Does hospital work constitute a risk factor for Helicobacter pylori infection?

The aim of this study was to assess whether clinical work constitutes a risk factor for Helicobacter pylori infection among employees in hospitals. The prevalence of H. pylori infection was analysed in 249 individuals employed in a university teaching hospital according to three categories of hospital workers: (A) personnel from gastrointestinal endoscopy units (N=92); (B) personnel from other hospital units with direct patient contact (N=105); and (C) staff from laboratories and other units with no direct patient contact (N=52). Stool samples from each subject were examined with a validated enzyme-linked immunosorbent assay for the presence of H. pylori antigens. A questionnaire inquiring about sociodemographic and occupational characteristics was completed by each participant. The prevalence of H. pylori infection was 37.0% in group A, 35.2% in group B and 19.2% in group C (P<0.05). Among the different healthcare categories, nurses had a significant higher prevalence of H. pylori infection (P<0.01). No significant association was found between the length of employment or exposure to oral and faecal secretions, and H. pylori infection. Hospital work involving direct patient contact seems to constitute a major risk factor for H. pylori infection compared with hospital work not involving direct patient contact.

Cardiac troponin I in acute coronary ischemic syndromes. Epidemiological and clinical correlates.

UNLABELLED: The present study was aimed to investigate the variability of cardiac troponin I (cTnI) in the first week of acute myocardial infarction (AMI) course with regard to some epidemiological and clinical parameters and in patients with non-AMI acute coronary ischemic disease. Serum cTnI was assayed in 82 patients, 42 affected with AMI and 40 with non-AMI acute coronary ischemic disease, on admission in coronary care unit, within 6 h after the onset of symptoms, and, in AMI group, on 24 and 48 h and 7th day of illness course. cTnI is increased within the first 6 h, remaining above normal until 7th day. However, some distinctive features in the subgroups scheduled for this study are present. (1) The mean values of cTnI in AMI patients who died, >60 years old and with anterolateral necrosis are constantly higher than in survivors, <60 years old and with inferoposterior necrosis, respectively. (2) The cTnI concentration is already returned in normal range at 7th day of illness course in survivors and in patients with inferoposterior AMI. (3) The 24-h peak level of cTnI is significantly higher in fibrinolysed than in patients who didn't undergo fibrinolysis. (4) A direct correlation between the cTnI value and the Killip class is present either in the whole group or in any subset of patients and the progressive decrease of the cTnI concentration along the AMI course doesn't occur in Killip>2 group. (5) cTnI is higher in unstable than in stable anginous patients and normal subjects but not in stable angina with respect to healthy controls. CONCLUSIONS: (1, 2) The less increase and the early return in normal range of cTnI serum levels which occur in AMI subgroups with a better prognosis could be regarded as favourable prognostic signs. (3) The persistent higher values of cTnI in fibrinolysed subjects being associated with the angiographic finding of patent coronary arteries, it can be suggested that the large and persistent relase of cTnI from myocardium represents a reliable biochemical marker following the wash-out associated to a successful reperfusion. (4) The persistent increase of cTnI in AMI patients with advanced Killip class suggests that the high cTnI values are not only a strong index of myocardial necrosis but also of ongoing myocyte injury and hemodynamic impairment predictive of poor outcome. (5) The hypothesis can be reasonably advanced that the higher values of cTnI in unstable angina are due to focal areas of myocardial necrosis undetectable by the conventional serum markers or to a clinically silent AMI occurred in the week or so before in-hospital admission.

[Troponin I in acute ischemic cardiopathy]. / La troponina I nella cardiopatia ischemica acuta.

BACKGROUND: The present study was aimed at investigating cardiac troponin I values in the first week of acute myocardial infarction and in non-infarct acute coronary ischemic syndromes. METHODS: Eighty-two patients, 42 with acute myocardial infarction, 10 with stable angina and 30 with primary unstable angina, were enrolled in the study. Blood was collected within 6 hours of symptom onset and, in the group with acute myocardial infarction, after 24 and 48 hours, and on day 7. RESULTS: Serum troponin I increased within the first 6 hours of myocardial infarction, reached the peak after 24 hours, at 48 hours it decreased, and remained above the normal range until day 7. However, troponin I values 1) were constantly higher in patients who died, in those > 60 years old and in those with antero-lateral necrosis than in survivors, in those < 60 years old and in those with infero-posterior necrosis, respectively; 2) returned to normal range on day 7 in survivors and in patients with infero-posterior acute myocardial infarction; 3) were significantly higher in fibrinolysed patients than in those who did not undergo thrombolysis; 4) were higher in patients classified as Killip class > 2. Serum troponin I values were in the normal range in non-infarct acute coronary ischemic syndromes, but were higher in unstable than in stable angina. CONCLUSIONS: The lesser increase and the early return to the normal range of cardiac troponin I levels in the subgroups of patients with myocardial infarction having a better clinical course could be regarded as a favorable prognostic sign. Since the persistent higher values of cardiac troponin I in fibrinolysed subjects are associated with the angiographic finding of patent coronary arteries, it can be suggested that the large and persistent post-thrombolysis release of cardiac troponin I from the myocardium represents a biochemical marker of a successful reperfusion. The persistent high cardiac troponin I values in patients with advanced Killip class suggest that the neuropeptide is an index of ongoing myocyte injury and hemodynamic impairment as well. The higher values of cardiac troponin I in unstable angina are probably due to focal areas of myocardial necrosis undetectable by conventional enzymatic serum markers.

