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. 1985 Feb;26(2):151–157. doi: 10.1136/gut.26.2.151

Familial occurrence of complement dysfunction in Crohn's disease: correlation with intestinal symptoms and hypercatabolism of complement.

J Elmgreen, H Both, V Binder
PMCID: PMC1432432  PMID: 3967833

Abstract

Complement was studied in Crohn's disease probands with early onset and in their first degree relatives. Controls included 24 healthy volunteers and 24 patients with ulcerative colitis or peptic ulcers. Subnormal generation of chemotactic activity by the alternative pathway was shown in eight of 21 probands and in six of 33 relatives, a frequency in both groups significantly different from controls (p less than 0.005), with a strong connection between findings in patients and relatives. As previously shown in patients with Crohn's disease, the subnormal generation was related to decreased utilisation of complement C3 in relatives. Raised levels of circulating complement C3c split products suggested complement involvement in Crohn's disease probands. In contrast, plasma C3c was normal in all relatives, and none of the six cases with complement dysfunction had gastrointestinal symptoms or a history of inflammatory bowel disease. Our data suggest, that complement abnormality seen in Crohn's disease patients does not simply reflect mucosal inflammation or hypercatabolism of complement.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Ament M. E., Ochs H. D. Gastrointestinal manifestations of chronic granulomatous disease. N Engl J Med. 1973 Feb 22;288(8):382–387. doi: 10.1056/NEJM197302222880802. [DOI] [PubMed] [Google Scholar]
  2. Berkowicz A., Rosenkvist J., Sørensen H. A single step immunoelectrophoresis method for the quantitation of complement C3c in biological fluids. J Immunol Methods. 1983 Jun 10;60(3):277–288. doi: 10.1016/0022-1759(83)90286-7. [DOI] [PubMed] [Google Scholar]
  3. Binder V. A comparison between clinical state, macroscopic and microscopic appearances of rectal mucosa, and cytologic picture of mucosal exudate in ulcerative colitis. Scand J Gastroenterol. 1970;5(7):627–632. [PubMed] [Google Scholar]
  4. D'Amelio R., Rossi P., Le Moli S., Ricci R., Montano S., Pallone F. In vitro studies on cellular and humoral chemotaxis in Crohn's disease using the under agarose gel technique. Gut. 1981 Jul;22(7):566–570. doi: 10.1136/gut.22.7.566. [DOI] [PMC free article] [PubMed] [Google Scholar]
  5. Elmgreen J., Berkowicz A., Sørensen H. Defective release of C5a related chemo-attractant activity from complement in Crohn's disease. Gut. 1983 Jun;24(6):525–531. doi: 10.1136/gut.24.6.525. [DOI] [PMC free article] [PubMed] [Google Scholar]
  6. Elmgreen J., Berkowicz A., Sørensen H. Hypercatabolism of complement in Crohn's disease--assessment of circulating C3c. Acta Med Scand. 1983;214(5):403–407. doi: 10.1111/j.0954-6820.1983.tb08615.x. [DOI] [PubMed] [Google Scholar]
  7. Elmgreen J. Subnormal activation of phagocytes by complement in chronic inflammatory bowel disease? Neutrophil chemotaxis to complement split product C5a. Gut. 1984 Jul;25(7):737–742. doi: 10.1136/gut.25.7.737. [DOI] [PMC free article] [PubMed] [Google Scholar]
  8. Farmer R. G., Michener W. M., Mortimer E. A. Studies of family history among patients with inflammatory bowel disease. Clin Gastroenterol. 1980 May;9(2):271–277. [PubMed] [Google Scholar]
  9. Hodgson H. J., Potter B. J., Jewell D. P. C3 metabolism in ulcerative colitis and Crohn's disease. Clin Exp Immunol. 1977 Jun;28(3):490–495. [PMC free article] [PubMed] [Google Scholar]
  10. Laurell C. B. Quantitative estimation of proteins by electrophoresis in agarose gel containing antibodies. Anal Biochem. 1966 Apr;15(1):45–52. doi: 10.1016/0003-2697(66)90246-6. [DOI] [PubMed] [Google Scholar]
  11. Lewkonia R. M., McConnell R. B. Progress report. Familial inflammatory bowel disease--heredity or environment? Gut. 1976 Mar;17(3):235–243. doi: 10.1136/gut.17.3.235. [DOI] [PMC free article] [PubMed] [Google Scholar]
  12. Potter B. J., Brown D. J., Watson A., Jewell D. P. Complement inhibitors and immunoconglutinins in ulcerative colitis and Crohn's disease. Gut. 1980 Dec;21(12):1030–1034. doi: 10.1136/gut.21.12.1030. [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. Rhodes J. M., Potter B. J., Brown D. J., Jewell D. P. Serum inhibitors of leukocyte chemotaxis in Crohn's disease and ulcerative colitis. Gastroenterology. 1982 Jun;82(6):1327–1334. [PubMed] [Google Scholar]
  14. Singer H. C., Anderson J. G., Frischer H., Kirsner J. B. Familial aspects of inflammatory bowel disease. Gastroenterology. 1971 Oct;61(4):423–430. [PubMed] [Google Scholar]
  15. Teisberg P. In vivo activation of C3 revealed by crossed immunoelectrophoresis as a parameter of immunological activity in disease. Clin Chim Acta. 1975 Jul 9;62(1):35–41. doi: 10.1016/0009-8981(75)90277-6. [DOI] [PubMed] [Google Scholar]
  16. Zigmond S. H., Hirsch J. G. Leukocyte locomotion and chemotaxis. New methods for evaluation, and demonstration of a cell-derived chemotactic factor. J Exp Med. 1973 Feb 1;137(2):387–410. doi: 10.1084/jem.137.2.387. [DOI] [PMC free article] [PubMed] [Google Scholar]

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