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Biomedical subjects

L Santarelli

Publications and source records attributed to L Santarelli.

At least 19 recordsLinked to original sources
PubMed2004

Atrophic gastritis as a cause of hyperhomocysteinaemia.

BACKGROUND: Hyperhomocysteinaemia is an independent risk factor for atherosclerosis. It is often related to low levels of vitamin B12 and/or folate, enzymatic co-factors of methionine metabolism. Atrophic gastritis, often caused by Helicobacter pylori infection, may impair vitamin absorption. AIM: To assess whether the presence of atrophic gastritis is associated with hyperhomocysteinaemia via deficiency of its vitamin co-factors. METHODS: Thirty-one patients with atrophic gastritis were recruited. The control group consisted of 28 patients with non-atrophic gastritis, matched with patients for sex, age and body mass index. The presence and degree of gastric atrophy were assessed by histology. H. pylori infection was assessed by histology/serology. Blood samples were collected for the measurement of homocysteine, vitamin B12 and folates. RESULTS: Multiple logistic regression analysis showed that atrophic gastritis (odds ratio, 5.3; 95% confidence interval, 1.23-25.26; chi2=5.2; P=0.01) and low vitamin B12 (odds ratio, 3.7; 95% confidence interval, 1.03-22.08; chi2=3.6; P<0.05) were both predictors of hyperhomocysteinaemia. None of the other variables considered in the analysis, including H. pylori status, showed a significant association with hyperhomocysteinaemia. CONCLUSIONS: The present study suggests that atrophic gastritis, rather than H. pylori infection per se, may be a contributing factor to hyperhomocysteinaemia, possibly via vitamin B12 malabsorption.

Female↗
PubMed2004

Crystalline silica induces apoptosis in human endothelial cells in vitro.

We investigated whether incubation of cultured human aortic endothelial cells (HAEC) with crystalline silica at the concentration 1 cm2/ml (chosen on the basis of a pilot experiment) leads to alterations typical of apoptosis. The binding of annexin V as early, and DNA fragmentation as late events of apoptosis were measured besides the number of cells with depolarized mitochondria. The generation of reactive oxygen species (ROS) by HAEC in presence of silica was determined as well as silica ability to in vitro generate hydroxyl radicals was investigated. After 18 h of silica incubation, about 30% of viable cells bound annexin V. After 24 h of silica treatment, the percentage of cells with fragmented DNA (Tunel positive) was 27% and it increased up to 50% after 48 h, whereas in untreated cells this percentage was 7% and 11% after 24 and 48 h, respectively. The presence of fragmented DNA in cells treated with silica was confirmed by agarose gel electrophoresis. In agreement with these results showing an induction of HAEC apoptosis by silica incubation, the number of cells with depolarized mitochondria was significantly higher after silica treatment as compared to the control. Apoptosis was also obtained with silica added to aliquots of anti-C5a-absorbed-medium. In the cells exposed to silica there was a significant increasing of ROS generation in comparison to the untreated cells. Apoptosis might be due to peroxidative stress since silica can generate hydroxyl radicals.

Annexin A5↗
PubMed2003

Levofloxacin-based triple therapy vs. quadruple therapy in second-line Helicobacter pylori treatment: a randomized trial.

BACKGROUND: Levofloxacin has been shown to be effective in Helicobacter pylori eradication. Two 10-day levofloxacin-based triple therapies were compared with standard 7- and 14-day quadruple regimens in second-line treatment. METHODS: Two hundred and eighty consecutive patients who failed to respond to standard triple therapy (clarithromycin, amoxicillin, rabeprazole) were randomly assigned to four groups: (1) levofloxacin 500 mg o.d., amoxicillin 1 g b.d., rabeprazole 20 mg b.d. for 10 days (LAR, n = 70); (2) levofloxacin 500 mg o.d., tinidazole 500 mg b.d., rabeprazole 20 mg b.d. for 10 days (LTR, n = 70); (3) tetracycline 500 mg q.d.s., metronidazole 500 mg t.d.s., bismuth salt 120 mg q.d.s., rabeprazole 20 mg b.d. for 7 days (7TMBR, n = 70); and (4) for 14 days (14TMBR, n = 70). Helicobacter pylori status and side-effects were assessed 6 weeks after treatment. RESULTS: The eradication rate was 94% in the LAR group and 90% in the LTR group in both intention-to-treat and per protocol analyses. Helicobacter pylori eradication was achieved in 63 and 69% of the 7TMBR group and in 69 and 80% of the 14TMBR group in intention-to-treat and per protocol analysis, respectively. Side-effects were significantly lower in the LAR and LTR groups than in the 14TMBR group. CONCLUSION: Ten-day levofloxacin-based therapies are better than standard quadruple regimens as second-line option for H. pylori eradication.

