Coeliac disease is a common disorder that can arise at any age and typically presents with a broad spectrum of symptoms. The disease is thought to be underdiagnosed, in part owing to the fact that coeliac disease is often characterized by associated conditions and extraintestinal manifestations that can misdirect and impede diagnosis. Some of these manifestations are direct consequences of autoimmunity, such as dermatitis herpetiformis or gluten ataxia, whereas others are indirectly related to inflammation and/or malabsorption including anaemia, osteoporosis, short stature and delayed puberty. Any organ from the central nervous system to joints, liver or teeth can be affected. In some cases, extraintestinal symptoms are the only clinical manifestations of coeliac disease or occur in conjunction with diarrhoea and malabsorptive symptoms. An increased awareness among medical practitioners of the variety of extraintestinal manifestations of coeliac disease is essential to improve diagnosis and treatment.
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... Symptoms of CD are highly variable and may occur at any age. Diseases like type I diabetes, Hashimoto's thyroiditis, Grave's disease, Sjogren's syndrome, Down syndrome, Turner syndrome, primary biliary cirrhosis, and neurologic disorders like unexplained peripheral neuropathy, epilepsy, and ataxia are also sometimes associated with CD (57)(58)(59)(60)(61)(62)(63). ...
... Determination of HLA-DQ2 and HLA-DQ8 types is useful along with histological findings (129). HLA-DQ2 and HLA-DQ8 molecules are associated with ∼95 and 5% CD patients, respectively (59). ...
Wheat is a major cereal crop providing energy and nutrients to the billions of people around the world. Gluten is a structural protein in wheat, that is necessary for its dough making properties, but it is responsible for imparting certain intolerances among some individuals, which are part of this review. Most important among these intolerances is celiac disease, that is gluten triggered T-cell mediated autoimmune enteropathy and results in villous atrophy, inflammation and damage to intestinal lining in genetically liable individuals containing human leukocyte antigen DQ2/DQ8 molecules on antigen presenting cells. Celiac disease occurs due to presence of celiac disease eliciting epitopes in gluten, particularly highly immunogenic alpha-gliadins. Another gluten related disorder is non-celiac gluten-sensitivity in which innate immune-response occurs in patients along with gastrointestinal and non-gastrointestinal symptoms, that disappear upon removal of gluten from the diet. In wheat allergy, either IgE or non-IgE mediated immune response occurs in individuals after inhalation or ingestion of wheat. Following a lifelong gluten-free diet by celiac disease and non-celiac gluten-sensitivity patients is very challenging as none of wheat cultivar or related species stands safe for consumption. Hence, different molecular biology, genetic engineering, breeding, microbial, enzymatic, and chemical strategies have been worked upon to reduce the celiac disease epitopes and the gluten content in wheat. Currently, only 8.4% of total population is affected by wheat-related issues, while rest of population remains safe and should not remove wheat from the diet, based on false media coverage.
... Systemic manifestations may include infertility, dermatitis herpetiformis, and malignancy. 4,5 While gluten avoidance is necessary in CeD, achieving a strict gluten-free diet (GFD) is difficult, because gluten contamination appears to be common when using objective measures of gluten exposure.  Therefore, many patients attempting to follow a GFD still experience signs and symptoms of active disease. ...
BACKGROUND & AIMS
Gluten challenge is used to diagnose celiac disease (CeD) and for clinical research. Sustained gluten exposure reliably induces histological changes but is burdensome. We investigated the relative abilities of multiple biomarkers to assess disease activity induced by two gluten doses, and aimed to identify biomarkers to supplement or replace histology.
In this randomized, double-blind, 2-dose gluten-challenge trial conducted in two US centers (Boston, MA), 14 adults with biopsy-proven CeD were randomized to 3 g or 10 g gluten/day for 14 days. The study was powered to detect changes in villous height:crypt depth (Vh:Cd), and stopped at planned interim analysis on reaching this endpoint. Additional endpoints included gluten-specific cluster of differentiation (CD)4 T-cell analysis with human leukocyte antigen (HLA)-DQ2-gluten tetramers and enzyme-linked immune absorbent spot (ELISpot), gut-homing CD8 T cells, interleukin (IL)-2, symptoms, video capsule endoscopy (VCE), intraepithelial leukocytes (IELs), and tissue multiplex immunofluorescence.
