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R Pellicano

Publications and source records attributed to R Pellicano.

At least 37 records · Page 2Linked to original sources
PubMed2005

How accurate is the culture of Helicobacter pylori in a clinical setting? An appraisal.

AIM: The trend towards increasing prevalence of Helicobacter pylori (H. pylori) antibiotic resistance may jeopardize the efficacy of most regimens. Culture of the bacterium, the useful method able to address therapy, is influenced by various factors. Thus, validation of the procedure is fundamental. Most studies have been carried out in microbiological settings, while only few have been conducted in clinical frames. We evaluated the accuracy of culture for detection of H. pylori in a clinical dedicated laboratory. METHODS: Forty-six patients (28 females, 18 males, mean age 56+/-4.7 years) were included. Thirty experienced failure to H. pylori eradication after at least 3 courses of treatment. The control group included 16 subjects suffering from gastroesophageal reflux disease and negativity for H. pylori infection. Diagnostic strategy was based on histology, culture testing, serology and 13C-urea breath test. A patient was considered infected if 2 tests were positive. A commercial culture medium in microaerophilic atmosphere was utilized. RESULTS: Out of 30 positive specimens, culture correctly identified 29. In 1 case, no growth of micro-organisms occurred. In the control group, bacterial culture accurately identified all negative samples. One of them indicated growth but neither aspect nor confirmation tests identified H. pylori. Sensitivity was 96.7%, specificity 100%, and accuracy 97.8%. Positive and negative predictive values were 100% and 94.1%, respectively. CONCLUSIONS: Culture of H. pylori is a feasible method and provides a good level of diagnostic accuracy even in a clinical setting by following international guidelines combined with training of specialized personnel.

Breath Tests↗
PubMed2004

Gastro-oesophageal reflux disease and asthma: would be possible to improve therapy on the basis of what is now known?

Gastro-oesophageal reflux disease (GORD) is a chronic and relapsing clinical condition, associated or not to histopathologic alteration resulting from repeated contact of oesophageal mucosa with gastric content. This condition occurs with high prevalence in the general population and represents one of the most frequent reasons for health care-seeking addressed to primary care physician and gastroenterologists. A plethora of extra-oesophageal manifestations have been described in patients suffering from GORD and a causal relationship has been postulated by many investigators. A large cohort of studies has focused on the possible cause-effect interaction between GORD and asthma. However, despite the improvement in both asthma symptoms and medication requirements after anti-secretory therapy, no change in pulmonary function is evident. Furthermore, the pathogenetic mechanism, a vagally mediated reflex, microaspiration or increasing reactivity to the stimuli, is yet unclear. Since conflicting conclusions and the failure to find a causal relationship are generally due to the heterogeneity of the studies, further research is needed to clarify the role of GORD in asthma pathogenesis, or viceversa, and whether a medical or surgical anti-secretory treatment may be an approach to curing the asthma patients non-responders to the classical therapy.

Asthma↗
PubMed2004

Is hepcidin the bridge linking Helicobacter pylori and anemia of chronic infection? A research proposal.

Since the last decade, several studies have reported on the link between chronic Helicobacter pylori (H. pylori) or Helicobacter species (H. species) infection and a variety of extragastric manifestations, comprising iron-deficiency anemia. A crucial question concerns which possible pathogenic mechanism of H. pylori infection may be involved in chronic anemia. Recent findings support the hypothesis that in subjects with H. pylori-positive gastritis, concomitant changes in intragastric pH and ascorbic acid are present that might play a role in impairing alimentary iron absorption with consequent sideropenic anemia. It has also been speculated that H. pylori infected antrum could act as a sequestering focus for iron. The bacterium enhances gastric lactoferrin, which captures iron from transferrin. The iron thus bound to lactoferrin is in turn picked up by the bacterium, by means of its outer membrane receptors, for its own growth. These models, however, are not able to answer why iron-deficiency anemia does not develop in all infected subjects. Recently, a new anti-microbial liver-made peptide, namely hepcidin, has been characterised. The link between hepcidin induction, inflammation and anemia both in humans and in animal models supports its key role as mediator of anemia of inflammation. In the present paper, we highlight the data available on the association between H. pylori and iron-deficiency anemia and, we propose to evaluate a possible mechanism involving hepcidin in a bridging role linking the infection to the anemia.

