الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Autoimmune and immune-related diseases (AID) are a heterogeneous group of disorders that occur in 7-9% of people worldwide. These disorders can be very debilitating and are relatively common, affecting roughly 1 in 20 individuals (5%).
The chronic nature of these relatively common disorders, lack of curative therapy and their associated morbidity and mortality, all make them represent a major threat to public health. These diseases are caused by an inappropriate response of the human immune system against self-antigens.
Autoimmunity develops over time, and preclinical autoimmunity precedes clinical disease by many years and can be detected in the peripheral blood in the form of circulating autoantibodies. Initially, symptoms of autoimmune disorders are vague and include fatigue, low-grade fever, muscle and joint aches, and malaise. They usually progress and become debilitating with significant morbidity.
Autoantibodies can be found in the serum of asymptomatic individuals who are prone to develop an autoimmune disease. These antibodies could be used for prognostic purposes or as a screening tool, as their appearance can precede the clinical manifestations of the disease by years.
Gastrointestinal complaints are common in patients with rheumatic diseases, and some authors have related inflammatory response in the gut of patients to rheumatic diseases.Although many of these complaints may be due to the use of medications such as NSAIDs, MTX or leuflonamide. They may also be caused by the disease itself.
Gluten sensitivity is a state of heightened immunological responsiveness to ingested gluten in genetically susceptible people. It represents a spectrum of diverse manifestations, of which gluten sensitive enteropathy (also known as celiac disease (CD) is one of many.
The classical presentation of CD includes diarrhoea, abdominal pain and nutritional deficiencies due to malabsorption.However, clinical symptoms could be misleading in most of the patients presenting subclinical forms with only minor gastroenterological symptoms, such as dyspepsia.
Gastrointestinal symptoms (i.e. diarrhoea, poor appetite, painful abdomen and weight loss or difficulty gaining weight) in older children are usually less dramatic. The classical description of a child with life-threatening malabsorption often is replaced by atypical presentation of celiac disease in older children.
In many patients, non-gastrointestinal symptoms including anaemia, osteoporosis, arthritis, and a number of neurological, psychiatric and dermatologic manifestations are the presenting complaint and should prompt the consideration of serologic testing. Establishing the diagnosis of subclinical celiac disease is of potential importance for three reasons: the danger of malignancy, the presence of unsuspected nutritional deficiencies and the occurrence of other autoimmune disorders.
An association between celiac disease and autoimmune rheumatologic diseases has been posited by various authors, but this possibility remains controversial, since these reports are usually based on descriptive case reports. Thus, most celiac disease patients show atypical symptoms and may remain undiagnosed, which makes screening justified in high-risk patients with autoimmune diseases. This collectively highlights the need to check for clinical evidence of celiac disease among patients suffering from juvenile rheumatic diseases and to confirm this by detection of presence of celiac disease antibodies (i.e. anti-tissue transglutaminase IgA and IgG) which is the most sensitive and highly specific in every patient with juvenile rheumatic diseases.
The aim of our study was to to screen for celiac disease antibodies (anti-tissue transglutaminase IgA and IgG auto-antibodies) in the serum of patients suffering from juvenile onset rheumatic diseases and comparing the results with normal subjects in general population.
This study was conducted on two groups. The first consisted of juvenile onset rheumatic patients diagnosed according to the relevant classification criteria for each disease.There were 23 with JIA,31 with juvenile SLE, 4 with juvenile scleroderma and 2 with Juvenile behcet disease.
The second consisted of twenty age and sex matched healthy subjects as control group.
All patients were subjected to the following:
• Detailed history taking with stress on age, sex, duration of the disease, and the history of clinical manifestations that diagnoses juvenile onset rheumatic disease with stress also on that all patients were not known to have CD and had no significant GIT symptoms.
• Clinical examination with throughout joint examination: The clinical examination stressed on the physical signs of rheumatic disease.
• Clinical assessment of juvenile rheumatic disease activity by the following:-
1. SLE disease activity by Systemic Lupus Erythermatosus Index (SLEDAI) score
2. JIA disease activity by DAS 28 –CRP score
3. SCLERODERMA disease activity by Modified Rodnan skin Score
4. BEHÇET’S disease activity by BEHÇET’S DISEASE ACTIVITY INDEX
• Laboratory evaluation of juvenile rheumatic disease which included the measurement of the levels of CBC, ESR, CRP, RF, ANA, anti-CCP.
• Laboratory screening for CD where the serum level of human recombinant anti-tTG autoantibodies (both IgA and IgG) was measured for all the subjects of both groups using Demeditec German kits.