Coeliac disease is associated with chronic inflammation of the
small intestine which can lead to malabsorption of nutrients. 1 It is
an immune-mediated enteropathy caused by consuming gluten, a mix of proteins found in wheat, barley and rye. 2 It is a permanent condition
in
genetically
predisposed
individuals
causing
precipitation in small intestine as a result of ingestion of gluten. 3
Coeliac disease is common disorder among Caucasians of European ancestry with estimated prevalence of 0.5% to 1%. 2 It affects approximately 1 in a 100 in the European countries. 3 Gliadin is alcohol-soluble fraction of gluten which contains most of disease-producing components.2 Gluten is digested by luminal and brush-border enzymes into amino acids and peptides. 2 Both innate and adaptive immune mechanism involved.2 Some gliadin peptides induce epithelial cells to express IL-15 that triggers activation and proliferation of CD8+ intraepithelial lymphocytes. 2 NKG2D, a receptor for MIC-A and is expressed by the lymphocytes. 2 These lymphocytes become cytotoxic and kill enterocytes with surface MIC-A.2 Epithelial damage cause other gliadin peptides to cross the epithelium to be deamidated by tissue transglutaminase. 2 Deamidated gliadin peptides will interact with HLA-DQ2 or HLADQ8 on antigen-presenting cells and they will presented to CD4+ T cells.2 These T cells will produce cytokines causing tissue damage.2 Patients blood test shows that she has low ferritin and folate level but normal B12 level. Thus, the patient can be given folic acid and iron.3 Additional blood tests that can be used are anti-endomysial antibody (EMA) test and tissue transglutaminase (tTG) test. 3 In EMA test, an antibody made up of immunoglobulin by the coeliac
disease patient reacts against an antigen, endomysium which is a
body tissue that supports and joins cells together.3 tTG test looks for antibodies to tTG, an enzyme produced when coeliac-affected gut repairs and remodels its tissues.3 DEXA scan is a type of X-ray scanning which measures density of the bones.3 A T score of -2.6 shows that the patient has osteoporosis. Treatment may include vitamin D tablets to strengthen the bones.3 Regular exercise and stopping smoking can help to improve bone health.3 Hormone replacement therapy can be offered for postmenopausal women. 4 Another alternative is bisphosphonates that inhibit bone resoprtion. 4 However, steroids suppress circulating oestrogen and inhibit osteoblast maturation, synthetic ability, calcium absorption and increase urinary loss. 4 Hormone replacement therapy can increase risk of breast cancer after 5 years or 10 years treatment. 4
It is also reported that
bisphosphonates can cause nausea, diarrhoea and constipation. 4
Extra intestinal manifestation of coeliac disease in childhood are delayed growth and delayed puberty, developmental abnormalities of the enamel on teeth, anaemia and behavioural or learning difficulties.3 Adults with coeliac disease may have osteoporosis, joint or muscle pain, ataxia, arthritis, peripheral neuropathy, dermatitis herpetiformis and hyposplenism.3 Problems with fertility can occur in untreated coeliac disease. 3 Adolescent girls will have late puberty and late menstrual periods. 3 Malnourished women with chronic, untreated disease have scanty, irregular periods.3 Menopause may occur earlier than expected. 3 Pregnant women with untreated coeliac disease have an
increased risk of miscarriage and smaller babies. 3 The untreated
patient will also have a swollen abdomen, swollen ankles, weight loss around upper body and weakness.3 The villi are absent or lack and there are openings into vestibules at the top of the crypts.3 The microvilli are short and fragmented. 3 The coeliac mucosa looks flat in appearance or has a mosaic pattern.3 The individual cells of enterocytes more cube-like or flattened.3 The enterocytes are smaller and irregular.3 More intraepithelial lymphocytes than normal.3 It is caused by nonresponsive coeliac disease which is a clinical diagnosis defined by persistence of signs, symptoms typical of coeliac disease despite adherence to a gluten-free diet at least 6 months.5 It is caused by refractory coeliac disease. 5 The patient can be managed with nutritional supplementation and possibly low level immunosuppressive therapy.5 Refractory coeliac disease is defined as the persistence of severe villous atrophy on small intestinal biopsy despite strict gluten withdrawal for at least 6 months with no evidence of other pathology.5 The patients do not respond to treatment and they remain clinically unwell.3 Specialist follow-up is needed for a more serious progression.3 Steroids or immuno-suppressive drugs such as azathiopine, nutritional replacement with special supplements and additional vitamins and minerals are necessary.3 Sometimes, surgery to look directly at the intestine is also done. 3 Guidelines for osteoporosis in coeliac disease and inflammatory bowel disease
NICE guidelines : Coeliac disease: recognition, assessment and
management Google scholar NICE guidelines : Coeliac disease: recognition, assessment and management.
Because
it
recommends
how
heathcare
professionals can recognize, diagnose, treat patients with coeliac