Anemia, Iron-Deficiency↗
PubMed2004

The epidemiology of hepatitis C virus infection. An update for clinicians.

Since the advent of sensitive diagnostic blood tests for the detection of antibody to hepatitis C virus (HCV) in donors, there has been a large decline in the incidence of transfusion-related hepatitis. Globally, the infection has an estimated prevalence of 3%, with a prevailing 1% in Europe while varying geographically within a North-South gradient, ranging from around 0.5% in Northern countries to 2% in Mediterranean area. The incidence is very difficult to estimate accurately as many patients with acute HCV infection are asymptomatic and, thus, do not present for diagnosis. Data from the US report a fall in the annual occurrence of new cases per year from 230,000 in the late 1980s to approximately 35,000 in the 1990s. Therefore, a reduction in incident cases might eventually lead to lower prevalence of HCV infection. Although the incidence of viral infection may be decreasing, the prevalence of liver disease caused by HCV is on the rise. This is due to the significant lag, often 20 years or longer, between the onset of infection and clinical manifestation of liver disease. HCV can be transmitted by a variety of routes. It is most efficiently passed on by large or repeated percutaneous exposures such as through transfusions, transplantation from an infected donor or intravenous drug use. Transmission may also occur from contacts with infected subjects in the household, through perinatal and parenteral exposures in the health care setting. The risk of sexual transmission of HCV is low. Despite this knowledge, nearly half of infected patients do not have a history suggesting a parenteral route of acquisition. Since a prophylactic vaccine is hitherto not available, prevention becomes extremely important: identification of infected persons and of risk factors associated with acquiring HCV allow to develop strategies for preventing the spread of infection as well as its complications, and for planning appropriate care and support services.

Hepatitis C↗
PubMed2004

[The diagnosis of helicobacter pylori infection: guidelines from the Maastricht 2-2000 Consensus Report].

The European Helicobacter pylori Study Group (EHPSG), during the Maastricht 2-2000 Workshop, revised and updated the original guidelines on the management of Helicobacter pylori (H. pylori) infection. The present review focuses on the diagnostic approach for patients referred to the primary care as well as to the specialist. Currently, two diagnostic methods can be used to detect H. pylori: invasive (urease test, histological detection, culture, polymerase chain reaction, smear examination, string test) or non-invasive (serology, urea breath test, antigen stool assay, ''doctor's tests'') tests. These methods vary in their sensitivity and specificity, and the choice depends on the situation, for example, whether the aim is to detect infection or the success of eradication treatment. Urea breath test (UBT) and antigen stool assay are recommended from EHPSG in patients without alarm symptoms or under 45 years of age, at low risk of malignancy in the ''test and treat strategy''. Confirmation of H. pylori eradication following treatment should be tested by UBT; a stool antigen assay is the alternative if the former is not available. Important added value can be gained from other tests: histology allows evaluation of the status of the mucosa while culture allows strain typing and tests for antibiotic susceptibility.

Adult↗
PubMed2004

Strategies for the diagnosis of gastro-esophageal reflux disease.

With patients referring symptoms of gastro-esophageal reflux disease (GERD), 2 initial approaches should be considered: an empiric therapy (treat and test strategy) or a strategy based on instrumental investigations (test and treat). In most cases a well-taken history is usually sufficient to confirm the diagnosis of GERD and initiate treatment. However, some patients may present with ''atypical'' symptoms, classic symptoms refractory to standard medical therapy or ''alarm'' symptoms. In these cases, one must rely on diagnostic studies to document the presence of mucosal damage related or not to GERD and/or quantify the degree of gastro-esophageal reflux. The most relevant test to diagnose esophageal injury and complications of GERD is represented by upper gastrointestinal endoscopy, while the most diffuse procedure to quantify the degree of acid reflux is pH monitoring. Further studies are required to delineate the appropriate use and the possible impact of new techniques, such as intraluminal impedance monitoring, Bilitec and, wireless ambulatory pH monitoring in the management of GERD.

Algorithms↗
PubMed2003

Helicobacter pylori infection in patients with Hepatitis C Virus positive chronic liver diseases.

