Short- and long-term follow-up of treatment for lymphocytic and collagenous colitis.

Collagenous colitis and lymphocytic colitis cause chronic watery diarrhea. Multiple therapies have been found to improve symptoms but there have been few long-term follow-up studies. Our goal was to obtain long-term clinical follow-up on a cohort of patients with independently confirmed typical histopathologic changes. Pathology slides from 32 cases of collagenous or lymphocytic colitis patients from 1988-1992 were independently reviewed. Twenty-five cases were confirmed by both groups of pathologist as collagenous or lymphocytic colitis. For these 25 patients, charts were reviewed and telephone follow-up interviews were performed in 1992 and 1995. Seven of 32 (22%) of the original cases were not confirmed on independent pathologic interpretation. A 15.8% discordance rate was found between the different groups of pathologists. Patient demographics were similar to previously published reports except one-half of our patients had diarrhea of only 6 months or less. Eighty-one percent of patients receiving 5-ASA agents reported improvement as well as 100% of those receiving prednisone. At 23 month follow-up 86% of patients reported improvement in diarrhea and only 32% required routine medications. At 47 month follow-up all patients reported improved diarrhea and only 29% required routine medications. Collagenous and lymphocytic colitis can sometimes be identified in patients with relatively brief duration diarrhea. Clinical parameters and response to therapy are similar for collagenous or lymphocytic colitis. Most patients with lymphocytic and collagenous colitis improve with therapy such as 5-ASA preparations or steroids. Over a follow-up period of several years, most patients have improvement in diarrhea and generally do not require maintenance medications. Independent pathologic confirmation of the diagnosis should be obtained in patients not responding to therapy.

An evaluation of the need for shared blood donor deferral registries.

OBJECTIVE: This study examined the frequency with which allogeneic, volunteer blood donors who had been deferred from donation at one blood collection facility donated, or attempted to donate, at a second blood collection facility. METHODS: The blood donor computer files of two local blood collection facilities were-combined and matched donors on the donor deferral registry of each blood collection facility were identified. RESULTS: Of 26,300 donors in the hospital-based blood bank file, 6732 (25.6%) were matched to the community blood center donor file (active donor base approximately 275,000). Matched donors on the donor deferral registry at each blood collection facility numbered 427 (6.3% of total matched donors). A total of 103 evaluable donors (1.5% of total, or 24.1% of deferred, matched donors) had been deferred at one blood collection facility and then later donated, or attempted donation, at the other blood collection facility. Of these 103, 51 were allogeneic donors who had been notified of their deferral status and should not have subsequently attempted blood donation. Thirty-two donors on the donor deferral registry of one blood collection facility made donations at the second blood collection facility which entered the general blood inventory. CONCLUSION: Shared donor deferral registries may be valuable at the local or regional level to prevent deferred blood donors from donating at other blood collection facilities. Whether or not a national donor deferral registry would be efficacious remains to be proven and deserves further study.

Leukocyte adhesion molecules and x-ray energy dispersive spectroscopy in Sturge-Weber disease.

We examined the light microscopic and ultrastructural features associated with Sturge-Weber disease, including x-ray energy dispersive spectroscopy to evaluate the chemical composition of the mineralized deposits and immunofluorescence microscopy with leukocyte adhesion molecules to examine the blood vessel proliferation further. Two patients (a 17-year-old girl and a 9-month-old boy) with Sturge-Weber disease comprise this series. Mineralized deposits stained strongly positive with von Kossa and negative with Prussian blue. Transmission electron microscopy of tissue removed during a functional hemispherectomy procedure in both cases indicated that most concretions were adjacent to or in the basal lamina of parenchymal vessels; no deposits were observed in leptomeningeal vessels. Energy dispersive spectroscopy of the deposits showed emission peaks corresponding predominantly to calcium, with lesser amounts of phosphorus. Fluorescent monoclonal antibodies to leukocyte adhesion molecules (endothelial cell, vascular cell, and intercellular: ELAM-1, VCAM-1, and ICAM-1) demonstrated strong positive staining of the meningeal vessels with all three antibodies. Cortical vessels were positive only for ICAM-1. Findings based on routine staining and energy dispersive spectroscopy indicate that the mineralized deposits detected in Sturge-Weber disease are composed primarily of calcium phosphate and are located primarily in and adjacent to the vascular basal lamina. There is an aberrant expression of ELAM-1 and VCAM-1 in the meningeal vascular proliferation similar to what is observed with other vascular malformations and tumors. Parenchymal vessel changes may be secondary to the meningeal vascular proliferation.