We report the first description of sevelamer crystals (Renagel and Renvela, Genzyme; phosphate-lowering agents) in the gastrointestinal tract. We prospectively collected cases with novel, histologically identical crystals from 4 major academic centers over a 1-year period and studied pertinent clinicopathologic features. Sevelamer usage in the setting of chronic kidney disease was demonstrated in all cases (n=15 total cases, 7 patients). Sites of involvement included the esophagus (n=2), small bowel (n=2), and colon (n=11). The background mucosa was normal in only 1 case. Notable mucosal abnormality included chronic mucosal damage (n=5), acute inflammation (n=4), inflammatory polyp (n=2), extensive ulceration (n=2), ischemia (n=1), and necrosis (n=1). In general, sevelamer crystals displayed broad, curved, and irregularly spaced "fish scales" with a variably eosinophilic to rusty brown color on hematoxylin and eosin (H&E) staining and violet color on periodic acid-Schiff-alcian special staining with diastase (PAS/D). To validate these findings, sevelamer tablets (Renvela) were crushed and submitted for histologic processing; the findings were identical to those in the patient specimens. The possibility of Kayexalate (sodium polystyrene sulfonate) and cholestyramine had been raised in error. However, Kayexalate has narrow, rectangular "fish scales" and is violet on H&E and magenta on PAS/D; cholestyramine lacks internal "fish scales," is bright orange on H&E, variably gray or hot pink on PAS/D, and is unassociated with mucosal injury. Further study is required to determine whether sevelamer plays a causal role in these injuries; however, its crystal is an important mimic of both Kayexalate and choleystyramine. As the history of sevelamer administration was not documented in any pathology requisition, awareness of sevelamer's characteristic morphology is crucial to avoid the diagnostic pitfalls of its mimics.
The present study was undertaken to investigate how a somatostatin analog (201-995 Sandoz), which is now commonly used for treatment of patients with gut hormone-producing tumors, affects water and ion absorption and transit time in the normal jejunum. Six healthy volunteers were given somatostatin analog intravenously at a dose of 1 microgram/kg/hr. At the same time, jejunal water and ion movement and transit time were measured using the triple-lumen tube technique [perfusion of a plasma-like electrolyte solution with PEG as a nonabsorbable marker at a rate of 15 ml/min; dye dilution curves ([3H]mannitol, [14C]PEG, BSP) for determination of jejunal transit time]. During somatostatin analog administration, transit time through a 30-cm segment of perfused jejunum increased from 4.0 min to 17.0 min. While the somatostatin analog increased jejunal transit time, it had no effect on net water and electrolyte absorption under steady-state conditions. The effect of somatostatin analog on the proximal small bowel is similar to the action of an eight-times higher dose of intravenous native somatostatin previously studied. The effect of the analog on transit time suggests a potentially beneficial effect in patients with large-volume diarrhea in which no tumor or circulating secretagogue can be identified, such as in pseudopancreatic cholera syndrome.
We randomly assigned 95 patients with large esophageal varices (Grade 3 or 4) who had not previously had upper gastrointestinal tract bleeding to two groups: 49 received intravariceal sclerotherapy, and 46 were followed as controls. Over a mean follow-up of 13 months there was no difference between the sclerotherapy group and the control group in mortality (24.4 percent) or any significant difference in average hospital stay per month (3.0 vs. 2.6 days). Sclerotherapy was associated with significantly more episodes of upper gastrointestinal bleeding (26 vs. 10 episodes, P less than 0.05); 75 percent of deaths in the sclerotherapy group were related to bleeding, as compared with 18 percent in the control group. An additional 54 patients with cirrhosis who did not qualify for the study were also followed--20 with small varices and 34 with none. Mortality was 20 and 15 percent, respectively; no deaths were due to bleeding. We conclude that prophylactic sclerotherapy does not provide clinical benefit to patients with large esophageal varices.
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