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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The frequency of renal vascular lesions (RVL) and their relevance in the progression of renal damage were evaluated by the Pathology Group of the "Gruppo Italiano per lo Studio della Nefrite Lupica" (GISNEL). Of 285 patients with lupus nephritis collected from 20 nephrology centers in Italy and classified according to World Health Organization (WHO) criteria, 79 cases (27.7%) with RVL were identified and classified as follows: (1) lupus vasculopathy (n = 27); (2) hemolytic-uremic syndrome/thrombotic thrombocytopenic purpura (HUS/TTP) malignant hypertension-like lesions (n = 24); (3) vasculitis (n = 8); (4) arterio-arteriosclerosis (n = 20). At the time of renal biopsy, patients with RVL had mean serum creatinine levels significantly higher than patients without RVL (201.8 +/- 195.9 mumol/L [2.2 +/- 2.2 mg/dL] v 108.1 +/- 108.0 mumol/L [1.2 +/- 1.2 mg/dL]; P less than 0.01). Hypertension was more frequent in patients with RVL than in those without (68.4% v 30.5%; P less than 0.01). The probability of kidney survival assessed according to the Kaplan-Meier method at 5 and 10 years was, respectively, 74.3% +/- 5.9% and 58.0% +/- 8.9% in patients with RVL, compared with 89.6% +/- 2.7% and 85.9% +/- 3.7% in patients without RVL. However, the two groups did not differ significantly as regards overall survival, the probability of survival at 5 and 10 years being 86.5% +/- 4.5% and 78.8% +/- 6.6% in patients with RVL and 92.2% +/- 2.2% and 83.3% +/- 4.4% in patients without RVL.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal vascular lesions as a marker of poor prognosis in patients with lupus nephritis. Gruppo Italiano per lo Studio della Nefrite Lupica (GISNEL). 186 81

We examined the thymic reticulum of three strains of mice showing symptoms of lupus-like disease. Ultrastructural pathology revealed several features common to the three mouse strains in varying degrees according to sex and age of the mice. Main anomalies included vacuolized aspect of the thymic epithelium, an increased number of macrophages, interdigitating cells and cystic cavities, the presence of a great number of plasmocytes and mastocytes and extensive interstitial fibrosis and arteriosclerosis. The most intriguing finding was the presence of crystal-like inclusions in epithelial cells. Some thymuses also showed premature histologic modifications similar to those observed in the ageing involuted thymus. Dysfunction of the epithelial cell secretory system, accumulation of denatured thymic hormone as well as premature organ ageing associated with a loss of thymic function could contribute significantly to the autoimmune phenomenon observed in lupus mice.
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PMID:Thymic reticulum of autoimmune mice. II: Ultrastructural studies of mice with lupus-like syndrome (NZB, BXSB, MRL/l). 233 2

Acute ischemic neuropathy is the acute ischemic necrosis of the optic nerve fibers occurred by the occlusion of small vessels which distribute widely to lamina cribrosa and anterior et posterior area of lamina cribrosa. Pale coloured edema and light swelling are seen generally on the optic disc, and after a few months falls in simplex nerve atrophy. I have explained my 3 cases of ischemic neuropathies. They have some things in common, and causes are considered arteriosclerosis or temporal arteritis in old people, and often takes place based on diabetes mellitus, lupus erythematosis or another many diseases etiologically.
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PMID:Acute ischemic atrophy of papilla disc and diabetes. 345 15

The electroencephalograms (EEGs) of 120 patients with systemic lupus erythematosus (SLE), were evaluated with regard to clinical manifestations and laboratory findings. On the initial 120 records, abnormal EEGs were observed in 109 patients (90.8%). Epileptiform patterns were also observed in 33 patients (27.5%). Diffuse alpha wave, theta wave, and delta wave appeared to be unique findings of basic wave activity in EEGs of SLE patients. Paroxysmal abnormalities of spike and wave complex, spike, and sharp wave were frequently observed. These paroxysmal abnormalities appeared to be easily exaggerated by hyperventilation or sleep. Focal abnormal discharges were also observed. The incidence of abnormal EEGs of the patients with central nervous system involvement (CNS lupus), did not differ from that of non-CNS lupus i.e. 24/30 (80.0%) vs 82/93 (88.2%). On the other hand, regarding the severity of abnormal EEGs, CNS lupus manifested severer findings than those of non-CNS lupus. As to the EEG abnormality, female patients, younger patients less than 30 years old, flared patients, and patients receiving prednisolone more than 30 mg/day had severer EEG findings than those of each counterparts. The patients who had once manifested neuropsychiatric disorders and/or immunologic abnormalities (anti-deoxynucleic acid antibody, anti-DNA antibody), showed severe findings on EEG. Epileptiform patterns were frequently observed in patients receiving lower prednisolone doses (30 mg/day or less), although they did not correlate with disease activity. Patients with arteriosclerosis obliterans or aortitis syndrome, demonstrated only mild abnormalities on EEGs and they had not shown any epileptiform patterns.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical significance of electroencephalograph in patients with systemic lupus erythematosus]. 849 81