All assessments showed changes with gluten challenge. However, time to maximal change, change magnitude, and gluten dose–response relationship varied. Vh:Cd, VCE enteropathy score, ELISpot, gut-homing CD8 T cells, IEL counts, and HLA-DQ2-restricted gluten-specific CD4 T cells showed significant changes from baseline only at 10 g gluten; symptoms were significant at 3 g. Symptoms and plasma IL-2 levels increased significantly or near significantly at both doses. IL-2 appeared to be the earliest, most sensitive marker of acute gluten exposure.
Modern biomarkers are sensitive and responsive to gluten exposure, potentially allowing less invasive, lower-dose, shorter-duration gluten ingestion. This work provides a preliminary framework for rational design of gluten challenge for CeD research.
... Classical gastrointestinal symptoms are chronic diarrhea, abdominal pain, vomiting, and steatorrhea. Extraintestinal manifestations include chronic fatigue, night blindness, anemia, osteoporosis, thyroid dysfunction, and reproductive disease (93) and are usually caused by generalized malabsorption of essential nutrients, e.g., vitamins and minerals. Slow growth rates and delayed sexual maturation are known complications of CD in children and adolescents. ...
Wheat-based foods have been staple foods since about 10,000 years and constitute a major source of energy, dietary fiber, and micronutrients for the world population. The role of wheat in our diet, however, has recently been scrutinized by pseudoscientific books and media reports promoting the overall impression that wheat consumption makes people sick, stupid, fat, and addicted. Consequently, numerous consumers in Western countries have started to question their dietary habits related to wheat consumption and voluntarily decided to adopt a wheat-free diet without a medical diagnosis of any wheat-related disorder (WRD), such as celiac disease, wheat allergy, or non-celiac gluten sensitivity. The aim of this review is to achieve an objective judgment of the positive aspects of wheat consumption as well as adverse effects for individuals suffering from WRDs. The first part presents wheat constituents and their positive nutritional value, in particular, the consumption of products from whole-grain flours. The second part is focused on WRDs that affect predisposed individuals and can be treated with a gluten-free or -reduced diet. Based on all available scientific knowledge, wheat consumption is safe and healthy for the vast majority of people. There is no scientific evidence to support that the general population would benefit from a wheat-free diet.
... 4 Systematic CD manifestations include anaemia, arthritis, dermatitis herpetiformis, delayed puberty, infertility, peripheral neuropathy and decreased bone density. 5 Complications of untreated CD may include psychiatric and neurologic disorders including ataxia, epilepsy and seizures, schizophrenia and depression. 6 Iron-deficiency anaemia is the most common non-gastrointestinal manifestation of CD. ...
Background & Aims
It is not clear whether alterations in the intestinal microbiota of children with celiac disease cause the disease or are a result of disease and/or its treatment with gluten-free diet (GFD).
We obtained 167 fecal samples from 141 children (20 with new-onset celiac disease, 45 treated with a GFD, 57 healthy children, and 19 unaffected siblings of children with celiac disease) in Glasgow, Scotland. Samples were analyzed by 16S rRNA sequencing and diet-related metabolites were measured by gas chromatography. We obtained fecal samples from 13 of the children with new-onset CD after 6 and 12 months on GFD. Relationships between microbiota with diet composition, gastrointestinal function, and biomarkers of GFD compliance were explored.
