Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with idiopathic ulcerative colitis (UC) have a colonbound antibody (CCA-IgG) that reacts with colon tissue extracts. We have partially characterized a colonic protein that is specifically recognized by CCA-IgG. CCA-IgG was eluted from operative colon specimens from 10 patients with UC. A colon tissue-bound IgG was similarly eluted from six patients with Crohn's colitis, two with ischemic colitis, and one with diverticulitis. Purified serum IgG from patients with Crohn's disease, from normal subjects and a patient with myeloma were also used as additional controls. For detection of antigen(s), tissue extracts were prepared from 26 specimens of colon (UC, 12; Crohn's disease, 6; normal, 4; other controls, 4), 8 specimens of human normal stomach, duodenum, ileum, and liver (2 each). Tissue extracts were also prepared from rats and mice, including germ-free rat colons and rat's fetal colons. Immunorecognition of CCA-IgG to the tissue extracts was examined by affinity-column chromatography and by transblot analysis. Tissue-extracted proteins were electrophoresed in SDS-polyacrylamide gel, transferred to nitrocellulose sheet, and probed with iodinated CCA-IgG, colonic IgG from other inflammatory bowel disease patients, UC serum IgG, and control serum IgG. Although many proteins were present in colon tissue extracts, 9 of 10 CCA-IgG consistently recognized a protein of 40 kD. None of the nine IgG preparations from colon specimens of patients with Crohn's colitis and other colonic inflammatory diseases reacted with the 40-kD protein. Five of six symptomatic UC serum IgG and none of eight control serum IgG reacted with the 40-kD protein. The 40-kD protein was present in all colon specimens and it appeared to be organ specific. It was absent in mouse and rat tissues, including colon. The 40-kD protein is not actin and nor a part of the Ig molecule. These results suggest that the 40-kD protein is a colonic "autoantigen" that may initiate a specific IgG antibody response in UC.
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PMID:Isolation and characterization of a colonic autoantigen specifically recognized by colon tissue-bound immunoglobulin G from idiopathic ulcerative colitis. 401 82

A significant increase has been reported in reticuloendothelial neoplasms in patients with inflammatory bowel diseases. We present two rare cases of multiple myeloma in patients with inflammatory bowel diseases. One was in a 58-year-old woman with ulcerative colitis, and the other was in a 59-year old woman with Crohn's disease. In both patients, multiple myeloma occurred during long-term observation of inflammatory bowel disease and during the inactive stage of intestinal inflammation. The multiple myeloma appeared to have resulted from monoclonal gammopathy of undertermined significance in both patients, and was diagnosed by characteristic serum and bone marrow findings. Our findings suggested that multiple myeloma should be particularly considered in women of middle or advanced age with ulcerative colitis or Crohn's colitis and serum monoclonal gammopathy.
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PMID:Two cases of inflammatory bowel disease with multiple myeloma. 1053 94

Under normal conditions, the colorectal mucosa exhibits small numbers of scattered lymphocytes and plasma cells in the lamina propria and only few mucosal lymphoid aggregates (MLAs). In Crohn's colitis, the number of lymphocytes and plasma cells in the lamina propria and of MLA is substantially increased. In addition, multiple lymphoid aggregates are newly formed in the submucosa (submucosal lymphoid aggregate (SLA)) and deeper. The aim of the present study was to investigate the cellular immune response in MLA, in SLA, and in the lamina propria in Crohn's colitis. Fifty-nine colorectal biopsies/surgical specimens with or without inflammatory diseases were challenged with multiple myeloma 1 (MUM1) that highlights activated T cells, committed B cells, and plasma cells (aT/cB/PC). The number of MUM1-positive aT/cB/PC per high-power field (HPF) in MLA and in SLA was significantly lower in Crohn's colitis than in controls (p < 0.05). In contrast, the number of MUM1-positive aT/cB/PC per HPF in the lamina propria was significantly higher in Crohn's colitis and in other forms of chronic colitis than in controls (p < 0.05). The paucity of MUM1-positive cells in MLA and in SLA in Crohn's colitis might be caused by an increased number of MUM1-negative precursors. These precursors would eventually migrate into the lamina propria to differentiate into aT/cB/PC, complying thereby with the immunological mucosal demands generated by the on-going chronic inflammation.
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PMID:Lymphoid aggregates in Crohn's colitis and mucosal immunity. 2397 5