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Abstract

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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... There are various extraintestinal manifestations of celiac disease (CD), which are common and sometimes more prominent than readily recognized intestinal symptoms and signs, such as abdominal pain, chronic diarrhea, and malabsorption [1][2][3]. Cutaneous (dermatitis herpetiformis), hepatic (celiac hepatitis), neurologic (gluten ataxia), and musculoskeletal (arthritis and myopathies) manifestations are well recognized and widely described [1][2][3][4]. It has also been recognized that CD is associated with other autoimmune diseases, such as type 1 diabetes mellitus and autoimmune thyroiditis [1][2][3]. ...
... There are various extraintestinal manifestations of celiac disease (CD), which are common and sometimes more prominent than readily recognized intestinal symptoms and signs, such as abdominal pain, chronic diarrhea, and malabsorption [1][2][3]. Cutaneous (dermatitis herpetiformis), hepatic (celiac hepatitis), neurologic (gluten ataxia), and musculoskeletal (arthritis and myopathies) manifestations are well recognized and widely described [1][2][3][4]. It has also been recognized that CD is associated with other autoimmune diseases, such as type 1 diabetes mellitus and autoimmune thyroiditis [1][2][3]. ...
... Cutaneous (dermatitis herpetiformis), hepatic (celiac hepatitis), neurologic (gluten ataxia), and musculoskeletal (arthritis and myopathies) manifestations are well recognized and widely described [1][2][3][4]. It has also been recognized that CD is associated with other autoimmune diseases, such as type 1 diabetes mellitus and autoimmune thyroiditis [1][2][3]. Hematologic ...
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Extraintestinal manifestations of celiac disease (CD) should be considered, even in patients without typical intestinal symptoms. The aim of our study is to examine the literature regarding the occurrence of thrombotic events in CD, and to synthesize the data from case reports and case series. A systematic review of the literature was conducted by searching the Pub-Med/MEDLINE database, from the date of database inception to January 2022, to identify published cases and case series on this topic, in accordance with the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. A total of 55 cases were included in the study. The majority of patients were previously healthy individuals, with no comorbidities. In less than one-third of the cases (30.91%), the diagnosis of CD was established before the onset of thrombosis, while in the remaining cases (34.54%), thrombosis preceded the diagnosis or was diagnosed concomitantly with CD. The most common sites for thrombosis occurrence were hepatic veins (30.91%), while thrombosis of cerebral blood vessels, deep venous thrombosis of lower extremities, and pulmonary thromboembolism were less frequent. Thrombosis was most commonly isolated to one site only (78.18%). In 69.09% of cases (n = 38), some form of anticoagulation, along with a gluten-free diet, was initiated.
... Celiac disease (CD) is characterized by gluten intolerance resulting in intestinal damage [1]. Over the last two decades, several extra-intestinal manifestations of CD have been identified solidifying the status of CD as a true multi-system disorder [2]. The liver is a frequently affected organ in CD but estimate of involvement can be variable. ...
... A previous metaanalysis more than a decade ago attempted to determine the prevalence of elevated LC in CD; however, numerous studies since have added to the literature in this area [14]. The aim of this study was to conduct a systematic review and meta-analysis to (1) estimate the prevalence of elevated LC at the time of CD diagnosis, (2) determine the response to GFD, (3) and identify factors associated with elevation of LC (e.g. age at diagnosis, gender, and Marsh grading). ...
... Our main outcomes of interest were as follows: (1) Pooled rate of elevated LC in newly diagnosed CD. This was further categorized into rate in patients with biopsy-proven CD. (2) Pooled rate of resolution of elevated LC where resolution was defined as normalization back into the reference range of each individual study after initiation of GFD. (3) Pooled rate of positive celiac serology and biopsy in patients with unexplained elevation of LC. ...
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Aims Previous studies have reported conflicting results regarding prevalence of elevated LC (2–70%) in celiac disease (CD). This systematic review and meta-analysis assessed the prevalence of elevated LC at time of CD diagnosis and associated response to GFD. We also report the prevalence of CD in patients with unexplained elevation of LC. Methods Studies assessing LC (aspartate aminotransferase [AST] and alanine aminotransferase [ALT]) in CD patients were eligible. Studies with < 50 cases or in pediatric populations were excluded. Results In total, 20 studies assessing prevalence of elevated LC in 4,265 participants with newly diagnosed CD (mean age = 35.6 ± 6.5 years, 69.8% female) were included. Pooled prevalence of elevated LC was 18.7% (95% CI 13.8–24.8; I2 = 95%). Normalization of elevated LC was seen in 83.1% (95% CI 73.4–89.7; I2 = 79%, 11 studies) of patients after GFD. On meta-regression, age at CD diagnosis, gender, and Marsh grading were not associated with elevated LC. Among 979 participants (7 studies) with unexplained elevation of LC, pooled seroprevalence and biopsy-proven CD was 6.4% (95% CI 2.9–10.3, I2 = 71%) and 4.5% (95% CI 2.6–7.7, I2 = 67%), respectively. Conclusion Elevated LC are seen in approximately one-fifth of patients at CD diagnosis with majority normalizing after GFD. Age, gender, and degree of intestinal damage are not predictive of elevated LC. In the appropriate clinical scenario, liver tests should be serially monitored in CD reserving workup for additional causes after a trial of GFD. Patients with unexplained elevation of liver tests should be screened for celiac disease.