Microbiota α diversity did not differ among groups. Microbial dysbiosis was not observed in children with new-onset celiac disease. In contrast, 2.8% (Bray-Curtis dissimilarity index, P=.025) and 2.5% (UniFrac distances, P=.027) of the variation in microbiota composition could be accounted for by the GFD. Between 3% to 5% of all taxa differed among all group comparisons. Eleven distinctive operational taxonomic units composed a microbe signature specific to celiac disease with high diagnostic probability. Most of the operational taxonomic units that differed between patients on GFD with new-onset celiac disease vs healthy children were associated with nutrient and food group intake (from 75% to 94%), and with biomarkers of gluten ingestion. Fecal levels of butyrate and ammonia decreased during the GFD.
Although several alterations in the intestinal microbiota of children with established celiac disease appear to be effects of a GFD, there are specific bacteria that are distinct biomarkers of celiac disease. Studies are needed to determine whether these bacteria contribute to pathogenesis of celiac disease.
... The clinical manifestations of CD can be directly related to autoimmunity or can indirectly derive from intestinal inflammation and/or malabsorption . ...
Celiac disease (CD) is an autoimmune disorder characterized by intolerance to dietary gluten in genetically predisposed subjects. Iron deficiency anemia (IDA) is a common sign in CD, being the only abnormality in approximately 40% of celiac patients. A multifactorial etiology leads to IDA in CD. The two main causes are the villous atrophy of the mucosa at the site of iron absorption (the duodenum) and the resulting inflammation, which triggers the mechanism that leads to the anemia of chronic disease. Until now, it has been unclear why some patients with CD continue to have IDA despite a careful gluten-free diet (GFD) and the normalization of villous atrophy. Furthermore, some celiac patients are refractory to oral iron supplementation despite the healing of the mucosa, and they thus require periodic intravenous iron administration. The Marsh classification evaluates the degree of inflammation and villous atrophy, but it does not assess the possible persistence of ultrastructural and molecular alterations in enterocytes. The latter was found in CD in remission after adopting a GFD and could be responsible for the persistently reduced absorption of iron and IDA. Even in non-celiac gluten sensitivity, anemia is present in 18.5–22% of patients and appears to be related to ultrastructural and molecular alterations in intestinal microvilli. It is possible that a genetic component may also play a role in IDA. In this review, we evaluate and discuss the main mechanisms of IDA in CD and the possible causes of its persistence after adopting a GFD, as well as their therapeutic implications.
... Although CD is primarily a disorder of the small intestine, it can affect other systems and has been associated with a wide spectrum of extraintestinal manifestations, including skin, liver, and neurological disturbances, which putatively result from immune-mediated mechanisms and/or malabsorption of vitamins and elements . In recent decades, the clinical presentation of CD tends to shift to a more mild presentation, with its extraintestinal manifestations being more prevalent than gastrointestinal symptoms. ...
Celiac disease (CD) is a chronic intestinal immune-mediated disease occurring in genetically susceptible individuals who are exposed to gluten. Although it primarily affects the small intestine, CD has been associated with a wide spectrum of extraintestinal manifestations, including thromboembolism and cardiovascular events. The risk of ischemic stroke, myocardial infarction, and thromboembolism, such as deep vein thrombosis and pulmonary embolism, is higher in patients with CD, while there is accumulating evidence that gluten-free diet in CD patients decreases the risk of these complications. The pathogenetic mechanism of increasing hypercoagulability in CD is multifactorial and involves hyperhomocysteinemia due to malabsorption of vitamins B12, B6, and folic acid; endothelial dysfunction; acceleration of atherosclerosis; chronic inflammation; thrombocytosis; and thrombophilia. Therefore, in cases of thromboembolic complications and cardiovascular disease of obscure etiology, clinicians’ awareness of possible celiac disease is warranted.
... Nagusiki heste meheari eragiten dio, bertako bilioen atrofia eta hantura sortuz eta paretaren iragazkortasuna handituz, modu horretan liseri hodiko sintomak eraginez. Hala ere, beste organo batzuk kaltetu daitezke eta hestez kanpoko sintomak eragin ditzake, hala nola, anemia, dermatitisa, neuropatíak, osteoporosia edo antzutasuna (51,52). Hesteko biloak erasanda daudenez, zaila egiten da elikagaietatik datozen bitaminak (azido folikoa, besteak beste) eta mineralak (hala nola, burdina eta kaltzioa) xurgatzeko gaitasuna mantentzea. ...