Bronchoalveolar lavage cell analysis in a child with chronic lipid pneumonia.

In an asymptomatic 4 yr old child with radiographic evidence of parenchymal lung disease, bronchoalveolar lavage (BAL) yielded the diagnosis of chronic lipid pneumonia caused by chronic aspiration of mineral oil given as a laxative. BAL analysis showed a marked reduction in the total number of alveolar macrophages; almost 70% of these cells contained intracytoplasmic lipid vacuoles. It also disclosed lymphocytic (cytotoxic/suppressor) alveolitis. A high percentage of lymphocytes expressed antigen markers of activation (human leucocyte antigen (HLA)-DR), CD54 and CD25). BAL analysis 18 months after mineral oil intake revealed that lymphocytes bearing antigen markers of activation had markedly decreased whereas alveolar macrophages (normal and lipid-laden) had increased. A subsequent whole lung BAL was considered unnecessarily invasive in this otherwise healthy child.

[Intestinal absorption of vitamin E in children with atrophy of the jejunal mucosa]. / Assorbimento intestinale della vitamina E in bambini con atrofia della mucosa digiunale.

The intestinal absorption of vitamin E is often thought to be closely correlated to that of fatty acids, but the biochemical mechanisms involved in the process are still not clear. For this reason, the present study aimed to assess the absorption of triglycerides and vitamin E, following oral administration, in 11 children with suspected malabsorption syndromes. Intestinal biopsy in 9 children showed the presence of a flat mucosa, whereas no changes were present in 2 patients. The results confirm the inverse correlation between the absorption of triglycerides and vitamin E, as if tocopherols used an independent system of transport. These findings contrast with those reported in the literature perhaps due to the low level of precision of colorimetric techniques previously used to assay vitamin E.

[Sensitivity to antibiotic drugs of isolated bacteria in urinary infections in children]. / Studio della sensibilità ai chemioantibiotici dei batteri isolati nelle infezioni urinarie in età pediatrica.

The need for an early start to antibiotic therapy during infections of the urinary ways in paediatrics, even before knowing the infecting strain and chemosensitivity tests, often makes it difficult to choose the drug to be used. The present study examines all the urine samples reaching the Microbiology Laboratory of Rome University's Paediatrics Clinic between 1986 and 1988, highlighting infecting species and respective chemosensitivity. The samples were also distinguished on the basis of sex and origin (hospitalised patients and out-patients). From the data so examined it was noted that some antibiotics give a broader cover against the species most frequently encountered during urinary way infections.

Opsonized-zymosan induces a respiratory burst in human blood platelets.

Opsonized-zymosan-stimulated polymorphonuclear cells show a cyanide-insensitive oxygen consumption. We have investigated whether opsonized-zymosan could induce similar metabolic change in human blood platelets. Preparation of intact human blood platelets, obtained by separation through a Ficoll layer (23% w/v) were challenged with opsonized-zymosan. The polymorphonuclear cell contamination was less than 1/10(8) platelets. The opsonized-zymosan-stimulated platelets showed an increase of oxygen consumption. The mean of oxygen burst measured by a polarographic method with a Clark electrode was 11 nmole/10(9) platelets/min (S.E.M. 4; n = 15). The duration of the burst was 2 min. Unstimulated platelets did not show the oxygen burst. The inhibitors of respiratory chain and prostaglandin synthesis completely abolished the oxygen consumption by opsonized-zymosan-stimulated platelets. The simultaneous addition of NADH (1 mM) and opsonized-zymosan induced a burst of oxygen consumption, which occurred after a variable lag phase (10-12 min) from the stimulation, also in the presence of inhibitors. This burst, which lasted about 1 min, amounted to 10 nmole/10(9) platelets/min (S.E.M. 2; n = 15) and it was higher in the presence of NAN3, a catalase inhibitor. Zymosan treated with hydrazine or heated plasma (56 degrees C) did not cause increased oxygen consumption. Inulin or inulin-treated serum did not stimulate platelets. In these experimental conditions some NADH disappeared, as shown by isotachophoresis. The results demonstrated that an immunological stimulus may activate a membrane-linked cyanide-insensitive oxygen metabolizing system.

The in vitro inhibitory effect on thrombin by 2,3-diphosphoglycerate.

Thrombin incubated with 2,3-diphosphoglycerate (150 nmol 2,3-DPG/1 NIH thrombin unit) lost up to 70% of its clotting activity, whereas the esterase activity remained unchanged. No fibrinopeptide release by thrombin was observed in the presence of 2,3-DPG. The fibrin polymerization was normal. By chromatography on Amberlite IRC-50, alpha-thrombin was eluted at pH 8.0. In presence of 2,3-DPG, alpha-thrombin was not eluted. Likely, 2,3-DPG can interfere with thrombin.