Adolescent↗
PubMed2002

Probiotics in antibiotic-associated diarrhoea.

Antibiotic-associated diarrhoea is a common event. In some cases, it could represent a life-threatening event. Clostridium difficile colitis is a further distinct complication of antibiotic administration. Treatment options for antibiotic-associated diarrhoea and Clostridium difficile colitis include supplementation with several types of probiotics, as overviewed in this paper. Three randomised, double-blind, controlled clinical trials show a therapeutic effect of Saccharomyces boulardii in antibiotic-associated diarrhoea. The efficacy of Lactobacillus acidophilus and bulgaricus has also been ascertained in two double-blind controlled studies. Other studies focusing on Lactobacillus as a new preventive agent for antibiotic-associated diarrhoea are not double-blind. Among these, a positive effect of Lactobacillus rhamnosus GG, Bifidobacterium longum and Enterococcus faecium SF68 has been reported. Effectiveness of probiotics in antibiotic-associated diarrhoea has, therefore, a consistent scientific rationale, however few studies have performed an assessment of bacterial recovery in stools, and this approach may be helpful in deciding a more rigorous dose standardisation.

Bifidobacterium↗
PubMed2002

Probiotics and Helicobacter pylori eradication.

The need for new strategies for Helicobacter pylori eradication, alternative or complementary to antibiotic therapy, has recently claimed the attention of many investigators. Pre-clinical studies have shown the inhibition of Helicobacter pylori growth by Lactobacilli and the anti-Helicobacter pylori action of Lactobacillus salivarius, Lactobacillus acidophilus and Lactobacillus casei subspecies rhamnosus strains, possibly due to the production of lactic acid or to the secretion of an autolysin. Clinical studies have demonstrated a persistent reduction in delta over baseline values at the 13C urea breath test independently of omeprazole administration with Lactobacillus acidophilus La1, the eradication in 6 out of 14 patients with Lactobacillus acidophilus alone, positive results in patients in which a standard Helicobacter pylori triple therapy was randomly supplemented with Lactobacillus acidophilus.

Helicobacter Infections↗
PubMed2001

In vitro inhibition of thymulin production in mercury-exposed thymus of young mice.

Lymphocyte differentiation, maturation and peripheral functions are affected by the thymic protein hormone thymulin. Mercury at very low concentrations has been seen to impair some lymphocytic functions causing subclinical manifestations in exposed workers. The present study was performed to test in vitro the effect of mercury on the production kinetics of thymulin using cultures of whole thymuses from young mice. Exposure to mercury (10(-8) M and 10(-6) M) added to the cultures, reduced kinetic thymulin production at all time intervals considered (1, 2, 4, 5 and 6 h) as compared to kinetic thymulin production of thymuses from young control mice. After the first hour the inhibition is more evident at the highest mercury concentration. Thymulin production decreased by 70, 74, 82 and 86% and by 55, 66, 73 and 81% for mercury concentrations of 10(-6) M and 10(-8) M, respectively, after 2, 4, 5 and 6 h. Mercury toxic effect on thymulin kinetics may be directly exerted to thymulin synthesis in epithelial cells, although it is less dramatic than that of cycloheximide (CHX), known as a potent inhibitor of protein synthesis in such cells. The toxic effect of mercury on thymic endocrine activity might cause the subclinical effects on cell-mediated immunological status observed in mercury exposed workers.

Animals↗
PubMed2001

Monocyte-macrophage system and polymorphonuclear leukocytes in workers exposed to low levels of metallic mercury.

Our previous research (Soleo L, Vacca A, Vimercati L et al. Occup Environ Med 1997;54:437-442) showed a reduction in tumor necrosis factor-alpha (TNF-alpha) serum levels in workers with prolonged exposure to low doses of inorganic mercury, suggesting an in vivo functional defect of the monocyte-macrophage system. On this basis, here we wondered whether workers exposed to lower doses of metallic mercury displayed possible changes in the monocyte-macrophage system. In this particular cohort of workers, we also sought for the effects of the exposure on the polymorphonuclear leukocytes (PMNL) chemotaxis. The monocyte-macrophage system and the natural killer (NK) cells were examined in 19 exposed workers and in 25 unexposed workers, as the control group (controls). Specifically, the circulating monocyte-macrophage cells and their CD13, CD15 and CD33 subsets, serum cytokines (IL-8, GM-CSF and TNF-alpha) and the NK cells were analyzed. In seven exposed and seven controls randomly chosen workers the PMNL chemotaxis was also assessed. The selected indicator of mercury exposure were the levels of mercury in the urine (U-Hg), that was significantly higher in exposed workers than the controls (9.7 +/- 5.5 microg/l and 2.4 +/- 1.2 microg/l, respectively). None of the exposed workers had shown signs of either acute or chronic inorganic mercury toxicity or any form of hypersensitivity. Several immunological variables tested, monocyte-macrophage cells and their subsets, NK cells and serum cytokines overlapped between the exposed and the control workers. When the workers were considered as a whole (exposed plus controls), no correlation was found between current U-Hg and all immunological parameters. However, when exposed workers were studied separately, an inverse correlation was disclosed between cumulative U-Hg and cells (as percentage) expressing the CD13 (r = -0.599; P = 0.007) and CD15 (r = -0.614; P = 0.005) molecules, and NK cells (r = -0.455; P = 0.05). Moreover, a significant impairment in the PMNL chemotaxis (t = 3.70; P = 0.003) was observed in the exposed workers. The results of our study suggest that the exposure to very low levels of metallic mercury led to subtle impairment of circulating monocyte and NK cells (as percentages) according to the increase in U-Hg levels, as well as of the PMNL chemotactic function in this particular group of workers, even though they remain clinically asymptomatic. Therefore, we suggest that impairment of these parameters provide a sensitive indicator of metallic mercury and other chemical contaminants present in the environment.

