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To:
Journal of NEUROL NEUROSURG PSYCHIATRY Letters
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Letter from Rome: Celiac disease and brain
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Ludovico Abenavoli, medicine doctor Institute of Internal Medicine, Catholic University of Rome, Italy
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l.abenavoli{at}yahoo.it Ludovico Abenavoli
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Dear Editor
The history of celiac disease (CD) is very long. The cultivation of grains, developed in the Neolithic period after the last ice age, particularly in the “Fertile Crescent” of the Near East including the Tigris, the Euphrates and the Upper Nile. With the development of cooking, agriculture came into its own and wheat became a main support of the vast growth in population in successive millennia. Thus arose the possibility of development of syndromes, including CD, reflecting intolerance of wheat. In this context is interesting that the generally accepted earliest description of CD, is attributed to “Aretaeus the Cappadocian” (I-II century A.D.), and Cappadocia is a region in the eastern part of Turkey near to the ‘Fertile Crescent’. Further descriptions, which may have been of CD followed, by the Dutch physician Vincent Ketelaer, William Hillary of Yorkshire, England, and others. The origin of the modern history of CD is ascribed to Samuel Gee in a lecture in 1887 followed by his written account in the Saint Bartholomew’s Hospital Reports in 1888. He termed the condition ‘the Celiac Affection’ after the translation by Francis Adams, in 1856, of the description by Aretaeus. In a notably description, Gee refers to the appearance of the stools, the onset of the condition, the muscular weakness, the abdominal distension and the chronic course of the disease. Subsequent to the suggestion by Samuel Gee there were various attempts at dietary management which bore some relation to the eventual recognition of cereal grains as being responsible. Herter in 1908 suggested that fats were better tolerated than carbohydrates, Still in 1918 drew attention to the poor tolerance of bread, Howland in 1921 recognised intolerance to carbohydrates and Haas in 1924 suggested a banana diet which, even though it contains carbohydrates, excludes the damaging cereals. The great breakthrough was by Wim Dicke of The Juliana Children's Hospital in The Hague. In his doctoral thesis of 1950 to the University of Utrecht he showed that exclusion of wheat, rye and oats from the diet led to dramatic improvement in the general condition of the child and marked reduction in the fatty diarrhoea. Wheat starch did not have the same damaging effect. There are descriptions of how Dicke came across this association. During wartime the gruel supplied to children in hospital might, at different times, have contained wheat or other plant products, depending on what was available, which would have provided the clue. Confirmation came with Dicke's laboratory colleagues Weijers and Van de Kamer. With the chemical measurement of stool fat, it became possible to diagnose less severe cases showing that excluding wheat, rye, barley and oats led to reduction in the fat content of the stool and improvement in the clinical condition of the patient. French, showed that similar changes occurred in adults with otherwise unexplained steatorrhoea. Faecal fat is rarely estimated now because of the requirements for accurate diet and prolonged collection of stools, and the associated expense. Since wheat starch did not produce the effect, attention was drawn to the protein components of the relevant cereals, referred to as gluten since the work of Jacopo Bartolomeo Beccari in Bologna in 1745. At present the etiology and pathogenesis of these disorders is uncertain. In the recent years, same relevant studies concerning CD, are performed by Professor Giovanni Gasbarrini, Director to the Institute of Internal Medicine, Catholic University of Rome, and my chief. The research Group to Professor Gasbarrini, have been described pathophysiology mechanisms and clinical manifestations of CD and published more than 140 articles, on this topic, available in pub-med. In the May issue, Dr Grossman highlighted the relationship between CD and neurological disorders (1). Our group reported, a case of brain perfusion abnormalities, assessed by single photon emission computed tomography (SPECT) examination, in a 33-year-old CD patient with schizophrenia; regression of both cerebral hypoperfusion and schizophrenic symptoms was observed after 6 months of a gluten free diet (GFD) (2). On the basis of this case we performed a SPECT study evaluating regional cerebral perfusion in untreated CD adult patients (age: 37±9 years), comparing them with CD patients on GFD, and with healthy controls (3). The study showed the presence of regional cerebral hypoperfusion in 73% of the untreated CD patients, compared with only 7% of CD patients on GFD and none of the controls. An overall multivariate test showed a significant difference in cerebral perfusion among the three groups of subjects (p=0.01). Considering each single region, a significant lower cerebral perfusion was found in untreated celiac patients compared to controls in seven of the 26 cerebral regions evaluated. Perfusion defects were predominant in the superior and anterior areas of the frontal cortex with the involvement of the adjacent anterior cingulated cortex. We have been reported similar cerebral blood flow changes, in patients suffering from different neurological and psychiatric disorders (4,5). In according to the author, I suggest to early investigate the presence of CD in patients with neurological abnormalities. To conclude I want to give my gratitude to Professor Giovanni Gasbarrini, for his scientific commitment and to be a guide for us young researchers. Figure legend Professor Gasbarrini (first line, the 3rd from left ), coworkers (me, first line, the 2nd from right) and medicine school students
References:
1. Grossman G. Neurological complications of coeliac disease: what is the evidence? Pract Neurol. 2008; 8:77-89. |
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