Abstract
Giriş ve Amaç: Bu çalışmanın amacı çölyak hastalığı tanısı ile takip edilen
hastaların klinik, laboratuvar ve patolojik özelliklerinin araştırılmasıdır. Gereç
ve Yöntem: Kliniğimizde çölyak hastalığı tanısı ile takip edilen hastalar
retrospektif olarak değerlendirildi. Anti-gliadin antikor immunglobulin A,
anti-endomisyum, doku transglutaminaz immunglobulin A ve immunglobulin
G antikorları kaydedildi. Hastaların tanı anında klinik ve laboratuvar
özellikleri patolojik Marsh sınıflamasına göre gruplara ayrılarak gruplar arası
farklılıklar saptanmaya çalışıldı. Bulgular: Çalışmaya kliniğimizde takip edilen
toplam 174 hasta alındı. Hastaların 107’si (%61,5) kadın, 67’si (%38,5)
erkekti. Ortalama tanı yaşı 30,67 (min/mak:18/73)’tü. Tanı anında hastaların
%24’ünde anemi, 118 hastanın 24’ünde (%20,3) vitamin B12 eksikliği, 110
hastanın 27’sinde (%24,5) folik asit eksikliği mevcuttu. D vitamini eksikliği
84 hastanın 63’ünde (%75) saptandı. Kemik mineral dansitometresi bakılan
53 hastanın %49,1’inde (26/53) osteoporoz, %41,5’inde osteopeni (22/53)
saptandı ve %9,4’ü normaldi. Endoskopik biyopsi sonuçları Marsh sınıflamasına
göre; 17’si (%14) sınıf 1, 20’si (%16,5) sınıf 2, 71’i (%58,6) sınıf 3 ve
13’ü (%10,7) sınıf 4 grubundaydı. Marsh 1’de sırasıyla anti-gliadin antikor
immunglobulin A, anti-endomisyum, doku transglutaminaz immunglobulin
A, doku transglutaminaz immunglobulin G pozitiflik oranları %22.2, %50,
%54.5 ve %20 iken Marsh 4’te pozitiflik oranları sırası ile %100, %100,
%81.8 ve %87’ye çıkmaktadır. Antikor pozitifliğinin Marsh 1’den Marsh 4’e
giderek arttığı gözlendi. Sonuç: Marsh 1 hastalarında düşük oranda antikor
pozitifliği saptanması bu grup hastaların bir kısmının çölyak olmayabileceğini
düşündürmektedir. Marsh 1 saptanan olguların kesin çölyak hastalığı
tanısı öncesi, diğer hastalıklar yönünden irdelenmesi gerekmektedir.
Keywords
References
- 1. Farrel RJ, Kelly CP. Celiac sprue. N Engl J Med 2002;346:180-8. 2. Green PH, Cellier C. Celiac disease. N Engl J Med 2007;357:1731-43. 3. Fasano A. Where have all the American celiacs gone? Acta Paediatr Suppl 1996;412:20-4. 4. Murray JA, Van Dyke C, Plevak MF, et al. Trends in the incidence and clinical features of celiac disease in a North American community, 1950-2001. Clin Gastroenterol Hepatol 2003;1:19-27. 5. Rampertab SD, Pooran N, Brar P, Singh P, Green PH. Trends in the presentation of celiac disease. Am J Med 2006;119:355.e9-14. 6. Rubio-Tapia A, Hill ID, Kelly CP, et al and; American College of Gastroenterology. ACG clinical guidelines: diagnosis and management of celiac disease. Am J Gastroenterol 2013;108:656-77. 7. Ludvigsson JF, Brandt L, Montgomery SM, et al. Validation study of villous atrophy and small intestinal inflammation in Swedish biopsy registers. BMC Gastroenterology 2009;9:19. 8. Gümürdülü Y, Serin E, Ozer B, et al. Predictors of vitamin B-12 deficiency: Age and Helicobacter pylori load of antral mucosa. Turk J Gastroenterol 2003;14:44-9. 9. Chakravarthi SD, Jain K, Kochhar R, et al. Prevalence and predictors of abnormal bone mineral metabolism in recently diagnosed adult celiac patients. Indian J Gastroenterol 2012;31:165-70. 10. Uyanıkoğlu A, Coşkun M, Binici DN, Öztürk Y. The incidence of endoscopic celiac (gluten) disease in the Erzurum area in an adult population. Akademik Gastroenteroloji Dergisi 2013;1:13-6. 11. Uyanıkoğlu A, Aydoğan T, Nar H, et al. Şanlıurfa yöresi çölyak hastalarının demografik ve laboratuvar özellikleri. Güncel Gastroenteroloji 2014;18:339-41. 12. Hopper AD, Hadjivassiliou M, Butt S, Sanders DS. Adult celiac disease. BMJ 2007;335:558-62.
