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M C Amigo

Publications and source records attributed to M C Amigo.

At least 19 recordsLinked to original sources
PubMed2006

Myocardial perfusion defects in patients with autoimmune diseases: a prospective study. Analysis of two diagnostic tests.

A significant correlation between autoimmune diseases and premature or accelerated coronary atherosclerosis has been found. The objectives of the study were: (a) to evaluate myocardial perfusion defects in patients with autoimmune diseases by contrast echocardiography and nuclear imaging; and (b) to evaluate the prevalence of alterations in subclinical myocardial perfusion defects in autoimmune diseases. Myocardial perfusion in 37 patients was evaluated by contrast echocardiography at rest and with dobutamine and with nuclear imaging. The agreement between the two diagnostic tests at rest was 0.72 (P < 0.0001) and with dobutamine was 0.65 (P < 0.0001). The prevalence of abnormalities in myocardial perfusion in autoimmune diseases by contrast echocardiography and nuclear imaging was 27% and in patients with primary antiphospholipid syndrome was 30%. We concluded that there is a high level of agreement between contrast ecocardiography and nuclear imaging for assessment of myocardial perfusion defects in patients with autoimmune diseases, and their prevalence is similar to that reported in the literature.

Adolescent↗
PubMed2004

Libman-Sacks endocarditis associated with antiphospholipid syndrome and infection.

INTRODUCTION: Antiphospholipid syndrome (APS) is a systemic autoimmune disease, associated not only with a hypercoagulable state and recurrent fetal loss but with many diverse clinical manifestations including heart involvement, neurological manifestations, as well as skin, kidney and hematologic abnormalities. Cardiac manifestations include coronary by-pass graft and angioplasty occlusions, cardiomyopathy, cyanotic congenital heart disease, intracardiac thrombus and complications of cardiovascular surgery. The valvular heart disease was defined as Libman-Sacks nonbacterial endocarditis. Previously, we have shown a linear subendothelial deposition of anti-cardiolipin/beta2 glycoprotein I (beta2GPI) antibodies in the valve specimens derived from APS patients. The involvement of complement C3c in the pathogenesis was documented. We assessed the beta2GPI-related target epitope recognized by the anti-beta2GPI Abs on the valves. MATERIALS AND METHODS: In order to find the beta2GPI-related target epitopes recognized by the anti-beta2GPI antibodies on the valves, we used beta2GPI-related synthetic peptides. The presence of anti-beta2GPI Abs on the studied valves was detected by anti-idiotypic antibody, followed by immunoperoxidase analysis. Biotin attached to the N-terminal of beta2GPI-related synthetic peptides and control peptide were used to identify the epitope addressed by the anti-beta2GPI Abs deposited on the patient's valve. The binding was probed by streptavidin-peroxidase and appropriate substrate. The specificity was confirmed by competition assays with control peptide and anti-idiotypic antibody. RESULTS: Among the beta2GPI-related synthetic peptides, two peptides were found in previous studies to mimic common pathogens either bacteriae or viruses, which raised a possible infectious origin for APS. One of these peptides, TLRVYK, is a specific target for anti-beta2GPI Abs deposited on the APS valves. This synthetic peptide was able to displace the anti-anti-beta2GPI anti-idiotypic Abs for binding the anti-beta2GPI Abs on the valve by a competition assay. CONCLUSION: We point to the possibility that Libman-Sacks nonbacterial endocarditis may have an infectious origin.

Antibodies, Anticardiolipin↗
PubMed2002

Vascular endothelial growth factor plasma levels in patients with systemic lupus erythematosus and primary antiphospholipid syndrome.

