Digestive Diseases and Sciences

, Volume 53, Issue 6, pp 1564–1572 | Cite as

Serum Copper, Ceruloplasmin and 24-h Urine Copper Evaluations in Celiac Patients

  • Ali Tüzün InceEmail author
  • Hüseyin Kayadibi
  • Aliye Soylu
  • Oya Ovunç
  • Mustafa Gültepe
  • Ahmet Burak Toros
  • Bülent Yaşar
  • Tulin Kendir
  • Evren Abut
Original Research


The aim of the study is to evaluate the serum copper, ceruloplasmin and 24-h urine copper levels in celiac patients.Serum copper, ceruloplasmin and 24-h urine measurements were evaluated in patients with celiac (n = 32), Crohn’s (n = 25), Wilson’s (n = 11) and in a healthy group (n = 35). Serum and 24-h urine zinc levels, AST, ALT, BUN, creatinine, iron, hemoglobin, hematocrit, lymphocyte, sedimentation and CRP levels were also measured. Results were evaluated statistically and significance was accepted as meaningful if P < 0.05. In celiacs, levels of urine copper were high (52 ± 29 μg/day, P < 0.000) but serum copper was the same as in controls (105 ± 16 μg/dl, P < 0.158). High urinary copper of celiacs were coming out in women (56 ± 30 μg/day) and in man (33 ± 17 μg/day, P < 0.115). Most celiacs were female (P < 0.001). Serum copper and ceruloplasmin levels in all groups were higher in women than in men and this was meaningful for serum copper in the control group (P < 0.045) and for ceruloplasmin in Crohn’s (P < 0.055) and control groups (P < 0.031). Serum (70 ± 14 μg/dl, P < 0.000) and urine zinc levels (25 ± 15 μg/dl, P < 0.039) of celiacs were low. Ceruloplasmin levels were higher in celiacs (337 ± 64 U/l) and Crohn’s patients (366 ± 47 U/l, P < 0.000). Correlations observed in the groups of celiac (P < 0.029) and Crohn’s (P < 0.024), celiac and Wilson’s (P < 0.001) and Crohn’s and Wilson’s (P < 0.001) between the ceruloplasmin and 24-h urine copper parameters. AST and ALT levels were higher in celiac and Wilson’s patients than in Crohn’s patients and controls. Mean CRP levels were significantly higher in Crohn’s than others. Lymphocyte counts were meaningfully higher in celiacs. Statistically, while mean iron, hemoglobulin and hematocrit levels of celiac and Crohn groups were meaningfully lower than the normal and Wilson’s group, it was similar in Wilson’s and the control group. Serum copper (85 ± 26 μg/dl, P < 0.158) and ceruloplasmin (219 ± 83 U/l, P < 0.001) levels were low and 24-h urine copper levels were high (415 ± 346 μg/day) in Wilson’s group. Increased urinary loss may be another cause of copper deficiency in female celiacs besides malabsorption and this topic needs more investigation. Increased urinary copper levels in celiac women should not always be regarded as a diagnosis of Wilson’s disease.


Copper Ceruloplasmin Celiac Crohn’s disease Wilson’s disease 



We would like to thank the “Istanbul branch of Society of Living with Celiac” for their contribution and support.


