Prevalence of hyperhomocysteinemia in adult gluten-sensitive enteropathy at diagnosis: Role of B12, folate, and genetics

Simone Saibeni, Anna Lecchi, Gianmichele Meucci, Marco Cattaneo, Liliana Tagliabue, Emanuele Rondonotti, Sara Formenti, Roberto De Franchis, Maurizio Vecchi

Research output: Contribution to journalArticle

Abstract

Background & Aims: Hyperhomocysteinemia, a risk factor for thrombosis, recurrent miscarriages, and osteoporosis, might derive from acquired folate and vitamin B12 deficiencies and from a C677T mutation in methylene-tetrahydrofolate reductase (MTHFR) gene. Undiagnosed gluten-sensitive enteropathy (GSE) is associated with vitamin deficiencies, osteoporosis, and recurrent miscarriages. We evaluated the prevalence and the risk factors for hyperhomocysteinemia in patients with newly diagnosed GSE. Methods: In this prospective study performed in a tertiary care setting, 40 consecutive subjects with newly diagnosed GSE were evaluated for homocysteine, folate, and vitamin B12 levels and for C677T polymorphism. One hundred twenty sex- and age-matched healthy control subjects were studied. Nonparametric tests and multiple regression analysis were used to evaluate the risk factors in inducing hyperhomocysteinemia in the GSE population. Results: Hyperhomocysteinemia was more frequent in GSE patients than in control subjects (8/40, 20.0% vs 7/120, 5.8%) (relative risk, 3.4; 95% confidence interval, 1.3-8.9), as well as folate deficiency (17/40, 42.5% vs 10/120, 8.3%) (relative risk, 5.1; 95% confidence interval, 2.5-10.2). Multiple regression analysis showed that folate and B 12 levels were independently and inversely associated with homocysteine levels, whereas homozygosity for the MTHFR thermolabile variant was not. The prevalence of MTHFR variant in GSE population was not different from that reported in racially comparable control groups. Gluten-free diet was able to normalize folate, vitamin B12, and homocysteine levels. Conclusions: Hyperhomocysteinemia is frequent in newly diagnosed GSE. Vitamin deficiencies caused by malabsorption are the most important determinants of this condition. Hyperhomocysteinemia might contribute to the occurrence of common complications of undiagnosed GSE.

Original languageEnglish
Pages (from-to)574-580
Number of pages7
JournalClinical Gastroenterology and Hepatology
Volume3
Issue number6
DOIs
Publication statusPublished - Jun 2005

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Hyperhomocysteinemia
Celiac Disease
Folic Acid
Methylenetetrahydrofolate Reductase (NADPH2)
Homocysteine
Avitaminosis
Habitual Abortion
Vulnerable Populations
Vitamin B 12
Osteoporosis
Regression Analysis
Confidence Intervals
Vitamin B 12 Deficiency
Gluten-Free Diet
Tertiary Healthcare
Healthy Volunteers
Thrombosis
Prospective Studies
Control Groups
Mutation

ASJC Scopus subject areas

  • Gastroenterology

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Prevalence of hyperhomocysteinemia in adult gluten-sensitive enteropathy at diagnosis : Role of B12, folate, and genetics. / Saibeni, Simone; Lecchi, Anna; Meucci, Gianmichele; Cattaneo, Marco; Tagliabue, Liliana; Rondonotti, Emanuele; Formenti, Sara; De Franchis, Roberto; Vecchi, Maurizio.

In: Clinical Gastroenterology and Hepatology, Vol. 3, No. 6, 06.2005, p. 574-580.

Research output: Contribution to journalArticle

Saibeni, Simone ; Lecchi, Anna ; Meucci, Gianmichele ; Cattaneo, Marco ; Tagliabue, Liliana ; Rondonotti, Emanuele ; Formenti, Sara ; De Franchis, Roberto ; Vecchi, Maurizio. / Prevalence of hyperhomocysteinemia in adult gluten-sensitive enteropathy at diagnosis : Role of B12, folate, and genetics. In: Clinical Gastroenterology and Hepatology. 2005 ; Vol. 3, No. 6. pp. 574-580.
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abstract = "Background & Aims: Hyperhomocysteinemia, a risk factor for thrombosis, recurrent miscarriages, and osteoporosis, might derive from acquired folate and vitamin B12 deficiencies and from a C677T mutation in methylene-tetrahydrofolate reductase (MTHFR) gene. Undiagnosed gluten-sensitive enteropathy (GSE) is associated with vitamin deficiencies, osteoporosis, and recurrent miscarriages. We evaluated the prevalence and the risk factors for hyperhomocysteinemia in patients with newly diagnosed GSE. Methods: In this prospective study performed in a tertiary care setting, 40 consecutive subjects with newly diagnosed GSE were evaluated for homocysteine, folate, and vitamin B12 levels and for C677T polymorphism. One hundred twenty sex- and age-matched healthy control subjects were studied. Nonparametric tests and multiple regression analysis were used to evaluate the risk factors in inducing hyperhomocysteinemia in the GSE population. Results: Hyperhomocysteinemia was more frequent in GSE patients than in control subjects (8/40, 20.0{\%} vs 7/120, 5.8{\%}) (relative risk, 3.4; 95{\%} confidence interval, 1.3-8.9), as well as folate deficiency (17/40, 42.5{\%} vs 10/120, 8.3{\%}) (relative risk, 5.1; 95{\%} confidence interval, 2.5-10.2). Multiple regression analysis showed that folate and B 12 levels were independently and inversely associated with homocysteine levels, whereas homozygosity for the MTHFR thermolabile variant was not. The prevalence of MTHFR variant in GSE population was not different from that reported in racially comparable control groups. Gluten-free diet was able to normalize folate, vitamin B12, and homocysteine levels. Conclusions: Hyperhomocysteinemia is frequent in newly diagnosed GSE. Vitamin deficiencies caused by malabsorption are the most important determinants of this condition. Hyperhomocysteinemia might contribute to the occurrence of common complications of undiagnosed GSE.",
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T2 - Role of B12, folate, and genetics

