First-degree Relatives of Celiac Disease Patients Have Increased Seroreactivity to Serum Microbial Markers

Risk of celiac disease (CD) is increased in relatives of CD patients due to genetic and possible environmental factors. We recently reported increased seropositivity to anti-Saccharomyces cerevisiae (ASCA), Pseudomonas fluorescens-associated sequence (anti-I2) and Bacteroides caccae TonB-linked outer membrane protein (anti-OmpW) antibodies in CD. We hypothesized these markers also to be overrepresented in relatives. Seropositivity and levels of ASCA, anti-I2 and anti-OmpW were compared between 463 first-degree relatives, 58 untreated and 55 treated CD patients, and 80 controls. CD-associated human leukocyte antigen (HLA)-haplotypes and transglutaminase (tTGab) and endomysium (EmA) antibodies were determined. One or more of the microbial antibodies was present in 75% of relatives, 97% of untreated and 87% of treated CD patients and 44% of the controls. The relatives had higher median ASCA IgA (9.13 vs. 4.50 U/mL, p < 0.001), ASCA IgG (8.91 vs. 5.75 U/mL, p < 0.001) and anti-I2 (absorbance 0.74 vs. 0.32, p < 0.001) levels than controls. There was a weak, positive correlation between tTGab and ASCA (r = 0.31, p < 0.001). Seropositivity was not significantly associated with HLA. To conclude, seropositivity to microbial markers was more common and ASCA and anti-I2 levels higher in relatives of CD patients than controls. These findings were not associated with HLA, suggesting the role of other genetic and environmental factors

First-degree Relatives of Celiac Disease Patients Have Increased Seroreactivity to Serum Microbial Markers

Risk of celiac disease (CD) is increased in relatives of CD patients due to genetic and possible environmental factors. We recently reported increased seropositivity to anti-Saccharomyces cerevisiae (ASCA), Pseudomonas fluorescens-associated sequence (anti-I2) and Bacteroides caccae TonB-linked outer membrane protein (anti-OmpW) antibodies in CD. We hypothesized these markers also to be overrepresented in relatives. Seropositivity and levels of ASCA, anti-I2 and anti-OmpW were compared between 463 first-degree relatives, 58 untreated and 55 treated CD patients, and 80 controls. CD-associated human leukocyte antigen (HLA)-haplotypes and transglutaminase (tTGab) and endomysium (EmA) antibodies were determined. One or more of the microbial antibodies was present in 75% of relatives, 97% of untreated and 87% of treated CD patients and 44% of the controls. The relatives had higher median ASCA IgA (9.13 vs. 4.50 U/mL, p < 0.001), ASCA IgG (8.91 vs. 5.75 U/mL, p < 0.001) and anti-I2 (absorbance 0.74 vs. 0.32, p < 0.001) levels than controls. There was a weak, positive correlation between tTGab and ASCA (r = 0.31, p < 0.001). Seropositivity was not significantly associated with HLA. To conclude, seropositivity to microbial markers was more common and ASCA and anti-I2 levels higher in relatives of CD patients than controls. These findings were not associated with HLA, suggesting the role of other genetic and environmental factors

Endomysial antibodies predict celiac disease irrespective of the titers or clinical presentation