Adult↗
PubMed2001

Genetic and pharmacological disruption of neurokinin 1 receptor function decreases anxiety-related behaviors and increases serotonergic function.

Alterations in serotonin (5-hydroxytriptamine, 5-HT), norepinephrine, and gamma-aminobutyric acid have been linked to the pathophysiology of anxiety and depression, and medications that modulate these neurotransmitters are widely used to treat mood disorders. Recently, the neuropeptide substance P (SP) and its receptor, the neurokinin 1 receptor (NK1R), have been proposed as possible targets for new antidepressant and anxiolytic therapies. However, animal and human studies have so far failed to provide a clear consensus on the role of SP in the modulation of emotional states. Here we show that both genetic disruption and acute pharmacological blockade of the NK1R in mice result in a marked reduction of anxiety and stress-related responses. These behavioral changes are paralleled by an increase in the firing rate of 5-HT neurons in the dorsal raphe nucleus, a major source of serotonergic input to the forebrain. NK1R disruption also results in a selective desensitization of 5-HT1A inhibitory autoreceptors, which resembles the effect of sustained antidepressant treatment. Together these results indicate that the SP system powerfully modulates anxiety and suggest that this effect is at least in part mediated by changes in the 5-HT system.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2001

Link between Helicobacter pylori infection and iron-deficiency anaemia in patients with coeliac disease.

BACKGROUND: Iron-deficiency anaemia is a frequent finding in coeliac disease. Recent investigations have identified Helicobacter pylori infection as a factor responsible for iron deficiency. We investigated the potential relationship between H. pylori and iron-deficiency anaemia in patients with coeliac disease. METHODS: We conducted a prospective observational cohort study on coeliac patients evaluated for iron-deficiency anaemia. An upper gastrointestinal endoscopy was performed and biopsy specimens of duodenal and gastric mucosa were taken for histological examination and assessment of Helicobacter pylori status. RESULTS: The initial database was 386 subjects. Of these, 24 were excluded because of concomitant potential causes of iron deficiency. Of the 362 enrolled patients, H. pylori was detected in 77 (21%) subjects; of these 55 (71%) had iron-deficiency anaemia. Among the 285 H. pylori-negative subjects, 81 (28%) showed anaemia (P < 0.001). We did not find significant differences in gastric histological aspects between patients with or without iron deficiency anaemia. CONCLUSIONS: This study shows a significant association between H. pylori infection and iron-deficiency anaemia in patients with coeliac disease. The discovery of iron-deficiency anaemia in coeliac subjects may constitute another indication for the diagnosis and treatment of this worldwide infection.

Adult↗
PubMed2001

Helicobacter pylori treatment: a role for probiotics?

Many new therapeutic strategies are studied to improve Helicobacter pylori eradication rate. Probiotics are live microorganisms which, upon administration, may interact with the human microflora and positively affect the health status. The use of probiotics in the field of H. pylori infection has been proposed for improving eradication rate and tolerability and for compliance of multiple antibiotic regimens used for the infection. Results from laboratory studies and from clinical trials seem to confirm the expectancies, but there is lack of standardization in terms of type of probiotic strain used, dosage and timing of supplementation. Before further ongoing trials and future studies will clarify these points, probiotics could remain a useful adjunct to standard anti-H. pylori therapies, but cannot take the place of other validated options.

Anti-Bacterial Agents↗
PubMed2001

Effect of Lactobacillus GG supplementation on antibiotic-associated gastrointestinal side effects during Helicobacter pylori eradication therapy: a pilot study.