The objective of this study was to assess the possible role of vascular endothelial growth factor (VEGF) in the pathogenesis of systemic lupus erythematosus (SLE) and primary antiphospholipid syndrome (PAPS). We studied 28 patients with SLE, 10 patients with PAPS, and 24 healthy controls. VEGF plasma levels were measured by ELISA. Immunolocalization of VEGF was done in renal tissue from SLE patients and cadaveric controls. Our results showed that VEGF plasma levels were increased in SLE patients compared with PAPS and controls. The correlation between clinical manifestations and VEGF levels revealed that SLE patients with renal failure had significantly increased plasma VEGF levels (134.1 + 91.0 pg/ml) compared with SLE patients with normal renal function (42.9 + 19.0 pg/ml), PAPS patients (41.9 + 26.6 pg/ml), and controls (36.2 + 27.0 pg/ml; P < 0.01). Immunostaining showed a strong expression of VEGF in SLE renal tissue samples. Our preliminary results indicate that VEGF is increased in plasma from patients with lupus nephritis and a moderate degree of renal failure and is overexpressed in renal tissue from these patients.

Adult↗
PubMed2001

Prognosis in antiphospholipid syndrome.

The results of prospective large cohort studies of patients with different clinical subsets of APS have been reported recently. A significant impact of the disease on long-term survival has been documented in these studies. Cumulative irreversible damage secondary to thrombosis results in organ dysfunction and morbidity. To assess prognosis and treatment in APS, it is imperative to quantify damage. We have recently created and validated an Antiphospholipid Damage Index, which is currently undergoing improvements. Having APS, whether primary or secondary, definitely confers a poor prognosis.

Adult↗
PubMed2000

Morphology of vascular, renal, and heart lesions in the antiphospholipid syndrome: relationship to pathogenesis.

A growing body of evidence suggests that aPL are not only serological markers of the antiphospholipid syndrome (APS), but may also directly contribute to the development of thrombosis and other manifestations, including the APS vasculopathy. The latter has been documented in leptmeninges, lung, skin, myocardium, peripheral arteries, and kidney. Renal lesions, a common feature of primary antiphospholipid syndrome (PAPS), include occlusion of principal renal arteries or their main branches, TMA, cortical ischemia, and renal vein thrombosis. Within the cardiac manifestations associated with aPL, valvular involvement is the most common. Histologic findings in valve specimens are consistent with a noninflammatory lesion characterized by intravalvular capillary thrombosis, laminar or verrucous superficial thrombosis, vascular proliferation, fibrosis, and calcification. Even though there is general consensus that endothelial damage triggers the chain of events that results in valve thickening, fusion, rigidity, and ultimately functional abnormalities, we believe that more experimental work remains to be done on the initial valve insult in APS.

Antibodies, Antiphospholipid↗
PubMed2000

Antiphospholipid (Hughes) syndrome in systemic lupus erythematosus.

APS is found in 20% to 35% of patients with SLE. PAPS and secondary APS have similar features and aPL specificities. The clinical course of the secondary syndrome is independent of the activity and severity of lupus, but the presence of APS worsens the prognosis of patients with lupus. Some features of SLE may result from thrombosis in patients with APS; thus, these patients require anticoagulation rather than corticosteroids. Novel preliminary classification criteria for APS were formulated during a postconference workshop held in Sapporo, Japan, following the Eight International Symposium on Antiphospholipid Antibodies. Treatment of APS remains empirical because of limited controlled prospective data. There is strong evidence that patients with aPL-associated thrombosis are subject to recurrences and require prophylactic therapy. APS is a treatable cause of recurrent fetal loss in women with SLE. The treatment of choice is anticoagulation with heparin, either standard unfractionated heparin or LMWH. One of the main reasons for the improving outcomes in APS pregnancies is closer obstetric surveillance.

Antiphospholipid Syndrome↗
PubMed1999

Echocardiographic evaluation of patients with primary antiphospholipid syndrome.

