[Aplastic anemia and nocturnal paroxysmal hemoglobinuria].
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Biomedical subjects
Publications and source records attributed to S De Castro.
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Intravenous drug abusers (IDA) normally show functional defects in monocyte activity, in particular their chemotactic response. The aim of the present work was to study the action of several opioids on monocyte chemotaxis. To do so, monocytes from healthy individuals were incubated with heroin and morphine at three different concentrations (10(-5) M, 10(-6) M and 10(-7) M), with the finding of a significant depression in monocyte chemotaxis in all cases. This alteration could be due to a receptor effect or, conversely, to a non-specific effect. Accordingly, in the second phase of the study, monocytes from controls were incubated with a selective agonist of mu receptors (DAGO) and a selective agonist of delta receptors (DPDPE). In both cases a decrease in chemotactic function was observed similar to that following incubation with morphine or heroin. Preincubation of the monocytes with naloxone prevented the depression induced by both specific agonists. These findings suggest that opioids play an important role in the depression of monocyte chemotaxis observed in IDA. The results also suggest the presence of mu and delta opiate receptors in the cells of the phagocytic mononuclear system.
Paradoxical embolism is considered a relatively uncommon disease. Continuous biplane transesophageal echocardiography (TEE) was performed in a 64-year-old woman who had an acute pulmonary embolism. TEE showed an elongated formation highly mobile within both atria. It was trapped in the interatrial septum, passing through a patent foramen ovale. Systemic embolism of the right arm was noted. The patient died 5 hours after admission, and postmortem examination confirmed the diagnosis of pulmonary embolism. This case demonstrates the potential utility of TEE in the study of patients with suspected paradoxical embolism.
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OBJECTIVE: To evaluate the prevalence of cardiac alterations by trans thoracic echocardiography (TTE) and the possible role of aPLs in determining heart damage in SLE patients. PATIENTS AND METHODS: We investigated 34 consecutive Caucasian SLE patients and 34 age and sex- matched controls. All patients underwent TTE. Lupus anticoagulant (LA) was assayed. IgG and IgM antiphospholipid antibodies against cardiolipin (aCL), phosphatidylinositol (aPI), phosphatidylserine (aPS), phosphatidic acid (aPA), and anti-Beta2-glycoprotein I antibodies (aBeta2GPI) were determined by ELISA. RESULTS: Nineteen (56%) SLE patients showed at least one cardiac abnormality (P < 0.0001 - RR 19; OR 41.8; 95% CI 5.1-342). The predominant valve dysfunctions were represented by mitral (21%) and tricuspidal (18%) regurgitation. Aortic regurgitation was observed in 12% of patients, pericardial effusion and left atrial enlargement were identified in 15% and 12% of cases, respectively. Mitral valvular strands were detected in one patient. The prevalence of cardiac abnormalities correlated with disease duration. Echocardiographic alterations were more common in aPLs positive than in aPLs negative patients (P = 0.02 - RR 2.5; OR 6.1; 95% CI 1.2-30.1). Patients with IgG-aPA, -aPI and -aPS had a higher prevalence of left atrial enlargement (P < 0.05); IgG-aPA and -aPI were significantly associated with increased interventricular septum thickness (P < 0.05). CONCLUSION: Our findings confirm that the heart is one of the main target in SLE patients. The association between aPLs and cardiac impairment suggests an adjunctive role of these autoantibodies in determining heart damage. SLE vasculopathy is a multifactorial process leading to accelerated atherosclerosis. Heart involvement over the course of disease requires a comprehensive screening and management of traditional and new cardiovascular risk factors to prevent cardiac damage, which represents the primary cause of morbidity and mortality in SLE patients.
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