FODMAPak, modu naturalean esnekietan eta landare jatorriko zenbait elikagaietan aurki daitezkeen konposatuak, zenbait heste gaixotasunetako sintomekin erlazionatu dira. Kate laburreko karbohidrato hartzigarri hauek zuntzaren antzeko efektuak eragiten dituzte, ur-atxikipena eragiten dute eta koloneko mikrobiotak hartzitzen dituzte, kate laburreko gantz azidoak eta gasak sortuz. Azken urteetan egin diren ikerketetan ikusi da FODMAP kontsumoak beherakoa eta flatulentzia moduko sintomak eragiten dituela heste funtzioaren aztoratzea duten gaixotasunetan, Heste Narritakorraren Sindromean, Hesteetako Hanturazko Gaixotasunean eta Zeliakian esaterako. Horregatik, FODMAP baxuko dieta eraginkorra dela ikusi da gaixotasun horien maneiuan, baina dietaren ezarpena zaila da. FODMAPen iturri diren elikagai asko murriztearen ondorioz dieta desorekatu eta gabezia nutrizionalak ager daitezke eta beraz, dietaren maneiu egokirako Dietista-Nutrizionista baten kontrola ezinbestekoa da. Nahiz eta dieta epe laburrean heste sintomak murrizteko eraginkorra izan, epe luzera dituen ondorioak jakiteko ikerketa gehiagoren beharra dago, dieta oso murriztailea izan baitaiteke.
... CD patients can present a certain grade of mucosal atrophy and crypt hyperplasia, including an increase of the intra-epithelial lymphocytes infiltrate . Besides classical intestinal manifestations of the disease (diarrhea, malabsorption, anemia, weight loss, growth delay, etc.), there is a wide range of possible extra-intestinal symptoms including bone, liver, skin and neurological manifestations [4,5]. An important hallmark of CD is the presence of an auto-immune response towards one main auto-antigen represented by the enzyme TG2 . ...
Celiac disease (CD) is a common intestinal inflammatory disease involving both a genetic background and environmental triggers. The ingestion of gluten, a proteic component of several cereals, represents the main hexogen factor implied in CD onset that involves concomitant innate and adaptive immune responses to gluten. Immunogenicity of some gluten sequences are strongly enhanced as the consequence of the deamidation of specific glutamine residues by type 2 transglutaminase (TG2), a ubiquitous enzyme whose expression is up-regulated in the intestine of CD patients. A short gluten sequence resistant to intestinal proteases, the α-gliadin peptide 31-43, seems to modulate TG2 function in the gut; on the other hand, the enzyme can affect the biological activity of this peptide. In addition, an intense auto-immune response towards TG2 is a hallmark of CD. Auto-antibodies exert a range of biological effects on several cells, effects that in part overlap with those induced by peptide 31-43. In this review, we delineate a scenario in which TG2, anti-TG2 antibodies and peptide 31-43 closely relate to each other, thus synergistically participating in CD starting and progression.
The treatment for coeliac disease (CD) has a considerable psychological impact on patients, which may vary depending on subjects and clinical characteristics. The aim of this study was to describe the quality of life (QoL) in CD patients during follow-up, evaluating which factors can influence it. Patients with CD who consecutively visited the outpatient clinic of CD Unit of the University Hospital of Padua from January to September 2019 were enrolled. Demographics and clinical information were collected, and all patients were asked to answer the CD-QoL and Biagi's validated questionnaires. Student's t-test and chi-square test were used to compare the continuous and categorical variables, respectively. One hundred patients were enrolled (86 females, mean age at test ± SD: 39.73 ± 13.51; mean age at diagnosis ± SD: 33.09 ± 12.92), with 61% of them having been diagnosed with CD within the previous 5 years. At the time of diagnosis, 43 CD patients reported classical CD presentation, 32 non-classical features, 16 only anaemia and 9 were asymptomatic. The mean CD-QoL value was overall high (80.54 ± 11.91). We found that the "health concerns" subscale score was significantly lower in subjects aged more than 35 years compared to younger subjects (p = 0.03). We also observed that the CD-QoL score in gluten-free diet (GFD)-adherent patients tended to be higher compared to subjects who were non-compliant, with a significantly higher percentage of patients with low score for the "dysphoria" subscale (p = 0.05). This study showed an overall good QoL in subjects on a GFD. However, subjects older and non-compliant to GFD appear to experience more health concerns and suffer from dysphoria, respectively.