BACKGROUND AND GOALS: One-third of patients with liver cirrhosis suffers from acute peptic ulcer, a disease strongly correlated with Helicobacter pylori (H. pylori) infection. We report the seroprevalence of antibodies to H. pylori in 179 patients with Hepatitis C Virus (HCV)-related chronic active hepatitis and cirrhosis. MATERIALS AND METHODS: Among patients, 135 (86 males and 49 females, mean age 51.2 +/- 13.28, range 27-77 years) had chronic active hepatitis (CAH) and 44 cirrhosis (28 males and 16 females, mean age 62.4 +/- 9.2, range 37-77 years). Serum antibodies to H. pylori were tested using a commercial enzyme immunosorbent assay. The control population consisted of 619 consecutive blood donors (523 males, 96 females, mean age 47 +/- 5.3 years, range 18-65). RESULTS: The overall prevalence of antibodies to H. pylori was 73.1% (131/179) among patients and 47% (291/619) among blood donors (p<0.0001; OR 3.08 [95%CI, 2.10-4.51]). 70.5% (24/34) of patients aged less than 40 years were seropositive for H. pylori versus 34.2% (90/263) of controls (p<0.0001; OR 4.61[95%CI, 2.0-10.85]). Among cirrhosis patients, the prevalence of antibodies to H. pylori was 79.5% (35/44) versus 47% (291/619) of controls (p<0.0001; OR 4.38 [95%CI, 1.98-9.98]). Overall seroprevalence among CAH patients was 71.1% (96/135) versus 47% (291/619) of blood donors (p<0.0001; OR 2.77 [95%CI, 1.82-4.24]). CONCLUSIONS: The high seroprevalence of antibodies to H. pylori in patients with HCV-positive liver diseases explains the elevated incidence of peptic ulcer, and warrants studies on the pathogenic role in human liver diseases of Helicobacter spp which is known to cause chronic hepatitis and hepatocellular carcinoma in mice.

Adult↗
PubMed2003

Infectious agents and gastric tumours. An increasing role for Epstein-Barr virus.

Helicobacter pylori (H. pylori) and Epstein-Barr virus (EBV) are 2 common and widely disseminated agents throughout the world. H. pylori has been classified, by the International Agency for Research on Cancer conference, as a class I carcinogen, i.e. undoubted cause of gastric cancer. However, this infection does not explain all the epidemiological and histological variations of the malignancies affecting the stomach. EBV has been identified, in the last decade, in the tumour cells of patients with gastric carcinoma and recent findings suggest the possibility of distinct mechanisms in its pathogenesis. A prevalent role of the virus has been described in a subset of stomach cancers, namely lymphoepithelioma-like carcinomas. The present update attempts to focus on the epidemiological evidence and the biological plausibility for a causal role of H.pylori and EBV infection in the pathogenesis of gastric cancer.

Epstein-Barr Virus Infections↗
PubMed2003

Helicobacter pylori seropositivity in patients with unstable angina.

AIM: The pathogenesis of ischemic heart diseases has been correlated, on epidemiological and pathogenetic grounds, with infections by viruses and bacteria, including Helicobacter pylori (H. pylori). THE AIM: of this study were to investigate the association of unstable angina (UA) with anti-H. pylori seropositivity in a case-control study and to search for the classic cardiovascular risk factors in both infected and uninfected patients. METHODS: We studied 32 consecutive patients (20 males, 12 females), mean age 65 years (range 42-89), with final diagnosis of UA. A total of 64 subjects (40 males, 24 females, mean age 65 years, range 42-89) admitted to the Emergency Care Unit, age and sex-matched, served as controls. The presence of hypertension, serum levels of cholesterol and glucose, plasma levels of fibrinogen, smoking habit and social class were investigated in all patients. Cases and controls were inhabitants of NorthWestern Italy, and had similar socioeconomic status as based on working place and on instruction level. H. pylori seroprevalence was assessed by the presence of antibodies (IgG) against H. pylori by means of a commercial enzyme immunosorbent assay. RESULTS: Antibodies to H. pylori were found in 26/32 (81%) of the patients and in 34/64 (53%) of the controls (p=0.007); the odds ratio was 3.82 (95% confidence interval 1.27 to 12.04). Classical cardiovascular risk factors, such as socio-economic status, did not differ among patients with and without antibodies to H. pylori. CONCLUSION: Patients with unstable angina had a significantly higher seroprevalence of anti-H. pylori than the control population. Classical risk factors for ischemic heart disease, such as the indicators of socio-economic status, were equally distributed among infected or uninfected patients with UA.

