First case of multiple discitis and sacroiliitis due to Abiotrophia defectiva.
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Biomedical subjects
Publications and source records attributed to S Sire.
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We report the case of a 56-year-old HIV-seropositive man who presented a facial Demodex infection developed 2 months after initiation of highly active antiretroviral therapy. The Demodex infection was confirmed by scrapings and histopathologic examination and by the dramatic response to antiparasitic treatment with oral ivermectin associated with 5% permethrin cream.
In this study we assessed the short- and long-term effects of 4-weeks of exercise training (MI) soon after myocardial infarction in patients on beta-blocker treatment. Thirty-seven male patients < or = 65 years of age were included in the study, 19 of them randomized to exercise training (ET) and 18 to a control group (Ctr). Cumulated work (CW), calculated in kiloJoules (kJ), was recorded before immediately after the intervention period and again six months after the MI. In the short term the mean (SD) CW increased by 22% (from 65(20) to 79(25) kJ) in the ET group, compared with no change in the Ctr patients (65(24) vs 65(21) kJ) (p = 0.009). At late follow-up CW was 14% above baseline in the ET patients (65(20) vs 74(20) kJ) p = 0.036, compared with only 6% in the 15 Ctr patients who were still available for follow-up (68(24) vs 72(29) kJ), but without a significant between-group difference. In post-MI patients on beta-blocker treatment, and with a high baseline exercise capacity, physical training improved exercise capacity in the short term, but there was no significant between-group difference at long-term follow-up.
Coronary heart disease and beta-blocker treatment can increase the use of the Frank-Starling mechanism during exercise. The aim of the study was to assess whether this could be influenced by physical training. Male patients on beta-blocker treatment after myocardial infarction were randomised to four weeks of training (ET, n = 19) or to a control group (Ctr, n = 18). Cardiac output (CO) at rest and at identical submaximal exercise levels in each patient were determined by radionuclide ventriculography at baseline and after the intervention period. CO was calculated as end diastolic volume (EDV) x ejection fraction x heart rate, and deltaCO and deltaEDV as change in parameter from rest to exercise. The mean (SD) deltaCO decreased from 6.5 (2.1) L/min(-1) to 5.1 (2.4) in ET patients and increased from 5.0 (1.7) to 5.8 (2.7) in Ctr, p = 0.004. deltaEDV decreased from 30 (30) mL to 12 (35) in ET and increased from 11 (20) to 36 (33) in Ctr, p = 0.005. When adjusting for baseline dissimilarities between the groups in a multivariate linear regression analysis, these differences were still statistically significant, p = 0.018 and p = 0.044, respectively. Physical training reduces the CO increase needed to perform identical submaximal exercise, and this is accompanied by less left ventricular dilatation, with a potential for reducing exercise-induced ischaemia.
In a retrospective study, an increase in double-negative (CD3+ CD4- CD8-) (DN) T lymphocytes has been shown to be an independent predictor of disseminated Mycobacterium avium complex (D.MAC) infection in patients with less than 100 CD4+ T cells per mm3. To better characterize this cell expansion, a prospective study was designed. From July 1995 to April 1997, 206 HIV-infected patients with less than 100 CD4+ T cells per mm3 were prospectively followed up and immunophenotyped. The median followup was 1.1 year (+/-0.5 year), and 14 new D.MAC infections were diagnosed among 84 first AIDS-defining events. In univariate and multivariate analyses, D.MAC infections were the only opportunistic infection with a significant increase in DN T-cell percentage (median = 6.6; range = 1.7 to 24.5, P = 0.004) compared with patients without any opportunistic infection. This alteration in T-lymphocyte count could constitute a predictor for D.MAC infection in clinical practice.
Constrictive pericarditis is an uncommon condition. Previously, tuberculosis or other bacterial infections were prevalent causes, often with prominent pericardial calcification. Presently, many patients with constrictive pericarditis of other aetiologies have lesser degrees of structural changes in the pericardium. We report on a case with severe symptoms where the correct diagnosis was elusive because of absent or minimal preoperative pericardial pathology. The clinical, echocardiographic and haemodynamic features of constrictive pericarditis are reviewed. We recommend thorough echocardiographic evaluation of central haemodynamics in patients with symptoms of heart failure when the aetiology is not readily apparent (e.g. previous myocardial infarction dilated cardiomyopathy or valvular disease.
Cardiac-related death of HIV-positive patients is not rare. The etiology of AIDS-associated dilated cardiomyopathies often remains unknown, even at autopsy. We report an observation associated to a severe deficit in selenium. The patient had been diagnosed as HIV-positive 2 years before. He presented Pneumocystis carinii pneumonia then Cryptococcus meningitis. Two months later he was hospitalized for pancreatitis and cachexia. He presented global heart failure that lead to death. No microorganism was found in myocardium at autopsy but plasma selenium was dramatically decreased (24 micrograms/L). The deficit in selenium has been associated to a dilated cardiomyopathy in non-AIDS patients. HIV-positive patients have an early decrease in plasma selenium, this concentration is dramatically decreased in malnourished patients. Selenium deficit might be the cause of some of the AIDS-related dilated cardiomyopathies and selenium supplementation might be useful in these patients.
