Search

OBJECTIVES: The aims of the present study were to investigate the plasma concentration of endotoxin in patients with inflammatory bowel disease (IBD), the effect of metronidazole (MNZ) and of symbiotics on that concentration, and the relationship to IBD activity. METHODS: The study group comprised 26 patients with quiescent ulcerative colitis (UC), all of whom were on maintenance mesalazine treatment (1200− 2400 mg/day). The control group comprised 15 subjects. Blood samples were taken from all study subjects to measure: routine blood chemistry, endotoxin concentration, lipopolysaccharide binding protein (LBP) and macrophage-colony stimulating factor (M-CSF). All the IBD patients were randomly enrolled for a 2-week oral daily treatment regimen with either MNZ (250 mg t.i.d.) or the symbiotic mixture SCM-III (Lactobacillus acidophilus, L. helveticus and Bifidobacteria brevis in an ion- and vitamin-enriched medium; 3 mL t.i.d.). Following a 6-week washout period during which the patients continued their maintenance treatment, the cross-over study of the new treatments was begun. Blood parameters were checked at entry and 2 weeks after each treatment schedule. RESULTS: The concentration of endotoxin level in the UC patients, as a whole, was comparable with that of the control subjects. However, a separate group of patients with long-standing disease and pancolitis showed a statistically significant increase in toxin. SCM-III, but not MNZ, normalized this parameter. There was no statistical change in LBP and plasma endotoxin-inhibiting capacity in the IBD patients. The M-CSF concentration was increased in the UC group, particularly in the pancolitis subgroup. SCM-III, but not MNZ, significantly decreased the M-CSF concentration in the UC patients, but there was only an insignificant trend toward decrease in the subgroup. There was a significant correlation between M-CSF and endotoxin in the pancolitis subgroup (r: 0.74, P

AIM: The aim of the present study was to assess fecal organic acid excretion and gut flora changes in a group of patients with compensated liver cirrhosis without hepatic encephalopathy by comparing pro­biotic therapy with more common therapeutic approaches. METHODS: Thirty patients with compensated Child B liver cirrhosis were allocated into one of three matched groups, which were randomly given one of three 3-week oral treatments: (i) lactitol 20 g t.i.d.; (ii) 400 mg rifaximin b.i.d.; or (iii) the synbiotic SCM-III (Microflorana-F, Named, Lesmo, Italy) 10 mL t.i.d. Stool samples were collected at both the time of entry into the study and at the end of the trial period for the assessment of intestinal bacterial flora and for the determination of fecal pH and of organic acid concentration. RESULTS: All three tested compounds significantly increased the total anaerobic bacterial count to the same extent. The change was mainly due to a reduction in the Bacteriodes population and an expansion of the bifidobacteria population. However, only SCM-III significantly decreased the total count of Bacteroides and Clostridium. Lactitol and SCM-III decreased (to a similar extent) the fecal pH compared with healthy controls and with pretreatment values (P

Aim: The aim of the present investigation was to test study benzodiazepines (BZDs) profile in patients with viral cirrhosis under different combinations of rifaximine and of a novel symbiotic. Methods: Our study groups consisted of 30 patients with a confirmed diagnosis of HCV-related Child B liver cirrhosis. Patients were randomly allocated into three groups: rifaximine 400mg t.i.d. for 2 weeks; (B) SCM-III (Lactobacillus acidophilus, Lactobacillus helveticus and Bifidobacteria in a ion- and vitamin-enriched medium, Named srl, Italy) 10ml t.i.d. for 2 weeks; (C) rifaximine 400mg t.i.d. for 1 week followed by SCM-III 10ml t.i.d. for 5 weeks. At weekly interval, blood samples were withdrawn to test BZD-like substances, ammonia and endotoxin. Results: Rifaximine treatment brought about a significant early drop of BZDs ( [Formula: see text] versus pre-treatment and versus control) till fourth week of observation when a gradual increase took place with return to pre-treatment values at the sixth week. Symbiotic treatment was comparably effective while given to patients but significantly elevated BZDs level were noted starting from the third week. Similar phenomena were noted for endotoxin and ammonia although symbiotic seemed more effective against endotoxin and rifaximine against ammonia increase. However, the sequential treatment rifaximine-symbiotic brought about a sustained normalization of BZDs, ammonia and endotoxin throughout the 6-week study. Conclusion: The present pilot study suggests that a rifaximine-symbiotic regimen could be an effective tool in compensated liver cirrhosis to limit some triggering factors of hepatic encephalopathy while being amenable to long-term use and devoid of significant side effects.