Latent coeliac disease in a child with epilepsy, cerebral calcifications, drug-induced systemic lupus erythematosus and intestinal folic acid malabsorption associated with impairment of folic acid transport across the blood-brain barrier

Calvani, Mauro; Parisi, Pasquale; Guaitolini, Carlos Renato de Freitas; Parisi, Giovanna; Paolone, Giovanna

doi:10.1007/s004310100728

Cited by 25 publications

(21 citation statements)

References 21 publications

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“…Several case reports of patients with both CD and SLE were published in the 1980s and 1990s 11,12,13,14,15,16 . In a report by Rensch, et al , 24 of 103 patients (23.3%) with SLE tested positive for antigliadin antibodies but none were positive for endomysial antibodies nor had small intestinal changes consistent with CD 17 .…”

Section: Discussionmentioning

confidence: 99%

“…Several case reports and case series have suggested a possible association between CD and SLE 11,12,13,14,15, 16,17,18,19 , but earlier research has suffered from low statistical power. At least 2 studies have also reported a high prevalence of antigliadin antibodies in SLE but with substantially lower rates of histologically verified CD 17,19 , and because of their lack of a control group with non-SLE individuals, these studies were unable to estimate relative risks of SLE in CD.…”

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confidence: 99%

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Increased Risk of Systemic Lupus Erythematosus in 29,000 Patients with Biopsy-verified Celiac Disease

Ludvigsson

Rubio–Tapia²,

Chowdhary³

et al. 2012

J Rheumatol

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Objective To investigate a possible association between celiac disease (CD) and systemic lupus erythematosus (SLE). Case series have indicated a possible association, but population-based studies are lacking. Methods We compared the risk of SLE in 29,048 individuals with biopsy-verified CD (villous atrophy, Marsh 3) from Sweden’s 28 pathology departments with that in 144,352 matched individuals from the general population identified through the Swedish Total Population Register. SLE was defined as having at least 2 records of SLE in the Swedish Patient Register. We used Cox regression to estimate hazard ratios (HR) for SLE. Results During followup, 54 individuals with CD had an incident SLE. This corresponded to an HR of 3.49 (95% CI 2.48–4.90), with an absolute risk of 17/100,000 person-years and an excess risk of 12/100,000. Beyond 5 years of followup, the HR for SLE was 2.54 (95% CI 1.57–4.10). While SLE was predominantly female, we found similar risk estimates in men and women. When we restricted our outcome to individuals who also had a dispensation for a medication used in SLE, the HR was 2.43 (95% CI 1.22–4.87). The HR for having 2 records of SLE diagnoses, out of which at least 1 had occurred in a department of rheumatology, nephrology/dialysis, internal medicine, or pediatrics, was 2.87 (95% CI 1.97–4.17). Conclusion Individuals with CD were at a 3-fold increased risk of SLE compared to the general population. Although this excess risk remained more than 5 years after CD diagnosis, absolute risks were low.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Increased Risk of Systemic Lupus Erythematosus in 29,000 Patients with Biopsy-verified Celiac Disease

Ludvigsson

Rubio–Tapia²,

Chowdhary³

et al. 2012

J Rheumatol

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“…Some authors have speculated that mechanisms of metabolic deficiency may represent the principal cause of this association (2,23,30,31) . as being associated with celiac disease (50,52) .…”

Section: Introductionmentioning

confidence: 99%

Prevalence of Celiac Disease in Children With Epilepsy

Vieira

Jatobá

Matos

et al. 2013

Arq. Gastroenterol.

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-Context -Neurological symptoms have been well-documented in patients with celiac disease, nevertheless, the presumption of a greater prevalence of epilepsy in celiac patients remains controversial. Objectives -To determine the frequency of celiac disease in children and adolescents with idiopathic or cryptogenic epilepsy. Methods -A cross-sectional study. One hundred pediatric patients with non-symptomatic epilepsy were followed-up at two public pediatric neurology clinics in Salvador, Bahia, Brazil. Screening for celiac disease was performed by serial measurements of IgA anti-transglutaminase and IgA anti-endomysium antibodies, followed by bowel biopsy in positive cases. HLA DQ02 and DQ08 were investigated in seropositive individuals, assessing the type of seizures, the number of antiepileptic drugs used and the presence gastrointestinal symptoms. Results -Three (3.0%) patients tested anti-tTG-positive, two with normal duodenal mucosa (Marsh 0) and one with intraepithelial infiltrate (Marsh I). No villous atrophy of the duodenal mucosa (Marsh III) celiac disease was found. Two patients tested positive for HLA DQ02; none were DQ08 positive.Conclusion -The present study failed to prove the association between celiac disease and epilepsy. HEADINGS -Celiac disease. Epilepsy. Disabled children.

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“…Folate deficiency (serum and CSF) has been noted in many patients with CEC, 15 though is not universal. Folate deficiency has been suspected to be the cause of CEC in previous cases because of their co‐occurrence, and the link between folate deficiency and cerebral calcification in other situations (e.g.…”

Section: Discussionmentioning

confidence: 99%

Coeliac disease, epilepsy, and cerebral calcifications: association with TG6 autoantibodies

Johnson

Dale²,

Wienholt

et al. 2012

Develop Med Child Neuro

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ABBREVIATIONSCEC Coeliac disease, epilepsy, and cerebral calcifications TG6 Transglutaminase isoenzyme 6A 4-year-old boy presented with occipital seizures but normal initial neuroimaging and proved refractory to antiepileptic medications. On repeat neuroimaging after 1 year, he had developed bi-occipital calcification and was then found to have positive coeliac serology. He was diagnosed with coeliac disease, epilepsy, and cerebral calcifications (CEC) and became seizure free after starting the gluten-free diet. Positive antibody binding to neurons and glia was demonstrated on indirect immunofluorescence. High levels of immunoglobulin-A directed against transglutaminase isoenzyme 6 (TG6) were found in the patient's serum. The positive response to the diet, TG6 antibodies, and neuronal antibody binding suggest that CEC might be autoimmune in nature, as in other extra-intestinal manifestations of gluten-related diseases, such as gluten ataxia.Many neurological manifestations of gluten-related diseases have been shown to have an autoimmune basis, the best characterized being gluten ataxia. Antibodies to transglutaminase isoenzyme 6 (TG6) have previously been associated with gluten ataxia, with some evidence for a causative role.

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Latent coeliac disease in a child with epilepsy, cerebral calcifications, drug-induced systemic lupus erythematosus and intestinal folic acid malabsorption associated with impairment of folic acid transport across the blood-brain barrier

Abstract: Impairment of intestinal folic acid absorption with a defect in folic acid transport across the blood-brain barrier has been demonstrated in a case of epilepsy and cerebral calcifications associated with coeliac disease.

Cited by 25 publications

References 21 publications

Increased Risk of Systemic Lupus Erythematosus in 29,000 Patients with Biopsy-verified Celiac Disease

Increased Risk of Systemic Lupus Erythematosus in 29,000 Patients with Biopsy-verified Celiac Disease

Prevalence of Celiac Disease in Children With Epilepsy

Coeliac disease, epilepsy, and cerebral calcifications: association with TG6 autoantibodies

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