Adult↗
PubMed2003

The epidemiology of gastro-oesophageal reflux disease. A brief review.

During the last century, gastro-oesophageal reflux disease (GERD) has become increasingly observed in Western countries. The disorder is chronic and relapsing with a clinically significant impairment in quality of life. Symptoms of GERD are very common in the general population. However, reported symptoms under-represent the true prevalence of the disease, because these do not equate with mucosal damage, and this might lead to a bias in epidemiologic surveys. Several studies have been conducted in endoscopic centres, but these were able to focus on only some consequences of GERD (oesophagitis or Barrett's oesophagus) and not on nonerosive reflux disease (NERD). The latter is a clinical condition characterised by symptoms of reflux and intraesophageal gastric content reflux in the absence of visible endoscopic oesophageal mucosal injury. Moreover, the diffuse use of acid suppressing drugs in the population is able to mask some manifestations of GERD. Other studies have been conducted in the form of questionnaires investigating the presence and the frequency of symptoms typical of GERD. These estimates have taken into consideration and assumed that heartburn is an indicator of the disease. Taking into account the many faces of GERD, and its wide spectrum of manifestations, including atypical symptoms, this could represent a serious limitation. This brief review article fosters understanding of this issue by focusing on the epidemiology of GERD.

Journal Article↗
PubMed2002

Mixed cryoglobulinaemia and chronic hepatitis C virus infection: the rheumatic manifestations.

The prevalence of rheumatologic symptoms in patients with mixed cryoglobulinaemia associated to chronic hepatitis C virus (HCV) infection was investigated. One hundred fourteen patients (96 female, mean age 63.5 years) with chronic HCV infection and cryoglobulinaemia were recruited. The presence, concentration, and type of cryoglobulins were tested by immunofixation. Rheumatoid factor (RF) and antinuclear antibody (ANA) were also measured. Rheumatological related symptoms were investigated by anamnesis and clinical evaluation. HCV genotype was determined by polymerase chain reaction (PCR) with genotype specific primer. Type II cryoglobulinaemia was identified in 39 cases and it was of type III in 58. HCV-RNA genotype was determined in 62 patients: 47 (76%) were infected by genotype1b, 8 (13%) by genotype 2a, while other genotypes were less common. RF and ANA were, respectively, present in 36 (31.5 %) and 4 (3.5 %) patients at low titre (RF < 50 UI/ml, ANA < 1:80). Of the 114 patients, 51 (44.7%) complained for rheumatological symptoms. The mean cryocrit value in these patients was 2,6 %, while in patients with HCV infection, liver disease, and cryoglobulinaemia without rheumatological symptoms the cryocrit value was lower than 0.5% in 50% of cases. It is concluded that patients with chronic HCV infection reported a wide variety of rheumatological manifestations, impairing their quality of life, with discrete frequency. These results suggest that HCV infection should be considered in the differential diagnosis of rheumatological symptoms of unknown origin.

Antibodies, Antinuclear↗
PubMed2002

Elevated serum chromogranin A in patients with hepatocellular carcinoma.