AU - Saibeni, Simone

AU - Lecchi, Anna

AU - Meucci, Gianmichele

AU - Cattaneo, Marco

AU - Tagliabue, Liliana

AU - Rondonotti, Emanuele

AU - Formenti, Sara

AU - De Franchis, Roberto

AU - Vecchi, Maurizio

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N2 - Background & Aims: Hyperhomocysteinemia, a risk factor for thrombosis, recurrent miscarriages, and osteoporosis, might derive from acquired folate and vitamin B12 deficiencies and from a C677T mutation in methylene-tetrahydrofolate reductase (MTHFR) gene. Undiagnosed gluten-sensitive enteropathy (GSE) is associated with vitamin deficiencies, osteoporosis, and recurrent miscarriages. We evaluated the prevalence and the risk factors for hyperhomocysteinemia in patients with newly diagnosed GSE. Methods: In this prospective study performed in a tertiary care setting, 40 consecutive subjects with newly diagnosed GSE were evaluated for homocysteine, folate, and vitamin B12 levels and for C677T polymorphism. One hundred twenty sex- and age-matched healthy control subjects were studied. Nonparametric tests and multiple regression analysis were used to evaluate the risk factors in inducing hyperhomocysteinemia in the GSE population. Results: Hyperhomocysteinemia was more frequent in GSE patients than in control subjects (8/40, 20.0% vs 7/120, 5.8%) (relative risk, 3.4; 95% confidence interval, 1.3-8.9), as well as folate deficiency (17/40, 42.5% vs 10/120, 8.3%) (relative risk, 5.1; 95% confidence interval, 2.5-10.2). Multiple regression analysis showed that folate and B 12 levels were independently and inversely associated with homocysteine levels, whereas homozygosity for the MTHFR thermolabile variant was not. The prevalence of MTHFR variant in GSE population was not different from that reported in racially comparable control groups. Gluten-free diet was able to normalize folate, vitamin B12, and homocysteine levels. Conclusions: Hyperhomocysteinemia is frequent in newly diagnosed GSE. Vitamin deficiencies caused by malabsorption are the most important determinants of this condition. Hyperhomocysteinemia might contribute to the occurrence of common complications of undiagnosed GSE.

AB - Background & Aims: Hyperhomocysteinemia, a risk factor for thrombosis, recurrent miscarriages, and osteoporosis, might derive from acquired folate and vitamin B12 deficiencies and from a C677T mutation in methylene-tetrahydrofolate reductase (MTHFR) gene. Undiagnosed gluten-sensitive enteropathy (GSE) is associated with vitamin deficiencies, osteoporosis, and recurrent miscarriages. We evaluated the prevalence and the risk factors for hyperhomocysteinemia in patients with newly diagnosed GSE. Methods: In this prospective study performed in a tertiary care setting, 40 consecutive subjects with newly diagnosed GSE were evaluated for homocysteine, folate, and vitamin B12 levels and for C677T polymorphism. One hundred twenty sex- and age-matched healthy control subjects were studied. Nonparametric tests and multiple regression analysis were used to evaluate the risk factors in inducing hyperhomocysteinemia in the GSE population. Results: Hyperhomocysteinemia was more frequent in GSE patients than in control subjects (8/40, 20.0% vs 7/120, 5.8%) (relative risk, 3.4; 95% confidence interval, 1.3-8.9), as well as folate deficiency (17/40, 42.5% vs 10/120, 8.3%) (relative risk, 5.1; 95% confidence interval, 2.5-10.2). Multiple regression analysis showed that folate and B 12 levels were independently and inversely associated with homocysteine levels, whereas homozygosity for the MTHFR thermolabile variant was not. The prevalence of MTHFR variant in GSE population was not different from that reported in racially comparable control groups. Gluten-free diet was able to normalize folate, vitamin B12, and homocysteine levels. Conclusions: Hyperhomocysteinemia is frequent in newly diagnosed GSE. Vitamin deficiencies caused by malabsorption are the most important determinants of this condition. Hyperhomocysteinemia might contribute to the occurrence of common complications of undiagnosed GSE.

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