  1. 1.
    Ashwood ER, Burtis CA, Tietz NW (1994) Tietz textbook of clinical chemistry, 2nd edn. Saunders, Philadelphia, USA, pp 1335–1339Google Scholar
  2. 2.
    Al-Bitar Y, Azam J-S, Azam T (2005) Menke’s kinky hair syndrome: a rare medical condition. J Pak Med Assoc 55:40–42PubMedGoogle Scholar
  3. 3.
    Klevay ML (1998) Lack of recommended dietary allowance for copper may be hazardous to your health. J Am Coll Nutr 17:322–326PubMedGoogle Scholar
  4. 4.
    Reish O, Townsend D, Berry SA, Tsai MY, King RA (1995) Tyrosinase inhibition due to interaction of homocystein with copper: the mechanism for reversible hypopigmentation in homocystinuria due to cystathionine beta-sythase deficiency. Am J Hum Genet 57:127–132PubMedGoogle Scholar
  5. 5.
    Li Y, Wang L, Schuschke DA, Zhou Z, Saari JT, Kang YJ (2005) Marginal dietary copper restriction induces cardiomyopathy in rats. J Nutr 135:2130–2136PubMedGoogle Scholar
  6. 6.
    Britton RS, Bacon BR (1994) Role of free radicals in liver diseases and hepatic fibrosis. Hepatogastroenterology 41:343–348PubMedGoogle Scholar
  7. 7.
    Pan JJ, Chu CJ, Chang FY, Lee SD (2005) The clinical experience of Chinese patients with Wilson’s disease. Hepatogastroenterology 52:166–169PubMedGoogle Scholar
  8. 8.
    Beshgetoor D, Hambidge M (1998) Clinical conditions altering copper metabolism in humans. Am J Clin Nutr 67(suppl):1017S–1021SPubMedGoogle Scholar
  9. 9.
    Rossi T (2004) Celiac disease. Adolesc Med Clic 15:91–103. ReviewCrossRefGoogle Scholar
  10. 10.
    Yamamato-Furusho JK, Korzenik JR (2006) Crohn’s disease: innate immunodeficiency. World J Gastroenterol 14:6751–6755Google Scholar
  11. 11.
    Jameson S, Hellsing K, Magnusson S (1985) Copper malabsoption in celiac disease. J Pediatr Gastroenterol Nutr 4:677–680CrossRefGoogle Scholar
  12. 12.
    Goyens P, Brasseur D, Cadranel S (2006) Copper deficiency in infants with active celiac disease. Med Hypoteses 66:769–772CrossRefGoogle Scholar
  13. 13.
    Fisgin T, Yaralı N, Duru F, Usta B, Kara A (2004) Hematologic manifestations of childhood celiac disease. Acta Haematol 111:211–214PubMedCrossRefGoogle Scholar
  14. 14.
    Forget P, Grandfils C, Van Cutsem JL, Dandrifosse G (1986) Diamine oxidase in serum and small intestinal biopsy tissue in childhood celiac disease. J Pediatr Gastroenterol Nutr 5:379–383PubMedGoogle Scholar
  15. 15.
    Corazza GR, Falasca A, Strocchi A, Rossi CA, Gasbarrini G (1988) Decreased plasma postheparin diamino oxidase levels in celiac disease. Dig Dis Sci 33:956–961PubMedCrossRefGoogle Scholar
  16. 16.
    Schenker JH, Jungreis E, Polishuk WZ (1971) Oral contraceptives and serum copper concentration. Obstet Gynecol 31:233–237Google Scholar
  17. 17.
    Carruthers ME, Hobbs CB, Warren RL (1966) Raised serum copper and caeruloplasmin levels in subjects taking oral contraceptives. J Clin Pathol 19:498–500PubMedCrossRefGoogle Scholar
  18. 18.
    Yunice AA, Lindeman RD (1975) Effect of estrogen–progesteron administration on tissue cation concentrations in the rat. Endocrinology 97:1263–1269PubMedCrossRefGoogle Scholar
  19. 19.
    Ringstad J, Kildebo S, Thomsen Y (1993) Serum selenium copper and zinc concentrations in Crohn’s disease and ulcerative colitis. Scand J Gastroenterol 28:605–608PubMedCrossRefGoogle Scholar
  20. 20.
    Brewer GJ (2002) Diagnosis of Wilson’s disease: an experience of three decades. Gut 50:130CrossRefGoogle Scholar
  21. 21.
    Hinks LJ, Inwards KD, Lloyd B, Clayton B (1988) Reduced concentration in mild Crohn’s disease. J Clin Pathol 41:198–201PubMedCrossRefGoogle Scholar
  22. 22.
    Ritland S, Elgjo K, Johansen O, Steiness E (1979) Liver copper content in patients with inflammatory bowel disease and associated liver disorders. Scand J Gastroenterol 14:411–715CrossRefGoogle Scholar
  23. 23.
    Deflandre J, Weber G, Delbrouck JM, Roelandts I, Royabe G, Brassinne A (1985) Assay of trace elements in the serum by PIXE method with Crohn’s disease. Gastrenterol Clin Biol 10:719–725Google Scholar
  24. 24.
    Mulder TP, Verspaget HW, Janssens AR, de Bruin PA, Pena AS, Lamers CB (1991) Decrease in two intestinal copper/zinc containing proteins with antioxydant function in inflammatory bowel disease. Gut 32:1146–1150PubMedCrossRefGoogle Scholar
  25. 25.
    Abdo A, Meddings J, Swain M (2004) Liver abnormalities in celiac disease. Clin Gastroenterol Hepatol 2:107–112PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media, LLC 2007

Authors and Affiliations

  • Ali Tüzün Ince
    • 1
    Email author
  • Hüseyin Kayadibi
    • 2
  • Aliye Soylu
    • 3
  • Oya Ovunç
    • 1
  • Mustafa Gültepe
    • 2
  • Ahmet Burak Toros
    • 1
  • Bülent Yaşar
    • 1
  • Tulin Kendir
    • 4
  • Evren Abut
    • 5
  1. 1.Gastroenterohepatology ClinicHaydarpasa Numune Education and Research HospitalIstanbulTurkey
  2. 2.Biochemistry Laboratory and Clinical Biochemistry DivisionGATA Haydarpaşa Education HospitalIstanbulTurkey
  3. 3.Gastroenterology DivisionBakırkoy State HospitalIstanbulTurkey
  4. 4.Unimed Special Gastroenterology CenterIstanbulTurkey
  5. 5.Erdem HospitalIstanbulTurkey

Personalised recommendations