Post-feeding hyperammonaemia in patients with transjugular intrahepatic portosystemic shunt and liver cirrhosis: role of small intestinal ammonia release and route of nutrient administration.

BACKGROUND: Hyperammonaemia is a pathogenetic factor for hepatic encephalopathy that may be augmented after a transjugular intrahepatic portosystemic shunt (TIPS). Experimental data suggest that hyperammonaemia may be caused to a large extent by metabolism of small intestinal enterocytes rather than colonic bacteria. AIMS: To evaluate if ammonia release and glutamine metabolism by small intestinal mucosa contribute to hyperammonaemia in vivo in patients with liver cirrhosis. METHODS: Using TIPS to examine mesenteric venous blood, we measured mesenteric venous-arterial concentration differences in ammonia and glutamine in patients with liver cirrhosis before, during, and after enteral (n = 8) or parenteral (n = 8) isonitrogenous infusion of a glutamine containing amino acid solution. RESULTS: During enteral nutrient infusion, ammonia release increased rapidly compared with the post-absorptive state (65 (58-73) v. 107 (95-119) micromol/l after 15 min; mean (95% confidence interval)) in contrast with parenteral infusion (50 (41-59) v. 62 (47-77) micromol/l). This resulted in a higher portal ammonia load (29 (21-36) v. 14 (8-21) mmol/l/240 minutes) and a higher degree of systemic hyperammonaemia (14 (11-17) v. 9 (6-12) mmol/l/240 minutes) during enteral than parenteral infusion. The mesenteric venous-arterial concentration difference in glutamine changed from net uptake to release at the end of the enteral infusion period (-100 (-58 to -141) v. 31 (-47-110) micromol/l) with no change during parenteral nutrition. CONCLUSIONS: These data suggest that small intestinal metabolism contributes to post-feeding hyperammonaemia in patients with cirrhosis. When artificial nutrition is required, parenteral nutrition may be superior to enteral nutrition in patients with portosystemic shunting because of the lower degree of systemic hyperammonaemia.

Leukocyte counts in cerebrospinal fluid with the automated hematology analyzer CellDyn 3500 and the urine flow cytometer UF-100.

BACKGROUND: The counting of leukocytes and erythrocytes in cerebrospinal fluid (CSF) is still performed microscopically, e.g., using a chamber in most laboratories. This requires sufficient practical experience, is time-consuming, and may constitute a problem in emergency diagnostics. Specific automated systems for CSF cell counting are not available at present. METHODS: We tested the hematology analyzer CellDyn 3500 (CD) and the urine flow cytometer UF-100 (UF), which are not designed for CSF analysis. We studied >104 samples with both analyzers, and the counts obtained were compared with the reference method (Fuchs-Rosenthal chamber). RESULTS: Good linearity in the medically relevant range of 15 x 10(6) to 1000 x 10(6) leukocytes/L and a high degree of within-run accuracy were seen for both analyzers. Cell counting on the UF was excellent, especially when low cell counts were encountered (CV, 4. 9% compared with 28% observed for the CD). Method comparison showed that identical results could be detected for a majority of the count pairs. For a few samples, there was a discrepancy between the results from the analyzers and the counting chamber. In most cases, these were CSF samples containing a high proportion of lymphocytes. For these samples, the CD result led to a false-positive high leukocyte count, and on the UF these cells were not allocated to the leukocyte population, thus leading to false-negative counts. CONCLUSIONS: Both analyzers should not be used for CSF cell counting in all cases at present. However, once the technical and software problems have been solved, routine use of the two analyzers for CSF analysis should be seriously contemplated.