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, said Sara Manti, MD, of the unit of pediatric genetics and immunology at the University of Messina, Italy, and her associates.
Serum HMGB1 levels were significantly higher in 49 children with celiac disease, compared with 44 healthy children in the control group (16.4 ng/mL vs. 6.23 ng/mL; P less than .001). Children with typical form celiac disease had significantly higher serum HMGB1 levels (22.03 ng/mL) than both children with atypical form (14.83 ng/mL) and silent form celiac disease (12.3 ng/mL). There was no statistically significant difference in serum HMGB1 levels between children with atypical form and silent form celiac disease.
Higher serum HMGB1 levels were correlated with severity of Marsh-Oberhüber classification.
These data, which need to be confirmed in further studies, suggest that HMGB1 is upregulated and linked to the severity of histologic damage in celiac disease. If other studies confirm these findings, it could be hypothesized that “asymptomatic children only with positive familial history and abnormal serum anti–tTG-IgA levels as well as normal serum HMGB1 levels need not be subjected to endoscopy to rule out the CD diagnosis,” the investigators said.
Perhaps, “neutralizing HMGB1 activity might be identified as a potential therapeutic target,” Dr. Manti and her associates noted.
Read more in the journal Nutrition (2017 May;37:18-21).
, said Sara Manti, MD, of the unit of pediatric genetics and immunology at the University of Messina, Italy, and her associates.
Serum HMGB1 levels were significantly higher in 49 children with celiac disease, compared with 44 healthy children in the control group (16.4 ng/mL vs. 6.23 ng/mL; P less than .001). Children with typical form celiac disease had significantly higher serum HMGB1 levels (22.03 ng/mL) than both children with atypical form (14.83 ng/mL) and silent form celiac disease (12.3 ng/mL). There was no statistically significant difference in serum HMGB1 levels between children with atypical form and silent form celiac disease.
Higher serum HMGB1 levels were correlated with severity of Marsh-Oberhüber classification.
These data, which need to be confirmed in further studies, suggest that HMGB1 is upregulated and linked to the severity of histologic damage in celiac disease. If other studies confirm these findings, it could be hypothesized that “asymptomatic children only with positive familial history and abnormal serum anti–tTG-IgA levels as well as normal serum HMGB1 levels need not be subjected to endoscopy to rule out the CD diagnosis,” the investigators said.
Perhaps, “neutralizing HMGB1 activity might be identified as a potential therapeutic target,” Dr. Manti and her associates noted.
Read more in the journal Nutrition (2017 May;37:18-21).
, said Sara Manti, MD, of the unit of pediatric genetics and immunology at the University of Messina, Italy, and her associates.
Serum HMGB1 levels were significantly higher in 49 children with celiac disease, compared with 44 healthy children in the control group (16.4 ng/mL vs. 6.23 ng/mL; P less than .001). Children with typical form celiac disease had significantly higher serum HMGB1 levels (22.03 ng/mL) than both children with atypical form (14.83 ng/mL) and silent form celiac disease (12.3 ng/mL). There was no statistically significant difference in serum HMGB1 levels between children with atypical form and silent form celiac disease.
Higher serum HMGB1 levels were correlated with severity of Marsh-Oberhüber classification.
These data, which need to be confirmed in further studies, suggest that HMGB1 is upregulated and linked to the severity of histologic damage in celiac disease. If other studies confirm these findings, it could be hypothesized that “asymptomatic children only with positive familial history and abnormal serum anti–tTG-IgA levels as well as normal serum HMGB1 levels need not be subjected to endoscopy to rule out the CD diagnosis,” the investigators said.
Perhaps, “neutralizing HMGB1 activity might be identified as a potential therapeutic target,” Dr. Manti and her associates noted.
Read more in the journal Nutrition (2017 May;37:18-21).
FROM NUTRITION