... A classic presentation of CeD would often include diarrhea, bloating, and deficiency of micronutrients such as iron, folate, or vitamin B12 (4). However, nonclassic and extraintestinal symptoms can also be part of the clinical spectrum, including hematologic, dermatologic, and neurologic manifestations (5). ...
Article
OBJECTIVES: Anemia and micronutrient deficiencies are common in newly-diagnosed patients with celiac disease (CeD). We aim to determine the prevalence and etiology of anemia in a cohort of patients with CeD in the U.S. and examine the effect of a gluten-free diet (GFD) on the laboratory parameters related to anemia in CeD.METHODS: We analyzed a prospectively-collected cohort of adults with biopsy-proven CeD followed in a specialized CeD center between January 2000 and June 2016. We used the level of hemoglobin (Hb) and micronutrients suggested by the World Health Organization (WHO) to establish the diagnosis of anemia or deficiencies. Information on demographics and laboratory parameters related to anemia and micronutrients were recorded at the time of diagnosis and on a GFD. A celiac expert nutritionist or gastroenterologist evaluated all patients.RESULTS: In 572 patients with laboratory evaluation before starting a GFD, about 25% presented with anemia at the time of diagnosis of CeD. Iron-deficiency was present in 50.8% of the cohort and in 78.8% of the anemic patients. Within the anemic population, 84.4% of female as compared to 58.3% of male patients (p=0.02) showed iron deficiency. Folate deficiency (23.2%), vitamin B12 deficiency (11%), and anemia of chronic diseases (7.8%) were also part of both genders' anemia etiology. Of the initially anemic patients, 81% and 89% normalized their Hb level within one year and two years of beginning a GFD, respectively. All patients received appropriate supplementation when needed.CONCLUSIONS: About twenty-five percent of individuals have anemia at CeD diagnosis. The anemia etiology included iron deficiency, vitamin deficiencies, and anemia of chronic diseases. The majority of patients will normalize their Hb levels and the anemia laboratory parameters one year after starting a strict GFD.
... The induction of celiac disease was directly related to gliadin, and innate immune regulation played an essential role in the occurrence of the disease, which would aggravate the disease while other complications exist [31,32]. With the discovery of the ATI component in the daily diet, it had been determined that the component would seriously interfere with the immune system of gluten intolerant individuals and worsen chronic diseases [22,33]. ...
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Celiac disease (CD) is an autoimmune intestinal disorder caused by the ingestion of gluten in people who carry the susceptible gene. In current celiac disease research, wheat gluten is often the main target of attention, neglecting the role played by non-gluten proteins. This study aimed to describe the effects of wheat amylase trypsin inhibitors (ATI, non-gluten proteins) and gliadin in BALB/c mice while exploring the further role of relevant adjuvants (cholera toxin, polyinosinic: polycytidylic acid and dextran sulfate sodium) intervention. An ex vivo splenocyte and intestinal tissue were collected for analysis of the inflammatory profile. The consumption of gliadin and ATI caused intestinal inflammation in mice. Moreover, the histopathology staining of four intestinal sections (duodenum, jejunum, terminal ileum, and middle colon) indicated that adjuvants, especially polyinosinic: polycytidylic acid, enhanced the villi damage and crypt hyperplasia in co-stimulation with ATI and gliadin murine model. Immunohistochemical results showed that tissue transglutaminase and IL-15 expression were significantly increased in the jejunal tissue of mice treated with ATI and gliadin. Similarly, the expression of inflammatory factors (TNF-α, IL-1β, IL-4, IL-13) and Th1/Th2 balance also showed that the inflammation response was significantly increased after co-stimulation with ATI and gliadin. This study provided new evidence for the role of wheat amylase trypsin inhibitors in the pathogenesis of celiac disease.
... The increased risk of CVD is attributed to a combination of chronic inflammation, nutrient deficiencies, and an adaptive immune response. 9 Previous reports have established that the presence of chronic inflammation and autoimmune disease are associated with accelerated atherosclerosis due to endothelial dysfunction. 3 The resultant injury to the endothelium results in compensatory changes leading to procoagulant properties and recruitment of macrophages and T-lymphocytes.. ...