BACKGROUND: One-week triple therapy is currently regarded as the reference of anti-Helicobacter pylori treatment. However, antibiotic-associated gastrointestinal side effects are among the major pitfalls of such regimens. Probiotic supplementation may be regarded as a therapeutic tool to prevent or reduce these troublesome drug-related manifestations. AIM: To determine whether the addition of the probiotic Lactobacillus GG to an anti-H. pylori standard triple therapy could help to prevent or minimize the occurrence of gastrointestinal side effects. METHODS: One hundred and twenty healthy asymptomatic subjects screened positive for H. pylori infection and deciding to receive eradication therapy were randomized either to 1-week pantoprazole (40 mg b.i.d.), clarithromycin (500 mg b.i.d.), tinidazole (500 mg b.i.d.) or to the same regimen supplemented with Lactobacillus GG for 14 days. Patients filled in validated questionnaires during follow-up to determine the type and severity of side effects and to judge overall tolerability. RESULTS: Bloating, diarrhea and taste disturbances were the most frequent side effects during the eradication week and were significantly reduced in the Lactobacillus GG-supplemented group (RR = 0.4, CI 0.2-0.8; RR = 0.3, CI 0.1-0.8; RR = 0.3, CI 0.1-0.7, respectively). The same pattern was observed throughout the follow-up period. Overall assessment of treatment tolerability showed a significant trend in favor of the Lactobacillus GG-supplemented group (p = 0.03). CONCLUSIONS: Lactobacillus GG supplementation beneficially affects H. pylori therapy-related side effects and overall treatment tolerance.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2000

Altered fear circuits in 5-HT(1A) receptor KO mice.

The study of genetically altered mice has been used successfully to determine the influence of different neurotransmitter receptors on fear and anxiety. Mice with a genetic deletion of the serotonin 1A receptor (5-HT(1A)R knockout [KO]) have been shown to be more fearful in a number of behavioral conflict tests, confirming the important role of this receptor in modulating anxiety. Factor analysis of the behavior of WT and 5-HT(1A)R KO mice in the open field test shows that locomotion and anxiety measures segregate independently, supporting the idea that the anxious behavior of the KO mice is not the result of altered locomotion. KO mice also show increased anxiety in the novelty-suppressed feeding task, which differs from the other conflict tests in the motivational drive of the animals. In response to a discrete aversive stimulus, foot shock, the KO mice show increased freezing and increased tachycardia. However, activation of the hypothalamic-pituitary-adrenal axis in response to stress appears to be slightly blunted in the KO animals. Together, these data support the idea that the 5-HT(1A)R modulates an important fear circuit in the brain. The dual function of the 5-HT(1A)R as both a presynaptic autoreceptor, negatively regulating serotonin activity, and a postsynaptic heteroreceptor, inhibiting the activity of nonserotonergic neurons in forebrain structures, has complicated interpretation of the anxious phenotype of these KO mice. A more complete understanding of the function of the 5-HT(1A)R awaits further study of its role in behaving animals using tissue-specific antagonists and novel transgenic mice with tissue-specific expression of the receptor.

Animals↗
PubMed2000

Efficacy of two one-week rabeprazole/levofloxacin-based triple therapies for Helicobacter pylori infection.

BACKGROUND: One-week low-dose proton pump inhibitor-based triple therapies have usually proved to be effective treatments for Helicobacter pylori infection. AIM: To investigate the eradication efficacy, safety profile and patient compliance of two triple therapies containing a standard dose of rabeprazole and a new fluoroquinolone, levofloxacin. METHODS: One hundred patients referred to us for gastroscopy, who were H. pylori-positive, were consecutively recruited in a prospective, open-label study. The enrolled patients were randomised to receive a seven-day course of rabeprazole 20 mg o.d. plus levofloxacin 500 mg o.d. and either amoxycillin 1 g b.d. (RLA group) or tinidazole 500 mg b.d. (RLT group). Their H. pylori status was assessed by means of histology and rapid urease test at entry, and by 13C-urea breath test 8 weeks after the end of treatment. RESULTS: All 100 enrolled patients completed the study. Forty-six of 50 patients treated with RLA (both PP and ITT analysis: 92%; 95% CI: 81-98%) and 45 of 50 with RLT (both PP and ITT analysis: 90%: 95% CI: 78-97%), became H. pylori-negative. Slight or mild side-effects occurred in 4 (8%) patients of the RLA group and in 5 (10%) of the RLT group. CONCLUSIONS: This study demonstrates the efficacy of two 1-week rabeprazole-based triple therapies including levofloxacin to eradicate H. pylori. These regimens prove to be safe, well-tolerated, and achieved good eradication rates. Levofloxacin may be an effective alternative to clarithromycin in triple therapy regimens.

2-Pyridinylmethylsulfinylbenzimidazoles↗