scholarly journals Symptomatic Secondary Selective IgM Immunodeficiency in Adult Man with Undiagnosed Celiac Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-4
Author(s):  
Eli Magen ◽  
Viktor Feldman ◽  
Mishal Joseph ◽  
Hadari Israel

Selective IgM immunodeficiency (SIgMID) is a heterogeneous disorder with no known genetic background and may occur as a primary or a secondary condition. Celiac disease has been reported in association with several humeral immunodeficiencies, including isolated severe selective IgA deficiency, panhypogammaglobulinemia, and isolated combined IgA and IgM deficiency. There are only few reported cases of pediatric and adult patients with SIgMID and celiac disease. In this paper, we describe an adult patient with a symptomatic secondary SIgMID associated with undiagnosed celiac disease, with a resolution of clinical symptoms of immunodeficiency and serum IgM normalization following a gluten-free diet.

2009 ◽  
Vol 55 (1) ◽  
pp. 150-157 ◽  
Author(s):  
Daniela Basso ◽  
Graziella Guariso ◽  
Paola Fogar ◽  
Alessandra Meneghel ◽  
Carlo-Federico Zambon ◽  
...  

AbstractBackground: AGA IgA II and AGA IgG II have recently been suggested as reliable tools for celiac disease (CD) diagnosis. We compared their utility for diagnosis and monitoring CD in children with that of tTG IgA, an established CD marker.Methods: We studied a cohort of 161 CD and 129 control children in whom CD was histologically confirmed or ruled out. We followed 37 children with CD on a gluten-free diet for 12–84 months. In fasting sera, we measured AGA IgA II, AGA IgG II, and tTG IgA using ELISAs.Results: The best sensitivity (92.5%), specificity (97.6%), positive predictive value (98%), and negative predictive value (91.2%) were obtained using tTG IgA. AGA IgG II correctly identified 3 of 3 children with CD with total IgA deficiency who had negative AGA IgA II and tTG IgA results. In children <2 years old without total IgA deficiency, AGA IgG II and tTG IgA performed equally well (sensitivity 96.4% and specificity 100%). AGA IgA II, AGA IgG II, and tTG IgA concentrations diminished significantly (P < 0.0001) after 1 year of a gluten-free diet, reaching values below the cutoff in 87%, 70%, and 51% of cases, respectively.Conclusions: The best available index for diagnosing CD in children was tTG IgA. In infants <2 years old, AGA IgG II performed as well as tTG IgA in cases without total IgA deficiency and allowed detection of CD when total IgA was <0.06 g/L. Gluten-free diet monitoring can be achieved using any of the studied serum markers.


2018 ◽  
Vol 66 (4) ◽  
pp. 654-656 ◽  
Author(s):  
Roberta Mandile ◽  
Valentina Discepolo ◽  
Serena Scapaticci ◽  
Maria Rosaria Del Vecchio ◽  
Maria Antonia Maglio ◽  
...  

2020 ◽  
Vol 16 (3) ◽  
pp. 33-38
Author(s):  
O.Yu. Gubska ◽  
Yu.V. Chichula ◽  
A.K. Sizenko ◽  
L.M. Kupchik

