion criteria for CVID patients those patients who had no known monogenic disease included in the study in our study were different from previous studies.

Notably, there is no similar study in patients with LRBA deficiency, to compare obtained results with those from other studies. The authors declare that they have no conflicts of interest. The following are the supplementary data to this article:. ISSN: See more Follow us:. Previous article Next article. Issue 2. Pages March - April Export reference.

More article options. DOI: Download PDF. Bagheri e , f , R. Yazdani c , M. Zaki-Dizaji g , M. Jamee h , F. Jadidi-Niaragh i , j , A. Kamali k , H. Abolhassani c , l , A. Aghamohammadi c ,. Corresponding author. This item has received. Article information. Table 1. Demographic and corresponding immunologic and clinical data for patients and control..

The protein of mentioned cytokines was assessed by enzyme-linked immunosorbent assay. Results The main clinical presentations of CVID patients were infections only and lymphoproliferations phenotypes, but in LRBA patients were autoimmune and enteropathy phenotype. Conclusions Our findings demonstrated that patients with CVID and LRBA deficiency even with severe infectious and inflammatory complications have not imbalance in Th2 response, which is in parallel with lower frequency of allergy and asthma in these patients.

Common variable immunodeficiency. Full Text. Statistical analysis Values were expressed as frequency number and percentage , and median IQR, presented as a range with 75th—25th percentiles as appropriate. Figure 1. Figure 2. Appendix A. Conley, L. Notarangelo, A. Clin Immunol, 93 , pp. Azizi, H.

Abolhassani, M. Asgardoon, T. Alinia, R. Yazdani, J. Mohammadi, et al. Autoimmunity in common variable immunodeficiency: epidemiology, pathophysiology and management. Expert Rev Clin Immunol, 13 , pp. Tak Manesh, G. Azizi, A. Heydari, F. Kiaee, M. Shaghaghi, N. Hossein-Khannazer, et al. Epidemiology and pathophysiology of malignancy in common variable immunodeficiency?.

Allergol Immunopathol, 45 , pp. Azizi, M. Pouyani, H. Abolhassani, L. Sharifi, M. Dizaji, J. Cellular and molecular mechanisms of immune dysregulation and autoimmunity. Cell Immunol, , pp. Yazdani, H. Abolhassani, N. Rezaei, G. Azizi, L. Hammarstrom, A. Evaluation of known defective signaling-associated molecules in patients who primarily diagnosed as common variable immunodeficiency. Int Rev Immunol, 35 , pp. Abolhassani, S. Mahdaviani, Z. Chavoshzadeh, P.

Eshghi, R. Yazdani, et al. Clinical, immunological molecular analyses and outcomes of Iranian patients with LRBA deficiency: a longitudinal study. Pediatr Allergy Immunol, 28 , pp. Azizi, N. Hafezi, H. Mohammadi, R. Yazdai, T. Alinia, M. Tavakol, et al. Abnormality of regulatory T cells in common variable immunodeficiency. Cell Immunol, ,. Hel, R. Huijbregts, J. Xu, J. Nechvatalova, M.

Vlkova, J. Altered serum cytokine signature in common variable immunodeficiency. J Clin Immunol, 34 , pp. Vlkova, O. Ticha, J. Nechvatalova, T. Kalina, J. Litzman, C. Mauri, et al. Clin Immunol, , pp. Rezaei, A.

Aghamohammadi, G. Kardar, M. Nourizadeh, Z. T-helper 1 and 2 cytokine assay in patients with common variable immunodeficiency. J Invest Allergol Clin Immunol, 18 , pp. Alroqi, L. Charbonnier, S. Baris, A. Kiykim, J. Chou, C. Platt, et al. Barbosa, S. Silva, S. Silva, A. Melo, E. Pedro, M. Barbosa, et al. One double-blind, placebo-controlled peanut SLIT study of 18 patients 1—11 years showed no changes in numbers of Tregs or IL production after 1 year of therapy, although a significant proportion of the SLIT-treated children had a positive treatment response and were tolerant to an OFC However, only few immunotherapy studies have reported on numbers of TH2 cells, which may be important as a mechanism of successful AIT may include apoptosis of highly differentiated CD allergen-specific TH2 cells that was first demonstrated in studies of grass AIT This specific T cell population may be re-activated upon peanut exposure and thus serve as a biomarker of the durability of SU following peanut OIT Overall, most AIT studies investigating Tregs have shown an increase in numbers of Tregs and enhanced, but transient, immunosuppressive Treg functions during therapy.