Abstract
Background and Aims: The aim of this study is to investigate the clinical,
laboratory, and pathological findings of patients who were clinically diagnosed
and followed with celiac disease. Materials and Methods: Patients
with a diagnosis of celiac disease who were followed in our center were evaluated
retrospectively. Anti-gliadin immunoglobuline A, anti-endomysium,
and tissue transglutaminase immunoglobuline A and immunoglobuline G
antibodies were recorded. Clinical and laboratory characteristics of patients
at the time of diagnosis of celiac disease were studied to determine the differences
between groups according to the Marsh pathological classification. Results:
A total of 174 patients with celiac disease who were followed in-clinic
were recruited into the current study. One-hundred and seven patients
(61.5%) were female, and 67 (38.5%) were male. The mean age at the time of
diagnosis was 30.67 (min/max: 18/73). Twenty-four percent of patients had
anemia at the time of diagnosis. Vitamin B12 deficiency was found in 24 of
118 patients (20.3%). Folic acid deficiency was found in 27 of 110 patients
(24.5%). Vitamin D deficiency was found in 63 of 84 (75%) patients. Bone
mineral density measurements were available for 53 patients; 26 patients
(49.1%) had osteoporosis, 22 patients (41.5%) had osteopenia, and 9.4%
of patients had normal bone mineral densities. Endoscopic biopsy results
according to Marsh classification were as follows: 17 patients (14%) were
in class 1, 20 patients (16.5%) were in class 2, 71 (58.6%) were in class 3
and 13 (10.7%) were in class 4. While Marsh 1 Anti-gliadin immunoglobuline
A, anti-endomysium, tissue transglutaminase immunoglobuline A, and
tissue transglutaminase immunoglobuline G positivity rates were 22.2%,
50%, 54.5%, and 20%, respectively, in the Marsh 1 group, positivity rates
were increased to 100%, 100%, 81.8%, and 87%, respectively in the Marsh
4 group. Antibody positivity increased gradually from Marsh 1 to Marsh 4.
Conclusion: Lower rates of antibody positivity in patients with Marsh class
1 suggest that this group of patients might be misdiagnosed with Celiac disease.
Celiac disease must be confirmed strictly in Marsh class I patients. This
group of patients must be examined closely before a definite diagnosis of
celiac disease is made.
References
- 1. Farrel RJ, Kelly CP. Celiac sprue. N Engl J Med 2002;346:180-8. 2. Green PH, Cellier C. Celiac disease. N Engl J Med 2007;357:1731-43. 3. Fasano A. Where have all the American celiacs gone? Acta Paediatr Suppl 1996;412:20-4. 4. Murray JA, Van Dyke C, Plevak MF, et al. Trends in the incidence and clinical features of celiac disease in a North American community, 1950-2001. Clin Gastroenterol Hepatol 2003;1:19-27. 5. Rampertab SD, Pooran N, Brar P, Singh P, Green PH. Trends in the presentation of celiac disease. Am J Med 2006;119:355.e9-14. 6. Rubio-Tapia A, Hill ID, Kelly CP, et al and; American College of Gastroenterology. ACG clinical guidelines: diagnosis and management of celiac disease. Am J Gastroenterol 2013;108:656-77. 7. Ludvigsson JF, Brandt L, Montgomery SM, et al. Validation study of villous atrophy and small intestinal inflammation in Swedish biopsy registers. BMC Gastroenterology 2009;9:19. 8. Gümürdülü Y, Serin E, Ozer B, et al. Predictors of vitamin B-12 deficiency: Age and Helicobacter pylori load of antral mucosa. Turk J Gastroenterol 2003;14:44-9. 9. Chakravarthi SD, Jain K, Kochhar R, et al. Prevalence and predictors of abnormal bone mineral metabolism in recently diagnosed adult celiac patients. Indian J Gastroenterol 2012;31:165-70. 10. Uyanıkoğlu A, Coşkun M, Binici DN, Öztürk Y. The incidence of endoscopic celiac (gluten) disease in the Erzurum area in an adult population. Akademik Gastroenteroloji Dergisi 2013;1:13-6. 11. Uyanıkoğlu A, Aydoğan T, Nar H, et al. Şanlıurfa yöresi çölyak hastalarının demografik ve laboratuvar özellikleri. Güncel Gastroenteroloji 2014;18:339-41. 12. Hopper AD, Hadjivassiliou M, Butt S, Sanders DS. Adult celiac disease. BMJ 2007;335:558-62.
Details
| Primary Language | Turkish |
|---|---|
| Subjects | Health Care Administration |
| Journal Section | Articles |
| Authors | |
| Publication Date | August 31, 2016 |
| Published in Issue | Year 2016 Volume: 24 Issue: 2 |