Antonio Pietroiusti

C-reactive protein is increased in patients with degenerative aortic valvular stenosis

OBJECTIVES The goal of this study was to assess the presence of systemic inflammation in degenerative aortic valvular stenosis. BACKGROUND Local inflammatory changes, resembling those observed in atherosclerosis, have been recently reported in degenerative aortic valvular stenosis. It is presently unknown whether systemic signs of inflammation, similar to those observed in atherosclerosis, may be present in this disorder. METHODS C-reactive protein (CRP) was measured by enzyme immunoassay in 141 subjects: 62 with trileaflet degenerative valvular aortic stenosis and 79 volunteers with similar demographic and clinical characteristics. IgG antibodies against Helicobacter pylori (enzyme-linked immunosorbant assay) and Chlamydia pneumoniae (microimmunofluorescence assay) were also measured. RESULTS C-reactive protein levels (mg/dl, mean +/- SD) were 0.848 +/- 1.42 in patients and 0.394 +/- 0.50 in controls (p = 0.0001, Mann-Whitney U test). Seroprevalence of H. pylori was 68.7% in patients and 79.7% in controls (p = NS), whereas seroprevalence of C. pneumoniae infection was higher in patients than it was in controls (59.7% vs. 33%, p = 0.003; chi-square test). After adjustment for various covariates in multiple logistic regression, the odds ratio for degenerative aortic stenosis was 3.41 for C. pneumoniae infection (95% confidence intervals [CI]: 1.60 to 7.30) and 2.76 for CRP (95% CI: 1.08 to 7.05). There was no significant difference in patients or controls in CRP levels according to the serostatus for C. pneumoniae. CONCLUSIONS Systemic signs of inflammation, similar to those found in atherosclerosis, are present in patients with degenerative aortic valve stenosis. They do not seem to be linked to C. pneumoniae or H. pylori infection.

Leukocyte Count and Aggregation during the Evolution of Cerebral Ischemic Injury

We evaluated leukocyte aggregation by means of the leukergy test and count in 26 patients with atherothrombotic stroke and in 10 patients with transient ischemic attacks. The evaluation was performed within 24 h from the onset of symptoms and then repeated on day 2, 4, 6 and 8. Data were compared with those of 10 healthy controls. Stroke patients were followed until day 30 when a clinical examination and brain computed tomography were performed to evaluate the extent and outcome of cerebral damage. Both leukocyte aggregation and count were significantly increased in stroke patients with respect to controls. While leukocyte count was not able to differentiate the severity of neurological impairment in stroke patients, leukocyte aggregation was significantly higher in major than in minor stroke patients on days 2 and 4 (p < 0.05). Moreover, while values of leukocyte count recorded at entry remained substantially stable in the following determinations in all groups, leukocyte aggregation showed a significant increase (p < 0.05) on day 4 with respect to all the other determinations in major stroke patients. These findings show that the extent and temporal profile of changes in leukocyte count and aggregation are different in patients with cerebrovascular disease and suggest an involvement of altered leukocyte rheology in the development of cerebral ischemic injury.

Leukocyte aggregation in patients with a previous cerebral ischemic event.

Background and Purpose The role of leukocyte aggregation in ischemic stroke is controversial. In this study we investigated this hemorheologic alteration in patients at risk for stroke. Methods Leukocyte aggregation was evaluated with the leukergy test in 61 patients with a recent cerebral ischemic event and in 61 control subjects. Results In patients leukocyte aggregation was significantly higher than in control subjects (3.8±3.4% versus 2.5±2.2%; P=.01). In control subjects, the presence of vascular risk factors was associated with values of aggregation similar to those observed in patients. Conclusions These findings suggest an association between altered leukocyte aggregation and cerebrovascular disease. Further investigations are needed to evaluate whether this hemorheologic alteration can be considered a marker of increased risk for stroke. (Stroke. 1994;25:1390‐1392.)

Leucocyte aggregation in acute cerebrovascular disease

We evaluated leucocyte aggregation in 26 patients with ischemic stroke and in 10 patients with transient ischemic attacks (TIA), previously untreated, within 24 h from the onset of symptoms. The evaluation was also performed in 30 healthy subjects matched for age and sex. Leucocyte aggregation was significantly higher in patients than in controls (p<0.01 post hoc Tukey test). Within patients, those with stroke showed a significantly higher aggregation than those with TIA (p = 0.01 post hoc Tukey test). Moreover, stroke patients with the poorest outcome showed significantly higher values of leucocyte aggregation. These results indicate an involvement of leucocytes in cerebral ischemia and suggest that changes in their aggregability may play a role in the evolution of the disease.