BACKGROUND: A third to half of the patients with primary antiphospholipid syndrome have valve disease. METHODS AND RESULTS: The echocardiographic characteristics of primary antiphospholipid syndrome were analyzed, and the utility of treatment with anticoagulants and/or antiplatelet agents (acetylsalicylic acid) is examined with the use of transesophageal echocardiography in the evaluation of valvular lesions after 1 year of therapy. Twenty-nine patients, 22 women and 7 men with average age of 35.4 years, were studied. Transesophageal echocardiography was performed on all patients before beginning anticoagulant and/or antiplatelet treatment. Valve lesions were found in 22 (75.9%) patients. Of these, other cardiac abnormalities were found in 3 cases, myocardial infarction in 2, and atrial septal defect in 1. In 7 (24.1%) cases, no valvular abnormality was detected, although in 1 of these, alterations in left ventricular segmental wall movement secondary to myocardial infarction were found. One year after initiation of anticoagulant and/or antiplatelet therapy, it was possible to perform transesophageal echocardiograms on 13 patients. No modification of valve lesions was found in 6 (46.2%) cases; new lesions had appeared in the remaining 7 (53.8%) as well as left ventricular apical akinesis in 1 case. CONCLUSIONS: These results indicate that the predominant heart lesion in primary antiphospholipid syndrome is valvular; anticoagulant and/or antiplatelet treatment does not diminish the noninfective valve lesions, and on occasion this entity may be associated with myocardial infarction despite angiographically normal coronary arteries.

Adolescent↗
PubMed1999

Increased endothelial cell expression of alpha3beta1 integrin in cardiac valvulopathy in the primary (Hughes) and secondary antiphospholipid syndrome.

The objective of this work was to determine markers of endothelial cell activation in valves from patients with antiphospholipid syndrome (APS) and heart valve involvement, in order to establish a role for endothelial cells in the pathogenesis of the valvular disease. Sixteen valves from ten patients with APS, obtained from autopsies or removed during valve replacement, were studied. Two groups of valves were used as controls. One group included seven normal valves from patients who died from non-cardiac diseases. The other group of valves were obtained from patients with bacterial endocarditis during autopsies or valve replacement operations. Immunoperoxidase and immunofluorescence stainings with antibodies to human immunoglobulins, endothelial cells, alpha3beta1 integrin, collagen IV, laminin and fibronectin were employed. Three histopathological patterns were apparent: normal valves, valves with verrucous endocarditis and valves with fibrocalcific changes. In all the valves with verrucous endocarditis the following findings were observed: (1) increased expression of the alpha3beta1 integrin on the endothelial cells, (2) increased amount of collagen IV, laminin and fibronectin, (3) proliferation of blood vessels and (4) linear subendothelial deposition of immunoglobulins and complement. The valves with fibrocalcific changes were deformed and showed a thick layer of collagen IV, laminin and fibronectin, yet in two valves the indothelial cells showed an expression of the alpha3beta1 integrin. The control valves did not express the integrin and had only a thin subendothelial band of collagen IV. In valves from patients with APS, 1 markers of endothelial cell activation are upregulated while the inflammatory exudate is scant. There is also a prominent deposition of immunoglobulins in the valves from patients with APS, suggesting a possible association between the deposition of the antibodies and the activation of the endothelial cells in APS.

Actins↗
PubMed1998

Antiphospholipid syndrome in SLE.

The antiphospholipid syndrome, initially described in systemic lupus erythematosus (SLE), occurs in 20-35% of patients with this condition. Its clinical manifestations may precede, be concurrent with, or follow clinical features of SLE. There are no major differences between the primary antiphospholipid syndrome and the secondary form that associates with SLE. Several studies suggest that the presence of an antiphospholipid syndrome in patients with SLE conveys a worse prognosis. To prevent recurrence of thrombotic events (particularly arterial events), oral anticoagulation with an international normalized ratio (INR) close to 3 is recommended. Treatment of recurrent fetal loss is with aspirin, or with aspirin plus heparin. Controlled studies are underway to determine optimal treatment in patients with cerebral ischaemia as well as the optimal treatment in women with recurrent pregnancy loss.

Abortion, Spontaneous↗
PubMed1997

Absence of ANCA in Mexican patients with Takayasu's arteritis.