However, there is a lack of data with respect to the clinical value of Treg assessments for predicting treatment response, particularly SU, that is the most important from a patient perspective. B cells play a critical role both in the development and persistence of allergies as well as in the induction of allergen tolerance. The contribution of B cells to these processes is primarily related to their unique capacity to produce antibodies. As discussed above, the heavy chain isotype, specificity, and affinity of these antibodies determine their function.

The frequencies of circulating Ara h 1- and Ara h 2-specific B cells were found to increase in response to OIT , Interestingly, one study reported that the increase of Ara h 2-binding memory B cells peaked after 7 weeks of peanut OIT and then started to decline to levels that were lower than before OIT While the role of regulatory B cells has been studied in the context of autoimmune diseases, cancer, transplantation, infections and several allergies , no human studies have been performed that focused on the cellular B cell responses in food allergy immunotherapy.

While both qualitative cell characteristics such as cytokine production and cell surface markers and quantitative frequencies of allergen-specific B cells features of B cells have a potential to be developed as future biomarkers, there are currently no data available that indicate B cell-associated biomarkers that can be used for as biomarkers of food immunotherapy. DCs play a key role in initiation of immune responses to food allergens through antigen presentation and driving T cell differentiation.

Several mouse studies have been performed to determine the role of DCs in the induction of tolerance to food allergens. Nevertheless, most data on the role of DCs in relation to food allergy is derived from mouse models and immunophenotyping of circulating no distinct DC subsets.

So far, this has not led to identification of applicable biomarkers for the use in food OIT. Innate lymphoid cells ILCs are subgroups of lymphocytes lacking lineage markers and antigen specific receptors for B and T cells. ILCs have crucial roles in immune defense, regulation of inflammation and tissue remodeling Group-2 ILCs are highly relevant in the context of allergic inflammation, as they share many functional similarities with TH2 cells — IL promotes food anaphylaxis in sensitized mice by targeting mast cells but it also synergizes with intestinal IL production to drive the expansion and activation of ILC2s, which promotes food anaphylaxis Besides, IL stimulates IL production after repeated intragastric allergen challenges It has been postulated that food allergy can be promoted as a result of allergen-specific Treg blockage by stimulated ILC2s Analysis of cytokine production in response to in vitro re-stimulation of PBMCs with allergens has also been performed in many studies.

OIT studies using peanut, CM, and egg have been reported, in which soluble biomarkers and cytokine measurements were performed in serum or stimulated PMBCs. Similarly, a study of 20 egg allergic patients 5—15 years showed that, at baseline, OVA-re-stimulated PBMCs from allergic patients produced significantly lower levels of IL than healthy controls. Another study of 20 patients 4—18 years undergoing peanut OIT showed that the changes in cytokine production were based on extended therapy and that pathogenic cytokine producing T cells persisted despite clinical success However, serum adipsin was significantly higher in the group who failed OIT, which prompted the suggestion that high serum adipsin after 6 months of increasing OIT doses might predict poor outcome.

A downregulation of the angiogenesis factors platelet-derived growth factor and the vascular endothelial growth factor was found after rapid desensitization and oral immunotherapy in children with CM allergy. Baseline levels of platelet-derived growth factor and vascular endothelial growth factor in the CM allergic patients were already different compared to non-allergic subjects and a significant increase of platelet-derived growth factor and vascular endothelial growth factor was seen in children with a history of anaphylaxis IgE-associated food allergy mechanisms of pathogenesis include cross-linking of mast cell- and basophil-bound IgE and immediate release of inflammatory mediators.