Peer reviewe

Markers of Coeliac Disease Latency

Coeliac disease (CD) is a permanent intolerance to dietary cereals. It is the most common malabsorption syndrome in children in Finland, with a prevalence possibly as high as 1:100. In view of the increasing risk of developing malignancies and osteoporosis later in life, it is essential to diagnose CD at an early stage. CD is characterised by a gluten-triggered manifest small-bowel mucosal lesion in genetically susceptible individuals, biopsy specimens showing villous atrophy with crypt hyperplasia and lymphocytic infiltration. The timepoint of the first manifestations of CD has shifted to later ages due to the fact that the clinical presentation of CD has changed during recent years. Classic symptoms such as diarrhoea, loose stools and failure to gain weight have become rare. The symptoms can be atypical, or the patients may even be symptomless. CD can also develop on previously normal mucosa. Patients with such a latent form of CD express a normal jejunal mucosal morphology while on gluten-containing diet, but will later be found to have small-bowel villous atrophy healing on a gluten-free diet. The diagnosis of latent CD can be established only in retrospect. The purpose of present study was to identify markers of CD latency. The present study shows that in patients with normal jejunal mucosal morphology markers are due to be found indicative of development of CD. The study also revealed that CD frequently occurs in patients with primary Sjögren's syndrome. These patients may have asymptomatic gluten sensitve enteropathy which can be detected by serologic screening tests.Coeliac disease (CD) is a permanent intolerance to dietary cereals. It is the most common malabsorption syndrome in children in Finland, with a prevalence possibly as high as 1:100. In view of the increasing risk of developing malignancies and osteoporosis later in life, it is essential to diagnose CD at an early stage. CD is characterised by a gluten-triggered manifest small-bowel mucosal lesion in genetically susceptible individuals, biopsy specimens showing villous atrophy with crypt hyperplasia and lymphocytic infiltration. The timepoint of the first manifestations of CD has shifted to later ages due to the fact that the clinical presentation of CD has changed during recent years. Classic symptoms such as diarrhoea, loose stools and failure to gain weight have become rare. The symptoms can be atypical, or the patients may even be symptomless. CD can also develop on previously normal mucosa. Patients with such a latent form of CD express a normal jejunal mucosal morphology while on gluten-containing diet, but will later be found to have small-bowel villous atrophy healing on a gluten-free diet. The diagnosis of latent CD can be established only in retrospect. The purpose of present study was to identify markers of CD latency. The present study shows that in patients with normal jejunal mucosal morphology markers are due to be found indicative of development of CD. The study also revealed that CD frequently occurs in patients with primary Sjögren's syndrome. These patients may have asymptomatic gluten sensitve enteropathy which can be detected by serologic screening tests

Markers of Coeliac Disease Latency

Coeliac disease (CD) is a permanent intolerance to dietary cereals. It is the most common malabsorption syndrome in children in Finland, with a prevalence possibly as high as 1:100. In view of the increasing risk of developing malignancies and osteoporosis later in life, it is essential to diagnose CD at an early stage. CD is characterised by a gluten-triggered manifest small-bowel mucosal lesion in genetically susceptible individuals, biopsy specimens showing villous atrophy with crypt hyperplasia and lymphocytic infiltration. The timepoint of the first manifestations of CD has shifted to later ages due to the fact that the clinical presentation of CD has changed during recent years. Classic symptoms such as diarrhoea, loose stools and failure to gain weight have become rare. The symptoms can be atypical, or the patients may even be symptomless. CD can also develop on previously normal mucosa. Patients with such a latent form of CD express a normal jejunal mucosal morphology while on gluten-containing diet, but will later be found to have small-bowel villous atrophy healing on a gluten-free diet. The diagnosis of latent CD can be established only in retrospect. The purpose of present study was to identify markers of CD latency. The present study shows that in patients with normal jejunal mucosal morphology markers are due to be found indicative of development of CD. The study also revealed that CD frequently occurs in patients with primary Sjögren's syndrome. These patients may have asymptomatic gluten sensitve enteropathy which can be detected by serologic screening tests.Coeliac disease (CD) is a permanent intolerance to dietary cereals. It is the most common malabsorption syndrome in children in Finland, with a prevalence possibly as high as 1:100. In view of the increasing risk of developing malignancies and osteoporosis later in life, it is essential to diagnose CD at an early stage. CD is characterised by a gluten-triggered manifest small-bowel mucosal lesion in genetically susceptible individuals, biopsy specimens showing villous atrophy with crypt hyperplasia and lymphocytic infiltration. The timepoint of the first manifestations of CD has shifted to later ages due to the fact that the clinical presentation of CD has changed during recent years. Classic symptoms such as diarrhoea, loose stools and failure to gain weight have become rare. The symptoms can be atypical, or the patients may even be symptomless. CD can also develop on previously normal mucosa. Patients with such a latent form of CD express a normal jejunal mucosal morphology while on gluten-containing diet, but will later be found to have small-bowel villous atrophy healing on a gluten-free diet. The diagnosis of latent CD can be established only in retrospect. The purpose of present study was to identify markers of CD latency. The present study shows that in patients with normal jejunal mucosal morphology markers are due to be found indicative of development of CD. The study also revealed that CD frequently occurs in patients with primary Sjögren's syndrome. These patients may have asymptomatic gluten sensitve enteropathy which can be detected by serologic screening tests

Estrogeenireseptorin, PS-2:n ja katepsiini-D:n immunohisto-kemiallinen osoittaminen rintasyöpäsoluista.

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