A 31-year-old woman was admitted to the hospital for investigation of left lower limb thrombophlebitis. History, physical examination, and laboratory investigations led to the diagnosis of systemic lupus erythematosus (SLE), complicated by secondary antiphospholipid syndrome (APS). Treatment included steroids, azathioprine, aspirin, and low molecular weight heparin. Sixty-three days later, she was admitted to the hospital again because of high fever, macroscopic hematuria, and dyspnea. Laboratory testing showed anemia and impaired renal function. High-resolution chest computed tomography (CT) revealed bilateral multiple peribronchial infiltrates with hemorrhage. Magnetic resonance imaging (MRI) angiography of the kidneys revealed left renal vein thrombosis combined with ischemia of the left kidney. Cyclophosphamide and methylprednisolone pulse treatment as well as intravenous immunoglobulins were started immediately. Despite intensive immunosuppressive and supportive treatment, she suffered three relapses of alveolar hemorrhage and died on day 40, due to severe intracerebral bleeding. The final diagnosis was catastrophic APS with diffuse alveolar hemorrhage and kidney involvement. The unusual combination of recurrent alveolar hemorrhage and death from intracerebral hemorrhage rather than thrombosis in a CAPS patient is discussed.
The purpose of this study was to evaluate the changes in tissue-plasminogen activator (t-PA), plasminogen activator inhibitor - type 1 (PAI-1) and D-dimer (DD) antigen plasma levels in acute myocardial infarction (AMI) patients after thrombolytic therapy with two different thrombolytic agents, rt-PA or acetyl-streptokinase and to find out any correlation between the plasma t-PA, PAI-1 and DD levels with the infarct size as it is estimated from the peak of serum CPK levels. The plasma antigen levels of t-PA, PAI-1 and DD were measured by the enzyme immunoassay method (Stago), in 57 consecutive patients (M = 46, F = 11, mean age 55.6 +/- 8.8 years) and in 25 normal subjects (M = 18, F = 7, mean age 54.0 +/- 5.5 years). In 47 out of the 57 patients who were treated successfully with 100 mg of rt-PA (26 patients) or with 1.5 MU 21 of acetyl-streptokinase, as well as in 10 patients who were not treated, samples were obtained again 4 and 24 hours after the end of thrombolytic therapy or admission, respectively. During the acute phase of myocardial infarction the t-PA, PAI-1 and DD antigen plasma levels were significantly higher than in healthy people. There were no significant changes in the t-PA, PAI-1 and DD plasma levels of the patients who were not treated with a thrombolytic agent. We found a significant elevation of t-PA (p < 0.001), PAI-1 (p < 0.05) and DD (p < 0.001) after 4 hours in comparison with the baseline (at presentation, before therapy). After 24 hours the t-PA and DD plasma levels remained significantly higher (p < 0.001) while the PAI-1 plasma levels returned to the pre-therapy levels. There were no significantly different changes in the t-PA, PAI-1 and DD plasma levels of either group of patients, treated with rt-PA or acetyl-streptokinase while the t-PA and PAI-1 levels were positively correlated with infarct size as estimated from peak serum CPK levels.
There is a growing interest in immunologically-mediated lesions in the cardiovascular system, as there has been evidence that there are antimitochondrial antibodies (AMA) in patients with hypertrophic cardiomyopathy or hypertensives with left ventricular hypertrophy (LVH). We have also very recently published findings from our laboratory that hypertensives with LVH have a considerable quantity of anticardiac antibodies (ACA) in their serum. The aim of this study was to investigate the possible involvement of autoimmune mechanisms in the pathogenesis and evolution of hypertensive disease. Three groups of subjects were included in the study. Group A comprised 37 patients (20 men, 17 women, mean age 50.5 +/- 8.5 years) with mild to moderate essential hypertension, 19 without echocardiographic evidence of LVH, and 18 with LVH. Group B comprised 10 patients (6 men, 4 women, mean age 45.1 +/- 8.7 years) with secondary hypertension. The control group (C) comprised 15 normotensive subjects (8 men, 7 women, mean age 47.7 +/- 8.7 years). Cellular immunity against arterial wall antigen was studied in all subjects by means of migration inhibitory factor (MIF) against relevant antigen preparation. Sera from Group A and C subjects were tested for the presence of autoantibodies against both specific (myocardial) and nonspecific antigens, by means of the indirect immunofluorescence technique. Eighty per cent of patients with essential hypertension showed a positive cellular response (MIF) against an arterial wall antigen compared to the patients with secondary hypertension or the control group. Moreover, patients with essential hypertension and LVH had the highest incidence of specific (anticardiac, ACA) and nonspecific autoantibodies and the highest C3c and C4 complement component levels compared to patients without LVH or the control group. Most of the ACA positive patients were also AMA positive, while the ACA negative patients were AMA negative as well. Defects in cell-mediated immunity against arterial wall antigen(s) may be the cause or the effect of hypertension. On the basis of our findings that there was no delayed type hypersensitivity response to arterial wall antigen(s) in the patients with secondary hypertension, we suggest that, in some cases of essential hypertension, delayed hypersensitivity reactions possibly contribute to the pathogenesis of hypertension. Autoimmune mechanisms are discussed on the basis of common epitopes shared between heart and arterial tissue.
The purpose of the study was to investigate the possible role of autoantibodies in the development and type of left-ventricular hypertrophy (LVH). Three groups of subjects were studied:15 patients with hypertrophic cardiomyopathy (HCM; 11 males, 4 females; mean age 50.0 ± 16..3 years); (b) 15 patients with essential hypertension (10 males, 5 females; mean age 56.8 ± 13.5 years) with normal renal function and serum electrolytes and (c) 15 male athletes (mean age 20.8 ± 5.9 years). The control group consisted of 15 normal subjects with no sign of heart disease. The following indices of cardiac performance were determined by means of echocardiography: end-diastolic and end-systolic diameters, interventricular septum thickness, left-ventricular (LV) wall thickness, LV mass and LV mass index. The immunologic parameters studied included autoantibodies against (a) specific (anticardiac cell; ACA) and nonspecific (antimitochondrial cell; AMA) autoantigens according to a conventional indirect immunofluorescence technique. (1) Higher values for LV mass and LV mass index were observed in HCM. (2) The incidence of specific and nonspecific autoantibodies in hypertensive patients and in patients with HCM was significantly higher compared to athletes and controls. All ACA-positive individuals (5 with HCM, 3 with hypertension and 1 athlete) were AMA positive as well, while all ACA-negative individuals were also AMA negative. The ACA-positive individuals had higher C3c and C4 levels compared to the ACA-negative individuals. An autoantibody-mediated immunopathogenic role is discussed in the development and type of myocardial hypertrophy. Left-ventricular hypertrophy (LVH) due to heart disease (cardiomyopathies, hypertension or aortic stenosis) is considered as a pathological process followed by fibrosis and structural muscle changes [1]. On the contrary, LVH in athletes is considered as a ‘physiological’ myocardial response to exercise [2]. On the other hand, Autore et al. [3] have reported the presence of autoantibodies against mitochondria in patients with cardiomyopathies or hypertension with LVH, but not in athletes with LVH. These findings suggest the possibility that autoimmune mechanisms might be involved in the pathogenesis of LVH due to heart disease In this study we sought for the presence of autoantibodies against both specific and nonspecific antigens in athletes and patients with LVH of different origins, such as hypertrophic cardiomyopathy (HCM) or hypertension, in order to investigate the possible involvement of these autoantibodies in the development of LVH.
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