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Background and Aims We aimed to study the impact of acute myocardial infarction (AMI) in patients with celiac disease (CD) Methods We used the National Inpatient Sample (NIS) 2011-2018 to identify patients 18 and older with a history of CD who presented with AMI using International Classification of Disease (ICD) 9 & 10. Primary outcome of interest was mortality differences in AMI patients with and without CD. Secondary outcomes were in-hospital length of stay (LOS), hospital costs, and coronary revascularization. Results A total of 2,287,840 weighted patients were included in this study with a principal diagnosis of AMI. Among this population, 183,027 weighted patients had a history of CD (0.08%), and 2,286,010 weighted patients had AMI without a history of CD (99.92%) (Table 2). Majority of AMI patients with and without CD were older (69.57 +/-13.21 vs. 67.08 +/-13.87), whites (92.55% vs. 75.39%), respectively. Patients with AMI and CD were more likely to be female compared to patients without CD (53.76% vs. 38.47%; p<0.05). In our study, we found that the difference for hospital charges [adjusted mean difference (aMD) $-2,644.7) was lower among AMI and CD, however, length of stay was higher among patients with CD (aMD 0.36 day), though they were not statistically significant (p>0.05) (Table 3). Both cohorts had higher recipients of Medicare and lower recipients of self-pay (Table 2). Our study also found that smoking was more prevalent among patients with CD, 12.14% vs patients without CD, 2.51%. Moreover, patients with CD who developed AMI had a lower adjusted odds of mortality compared to those without CD (adjusted odds ratio (aOR) 0.41; p<0.05) (Table 2). Patients with CD and AMI also had lower odds of coronary revascularization (aOR 0.80; p<0.05) (Table 2). In addition, we found that adults with CD had a lower odds of developing AMI (aOR 0.78; p< 0.05) (Table 2). Conclusion CD is a chronic disease leading to chronic inflammation and various nutrition related problems which can lead to increased morbid conditions. However, we found lower odds of AMI among patients with CD, as well as lower mortality and comorbidities related to AMI thus contradicting previous assumptions.
Article
Celiac disease (CD) is well recognized as a systemic, chronic autoimmune disease mainly characterized by gluten-sensitive enteropathy in genetically predisposed individuals but with various extraintestinal features. One of the affected organs in CD is the pancreas, consisting of both endocrine and exocrine alterations. Over the last decades there has been increasing interest in the pancreatic changes in CD, and this has been reflected by a great number of publications looking at this extraintestinal involvement during the course of CD. While pancreatic endocrine changes in CD, focusing on type 1 diabetes mellitus, are well documented in the literature, the relationship with the exocrine pancreas has been less studied. This review summarizes currently available evidence with regard to pancreatic exocrine alterations in CD, focusing on risk of pancreatitis in CD patients, association with autoimmune pancreatitis, prevalence and outcomes of pancreatic exocrine insufficiency in newly diagnosed and gluten-free diet treated CD patients, and the link with cystic fibrosis. In addition, we discuss mechanisms behind the associated pancreatic exocrine impairment in CD and highlight the recommendations for clinical practice.
Article
Introduction Coeliac disease and dermatitis herpetiformis are immune-mediated diseases triggered by the consumption of gluten in genetically predisposed individuals. These guidelines were developed to provide general practitioners, paediatricians, gastroenterologists, and other clinicians with an overview on the diagnosis, management and follow-up of coeliac patients and those with dermatitis herpetiformis. Methods Guidelines were developed by the Italian Societies of Gastroenterology. Following a systematic literature review, the Grading of Recommendations Assessment, Development and Evaluation methodology was used to assess the certainty of the evidence. Statements and recommendations were developed by working groups consisting of gastroenterologists and a paediatrician with expertise in this field. Results These guidelines provide a practical guidance for the diagnosis, management and follow-up of coeliac patients and dermatitis herpetiformis in children and adults, both in primary care and in specialist settings. We developed four sections on diagnosis, gluten-free diet, follow-up and risk of complications in adults, one section focused on diagnosis and follow-up in children and one on the diagnosis and management of dermatitis herpetiformis. Conclusions These guidelines may support clinicians to improve the diagnosis and management of patients with coeliac disease.
