Extracorporeal Treatment in Severe Hypertriglyceridemia-Induced Pancreatitis.

Plasmapheresis is a well-accepted treatment option in severe hypertriglyceridemia-induced pancreatitis (HTGP). The rationale behind this approach is the depletion of triglycerides and the reduction of inflammatory cytokines. The time span between onset of clinical symptoms and start of plasmapheresis might have an important impact on mortality. Hyperviscosity of patients' plasma represents another special challenge for the applied separation technology. The procedures can be performed either by centrifugal device (CFD) or membrane based (MBS) units. The present study reports the outcome of 10 patients suffering from HTG. The expected mortality of the collective was 25%. Plasmapheresis was started after an average 16.3 h (SD ± 6.7 h) after onset of symptoms. No mortality occurred. Apheresis was statistically equally effective with both devices. A median of 3 sessions reduced the TG level to normal and correlated with patients' improvement. During follow up, three patients developed a pancreatic pseudocyst requiring surgical intervention without further complication.

The effect of hemodialysis on liver stiffness measurement: a single-center series.

BACKGROUND/AIMS: The noninvasive measurement of liver stiffness using transient elastography (TE) is increasingly being used alongside liver biopsy. However, several conditions may lead to higher liver stiffness values without reflecting more fibrosis. Such conditions (e.g. hepatitis, cholestasis, heart failure, mechanical ventilation) limit the interpretation of liver stiffness measurements. The influence of hemodialysis on the measurement of liver stiffness has not been investigated to date. Here, we analyzed liver stiffness assessed by fibroscan in 17 patients directly before and after a hemodialysis session. PATIENTS AND METHODS: Measurement of hepatic stiffness by TE was carried out using the Fibroscan device with the 'M probe' directly before and directly after one session of hemodialysis. Each measurement consisted of at least 10 individual and valid measurements, with a success rate of at least 60%, and an interquartile range of less than 25%. All measurements were carried out by one investigator not involved in patient management. RESULTS: Before dialysis, the median TE was 5.1 kPa (2.8-17 kPa). Ten patients had values below the threshold of 7.1 kPa and seven patients had TE>7.1 kPa. The median net fluid withdrawal by hemodialysis was 2.5 l (0.4-3.1 l) and did not differ between patients. After dialysis, the TE median was 7.4 kPa (3.5-12.5 kPa) and had changed in all patients except one. Liver stiffness increased significantly when the initial TE was lower than 7.1 kPa (P=0.05), but not when the initial TE was higher than 7.1 kPa. Furthermore, the magnitude of the change in TE after hemodialysis correlated inversely with the liver stiffness before hemodialysis (P=0.03) and with spleen length measured by ultrasound (P=0.03). CONCLUSION: This study is the first to report on the influence of hemodialysis on liver stiffness measurement. In contrast to previous reports, liver stiffness might increase after fluid withdrawal if patients do not show significant fibrosis. We conclude that before dialysis, TE possibly better differentiates between patients with or without significant fibrosis.

Serum levels of beta-trace protein and its association to diuresis in haemodialysis patients.

BACKGROUND: Beta-trace protein (BTP) has been proposed as an alternative endogenous marker of the glomerular filtration rate. However, possible determinants of BTP in ESRD patients undergoing regular renal replacement therapy have not been evaluated. METHODS: Serum levels of BTP, beta-2-microglobulin, creatinine and urea were analysed before and after dialysis treatment in 73 patients [haemodialysis (HD) n=52; haemodiafiltration (HDF) n=21]. Patients were categorized into four groups with residual diuresis (RD)<0.5 l/day (group 1; n=24), 0.5-1 l/day (group 2; n=18), 1.1-1.5 l/day (group 3; n=12) and >1.5 l/day (group 4; n=19). Subsequently RD was compared to pre-treatment levels of BTP. RESULTS: HD treatment did not affect BTP serum levels [pre-treatment 8.1+/-4.1 mg/l (mean+SD) vs post-treatment 7.7+/-4.1 mg/l; -0.6 +/- 16.1%; ns]. However, in 6 out of 21 patients undergoing HDF BTP levels were reduced by more than 20%. Overall, the resulting decrease in serum concentration was minuscule (9.6+/-6.2 vs 8.3+/-4.9 mg/l; -14+/-21.9%; P=0.03). BTP serum levels were tightly associated to RD of the four groups. Comparison of BTP levels showed significant differences between patients of groups 1 vs 3 and 4 as well as 2 vs 4. CONCLUSIONS: BTP serum levels may serve as a surrogate marker for residual renal function since HD and HDF do not exert clinical relevant alterations on them. Furthermore, BTP serum concentrations appear strongly associated to RD.