Celiac Disease: Pathophysiology, Clinical Manifestations, and Associated Autoimmune Conditions

Barker, Jennifer M.; Liu, Edwin

doi:10.1016/j.yapd.2008.07.001

Cited by 161 publications

(155 citation statements)

References 66 publications

(70 reference statements)

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“…Neurological abnormalities including hypotonia, developmental delay, learning disorders and ADHD, headache, and cerebellar ataxia have also been reported to be more common in children with CD (Zelnik et al 2004). Patients with CD have a slightly increased risk for developing gastrointestinal malignancies such as adenocarcinoma (Barker and Liu 2008). As noted above, complications from CD may also include reduced fertility and increased mortality (Corrao et al 2001;Soni and Badawy 2010).…”

Section: Presentation Pathophysiology and Genetics Of CDmentioning

confidence: 98%

“…Only since the 1950s have clinicians recognized that a gluten-free diet is an effective treatment (Barker and Liu 2008). Before that time, diagnosed and undiagnosed CD reduced the health and fitness of sufferers, with juvenile cases leading to malnutrition or death, and adult cases causing wasting, lack of adequate nutrition, greater susceptibility to infection, and direct reductions in fertility (Corrao et al 2001;Soni and Badawy 2010).…”

Section: Celiac Disease (Cd) Is a Multifactorial Chronic Inflammatorymentioning

confidence: 99%

“…The clinical presentation of CD is highly variable and depends on age (Fasano 2005;Barker and Liu 2008). Classical symptoms include abdominal pain and distension, diarrhea, malnutrition, and failure to thrive within the first few years of life (Barker and Liu 2008).…”

Section: Presentation Pathophysiology and Genetics Of CDmentioning

confidence: 99%

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Celiac Disease as a Model for the Evolution of Multifactorial Disease in Humans

Sams

Hawks

2014

Human Biology

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Abstract. Celiac disease (CD) is a multifactorial chronic inflammatory conditionthat results in injury of the mucosal lining of the small intestine upon ingestion of wheat gluten and related proteins from barley and rye. Although the exact mechanisms leading to CD are not fully understood, the genetic basis of CD has been relatively well characterized. In this review we briefly review the history of discovery, clinical presentation, pathophysiology, and current understanding of the genetics underlying CD risk. Then, we discuss what is known about the current distribution and evolutionary history of genes underlying CD risk in light of other evolutionary models of disease. Specifically, we conclude that the set of loci underlying CD risk did not cohesively evolve as a response to a single past selection event such as the development of agriculture. Rather, deterministic and stochastic evolutionary processes have both contributed to the present distribution of variation in CD risk loci. Selection has shaped some components of this network, but this selection appears to have occurred at different points in the past.Other parts of the CD risk network have likely arisen due to stochastic processes such as genetic drift. Celiac disease (CD) is a multifactorial chronic inflammatory condition that resultsin injury of the mucosal lining of the small intestine. The earliest descriptions of a condition with symptoms like CD date back to the first and second century writings of the Greek physician Arataeus (Simoons 1981;Losowsky 2008). The first modern description of CD is attributed to English physician Samuel Jones Gee, who was familiar with the writings of Arataeus. In 1888 (Dowd and Walker-Smith 1974;Simoons 1981;Losowsky 2008) Gee described the 'coeliac affection' as a condition of chronic indigestion associated with diarrhea, wasting, and weakness and common in people of all ages. Gee's report was the first to hypothesize dietary factors as a primary cause of the condition (Dowd and Walker-Smith 1974), and during the early twentieth century some workers noted the value of a starch free diet for prevention of CD (Haas 1924). Dicke and colleagues (1950, 1953) observed the detrimental effect of wheat flour (but not wheat starch) on CD patients experimentally confirming a role for diet as a driver of CD. Shortly thereafter, Anderson and colleagues (Anderson et al. 1952;Alvey et al. 1957) confirmed the effect of wheat on CD and identified wheat gluten as the primary culprit.CD appears to be an evolutionary paradox. Only since the 1950s have clinicians recognized that a gluten-free diet is an effective treatment (Barker and Liu 2008). Before that time, diagnosed and undiagnosed CD reduced the health and fitness of sufferers, with juvenile cases leading to malnutrition or death, and adult cases causing wasting, lack of adequate nutrition, greater susceptibility to infection, and direct reductions in fertility (Corrao et al. 2001;Soni and Badawy 2010). Despite these apparent costs, CD is common today (>1%) in several popul...

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Section: Presentation Pathophysiology and Genetics Of CDmentioning

confidence: 98%

Section: Celiac Disease (Cd) Is a Multifactorial Chronic Inflammatorymentioning

confidence: 99%

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Celiac Disease as a Model for the Evolution of Multifactorial Disease in Humans

Sams

Hawks

2014

Human Biology

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“…It is characterized by the presence of diverse clinical symptoms, CD-specific antibodies, the presence of HLA-DQ2 and/or -DQ8 molecules, and gastrointestinal tissue damage (1)(2)(3)(4)(5). While the presence of HLA-DQ2 and/or -DQ8 haplotypes constitutes a genetic risk for CD, several non-HLA genes, especially interleukin-21 (IL-21), IL-2, and KIAA1109 gene clusters, have been reported (6,7).…”

mentioning

confidence: 99%

Testing for Antireticulin Antibodies in Patients with Celiac Disease Is Obsolete: a Review of Recommendations for Serologic Screening and the Literature

Nandiwada

Tebo

2013

Clin Vaccine Immunol

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Celiac disease (CD) is an autoimmune disorder that occurs in genetically susceptible individuals of all ages and is triggered by immune response to gluten and related proteins. The disease is characterized by the presence of HLA-DQ2 and/or -DQ8 haplotypes, diverse clinical manifestations, gluten-sensitive enteropathy, and production of several autoantibodies of which endomysial, tissue transglutaminase, and deamidated gliadin peptide antibodies are considered specific. Although antireticulin antibodies (ARA) have historically been used in the evaluation of CD, these assays lack optimal sensitivities and specificities for routine diagnostic use. This minireview highlights the advances in CD-specific serologic testing and the rationale for eliminating ARA from CD evaluation consistent with recommendations for diagnosis.

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“…Although HLA haplotypes confer the highest genetic risk for CD, the fact that only about 3% of DQ2-⁄ DQ8-positive individuals develop the disease after exposure to gluten means that HLA is an essential genetic factor but insufficient by itself [34]. Hence, other genetic factors must be involved in the development of the disease to explain the familial clustering and the high concordance rate in monozygotic twins [35].…”

mentioning

confidence: 99%