POSSIBLE DIAGNOSTIC TEST FOR CROHN'S DISEASE BY USE OF BUCCAL MUCOSA

doi:10.1016/S0140-6736(78)92648-X

The Lancet

Volume 312, Issue 8093, 7 October 1978, Pages 759-760

https://doi.org/10.1016/S0140-6736(78)92648-X Get rights and content

Abstract

Immunofluorescent tracing was used on buccal mucosa from patients with Crohn's disease to investigate some of its immunological characteristics, and to compare these with those of mucosa from controls. Normal buccal mucosa from patients with Crohn's disease, incubated with its own serum then stained for deposited antibody by the fluorescent technique, showed a positive reaction, not observed in buccal mucosa from normal persons or patients with ulcerative colitis. These observations could provide the basis of a diagnostic test.

References (2)

R.C. Nairn
Fluorescent Protein Tracing
(1969)

There are more references available in the full text version of this article.

Cited by (10)

Autoimmunity in Crohn's Disease—A Putative Stratification Factor of the Clinical Phenotype
2016, Advances in Clinical Chemistry
Citation Excerpt :
IBD could be considered to be an autoimmune as autoantibodies against antigens expressed by enteric epithelial cells and leucocytes have been described as early as 1950 [12]. Early rudimentary immunofluorescent tracing assays demonstrated that sera from patients with CD possessed autoantibodies to buccal mucosa from same patients, as compared to matched controls [31]. While autoimmunity has been mostly demonstrated against intestinal neutrophilic and goblet cell antigens, Stöcker et al. have also reported the association of CD with pancreatic autoimmune antibody (PAb) responses [32–34].
Inflammation in inflammatory bowel diseases (IBD) has been linked to a loss of tolerance to self-antigens suggesting the existence of autoantibodies in specific disease phenotypes. However, the lack of clearly defined autoantigenic targets has slowed down research. Genome-wide association studies have identified an impressive number of immune-related susceptibility loci for IBD with no clearly discernible pattern among them. Growing evidence supports the hypothesis that innate immune responses to a low-diversity and impaired gut microbiota may be of key importance in initiating and perpetuating chronic inflammation in IBD. Increasing evidence suggests that reduced microbial diversity and microbial–mucosal epithelium interaction (including adhesion and clearance) are critically involved in IBD pathogenesis.
Along these lines the discovery of autoantigenic targets in Crohn's disease (CD) has refocused research in IBD on the possible role of autoimmune responses. The identification of the major zymogen granule membrane glycoprotein 2 (GP2) as an autoantigen in CD patients and its proposed role in the sensing of the microbiota lends credence to this trend. Loss of tolerance to GP2 occurs in up to 40% of patients with CD. Corresponding autoantibodies appear to be associated with distinct disease courses (types or phenotypes) in CD. Here, we critically review autoantibodies in CD for their impact on clinical practice and future IBD research. The immunomodulatory role of GP2 in innate and adaptive intestinal immunity is also discussed.
Diagnosis and classification of Crohn's disease
2014, Autoimmunity Reviews
Citation Excerpt :
Autoimmunity is assumed to be another major contributor to the pathogenesis in IBD. First reports of autoimmune responses in patients with CrD can be traced back to the late 1970s [12]. In 1984, loss of tolerance to exocrine pancreatic targets was detected in CrD [13].
Crohn's disease (CrD) is a chronic relapsing inflammatory bowel disease (IBD) potentially affecting any portion of the gastrointestinal tract from the mouth to the anus. CrD usually manifests between 15 and 30 years of age and presents typically with abdominal pain, fever, bloody or non-bloody diarrhoea, and weight loss. Paediatric patients may show failure to thrive, growth impairment, and delayed puberty additionally. Extraintestinal manifestations like arthritis, uveitis, and erythema nodosum are diagnosed in almost half of the patients. CrD is characterized by a discontinuous and ulcerous transmural inflammation often involving the ileocaecal region and leading to a stricturing or even fistulising phenotype in up to 50% of patients finally. Incidence and prevalence of CrD have been rising worldwide over the past decades. Although many details of the pathophysiology of CrD have been elucidated, no common aetiopathogenic model exists for all forms of CrD, presenting more an umbrella term for a phenotypically and genotypically heterogeneous clinical condition. In CrD, we see an inappropriate response of the innate and/or adaptive immune system to the intestinal microbiota in genetically predisposed individuals. The diagnosis of CrD is based mainly on patient's history and clinical examination and supported by serologic, radiologic, endoscopic, and histologic findings. Antibodies to Saccharomyces cerevisiae and autoantigenic targets such as glycoprotein 2 may aid in differentiating CrD from UC. Their single use, however, is limited by low sensitivity requiring antibody profiling for an appropriate serologic diagnosis. This review focuses on diagnostic and classification criteria of CrD.
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An unusual presentation of Wegener's granulomatosis is described in a 16.67-yr-old black woman with diarrhea, fever, weight loss, abdominal pain, arthralgias, and mouth ulcers, suggesting the diagnosis of inflammatory bowel disease. However, biopsy specimens of rectal mucosa, oro- and nasopharynx, and skin conclusively demonstrated the vasculitic lesion of Wegener's granulomatosis. Furthermore, cyclophosphamide therapy induced remission of clinical and histologic abnormalities. This case emphasizes the diagnostic value of taking biopsy specimens of oral lesions in patients with suspected inflammatory bowel disease and demonstrates that the presentation of Wegener's granulomatosis may mimic that of inflammatory bowel disease.
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POSSIBLE DIAGNOSTIC TEST FOR CROHN'S DISEASE BY USE OF BUCCAL MUCOSA

Abstract

Fluorescent Protein Tracing