Alimentary TractFrontal cortical perfusion abnormalities related to gluten intake and associated autoimmune disease in adult coeliac disease: -ECD brain SPECT study
Introduction
Coeliac disease (CD) is characterised by gluten-induced intestinal mucosal injury and malabsorption. Its clinical presentation may be variable [1]: while some symptoms may be related to malabsorption, others such as involvement of the joints and of the central nervous system (CNS) appear to be the consequence of autoimmunity. In particular, some neurological illness, peripheral neuropathy [2] and sporadic idiopathic ataxia [3], seem to be the result of gluten sensitivity with or without histological evidence of small bowel involvement, but with serologic markers (serum antiglidin-antibodies) and genetic susceptibility (HLA DQ2) [4]. Furthermore, it is well known that CD may be associated with other autoimmune disorders such as diabetes mellitus [5], dermatitis herpetiformis [6], thyroid autoimmune disease [7], [8] and Sjögren’s syndrome [9], as well as with migraine and neurological disorder [10] and primary biliary cirrhosis [11]. In some autoimmune disorders such as SLE [12], Sjögren’s syndrome [13], antiphospholipid antibody syndrome [14], and in sporadic cases of autoimmune thyroiditis [15], an involvement of the cerebrovascular system has recently been shown by brain perfusion single-photon emission computed tomography (SPECT), a sensitive method for detecting brain perfusion abnormalities [16].
The aim of this study was to evaluate the cortical brain perfusion in a group of adult coeliac patients by means of ethyl cysteinate dimer (ECD) brain SPECT, and to investigate the possible role of diet and of concomitant presence of other autoimmune diseases in the manifestation of cortical impairment.
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Study groups
The study population consisted of two groups:
- (A)
Thirty-four consecutive adult coeliac patients, recruited in our clinic departments of Cagliari University between 1999 and 2001, 16 (11 females and five males, aged 17–77 years, mean 37±16 years) diagnosed between 1980 and 1999 on gluten-free diet at least for 4 years (range 4–20, median 7 years) and 18 on gluten-containing diet (17 females and one male, aged 18–67 years, mean 41±15 years). The diagnosis of CD was based on clinical, serological and
Results
Neurological examination and MRI yielded normal findings. The clinical and serological data are detailed in Table 1. All patients on gluten-free diet were compliant as assessed by negative serum AGA-A and EMA. Positive anti-TPO values (>20 IU/ml) were observed in 17/34 (50%) coeliac patients, 14 women and three men. Anti-TPO prevalence was significantly higher (50%) than that found in healthy controls (9.6%) (P<0.001). Eight out of 17 anti-TPO positive patients were clinically euthyroid, seven
Discussion
The results of the present study provide clear evidence of high prevalence of cortical perfusion abnormalities in adult coeliac patients, up to 71% displaying brain perfusion defects. The prevalence of cortical abnormalities and the severity of AI values observed in our series of coeliac patients were similar to those observed by Sanna et al. [12] in systemic lupus erythematosus (SLE) with or without overt neuropsychiatric manifestation.
The origin of the described generalised cortical perfusion
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