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BACKGROUND AND AIMS OF THE STUDY: The hemodynamic function of the CarboMedics bileaflet mitral valve prosthesis was evaluated by Doppler echocardiography and by heart catheterization. The clinical state of the invasively examined patients was evaluated before and after surgery. METHODS: Doppler echocardiography was performed in 54 patients at six months after surgery. Further, combined right and left heart catheterization was performed in 22 of these patients before surgery and at six months thereafter. RESULTS: The Doppler mean gradients were small (3.6 +/- 1.2 mmHg), and corresponded well with Doppler mean gradients in the subgroup examined with both methods (3.5 +/- 1.1 mmHg) and with the invasive gradients (3.4 +/- 1.9 mmHg); there was also no difference between the different valve sizes. Clinically, pressure recovery distal to the valve is probably so small that no systematic difference between the two techniques of measurement is present. Only physiological regurgitation was found, and no case of valve dysfunction. The patients improved from functional NYHA class 3.1 +/- 0.4 to 1.4 +/- 0.6, regardless of preoperative diagnosis, with most pronounced improvement in those with mitral stenosis. Pulmonary artery pressure was normalized. Pulmonary vascular resistance and cardiac index improved slightly. CONCLUSIONS: In conclusion, the valvular prostheses demonstrated excellent hemodynamic function. There was striking agreement between the small invasive and non-invasive gradients. Finally, the functional status of the patients improved considerably, most distinctly in those patients with prior mitral stenosis.
The Kikuchi-Fujimoto's syndrome is an histiocytic necrotizing lymphadenitis which is observed at any ages but preferentially among young adults. The sex ratio is about 4:1 in favour of women. It is clinically characterized by cervical lymph nodes in a context of fever and asthenia. Sometimes, there is transitory leucopenia and an increase of the erythrocyte sedimentation rate. The course of the disease is spontaneously favourable in 1 or 3 months but recurrence is possible. The histology of the lymph node could mimic a malignant lymphoma and the immunohistochemical findings are of a great importance (Ki-M1P or KP1 antibody). The etiology remains unknown but some infectious diseases have been suspected (toxoplamosis, Epstein-Barr virus). Its association with a systemic lupus erythematous had been described and this set the problem of its physiopathology. We report two new cases of Kikuchi-Fujimoto's syndrome which one was attributed to Epstein-Barr virus primo-infection and the other associated with a systemic lupus erythematous.
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OBJECTIVES: The aim of the present study was to determine whether simple clinical variables can predict the effect of intensive exercise training in an unselected population early after myocardial infarction. METHODS: Starting 5 weeks after the qualifying myocardial infarction, 105 patients, 68 years old or younger, completed a 4 week period of intensive exercise training. The training effect was defined as an absolute increase in cumulative work at bicycle ergometry. Using univariate and multivariate analysis, 28 variables were tested against the training effect. RESULTS: The mean exercise capacity increased from 46.7 +/- 22.7 kJ to 69.5 +/- 31.1 kJ (P = 0.0001). Multivariate analysis identified five independent predictors of the training effect. Myocardial infarct size was associated with a better training effect (P = 0.0018), as was male gender (P = 0.0042) and ability to exercise to exhaustion at the baseline exercise test (P = 0.0124). Older age (P = 0.0017) and treatment with beta-adrenergic blocking agents (P = 0.0241) were associated with a lower effect from training. These five variables explained 33% of the variations in effect from training. Patients suffering in-hospital cardiac complications or congestive heart failure achieved a training effect at least as great as patients without cardiac complications. CONCLUSIONS: Five simple clinical variables, including infarct size, can assist in the selection of patients for exercise training after myocardial infarction.
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One hundred and two patients participated in a 4 week programme of intensive exercise training early after myocardial infarction. Lipid levels were measured before and after exercise training. The mean exercise capacity increased by 49% (P = 0.0001). Twenty-one patients who continued smoking and 25 non-beta-blocked patients were considered to have an increased risk of recurrent cardiac events, as were patients with high initial lipid levels. In the smokers and non-beta-blocked patients total cholesterol decreased by 0.30 mmol.l-1 (P = 0.031) and 0.37 mmol.l-1 (P = 0.042) respectively and triglycerides by 0.28 mmol.l-1 (P = 0.058) and 0.13 mmol.l-1 (P = 0.11). Patients with high initial cholesterol and triglyceride levels had the largest cholesterol and triglyceride decrease, r = 0.43 (P = 0.0001) and r = 0.38 (P = 0.001) respectively. After adjusting for initial lipid levels, cholesterol (P = 0.036) as well as triglycerides (P = 0.034) decreased in patients without beta-blocker treatment whereas smoking no longer had an independent effect on lipid level decrease. HDL-cholesterol did not change in any group. Thus, after 4 weeks of exercise training lipid profiles were improved in patients with an increased risk of recurrent cardiac events. Beta-blocker treatment, however, seemed to hinder the beneficial effects of exercise training on lipid levels.
The sequential interaction between the two components S and F of leukocidin from Staphylococcus aureus and the membrane of human polymorphonuclear neutrophils has been investigated in the presence of 1 mM Ca2+. With 125I-labeled components, it has been shown that binding of the F component occurred only after binding of the S component. The kinetic constants of binding of both components were not statistically different (Kd, approximately 5 nM; Bm, approximately 35,000 molecules per cell), and both Hill coefficients were 1. The application of increasing concentrations of leukocidin provoked a dose-dependent secretion of the granule content, as determined by hexosaminidase and lysozyme activity measurements. Furthermore, the separate perfusion of S and F components on human polymorphonuclear neutrophils deposited on a filter induced secretion of the granules content only when the perfusion of the S component preceded that of the F component. We conclude, therefore, that (i) S-component binding is a prerequisite for F-component binding and for subsequent activation of polymorphonuclear neutrophils and (ii) there is a specific binding site for the S component in the plasma membrane.