56 WORLD GASTROENTEROLOGY NEWS JULY 2016 Editorial | Expert Point of View | Gastro 2016: EGHS-WGO | WDHD News | WGO & WGOF News | WGO Global Guidelines | Calendar of Events cally, IgG-based tests are useful for detecting CD in selected IgA-deficient patients. It is recommended to test also the level of the serum total IgA, as IgA deficiency is present in 2% of population. In case of selective IgA deficiency in a second blood samples, IgG-based tests should be performed (anti- DGP, anti-tTG or EMA) be-cause negative IgA antibodies will not be diagnostic. Patients having a low titer of antibodies, and having histologically normal mucosa, may be a false posi-tive test. The recommendation is to repeat the serology after six months while on a gluten-containing diet. If serology remains to be positive, these patients may be called potential CD and they should be followed. Majority of potential CD patients later develop the disorder. The long-term follow up of such patients is not well known. The intestinal (duodenal) biopsy has been considered as essential for diagnosing CD. CD predominantly affects the mucosa of the proximal small intestine, with damage gradu-ally decreasing in severity towards the distal small intestine. Under light microscopy, the most characteristic histological findings in patients with CD who are taking a gluten-contain-ing diet are: • Increased density of intraepithelial lymphocyte (>25/100 epithelial cells) • Crypt hyperplasia with a decreased villi/crypt ratio • Blunted or atrophic villi • Mononuclear cell infiltration in the lamina propria • Epithelial changes, including structural abnormalities in epithe-lial cells A modified Marsh classification for villous abnormalities is now widely used for assessing the severity of villous atrophy in clinical practice. It is highly recommended that the pathologists include report changes in a structured format, including the abovementioned histological changes, intraepithelial lymphocytes count, and interpretation in terms of modi-fied Marsh´s classification. A negative histological diagnosis may justify a second biopsy in selected patients who have positive autoantibodies, such as high titre anti-tTG, anti-DGP, and/ or endomysial antibodies. Patients with dermatitis herpetiformis having a positive serology may have normal histology. Upper endoscopy, performed for other causes than biopsy procuration, may show scalloping and/or flattening of duodenal folds, fissuring over the folds, and a mosaic pattern of mucosa of folds. Four to six biopsy samples must be taken from the second part of the duodenum, and from the duode-nal bulb, even if the mucosa appears normal. Biopsies must be taken when patients are on a gluten-containing diet (e.g. two slices of toast per day during four weeks). The intestinal biopsy is always nec-essary if the antibodies are negative. However (and according to very new concepts for children), biopsies may be omitted in the presence of symp-toms and signs of malabsorption, very high tTG-IgA titer (>10 time upper limit of normal), and positive EMA in a second blood sample. When the country resources are low, CD diagno-sis can rely on the sole presence of positive serology or even of a histol-ogy demonstrating intestinal damage, followed both by the good clinical response to GFD. Presumptive GFD followed by dramatic clinical improve-ment has been considered an indirect diagnostic tool for CD. However, this strategy (sometimes useful in under-privileged countries) must be strongly discouraged as the GFD will by time decrease the specific antibody levels and restore the damaged mucosa, not allowing a proper CD diagnosis. IMPORTANCE OF GENETICS FOR DIAGNOSIS OF CD AND POPULATION AT RISK First-degree and (to a lesser extent) second-degree relatives have an increased risk for CD. Because of the genetic predisposition, in HLA posi-tive people the onset of the disease or symptoms, on a gluten-containing diet, may occur at any time in life. On the converse, a negative HLA test will exclude the possibility of CD. All first-degree relatives should be screened for celiac disease. Approxi-mately 7% to 10% of first-degree rela-tives may develop CD; the risk varies considerably with their relationship with the index patient (the maximum risk in presence of the HLA haplotype DR3-DQ2, especially homozygotes, the minimum in presence of DR4- DQ8).1 Some other conditions (even if they may not be related pathogenically to CD) are considered at higher risk for CD. Therefore, there is the recom-mendation to test for CD the patients affected with type 1 diabetes mellitus, autoimmune thyroid disease, autoim-mune liver disease, Down syndrome, Turner syndrome, Williams syn-drome, and selective immunoglobulin A (IgA) deficiency. TREATMENT, THE GLUTEN-FREE DIET Patients with CD should not eat products containing wheat for the rest of their lives. Patients should consult a dietitian who is knowledgeable about gluten-free diets, especially during the first year after diagnosis. The safe limit of gluten intake varies across patients and has been considered to be 10-100 mg/day, although a subsequent study indicated that the upper limit should be closer to more like 50 mg/day. Celiac patients cannot eat the fol-lowing cereals and flours: semolina, spelt, triticale, wheat germ, wheat starch, wheat bran, bulgur, couscous, durum flour, farro, gluten flour,
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