Chromogranin A is a cellular marker forneuroendocrine tumors. Elevated levels of chromogranin A are also found in patients with cancers of epithelial origin when neuroendocrine differentiation occurs, which is associated with a poor prognosis. We investigated the prevalence of serum levels of chromogranin A in patients with primary liver cancer. Seventy-nine patients (65 males, mean age 67.6 years, range 48-88 years) with liver cirrhosis and hepatocellular carcinoma were studied. The etiology of cirrhosis was identified as due to hepatitis C virus infection in 47 patients, to hepatitis C virus and alcohol in 7, to alcohol alone in 14, to hepatitis C and B virus in 2, and to hepatitis B virus alone in 4. Of the remaining patients, 2 suffered from hemochromatosis and 3 had cryptogenic cirrhosis. According to the Child-Pugh's score, 54 patients belonged to class A, 22 to class B, and 3 to class C. The concentration of chromogranin A was measured in serum with a commercial solid-phase two-site immunoradiometric assay. Elevated serum levels of chromogranin A were found in 32 of 79 patients (43%). Levels over 600 ng/ml were present in 7 of 76 patients (9.2%), all of whom had very high serum levels of alpha-fetoprotein. Hence, elevated serum levels of chromogranin A are present in over one third of patients with hepatocellular carcinoma. It is therefore possible that some hepatocellular carcinomas could acquire a neuroendocrine differentiation. We propose further studies to ascertain whether serum levels of chromogranin A are useful as a prognostic marker for hepatocellular carcinoma as in prostate cancer.

Aged↗
PubMed2002

The esophageal chest pain. An update for clinicians.

Chest pain is a common symptom and even when there is evidence of only minor obstructive coronary artery disease on angiography, it leads to disability and imposes a substantial economic burden on health care system. Gastroesophageal reflux disease (GERD) and esophageal dysmotility disorders are thought to play an important role in the genesis of non-cardiac chest pain. Its pathogenetic mechanism remains unclear. The esophageal origin of the symptom may be identified by an aggressive trial of high-dose antisecretory drugs or an abnormal prolonged ambulatory pH monitoring study. Endoscopy is often normal and less useful in this population than in those with heartburn as presenting symptom. The use of manometry, with provocative testing to evaluate for esophageal motility abnormalities or esophageal sensitivity, allows optimal evaluation of those who do not have GERD. Patients with non-cardiac chest pain of unknown origin should be carefully screened for the occurrence of esophageal disorders but further research is needed to clarify the role of the latter on the pathogenesis of this symptom.

Chest Pain↗
PubMed2002

Eradication of Helicobacter pylori infection with proton pump inhibitor-based triple therapy. A randomised study.

BACKGROUND: Helicobacter pylori (H. pylori) infection plays an important role in the pathogenesis of duodenal ulcer (DU) disease. Low DU recurrences and reinfection rates were universally described, when treatment was effective. It has been suggested that short-term triple therapy, comprising a proton pump inhibitor plus 2 antibiotics (clarithromycin, amoxycillin or a nitroimidazole), should be used as first choice in treating H. pylori infection. Nevertheless, conflicting results have been reported on using these treatment regimens in different countries. Our aim was to compare cure rates of H. pylori infection, with a 1-week triple therapy versus 10 and 15 day triple schedules, in patients with DU. METHODS: A total of 172 patients (91 males, mean age 56.2+/- 3.2 years) were randomly treated with a triple therapy including a standard dose of proton pump inhibitor, amoxicillin at a dose of 1 g twice daily and clarithromycin 500 mg twice a day. Sixty-six patients received a 1-week triple therapy (group I), 42 subjects were treated with a 10-day triple therapy (group II) and 64 others with a 14-day triple therapy (group III). H. pylori infection at entry and after eradication, at least 4 weeks after therapy had ended, were assessed by 13C urea breath test and histology on biopsies from the antrum and the corpus. RESULTS: At the end of the course of treatment, the overall H. pylori eradication rate was 68.2% (45/66) in group I, 76.2% (32/42) in group II and 71.9% (46/64) in group III, without any statistically significant difference between the 3 differing period regimens, although a trend for better results with the 10-day triple therapy was observed. Compliance was good and side effects infrequent and mild. CONCLUSIONS: None of the 3 periods of triple therapy achieved 80% eradication rate recommended by the Maastricht Consen-sus Conference. The 10-day triple therapy, although not significantly, provided a satisfactory treatment against H. pylori infection.

Adult↗
PubMed2002

Surgery for carcinoma of the gallbladder. Our experience.