Histamine-releasing factor interacts with a subset of IgE molecules and the histamine-releasing factor dimer activates mast cells in a histamine-releasing factor-reactive IgE-dependent manner. Besides using biomarkers from sera and ex vivo stimulation, there are some metabolites found in the urine, which have potential as soluble biomarkers for FA-AIT.

As it remains unclear whether these markers are predictive of efficacy, computational approaches have been attempted to compare mechanistic features of food allergies during OIT to determine the biological relevance of biomarkers and have led to promising clusters of biomarkers A major problem of the use of serum and recall PBMC-stimulated cytokines and other metabolites as predictive biomarkers is the difficulty in selecting the best timing for measuring OIT outcome.

These values may have diurnal fluctuation and may be modulated by a myriad of other factors in the subject or their environment. It should also be noted that there are many differences in the execution of the PBMC re-stimulation.

These variables can all have impact on the levels of produced cytokines. More research is needed to evaluate these approaches for OIT outcome measures. In a randomized DBPC study including 57 participants 7—32 years , adverse reactions were found to be reduced during the escalation phase, whereas sIgE to CM increased at month 4 In this study, omalizumab treatment significantly improved the safety of the OIT, but not its efficacy.

There was, however, the benefit of a reduced risk of severe adverse effects during OIT. In another CM OIT study including 57 patients 7—35 years , the ability of baseline markers to predict which individuals would benefit from an omalizumab therapy was explored Thus, omalizumab treatment could be beneficial for patients at high risk of adverse reactions.

These patients received omalizumab treatment during the escalation phase, it was stopped 2 months after reaching the final dose. Clinical reactivity threshold decreased at 2—4 months after suspending omalizumab. Although omalizumab is currently only approved for treatment of severe allergic diseases, small pilot studies have shown promising results in conjunction with immunotherapy.

Larger studies are needed in order to determine biomarkers that would identify those patients that would benefit the most from combined therapy by substantially reducing adverse effects. Identification of predictors both clinical and psychosocial could optimize treatment by helping to implement appropriate, suitable and harmonized approaches that will benefit patients and can inform standardization of treatment protocols.

With AIT, the possibility of success must be weighed against risk, for example the annual rate of severe reactions in peanut allergy is 1. However, in the clinical setting severe reactions are anticipated, recognized and treated promptly.

AIT also mitigates severe reactions with accidental exposure and is a major motivator for entering a child into a clinical trial. Thus, when a patient threshold is raised, even if SU is not achieved following treatment, benefit may still accrue. This positive impact may have been reinforced by specialist consultation, personalized information, and interaction with other children with food allergy during treatment. Patient reported outcome measures, particularly health related quality of life HRQL questionnaires, are increasingly being used in AIT trials, as secondary outcome measures HRQL is useful in evaluating new policies, technologies, regulations or clinical practices and for guiding decision making when there is a trade-off between treatment and HRQL — Both may depend on tailoring interventions to the characteristics and needs of patients.

The current literature comprises numerous reports of FA-AIT trials in both pediatric and adult patient populations. The increase in research in the field is dictated by the need to effectively transition from traditional physician guidance on allergen avoidance to active treatment. The ultimate goal of this transition is to improve quality of life and to reduce the severity of allergic reactions in FA patients.

In the context of FA-AIT trials, it is important to distinguish between the two major objectives of immunological outcome measurements: 1 To identify outcome measures that have predictive value for the probability of successful AIT that can be assessed at baseline. Achieving these objectives remains a challenge, in particular due to the absence of insufficient standardization of outcome measures employed in different clinical trials, and the high degree of uncertainty concerning the informative value of these different outcome measures.

Reduced basophil and mast cell reactivity are among the earliest changes that occur during AIT. This response typically occurs within the first months of AIT and precedes decreases in allergen specific-IgE levels and therefore cannot be attributed to that. During the initiation phase of FA-AIT, subthreshold dosing induces IgE internalization and actin rearrangement causing hyporesponsive effector cells.

