Hey, Bill:
They found "Crohn's-like microlesions" in a majority of people with AS who were studied. The problems with this are not limited to 1) where they were looking (the terminal ileum), 2) the method used (needle biopsy?), and 3) definitive criteria.
In fact, LGS cannot always be so easily identified and quantified, but the only way the germ can trigger a secondary immune response is to actually be present in blood/lymph (actually lymph in the case of AS, and twice as probable there due to the fact there are twice as many lymph ducts on the intestinal tract as there are blood capillaries.
The thing is that in Crohn's disease, the lesions might be much higher in the alimentary process, but in Reiter's-origin AS, they are certainly lower than typical--transverse colon, for example. The researchers did not take biopsies along the entire tract, and once they got these they might not have been able to determine whether there was an actual "lesion" or just wider than normal spaces between cells.
Dr. Dean (Edell) recently made the comment about needle biopsies: "bake an olive in a loaf of bread and shove a needle into the loaf. The chances of missing the olive are greater than the chances of hitting it."
I go with the fact of IgA-Kp being produced as proof of LGS and I do not think that Ebringer would object to this characterization--but we will ask him soon.
How is the Serpentine this year?
John
