PubMed · 11915427
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Jean Sutton. 2002. ABO incompatibility.. https://pubmed.ncbi.nlm.nih.gov/11915427/
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BACKGROUND: The major cause for chronic gastritis in human is the infection by the Helicobacter pylori. The blood group antigens present at the gastric mucous are described as possible receptor for this bacteria in the epithelium. The alterations in the expression of blood group patterns are associated with the development of gastric cancer. OBJECTIVES: Verify the H. pylori prevalence and examine the immunohistochemical distribution of the ABH and Lewis antigens expression to correlate with histopathological alterations. PATIENTS AND METHODS: From 63 chronic gastritis patients were investigated gastric biopsies, blood and saliva samples by dot-blot-ELISA, indirect immunoperoxidase and hematoxylin-eosin and Gram. RESULTS: No significant association between the presence of the bacteria and the ABH, Lewis and Secretor phenotype was found. For the majority of the patients the antigen expression of the ABH and Lewis blood group was restricted mainly to the foveola epithelium of the gastric mucosa, similar to the saliva. The inappropriate expression of these antigens occurred always in the presence of H. pylori and/or preneoplastic alterations of the gastric mucosa. In areas with intestinal metaplasias we also observed reduced reactivity for the H and Le b antigens and mainly the induced expression of Le . CONCLUSION: Alterations in the pattern of the glycosylation of this antigens are interesting, because they reflect different stages in the cellular differentiation and become potential markers in the diagnostic evaluation and prognosis of gastric pathologies.
BACKGROUND: Nonmyeloablative allogeneic hematopoietic stem-cell transplantation (NST) allows establishment of donor hematopoiesis without eradication of recipient stem cells by chemoradiotherapy. Quantification of donor chimerism may predict graft failure and relapse. METHODS: We quantified donor long-term culture-initiating cells (LTC-IC) in nine patients during the early phase after NST and lineage-specific donor cells of myeloid (CD33+, CD34+, granulocytes) and lymphoid lineage (CD3+, CD4+, CD8+, CD56+) in 38 patients with a median follow-up of 40 weeks after NST. Conditioning therapy consisted of fludarabine 90 mg/m2 followed by total body irradiation of 2 Gy. RESULTS: Only rapid establishment of donor T-cell chimerism was essential for stable donor engraftment. Patients with less than 90% of donor T cells 4 weeks after NST had a significantly higher risk of relapse, graft rejection, or both (14 of 18 patients) than patients with donor T-cell chimerism of 90% and higher (3 of 20 patients). Although conditioning therapy was nonmyeloablative, a significant decrease of repopulating stem cells defined as LTC-IC was seen after 2 weeks followed by rapid recovery of LTC-IC to pretransplant values. Interestingly, all LTC-IC were from donor origin 2 and 4 weeks after NST, but rapid establishment of donor LTC-IC was not predictive for progression-free survival. CONCLUSIONS: Rapid establishment of lymphoid but not myeloid donor chimerism is a prognostic factor for stable donor engraftment after NST. It seems that an immunologic shield of alloreactive donor T cells is essential for early hematopoietic progenitors.
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