Neurological manifestation of Coeliac disease in Iraqi patients

Authors

  • Mohammed Shanan Dhair Al Muthanna health directorate, Al Hussain teaching hospital. M.B.Ch.B., F.I.CM.S (neurologist) Author
  • Mustafa Makki Ajam Al Muthanna health directorate, Al Hussain teaching hospital. M.B.Ch.B., F.I.CM.S (neurologist) Author

DOI:

https://doi.org/10.61841/b2bmb209

Keywords:

neurological disability, neurological dysfunction.

Abstract

Background: Celiac disease (CD/Non-tropical sprue, gluten-sensitive enteropathy) is a malabsorptive conditioning in which an allergic reaction to the cereal grain-protein gluten (present in wheat, rye, and barley) causes small intestine mucosal injury.

 

Aims: The purpose of the present study was to evaluate neurological manifestations in association with celiac disease. The specific objectives were to study the neurological manifestations of celiac disease.

 

Methods: Seventy-five unselected consecutive patients (32 men, 43 women, mean age 25.51±8.473 years) with histologically proven CD were enrolled and prospectively investigated. The 75 patients were seen in the Department of Gastroenterology outpatient, medical, and neurological wards of Baghdad hospital. All patients were on a gluten-free diet at recruitment, and the median duration of disease was 2.56±1.670.

 

Results: The onset is in the first four decades of life, with a female to male ratio of 2:1. It may be associated with a wide spectrum of neurological manifestations, including cerebellar ataxia, epileptic seizures, dementia, neuropathy, myopathies, and multifocal leucoencephalopathy. We report three teen patients with neurological manifestations related to CD: two with cerebellar ataxia, two with epilepsy, two with carpel tunnel syndrome, two with myopathies, two with peripheral neuropathy, and one with cognitive impairment. The diagnosis of CD was confirmed by serologic tests (antiendomysial, antitransglutaminase antibodies, and antigliadin antibodies) and biopsy of the small intestine. In two patients the neurological symptoms preceded the gastrointestinal abnormalities, and in all of them gluten restriction failed to improve the neurological disability.

Conclusion: CD should be ruled out in the differential diagnosis of neurological dysfunction of unknown cause, including ataxia, epilepsy, and dementia. A gluten-free diet, the mainstay of treatment, failed to improve the neurological disability. 

Downloads

Download data is not yet available.

References

1. Marsh MN. Clinical and pathological spectrum of coeliac disease. Gut 1993;34:1740

2. Booth, CC. History of celiac disease. BMJ 1989; 298:527

3. Dicke, WK. Simple dietary treatment for the syndrome of GheeHerter. Ned Tijdschr Geneeskd

1941; 85:1715.

4. DICKE, WK, WEIJERS, HA, VAN DE, KAMER JH. Coeliac disease. II. The presence in

wheat of a factor having a deleterious effect in cases of coeliac disease. Acta Paediatr 1953;

42:34.

5. Van de Kamer, JH, Weyers, HA, Dicke, WK. Coeliac disease IV. An investigation into the

injurious constituents of wheat in connection with their action on patients with coeliac disease.

Acta Paediatr 1953; 42:232.

6. PAULLEY, JW. Observation on the aetiology of idiopathic steatorrhoea; jejunal and lymphnode biopsies. Br Med J 1954; 4900:1318.

7. RUBIN, CE, BRANDBORG, LL, PHELPS, PC, TAYLOR, HC Jr. Studies of celiac disease. I.

The apparent identical and specific nature of the duodenal and proximal jejunal lesion in celiac

disease and idiopathic sprue. Gastroenterology 1960; 38:28.

8. Hardwick, C. Prognosis in coeliac disease. Arch Dis Child 1939; 14:279

9. Fry, L, Seah, PP, McMinn, RM, Hoffbrand, AV. Lymphocytic infiltration of epithelium in

diagnosis of gluten-sensitive enteropathy. Br Med J 1972.

10. Troncone, R, Greco, L, Mayer, M, et al. Latent and potential coeliac disease. Acta Paediatr

Suppl 1996; 412:10.

11. Cellier, C, Patey, N, Mauvieux, L, et al. Abnormal intestinal intraepithelial lymphocytes in

refractory sprue. Gastroenterology 1998; 114:471

12. . Matysiak-Budnik, T, Malamut, G, de Serre, NP, et al. Long-term follow-up of 61 coeliac

patients diagnosed in childhood: evolution toward latency is possible on a normal diet. Gut 2007;

56:1379.

13. Arranz, E, Ferguson, A. Intestinal antibody pattern of coeliac disease: Occurrence in patients

with normal jejunal biopsy histology. Gastroenterology 1993; 104:1263

14. Marsh, MN, Crowe, PT. Morphology of the mucosal intestinal lesion in gluten sensitivity.

Baillieres Clin Gastroenterol 1995; 9:273.

15. Bottaro, G, Cataldo, F, Rotolo, M, et al. The clinical pattern of subclinical/silent celiac

disease: An analysis on 1026 consecutive cases. Am J Gastroenterol 1999; 94:691.

16. West, J, Logan, RF, Hill, PG, Khaw, KT. The iceberg of celiac disease: what is below the

waterline?. Clin Gastroenterol Hepatol 2007; 5:59.

17. Collin, P, Reunala, T, Pukkala, E, et al. Coeliac disease-associated disorders and survival.

Gut 1994; 35:1215.

18. Ventura, A, Magazzu, G, Greco, L, et al. Duration of exposure to gluten and risk for

autoimmune disorders in patients with celiac disease. Gastroenterology 1999; 117:297.

19. Sategna Guidetti, C, Solerio, E, Scaglione, N, et al. Duration of gluten exposure in adult

coeliac disease does not correlate with the risk for autoimmune disorders. Gut 2001; 49:502.

20. Holmes, GK. Non-malignant complications of coeliac disease. Acta Paediatr Suppl 1996;

412:68.

21. Lubrano, E, Ciacci, C, Ames, PR, et al. The arthritis of coeliac disease: Prevalence and

pattern in 200 adult patients. Br J Rheumatol 1996; 35:1314.

Downloads

Published

30.06.2021

How to Cite

Neurological manifestation of Coeliac disease in Iraqi patients. (2021). International Journal of Psychosocial Rehabilitation, 25(3), 1397-1404. https://doi.org/10.61841/b2bmb209