Article
Introducción: la enfermedad celíaca (EC) es una patología sistémica inmunomediada por el gluten en la dieta en personas genéticamente susceptibles con un amplio rango de manifestaciones clínicas, respuesta serológica específica y daño variable de la mucosa intestinal. Objetivo: revisar la fisiopatología, manifestaciones clínicas, diagnóstico, tratamiento, seguimiento y pronóstico de la EC, resaltando la importancia de reconocerla y proponer un algoritmo diagnóstico para la población colombiana. Materiales y métodos: revisión crítica de la literatura científica en las bases de datos Medline y buscadores específicos PUBMED, SCIENCE DIRECT, SCIELO, filtrando resultados a revisiones sistemáticas, metaanálisis, ensayos controlados aleatorios, ensayos clínicos y guías, con un total de 1209 artículos, de los cuales se priorizaron 53. Resultados y discusión: la prevalencia de la EC viene en aumento en países en vía de desarrollo. El diagnóstico tiene tres pilares fundamentales: identificación de casos de alto riesgo o sospecha por manifestaciones clínicas, perfil serológico de anticuerpos específicos y hallazgos histológicos característicos. El tratamiento se basa en dieta sin gluten, detección temprana de complicaciones y manejo de las alteraciones nutricionales. Conclusión: en Colombia no existen protocolos de diagnóstico y tratamiento de la EC, como tampoco una legislación clara con respecto al etiquetado de productos libres de gluten. Hay que establecer estrategias para impactar el curso natural de la enfermedad, las morbilidades asociadas y la calidad de vida de los pacientes.
Article
Background: Quinoa is a good gluten-free resource for food processing especially bread making which can improve and prevent the development of complications associated with celiac disease (CD). However, lack of gluten affected quinoa bread quality. Previous researches showed soy protein isolate (SPI) could improve gluten-free bread quality to some extent. Therefore, this study investigated the effects of SPI on the physical properties of quinoa dough and gluten-free bread quality characteristics. Results: Results showed that, with appropriate soy protein isolate (SPI) substitution, the farinograph properties of quinoa flour significantly improved (P<0.05). And the sample with 8% SPI substitution showed the better development time (DT, 3.30±0.20 min), stability time (ST, 8.80±0.10 min), softening degree (SD, 8.80±0.10 FU) which were close to those of wheat flour, although more water absorption (WA, 76.40±2.10%) was needed than wheat flour (66.30±3.10%). And the extensograph properties of quinoa flour also significantly improved after 8% SPI substitution (P<0.05). Furthermore, SPI substitution increased G' moduli of quinoa dough and decreased tanδ to some extent, providing better rheological properties nearly close to the wheat dough. SPI substitution also improved the quality and texture of quinoa bread and reduced the gap with wheat bread. When SPI substitution was 8%, the specific volume, hardness and springiness of quinoa bread were 2.29±0.05 ml/g, 1496.47±85.21 g and 0.71±0.03%, respectively. Conclusions: These results suggested that SPI substitution will be an effective way to develop higher-quality gluten-free bread. This article is protected by copyright. All rights reserved.
Article
Introduction: Anemia is a common complication of gastrointestinal (GI) disorders, with a prevalence up to 60% in celiac disease (CeD) and inflammatory bowel disease (IBD). Iron deficiency anemia (IDA) is the most prevalent form of anemia in these conditions, but chronic inflammation and vitamin B12 deficiency represent other common contributing mechanisms, especially in IBD. Areas covered: We discuss the pathogenesis of anemia in various medical GI disorders, the sometime problematic distinction between IDA, anemia of inflammation (AI) and the association of the two, and therapeutic and preventive measures that can be useful for the management of anemia in GI disorders. Unfortunately, with the exception of IDA and AI in IBD, large RCT concerning the treatment of anemia in GI disorders are lacking. Expert opinion: Anemia management strategies in GI disorders are outlined, with a focus on the main prevention, diagnostic and therapeutic measures. Specific problems and situations such as the role of gluten free diet for IDA treatment in CeD, the choice between oral and parenteral supplementation of iron or vitamin B12 in carential anemias, the use of endoscopic procedures to stop bleeding in intestinal angiodysplasia and preventive/treatment strategies for NSAID-associated GI bleeding are discussed.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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• Previous studies have suggested that a cereal-and milk-free diet may be beneficial to schizophrenics and that the gluten in regular diets is harmful to schizophrenics. In an effort to replicate these findings, with improved control vehicles, patients on a locked ward were placed on a cereal-and milk-free diet. Thirteen schizophrenics were given gluten-free peanut-flour supplementary cookies and 13 were given virtually identical cookies with gluten added. Tests and rating scales before and after the ten-day study period showed no greater improvement for those receiving the gluten-free cookies than for those receiving the gluten-added cookies. Contrary to expectations, the group receiving gluten-added cookies showed significantly greater improvement on Profile on Mood States measures of tension-anxiety and anger-hostility. Previous findings were not supported. Perhaps a longer time on the diet is required for any beneficial effects to appear.