Absolute alcohol in esophageal vein sclerosis

Absolute alcohol is a potentially optimal agent for sclerotherapy of esophageal varices. It is cheap and readily available. We compared the efficacy and safety of alcohol with those of a commonly used sclerosing agent, polidocanol. The study was planned to include patients with previous bleeding from esophageal varices randomly assigned to one of the two treatments. After the inclusion of the first 11 patients (6 in the polidocanol group and 5 in the alcohol group), however, the trial was interrupted because of serious complications in patients treated with alcohol (four major bleeding episodes and one esophageal stenosis). The two agents were of comparable efficacy in the small sample of patients studied. The complications were related to the presence of iatrogenic esophageal ulcers which were more frequent (100% vs. 30%) and significantly larger (mean, 1.4 cm vs. 0.7 cm, p less than 0.05) in patients treated with alcohol.

Cytotoxin-associated gene A and vacuolating cytotoxin A in human isolates of Helicobacter pylori and their association with the clinical status of ulcer disease.

Objective The aim of this study was to evaluate whether different Helicobacter pylori genotypes are associated with different clinical stages of peptic ulcer disease (PUD). Design We assessed the virulence characteristics of H. pylori isolates from patients with active PUD (presence of an ulcer crater at endoscopy) and from those with PUD in remission (normal endoscopic findings or scar not induced by drugs in PUD patients). Methods H. pylori isolates from biopsies of the gastric antrum were examined for cagA and vacA genotypes by PCR amplification and Western blot analysis. Descriptive statistical techniques and multivariate polytomous logistic regression were used to estimate adjusted odds ratio (OR) for cagA and vacA genotypes in patients with active PUD or PUD in remission. Patients with non‐ulcer dyspepsia (NUD) were used as negative controls. Results The cagA genotype and phenotype were found to be differently associated with disease status. In fact, the multivariate regression model showed that gastric colonization by CagA+ H. pylori strains was associated with an increased risk of active PUD (OR 2.58), whereas the OR for patients with PUD in remission was 0.94. Conclusions Our data indicate that the active ulcer status is more strongly associated with H. pylori strains carrying the pathogenicity island (PAI) than remission status. These results support the hypothesis that a dynamic equilibrium exists among bacterial populations with or without the PAI, and that the relapse of the peptic ulcer could be consequent to expansion of the H. pylori population carrying the PAI.

Paroxysmal atrial fibrillation after insect sting

We report an unusual cardiac reaction to insect sting, consisting in an episode of paroxysmal atral fibrillation in an otherwise healthy man. In order to validate the hypothesis that the cardiac complication was due to the chemical substance injected by the insect, we isolated the the venom and injected it subcutaneously to the subject under supervision of a cardiology team. The same cardiac complication was observed. The putative responsible of the reaction was represented by a peculiar pattern of released cytokines.

Comparison of an enzyme immunoassay versus a rapid latex test for serodiagnosis of Helicobacter pylori infection.

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Infection with Helicobacter pylori and leukocyte response in patients with myocardial infarction.

Abstract To test whether Helicobacter pylori may contribute to the inflammatory response following myocardial infarction, the levels of IgG antibodies to Helicobacter pylori and some parameters of leukocyte activity were measured in 63 patients and 61 comparable controls. Helicobacter pylori-positive patients showed a significantly higher expression of the adhesion molecule LFA-1 on neutrophils than Helicobacter pylori-negative patients (433±29.0 vs. 398.8±38.9 mean fluorescence channels; P<0.0001), whereas no significant difference for any parameters tested was found in control subjects. These data suggest a role of Helicobacter pylori in inducing a leukocyte response following myocardial infarction.

Leukocyte aggregation in patients with chronic cerebrovascular disease

It has been previously shown that an increase in leukocyte aggregation may represent a risk factor for the development of acute ischemic stroke. Little is known about the role of this parameter in patients with recurrent stroke. For this purpose, we evaluated monthly for two years the level of leukocyte aggregation in patients with a first episode of acute ischemic stroke, in order to assess if this factor may predict further cerebral ischemic events. Patients with recurrent stroke had significantly higher values of leukocyte aggregation than those free of recurrences. We conclude that the regular evaluation of leukocyte aggregation after ischemic stroke may hel in the identification of patients at risk of recurrence.