Celiac disease is a multiform, challenging condition characterized by extremely variable features. Our goal was to define clinical, serological and histopathological findings in a large cohort of celiacs diagnosed in a single referral center.
From January 1998 to December 2012, 770 patients (599 females, median age 36 years, range 18-78 years) were diagnosed as celiacs at St.Orsola-Malpighi Hospital (Bologna, Italy). The clinical phenotypes were classified as: 1) classical (malabsorption syndrome); 2) non-classical (extraintestinal and/or gastrointestinal symptoms other than diarrhea); 3) subclinical. Serology, duodenal histology, comorbidities, response to gluten-free diet and complications were evaluated.
Disease onset was symptomatic in 610 patients (79%), while 160 celiacs showed a subclinical phenotype. In the symptomatic group the non-classical prevailed over the classical phenotype (66% vs 34%). Diarrhea was found in 27%, while other gastrointestinal manifestations were bloating (20%), aphthous stomatitis (18%), alternating bowel habit (15%), constipation (13%) and gastroesophageal reflux disease (12%). Extraintestinal manifestations included osteopenia/osteoporosis (52%), anemia (34%), cryptogenic hypertransaminasemia (29%) and recurrent miscarriages (12%). Positivity for IgA tissue transglutaminase antibodies was detected in 97%. Villous atrophy was found in 87%, while 13% had minor lesions consistent with potential celiac disease. A large proportion of patients showed autoimmune disorders, i.e. autoimmune thyroiditis (26.3%), dermatitis herpetiformis (4%) and diabetes mellitus type 1 (3%). Complicated celiac disease was very rare.
Our study demonstrates that the clinical profile of celiac disease changed over time with an increasing rate of non-classical and subclinical phenotypes.
Celiac disease is an autoimmune enteropathy caused by gluten in genetically predisposed individuals. In celiac disease, adaptive and innate immune activation results in intestinal damage and a wide range of clinical manifestations. In the past, celiac disease was thought to result in signs and symptoms solely related to the gastrointestinal tract. Now, more than half of the adult population presents with extra-intestinal manifestations that can also be expected to improve on a gluten-free diet. For this reason, it is recommended that physicians have a low threshold of suspicion for celiac disease. Current knowledge of the immune pathogenesis of this autoimmune disease has served as a catalyst for the development of novel diagnostic tools and therapeutics.
Over the years, highly sensitive and specific serological assays, in addition to genetic markers, have been found to target specific steps in the cascade pathway of celiac disease. Also the advent of the gluten challenge has enabled experts to design diagnostic algorithms and monitor clinical responses in clinical trials. The gluten challenge has provided substantial benefit in the advance of novel therapeutics as an adjuvant treatment to the gluten free diet. Generally, a strict gluten-free diet is highly burdensome to patients and can be limited in its efficacy. Alternative therapies—including gluten modification, modulation of intestinal permeability and immune response—could be central to the future treatment of celiac disease.