Antineutrophil cytoplasmic autoantibodies (ANCA) were sought in 43 sera from 39 Mexican patients with typical Takayasu's arteritis (TA), (5 with active and 34 with inactive disease), and in a comparative group comprising 50 sera. Results were negative in all cases. This suggests that ANCA are not a serologic feature in TA per se, even during its active stage. ANCA positivity in TA, when present, may be a non-related phenomenon and probably identifies a subset of patients with atypical forms of TA or a polyangiitis overlap syndrome.

Adult↗
PubMed1997

[Morbidity in hospital admission for stroke].

INTRODUCTION: In spite of advances in the prevention and treatment of ischemic vascular disease, this continues to be one of the main causes of disablement and prolonged hospitalization in developed countries. Also, hospitalization itself leads to complications which have a negative effect on the morbi-mortality of these patients during the time spent in hospital. OBJECTIVE: We decided to study the effect of systemic complications during the period of hospital stay, on the functional recovery of patients which ictusl. MATERIAL AND METHODS: A prospective study was made of 47 patients admitted to our unit for neurological deficit of more than 24 hours evolution and of cerebrovascular aetiology. Functional recovery was evaluated by means of the index of Barthel on discharge and after a period of 3 months with respect to the degree of neurological involvement (Canadian scale on admission), glycemia on admission, time spent in hospital and the occurrence of systemic complications in hospital. RESULTS: These were no differences between the groups of patients with and without systemic complications regarding age, glycemia and Canadian scale on admission. Nor wes there any difference between the groups regarding the number of patients with significant deterioration of their neurological condition (decrease > 20% in the EC). Functional recovery on hospital discharge was worse in the group with systemic complications (IB: 43.05 +/- 34.1: as compared with IB: 72.8 +/- 22.7 in the group without complications). This difference persisted after 3 months. CONCLUSIONS: Systemic complications related to hospitalization have a negative effect on the functional recovery of patient with ictus and also prolong the time spent in hospital.

Adult↗
PubMed1996

The antiphospholipid/cofactor syndromes: a primary variant with antibodies to beta 2-glycoprotein-I but no antibodies detectable in standard antiphospholipid assays.

BACKGROUND: Most systemic lupus erythematosus (SLE) patients with two or more clinical manifestations of the antiphospholipid syndrome (APS) and negative antiphospholipid antibodies (aPL) have antibodies to beta 2-glycoprotein-I (a beta 2 GP-I). Herein we describe a similar set of circumstances, but in patients without evidence of SLE. PATIENTS AND METHODS: We studied 6 patients with recurrent venous and/or arterial thromboses without aPL as detected by routine assays nor clinical or serological evidence of other autoimmune disease. Immunoglobin (Ig) G and IgM antibodies to bovine and human phospholipid-free beta 2 GP-I were studied by Western blot test and by enzyme-linked immunosorbent assay (ELISA) utilizing radiated and nonirradiated plates. We also tested antibodies to cardiolipin, phosphatidylserine, and phosphatidylethanolamine by ELISA. As controls, 54 normal sera were studied. RESULTS: All 6 patients had recurrent arterial and/or venous thromboses. Three also had thrombocytopenia, 1 had livedo reticularis, and 2 had valvular heart disease. None of the patients had aPL, but all had serum IgG reactivity against human and bovine beta 2 GP-I (P < 0.001 versus controls for both). Titers of anti-bovine beta 2 GP-I were higher when studied in irradiated plates but were also higher than normal in nonirradiated plates (P < 0.001). These antibodies did not recognize human or bovine beta 2 GP-I bound to cardiolipin in solid phase. We confirmed by Western blot that these autoantibodies recognize human beta 2 GP-I. We found no IgM a beta 2 GP-I. CONCLUSIONS: We describe a primary condition akin to the antiphospholipid syndrome with negative aPL, but with serum IgG antibodies to human and bovine beta 2 GP-I. These antibodies recognize beta 2 GP-I epitopes that are not accessible when beta 2 GP-I is bound to cardiolipin.

Adult↗