Relevance. Although monotherapy with a gluten-free diet (BGD) for celiac disease is highly effective, it does not in all cases achieve complete remission of the disease. Therefore, an additional comprehensive examination of patients for the purpose of prescribing reasonable therapy is relevant. Objective: to study the causes of the persistence of clinical symptoms in patients with celiac disease who are on a gluten-free diet for 6 months. Materials and methods. Patients with celiac disease (n = 41) who were on a gluten-free diet (GFD) for 6 months were studied. The average age is 35.42 ± 0.45 years. Group 1 (n = 17) – patients who subjectively noted a positive dynamics of treatment and with a significant improvement in general condition, but without complete clinical remission. Group 2 (n = 24) – patients with unsatisfactory treatment results, no clinical effect from treatment, or weak positive dynamics on the background of GFD. The study included two stages: 1) assessment of patients' compliance and their diet (through the analysis of food diaries) in order to identify disorders of a gluten-free diet as the main cause of the persistence of clinical symptoms; 2) identification of other causes of the persistence of symptoms: exocrine pancreas insufficiency (EPI), lactase deficiency (LD) and the syndrome of increase bacterial growth (SIBR). A C13 triglyceride breath test (IRIS analyzer) was performed to diagnose EPI. To diagnose LD and SIBR in the small intestine, hydrogen breath tests (Micro H2-meter analyzer) were used – a test with lactose and D-xylose, respectively. Also, the titer of antibodies to tissue transglutaminase (TTG) to deaminated gliadin peptides (DPG) was determined in all patients, and their DPG/TTG ratio was calculated. Results. The main reason for the ineffectiveness of treatment is a violation of a gluten-free diet, found in 63.4% of subjects (incompletely formed mushy stool, polyfaeces, steatorrhea; recurrent abdominal pain, bloating, flatulence). Revision of food intake and elimination of sources of latent gluten from the diet of patients with celiac disease allowed to achieve complete serological remission (normalization of titers specific for celiac disease antibodies) in all patients, but complete clinical remission was achieved in only 34.6%. Therefore, it is concluded that there are other causes of incomplete remission of celiac disease associated with concomitant diseases of the digestive tract. Using carbon and hydrogen breath tests, it was found that, in addition to diet, the reasons for the lack of complete remission in patients with celiac disease are EPI (19%), SIBR in the small intestine (16%), LD (47%) and a combination of EPI with SIBR. Conclusion. The inclusion of respiratory tests (C13-triglyceride, hydrogen with lactose, and D-xylose) in a comprehensive examination of patients with celiac disease can significantly improve treatment outcomes and reduce the duration of clinical remission.


2008 ◽  
Vol 136 (Suppl. 2) ◽  
pp. 152-157
Author(s):  
Nedeljko Radlovic

Celiac disease presents a hereditary disorder of gluten tolerance, i.e. of gliadin and related prolamins of wheat, rye and barley. It primarily occurs in Caucasians (1:100-300), while it is considerably or exceptionally rare in colored races. It is particularly frequent in close relatives of the patient, as well as in persons with congenital IgA deficiency and in patients with autoimmune and some chromosomal diseases. The basis of the disease, as well as the key finding in its diagnostics, lies in small bowel inflammation, which withdraws on gluten free diet. Beside clinically manifest or non-manifest enteropathy, changes involving other organs and systems are also frequently seen. The diagnosis of the manifest form of the disease is based on characteristic pathohistological finding detected by the examination of small bowel mucosa in patients on standard diets and their clinical improvement after the introduction of gluten free diet. However, in the diagnosis of the asymptomatic form of the disease, it is necessary to perform enterobiopsy, which confirms the normalization of the appearance of small bowel mucosa in patients on the elimination diet. In children with gluten sensitive enteropathy detected in the first two years of life, as well as in cases in which mucosa samples taken on the first enterobiopsy do not have typical appearance or are inadequate for a reliable interpretation, a definite diagnosis is made based on biopsy finding during the provocation of gluten tolerance. As the quality of permanent teeth can be disturbed, this procedure is not suggested to be done before the completed age of 6 years, and due to adverse effects on the growth and development of the child, it should not be done during puberty. Due to incomplete sensitivity and specificity, the serological indicators of the disease do not have diagnostic value. Therefore, they are primarily used in the disclosure of asymptomatic and atypical forms of celiac disease, as well as in the assessment of the consistency of elimination diet in cases with already verified disease. In addition, the application of these tests makes easier passing the decision to perform pathohistological examination of small bowel mucosa in patients with provoked gluten tolerance, which also gives a more complete understanding into the remission of the disease during the initial phase of treatment.


Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2274
Author(s):  
Herbert Wieser ◽  
Ángela Ruiz-Carnicer ◽  
Verónica Segura ◽  
Isabel Comino ◽  
Carolina Sousa

Celiac disease (CD) is a chronic gluten-responsive immune mediated enteropathy and is treated with a gluten-free diet (GFD). However, a strict diet for life is not easy due to the ubiquitous nature of gluten. This review aims at examining available evidence on the degree of adherence to a GFD, the methods to assess it, and the barriers to its implementation. The methods for monitoring the adherence to a GFD are comprised of a dietary questionnaire, celiac serology, or clinical symptoms; however, none of these methods generate either a direct or an accurate measure of dietary adherence. A promising advancement is the development of tests that measure gluten immunogenic peptides in stools and urine. Causes of adherence/non-adherence to a GFD are numerous and multifactorial. Inadvertent dietary non-adherence is more frequent than intentional non-adherence. Cross-contamination of gluten-free products with gluten is a major cause of inadvertent non-adherence, while the limited availability, high costs, and poor quality of certified gluten-free products are responsible for intentionally breaking a GFD. Therefore, several studies in the last decade have indicated that many patients with CD who follow a GFD still have difficulty controlling their diet and, therefore, regularly consume enough gluten to trigger symptoms and damage the small intestine.


Author(s):  
Y.O. Trufanov ◽  
N.K. Svyrydova ◽  
M.M. Martynovsky

The objective of our research was to raise awareness of neurologists and family physicians about gluten ataxia and improve the diagnostic approaches. Methods. PubMed and Google Scholar resources were used to write the review article. Discussion. It is incredibly important not to overlook treatable courses of ataxia. One of these diseases is gluten ataxia. Early diagnosis and timely treatment (gluten-free diet) of gluten ataxia leads to a significant improvement of clinical symptoms and prevents their progression. Gluten ataxia is one of the most common and commonly misdiagnosed ataxia. Its prevalence among all ataxias is 15% and reaches 40% among all idiopathic sporadic ataxias (Hadjivassiliou M., Sanders D.D., Aeschlimann D.P., 2015). Keywords: gluten ataxia, celiac disease, gluten-related disorders.


1965 ◽  
Vol 48 (2) ◽  
pp. 155-172 ◽  
Author(s):  
I. Michael Samloff ◽  
John S. Davis ◽  
Eric A. Schenk

2016 ◽  
Vol 25 (4) ◽  
pp. 555-558
Author(s):  
Alina Popp

Background: Alveolar hemorrhage is a potentially life-threatening condition which is usually managed by the pulmonologist. When considering its etiology, there is a rare association that sets the disease into the hands of the gastroenterologist. Case presentation: We report the case of a 48 year-old female who was admitted to the intensive care unit for severe anemia and hemoptysis. On imaging, diffuse pulmonary infiltrates suggestive of alveolar hemorrhage were detected and a diagnosis of pulmonary hemosiderosis was made. She received cortisone therapy and hematologic correction of anemia, with slow recovery. In search of an etiology for the pulmonary hemosiderosis, an extensive workup was done, and celiac disease specific serology was found positive. After confirmation of celiac disease by biopsy, a diagnosis of Lane-Hamilton syndrome was established. The patient was recommended a gluten-free diet and at 6 months follow-up, resolution of anemia and pulmonary infiltrates were observed. Conclusion: Although the association is rare, celiac disease should be considered in a patient with idiopathic pulmonary hemosiderosis. In our case, severe anemia and alveolar infiltrates markedly improved with glucocorticoids and gluten-free diet. Abbreviations: APTT: activated partial thromboplastin time; BAL: bronchoalveolar lavage; CD: celiac disease; Cd: crypt depth; GFD: gluten-free diet; GI: gastrointestinal; IEL: intraepithelial lymphocyte; INR: international normalized ratio; IPH: idiopathic pu


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