Studies of leukocyte telomere length (LTL) and adiposity have produced conflicting results, and the relationship between body mass index (BMI) and telomere length throughout life remains unclear. We therefore tested association of adult LTL measured in 5,598 participants with: i) childhood growth measures (BMI and age at adiposity rebound (AR)); ii) change in BMI from childhood to adulthood and iii) adult BMI, waist-to-hip ratio (WHR), body adiposity index (BAI). Childhood BMI at AR was positively associated with LTL at 31 years in women (P = 0.041). Adult BMI and WHR in both men (P = 0.025 and P = 0.049, respectively) and women (P = 0.029 and P = 0.008, respectively), and BAI in women (P = 0.021) were inversely associated with LTL at 31 years. An increase in standardised BMI between early childhood and adulthood was associated with shorter adult LTL in women (P = 0.008). We show that LTL is inversely associated with multiple measures of adiposity in both men and women. Additionally, BMI increase in women from childhood to adulthood is associated with shorter telomeres at age 31, potentially indicating accelerated biological ageing.
Celiac disease (gluten sensitive enteropathy) is a common disorder affecting both children and adults. As many people with celiac disease do not present with the classic malabsorptive syndrome, delays in diagnosis are common. Dental enamel defects and recurrent aphthous ulcers, which may occur in patients with celiac disease, may be the only manifestation of this disorder. When dentists encounter these features, they should enquire about other clinical symptoms, associated disorders and family history of celiac disease. In suspected cases, the patient or family physician should be advised to obtain serologic screening for celiac disease and, if positive, confirmation of the diagnosis by intestinal biopsy. Dentists can play on important role in identifying people who may have unrecognized celiac disease. Appropriate referral and a timely diagnosis can help prevent serious complications of this disorder.
Iron deficiency anaemia in men and postmenopausal women is most commonly caused by gastrointestinal blood loss or malabsorption. Examination of both the upper and lower gastrointestinal tract is therefore an important part of the investigation of patients with such anaemia. In the absence of overt blood loss or any obvious cause, all patients should have upper gastrointestinal endoscopy, including small bowel biopsy, and colonoscopy or barium enema to exclude gastrointestinal malignancy. Further gastrointestinal investigation is only warranted in transfusion dependent anaemia or where there is visible blood loss. Treatment of an underlying cause will cure the anaemia but even when no cause is detected the long term outlook is good.
Guidelines recommend routine screening of liver function tests (LFTs) in patients diagnosed with celiac disease (CD). However, little is known about the prevalence of liver disorders in CD outside of Europe. Our aims were to estimate the prevalence of LFT abnormalities in CD and to evaluate the effect of a gluten-free diet (GFD) on LFTs.
Adult patients with biopsy-proven CD were identified from a prospectively maintained database and matched with healthy controls. LFT levels for women and men were defined as abnormal based on the Third National Health and Nutrition Examination Survey (NHANES III) criteria. Data on demographics, coexisting liver diseases, and laboratory work-ups including aspartate transaminase (AST) and alanine transaminase (ALT) values at the time of diagnosis and on a GFD were recorded. Subsequently, data from this cohort were compared with data from 7,789 individuals participating in the National Health and Nutrition Examination Survey, 2009-2010. Univariate logistic regression, Wilcoxon signed-ranks, Student's t-test, χ(2), and Fischer's exact test were used for statistical analysis.
In 463 CD patients with ALT or AST levels at the time of CD diagnosis, 40.6% had elevated LFTs compared with 24.2% of treated CD patients (P<0.001) and 16.6% of matched controls (P<0.001). Similarly, 36.7% of CD patients on the NHANES database had abnormal ALT values compared with 19.3% of non-celiac patients (P=0.03). Approximately, 78.6% of CD patients with elevated LFTs at diagnosis normalized LFTs on a GFD after a mean duration of 1.5±1.5 years.
Forty percent of individuals will have elevated LFTs at CD diagnosis; however, the majority will normalize with standard CD therapy. LFTs should be checked in all patients with CD and coexisting liver disorder should be considered in patients whose LFTs have not improved within a year on a GFD.Am J Gastroenterol advance online publication, 7 July 2015; doi:10.1038/ajg.2015.192.