Other mechanisms that may drive these early effects on include histamine receptor 2 upregulation in basophils leading to suppression of basophil activation 35 , and piecemeal basophil and mast cell degranulation occurring early during AIT, which may decrease their granule content and affect their threshold for activation Most studies reported reduced SPT reactivity after the start of therapy.

Changes in humoral responses during AIT include early increases in allergen-sIgE levels, which are observed during the first weeks and months of AIT, possibly resulting from an initial boost of allergen-specific B cell activation. This is followed by a reduction in allergen-sIgE and an increase in allergen-sIgG4 and IgA during the following months.

No consistent results emerged from these experiments, and changes in the production of TH2, TH1, and Treg-related cytokines differed substantially between studies. Increases in Treg frequencies were observed 1 year after the start of peanut OIT 67 , , while a temporary increase in the suppressive function of Tregs was reported in a small group of patients, suggesting a possible effect of FA-AIT on Treg suppressive capacity It should be emphasized that FA-AIT-induced immunologic changes may be temporary, even while patients receive continued maintenance treatment, highlighting inter-individual variability in immune suppression and clinical response.

The development of new technologies such as single-cell-omics approaches and high-dimensional platforms for detection of cell surface markers, allergen-specific antibodies as well as soluble biomarkers combined with sophisticated bioinformatics approaches, will enable the exploration of these mechanisms at an unprecedented level of detail potentially revealing novel candidates that may be used as immunological outcome measures in FA-AIT.

In this review, we critically appraised the utility of different immunological parameters as outcome measures in FA-AIT clinical trials. Based on these studies, we have summarized the following recommendations for biomarkers to be measured before, during and after FA-AIT. The biomarkers are also listed in Table 1.

The immunological parameters were grouped into four main categories: 1 functional tests, 2 humoral responses, 3 cellular responses, 4 cytokines, and other potential soluble biomarkers. Several studies found that lower allergen-induced CD63 expression at baseline correlated with successful AIT 63 , 99 and also with obtaining SU 98 , Most studies reported that allergen-induced CD63 expression was generally reduced during FA-AIT, both in patients showing clinical response to FA-AIT and non-responders 6 , 53 , 98 , 99 , except in one study where no change was observed The magnitude of the SPT response at baseline was not reported in any of the studies as having predictive value with respect to the clinical outcome of FA-AIT.

While some studies found no correlation 54 , , most studies observed a negative correlation between specific IgE levels and success of OIT 99 , , , , Most studies reported that increased specific IgG4 levels were associated with a successful outcome 53 , , , but one study observed no difference between groups and another study even found a reverse association However, an increased ratio of sIgG4:sIgE was consistently associated with successful outcome in several studies 99 , , , Studies in which allergen-specific IgA levels were determined found contradictory results for baseline levels of specific IgA and their correlation with a successful outcome of AIT , , However, it was consistently found that allergen-specific IgA levels increased during AIT and this increase was often more pronounced in responders than in non-responders , , There is a lack of data with respect to the clinical value of Treg assessments for predicting response to OIT, particularly SU.

It is a major limitation that all evidence is based on small studies with short follow-up periods, which are predominantly peanut OIT trials. Therefore, although Treg assessment seems promising to determine response to FA-AIT, there is a need for large-scale, long-term studies to properly assess the value of Tregs. Further studies of TH2 cells are needed to replicate these findings and confirm a clinical applicability. Only one study looked at cytokines in relation to clinical outcome and found no correlation with development of tolerance As it remains unclear whether these markers are predictive of efficacy, machine learning approaches have been attempted to compare mechanistic features of food allergies during OIT to determine the biological relevance of biomarkers and have led to promising clusters of biomarkers On the basis of currently available literature we conclude that the immunological parameters with the strongest evidence pertaining to both 1 predicting probability of successful FA-AIT and 2 monitoring the immune response to the intervention, both in the short-term i.

KK was employed by Danone Nutricia research. JG is part time employee of Nutricia research. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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