Immunology Case Reports

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Commentary - Immunology Case Reports (2023) Volume 6, Issue 2

Autoimmune disorders including thyroiditis and celiac disease are predicted by autoantibodies

Stella Christopher*

Department of Immunology & Microbiology, Kings College, London, United Kingdom

*Corresponding Author:
Stella Christopher
Department of Immunology & Microbiology
Kings College, London
UK
E-mail:stellachristopher@kcl.ac.uk

Received:31-Mar-2023, Manuscript No. AAICR-23-90267; Editor assigned:03-Apr-2023, PreQC No. AAICR-23-90267(PQ); Reviewed:17-Apr-2023, QC No. AAICR-23-90267; Revised:22-Apr-2023, Manuscript No. AAICR-23-90267(R); Published:29-Apr-2023, DOI:10.35841/aaicr-6.2.139

Citation: Christopher S. Autoimmune disorders including thyroiditis and celiac disease are predicted by autoantibodies. Immunol Case Rep. 2023;6(2):139

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Introduction

One of the main characteristics of many disease processes is immune response activation. Immune reactions can either be beneficial, as in the case of viral diseases, or harmful, as in the case of autoimmune inflammatory diseases, or both. Both T and B cells are often activated during the immune response, and the latter produces antibodies that may be found in the sera and can be utilised to direct the clinical care of some disorders. Here, we concentrate on autoantibodies as potential illness indicators [1].

The presence, character, and strength of the immune response may all be reflected in antibodies. Autoantibodies can be used as indicators of disease activity since the immune response in autoimmune disorders is a component of the disease process itself. In disorders with a lengthy prodrome and no clinical signs, autoantibodies can be found. Autoantibodies have the ability to anticipate the activity of certain of these diseases, or the likelihood of clinical disease and the rate at which the disease will develop. Autoantibodies can be found in peripheral blood in organ-specific autoimmune illnesses including type 1 diabetes and thyroiditis years before the death of hormone-secreting cells results in overt clinical signs [2].

Thyroiditis

Thyroid autoantibodies can help with illness classification and prediction by reflecting disease activity and progression. Hypothyroidism (also known as Hashimoto thyroiditis) and hyperthyroidism are the two main clinical conditions linked to thyroid autoimmunity (Graves disease). Thyroid peroxidase and thyroglobulin are two of the main thyroid autoantigens in the former. Before the age of 20, autoantibodies to these antigens are uncommon, although they may indicate future clinical illness (primary hypothyroidism). Less than 5% of women who are thyroid peroxidase antibody-negative and have TSH levels less than 2 mU/l may get overt hypothyroidism during the next 20 years [3].

This probability rises logarithmically to 55% when the thyroid stimulating hormone is above 6 mU/l in thyroid peroxidase antibody-positive subjects, representing a 4.3% annual rate of progression, as opposed to just 2.6% and 2.1%, respectively, for those with only elevated TSH and peroxidase autoantibodies. Men, who are five times more likely than women to progress to overt disease, women over the age of 45, patients with thyroid stimulating hormone levels larger than 20 mU/l, and patients with thyroid antibody titers greater than 1:100,000 have all been linked to higher rates of progression. In these investigations, 10% of people with thyroid antibodies became thyroid antibody-negative later on, and mildly increased thyroid stimulating hormone recovered to normal in some subjects.

Celiac disease

An autoimmune condition called celiac disease causes whole or partial villous atrophy, which impairs intestinal absorption. Similar to diabetes, antibodies linked to celiac disease can anticipate the development of the clinical condition and be used to identify the root of malabsorption. Endomysial antibodies, as well as antibodies to gliadin and reticulin, are linked to the condition. However, the majority of the pertinent studies have been cross-sectional, testing established cases and controls; as a result, these estimates are not true estimates of prediction but of identification. Gliadin antibodies, both IgA and IgG, have been used in screening and have a sensitivity and specificity for prediction of celiac disease of 70–100%. More than 90% of cases can be diagnosed using serum reticulin antibodies, particularly IgA antibodies against R1-type reticulin. Endomysial antibodies, which recognise the enzyme tissue transglutaminase (tTG), which prefers gliadin as a substrate, are also very predictive of celiac disease [4].

It has been discovered that the tTG antibody has a sensitivity of 95.6% and a specificity of 99.5% for celiac disease. In one study, IgA endomysial and anti-reticulin antibodies were used for population screening. When sera were persistently positive for the antibodies over a 4-year period, the sensitivity for the antibodies was 100%, but the positive predictive value was only 27% when based on positivity at the initial screening. None of the individuals with transitory antibodies exhibited villous atrophy, which raises the intriguing possibility that this characteristic only appears after long-term immunological activity. In another study, IgA endomysial antibodies exhibited 100% positive predictive value for celiac disease as determined by small intestinal biopsy in patients referred by general practitioners with nonspecific abdominal symptoms. Along with type 1 diabetes and thyroiditis, a sizeable majority of people have temporary autoantibodies; nevertheless, when these autoantibodies persist, there is a considerable chance of developing clinical celiac disease. Autoantibodies linked to celiac disease are now often employed for disease prediction and diagnosis. In fact, the preferred treatment for celiac disease at the moment is to eliminate the antigen, gluten [5].

References

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  5. Mottonen T, Paimela L, Leirisalo-Repo M, et al. Only high disease activity and positive rheumatoid factor indicate poor prognosis in patients with early rheumatoid arthritis treated with “sawtooth” strategy. Ann Rheum Dis. 1998;57(9):533-9.

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