The nosology and aetiology of sporadic adult‐onset ataxia are poorly understood. The aim of the present study was to answer the following questions: (i) How many sporadic ataxia patients have a genetic cause? (ii) How many sporadic ataxia patients suffer from multiple system atrophy (MSA)? (iii) Is there a specific association between sporadic ataxia and serum anti‐glutamic acid decarboxylase (GAD) or antigliadin antibodies? and (iv) What are the clinical features of patients with unexplained sporadic ataxia? The study was performed in 112 patients who met the following inclusion criteria: (i) progressive ataxia; (ii) onset after 20 years; (iii) informative and negative family history (no similar disorders in first‐ and second‐degree relatives; parents older than 50 years); and (iv) no established symptomatic cause. Thirty‐two patients (29%) met the clinical criteria of possible (7%) or probable (22%) MSA. The Friedreich’s ataxia mutation was found in five patients (4%), the spinocerebellar ataxia (SCA) 2 mutation in one (1%), the SCA3 mutation in two (2%) and the SCA6 mutation in seven (6%). The disease remained unexplained in 65 patients (58%). We did not detect anti‐GAD antibodies in any of our patients. Antigliadin antibodies were present in 14 patients, 10 patients with unexplained ataxia (15%) and 4 patients with an established diagnosis (9%). Patients with unexplained sporadic ataxia had a median disease onset of 56.0 years. Decreased vibration sense (62%), decreased or absent ankle reflexes (40%), increased ankle reflexes (39%), dysphagia (38%) and extensor plantar responses and/or spasticity (34%) were the most frequent extracerebellar symptoms. Compared with MSA, disease progression was significantly slower.
The prevalence of hypertransaminasemia and the effect of gluten-free diet (GFD) were evaluated in 158 consecutive adult celiac patients, 127 women and 31 men, aged 18 to 68 years (mean, 32). At diagnosis, 67 patients (42%) had raised aspartate and/or alanine transaminase levels (AST and ALT; mean, 47 IU/L, range, 30 to 190; and 61 IU/L, range, 25 to 470, respectively), whereas 91 patients had normal liver function tests (LFT). Patients with and without hypertransaminasemia were comparable for epidemiological data, body mass index (18.5 vs. 19.6), and severity of intestinal histological involvement. All patients were given a strict GFD and were followed for 1 to 10 years (median, 4). At 1 year, a highly significant improvement in intestinal histology was observed in both groups (P < .0001). In the 67 patients with raised transaminase levels body mass index (BMI) also increased significantly (from 18.5 to 21.0, P < .001), and transaminase levels normalized in 60 (95%). In the other seven cases liver biopsy showed fatty infiltration in two and chronic active hepatitis (CAH) in the other five, related to chronic infection with hepatitis B virus in three and hepatitis C virus in one, and to autoimmune type in the fifth. We conclude that in adult celiac patients elevated serum transaminases are a frequent finding and normalize in most cases after GFD. When they persist, liver biopsy is mandatory to further investigate hepatic involvement, which in our series was mainly attributable to CAH.
Objectives: To assess whether children with autism are more likely to have a history of gastrointestinal disorders than children without autism.
Design: Nested case-control study.
Setting: UK General Practice Research Database.
Subjects: Children born after 1 January 1988 and registered with the General Practice Research Database within 6 months of birth.
Outcome measures: Chronic inflammation of the gastrointestinal tract, coeliac disease, food intolerance, and recurrent gastrointestinal symptoms recorded by the general practitioner.
Results: 9 of 96 (9%) children with a diagnosis of autism (cases) and 41 of 449 (9%) children without autism (matched controls) had a history of gastrointestinal disorders before the index date (the date of first recorded diagnosis of autism in the cases and the same date for controls). The estimated odds ratio for a history of gastrointestinal disorders among children with autism compared with children without autism was 1.0 (95% confidence interval 0.5 to 2.2).
Conclusions: No evidence was found that children with autism were more likely than children without autism to have had defined gastrointestinal disorders at any time before their diagnosis of autism.