BACKGROUND: Carcinoma of the gallbladder is a gastrointestinal malignancy with a very poor prognosis. The 5-year survival rate amounts to less than 5% in most series. In this study we reviewed the results of surgical treatment for gallbladder carcinoma with special reference to extended radical procedures. METHODS: Between 1995 and 2000 we enrolled 36 patients (17 males and 19 females), 24 of whom were treated with simple cholecystectomy and 12 with radical resection (partial hepatectomy, regional lymphadenectomy, and common bile duct resection). The tumours were classified by stage using the criteria of the American Joint Committee on Cancer (AJCC). Stages, operative procedures, results of pathologic examinations and the outcome of the resected cases were reviewed. RESULTS: There were 2 postoperative deaths (0.55%). The mean follow-up period was 19.1 months (range 1-60). For stage I and II disease extended cholecystectomy had a better result than simple cholecystectomy: the 5-year survival rates were 38.4 versus 19%, respectively. For the patients with advanced stage III or IV gallbladder carcinoma, a significant advantage of survival resulted in case of liver resection as compared to surgical treatment without liver resection: the 5-year survival rates were 20 and 0%, respectively. CONCLUSIONS: The survival of stage I-II patients was good. For the patients in higher stages the prognosis was significantly worse. In these cases more aggressive surgery may be needed.

Aged↗
PubMed2002

The role of gastroesophageal reflux disease in chest pain.

Gastroesophageal reflux disease (GERD) is thought to play an important role in the pathogenesis of non-cardiac, unexplained, chest pain. The physiopathological mechanism of this extraesophageal manifestation, remains unclear but it is supposed that the ache could be triggered by the stimulation of acid-sensitive nociceptors of the mucosa. The esophageal origin of the symptom may be identified by an empiric trial of high-dose antisecretory drugs or an abnormal prolonged ambulatory pH monitoring study. Less important is the role of endoscopy especially in subjects without typical symptoms of GERD. The use of manometry or provocative tests can consent to evaluate for esophageal motility abnormalities. It is generally accepted that in clinical practice, in patients with non-cardiac chest pain, the administration of proton pump inhibitors, could serve as a first approach. It is cost-effective in the short-term period, when compared with investigation for gastrointestinal causes, with cost savings persisting beyond a year. In conclusion, patients with non-cardiac chest pain of unknown origin should be carefully screened for the occurrence of GERD, but further research is needed to clarify the role of the latter on the pathogenesis of this symptom.

Chest Pain↗
PubMed2002

Infection by Helicobacter pylori and acute myocardial infarction. Do cytotoxic strains make a difference?

The classical risk factors for acute myocardial infarction (AMI) fail to explain all the epidemiological variations of the disease. Among the risk factors recently reported, several infectious agents appear to increase the risk of AMI. Helicobacter pylori (H. pylori) infection, a bacterium involved in duodenal and gastric ulcer, gastric cancer and MALT-lymphoma, seems to be strongly associated with AMI. More virulent (anti-CagA positive) strains of the bacterium are almost exclusively the causative agents of such diseases. To determine the prevalence of H. pylori infection and of virulent strains, a case-control study was conducted in a group of male patients with AMI. A group of patients consecutively admitted to the Emergency Care Unit served as controls. We studied 223 consecutive male patients, mean age 60.2 (range 40-79) years, admitted for AMI to the Coronary Care Units at Hospitals in two towns of Northern Italy, 223 age matched male patients (mean age 61.8, range 40-79 years) admitted to the Emergency Care Unit, served as control. H. pylori seroprevalence was assessed by presence of antibodies (IgG) against H. pylori and anti-CagA in circulation. Among the patients we investigated the presence of hypertension, levels of cholesterol and glucose in serum, fibrinogen in plasma and smoking habits. H. pylori infection was present in 189/223 (84.7%) of the patients and in 138/223 (61.8%) of the control population (p < 0.0001 OR 3.42 [IC 95% 2.12-5.54]). The anti-CagA antibodies were detected in 33.8% of infected patients with AMI (64/189) versus 26.8% in the control subjects (37/138) (p:0.17, OR 1.40 [IC 95% 0.84-2.33]). Classical risk factors for AMI did not differ among patients with and without H. pylori infection. Patients admitted to the Coronary Care Unit for acute myocardial infarction had a notably higher prevalence of anti-H. pylori not restricted to virulent strains, when compared to a population of patients referred to the Emergency Care Unit. The classical risk factors for coronary disease were present in the patients with AMI irrespective of H. pylori status.

Adult↗