Postinterventional passive expansion of partially dilated transjugular intrahepatic portosystemic shunt stents.

PURPOSE: To investigate passive transjugular intrahepatic portosystemic shunt (TIPS) stent expansion in patients with intentional "underdilation" (eg, 10-mm stent, 8-mm balloon) during TIPS creation. MATERIALS AND METHODS: Custom in-house software was developed for objective quantification of cross-sectional stent area from computed tomography (CT) data. The technique was validated by in vitro experiments. The study included 39 patients (22 men; mean age, 59.2 y) who underwent TIPS creation (VIATORR stent graft [W. L. Gore & Associates, Flagstaff, Arizona]; n = 29; WALLSTENT endoprosthesis [Boston Scientific, Marlborough, Massachusetts], n = 10) with stent underdilation. Follow-up CT data of the patients were used to quantify in vivo stent area changes. Data were analyzed by variance analysis and entered into a general linear model to test for interrelations between stent area changes and clinical (eg, cirrhosis grade) and procedural parameters. RESULTS: In vitro validation of the in-house software showed good agreement and reproducibility without overestimation of stent area. Mean clinical follow-up time in patients was 787 days (range, 7-2,450 d). At the time of intervention, VIATORR stent grafts and WALLSTENT endoprostheses were dilated to an average of 64.4% ± 2.3% and 65.63% ± 8.52% of nominal area, respectively. At the last imaging follow-up evaluation, this value had increased in all stents to a mean of 87.8% ± 7.9% (VIATORR) and 82.34% ± 19.6% (WALLSTENT) in the TIPS tract (P < .05). Multivariate analysis revealed the time after intervention to be the only predictor of stent area in the TIPS tract. There was no significant association between stent expansion and clinical or procedure-related parameters. CONCLUSIONS: The area of self-expanding stents implanted in the liver for TIPS creation with dilation to less than nominal diameter significantly increases over time. This increase has to be considered as an additional factor influencing the long-term portosystemic gradient.

Serum leptin and cytokines in whole blood in relation to clinical and nutritional status in cystic fibrosis.

OBJECTIVES: Leptin plays an important role in the energy balance and may be affected by hormonal and metabolic derangement associated with chronic disease. The aim of this study was to assess the correlation between leptin, proinflammatory cytokines and nutritional status with regard to clinical status in homozygous delta F 508 cystic fibrosis patients. METHODS: Patients with mild (Shwachman score 71-100 points, group A) disease were compared with those with moderate disease (Shwachman score 41-55 points, group B) and age-matched controls (group C, n = 22). Leptin was assessed by enzyme-linked immunosorbent assay and cytokines (interleukin-8, tumor necrosis factor alpha) before and after stimulation with 5 ng lipopolysaccharide by a chemiluminescent immunometric assay. RESULTS: Twenty-two patients were recruited for each group (median A/B/C forced expiratory volume in 1 second 80%/59%/-; median age 12/13.5/12.5 years). Leptin (median 3.25/2.65/3.3 pg/mL; P = 0.083) and body mass index were lower (group A/B/C 18.55/16.75/20.5 kg/m(2); P = 0.023), but dietary intake was significantly higher (group A/B/C 50.5/68/43 kcal/kg body weight; P = 0.026) in moderate disease. Cytokines before stimulation with lipopolysaccharide were highest in moderate disease, but there was no significant difference after stimulation (interleukin-8 median A/B/C before--15/25.1/8.0 pg/mL, P < 0.005; after--570.5/573.5/415.5 pg/mL, not significant; tumor necrosis factor alpha median A/B/C 43/56/30 pg/mL, P < 0.0001; 580/427/720.5 pg/mL, not significant.). CONCLUSIONS: There is a physiological regulation of leptin even in more advanced states of disease with significantly lower body mass index than controls. However, our data do not support the idea of elevated cytokine levels inducing anorexia in homozygous delta F 508 cystic fibrosis patients.

Interleukin-8 in whole blood and clinical status in cystic fibrosis.

Cytokines and polymorphonuclear leukocytes play a key role in immune mediated inflammation in progressive pulmonary damage due to cystic fibrosis. The aim of this study is to establish a simple measure of the host's propensity to secrete inflammatory cytokines and to correlate this with clinical status. Patients (n=44, median age 16 years) with the DeltaF 508 mutation (homozygous) were grouped according to their Shwachman score: Patients with mild disease (Shwachman score 71-100 points, group A, n=22, median FEV(1) 79%) were compared with those with more severe disease (Shwachman score 41-55 points, group B, n=22, median FEV(1) 55%) and age-matched controls (group C, n=22, median FEV(1) 102%). Whole blood was stimulated with 5 ng of lipopolysaccharide (LPS). Interleukin-8 (IL-8) was measured by chemiluminescent immunometric assay (DPC, Bad Nauheim, Germany). Though there was a significant difference at baseline for IL-8 (median group A/B/C 6.1/30.5/5.8 pg/ml; p<0.001), there was no significant difference after stimulation. Moreover, in Pseudomonas aeruginosa positive (Psa+) patients (n=26) there was a significant negative correlation (r=-0.539; p<0.004) between baseline IL-8 and FEV(1) (%). Clinical course and lung function (in Psa+) correlate with IL-8 levels.

Lipopolysaccharide binding protein, cytokine production in whole blood, and lipoproteins in cystic fibrosis.

According to the endotoxin lipoprotein hypothesis, lipoproteins may down-regulate cytokine production by neutralizing lipopolysaccharide (LPS) binding protein (LBP) complexes. We investigated the correlation between lipoproteins, LBP, cytokine production, and clinical status in Delta F 508 (homozygous) individuals. Cystic fibrosis patients with mild disease were compared with those with more severe disease and age-matched controls. LBP, IL-8, and tumor necrosis factor-alpha, using a chemiluminescent immunometric assay, and fat intake, as well as serum triglycerides, cholesterol, very low density lipoprotein, LDL, and HDL were measured. In more severe disease there was a correlation between maximum expiratory flow at 25% of vital capacity and HDL. To adjust for the influence of colonization with Pseudomonas aeruginosa, those who were colonized with P. aeruginosa were analyzed separately. There was a significant correlation between LBP and forced expiratory volume in 1 s. Lipoproteins may have a modulating effect in more advanced disease and are not influenced by fat intake. LBP correlates those who were colonized with P. aeruginosa (Psa+) with clinical status as well as lung function and may be a critical molecule regulating LPS-induced inflammation.