The paradox of aerobic life, or the 'Oxygen Paradox', is that higher eukaryotic aerobic organisms cannot exist without oxygen, yet oxygen is inherently dangerous to their existence. This 'dark side' of oxygen relates directly to the fact that each oxygen atom has one unpaired electron in its outer valence shell, and molecular oxygen has two unpaired electrons. Thus atomic oxygen is a free radical and molecular oxygen is a (free) bi-radical. Concerted tetravalent reduction of oxygen by the mitochondrial electron-transport chain, to produce water, is considered to be a relatively safe process; however, the univalent reduction of oxygen generates reactive intermediates. The reductive environment of the cellular milieu provides ample opportunities for oxygen to undergo unscheduled univalent reduction. Thus the superoxide anion radical, hydrogen peroxide and the extremely reactive hydroxyl radical are common products of life in an aerobic environment, and these agents appear to be responsible for oxygen toxicity. To survive in such an unfriendly oxygen environment, living organisms generate--or garner from their surroundings--a variety of water- and lipid-soluble antioxidant compounds. Additionally, a series of antioxidant enzymes, whose role is to intercept and inactivate reactive oxygen intermediates, is synthesized by all known aerobic organisms. Although extremely important, the antioxidant enzymes and compounds are not completely effective in preventing oxidative damage. To deal with the damage that does still occur, a series of damage removal/repair enzymes, for proteins, lipids and DNA, is synthesized. Finally, since oxidative stress levels may vary from time to time, organisms are able to adapt to such fluctuating stresses by inducing the synthesis of antioxidant enzymes and damage removal/repair enzymes. In a perfect world the story would end here; unfortunately, biology is seldom so precise. The reality appears to be that, despite the valiant antioxidant and repair mechanisms described above, oxidative damage remains an inescapable outcome of aerobic existence. In recent years oxidative stress has been implicated in a wide variety of degenerative processes, diseases and syndromes, including the following: mutagenesis, cell transformation and cancer; atherosclerosis, arteriosclerosis, heart attacks, strokes and ischaemia/reperfusion injury; chronic inflammatory diseases, such as rheumatoid arthritis, lupus erythematosus and psoriatic arthritis; acute inflammatory problems, such as wound healing; photo-oxidative stresses to the eye, such as cataract; central-nervous-system disorders, such as certain forms of familial amyotrophic lateral sclerosis, certain glutathione peroxidase-linked adolescent seizures, Parkinson's disease and Alzheimer's dementia; and a wide variety of age-related disorders, perhaps even including factors underlying the aging process itself. Some of these oxidation-linked diseases or disorders can be exacerbated, perhaps even initiated, by numerous environmental pro-oxidants and/or pro-oxidant drugs and foods. Alternatively, compounds found in certain foods may be able to significantly bolster biological resistance against oxidants. Currently, great interest centres on the possible protective value of a wide variety of plant-derived antioxidant compounds, particularly those from fruits and vegetables.
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PMID:Oxidative stress: the paradox of aerobic life. 866 Mar 87

In the present review piece, we analyze the formation of free radicals as a consequence of the cellular metabolism in aerobe organism, and the beneficious and harmful actions thereof on cellular structures. The balance existing between free radicals and the so-called antioxidant defenses, is a key factor for preventing the development of noxious processes at the cellular and tissue level. In accordance with the present scientific knowledge, the excessive production of free radicals in the organism, and the imbalance between the concentrations of these and the antioxidant defenses, may be related to processes such as aging and several diseases, among which we find cancer, ischemic processes, senile dementia, diabetes, pulmonary and pancreatic diseases, lupus erythematosus, cirrhosis, intestinal inflammatory disease, multiple sclerosis, arthritis, arteriosclerosis, cardiovascular disease, diseases of the central nervous system and the brain. According to the results of numerous research works conducted with the administration of several molecules with an antioxidant activity, one is beginning to see what their role will be in the pharmacological therapeutics for the treatment of a large number of patients such as those with burns, traumas, septics, shock, surgery, transplantation, radiation or chemotherapy, respiratory distress syndrome, AIDS, etc. We may possibly be facing a therapeutic tool which is of great interest in the clinical area, which shall be developed in the near future, as clinical trials which permit confirmation of their efficacy are conducted.
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PMID:[Antioxidants: the therapy of the future?]. 961 71

A workshop to be held in Sapporo will attempt to upgrade criteria for the antiphospholipid syndrome (APS). These criteria should probably be based on a scoring system using both clinical and biological items. Clinical criteria could be categorized between 'major', that is thrombosis or obstetrical criteria, and 'minor', to be selected among livedo, heart valve lesions, chorea, adrenal hemorrhage, thrombocytopenia, and others. A similar approach could be proposed for biological criteria, with persistent strong LA, high IgG aCL or antibodies to beta2GPI as major criteria if the workshop accepts antibodies directed to co-factors as APS criteria. Minor criteria could include IgM aCL, low/medium IgG aCL, and VDRL. Whether anti-prothrombin, anti-oxidised LDL, and M5 anti-mitochondrial antibodies should be added to the minor criteria, is open to discussion. In our mind, other parameters should be taken into account such as: young age--a method to avoid the questionable exclusion of arteriosclerosis in cases of arterial thrombosis--and the presence of personal and/or first-degree familial features of auto-immunity. Lastly, a differential diagnosis section is probably needed.
Lupus 1998
PMID:Towards improved criteria for the antiphospholipid syndrome. 981 94

Vasospasm can have many different causes and can occur in a variety of diseases, including infectious, autoimmune, and ophthalmic diseases, as well as in otherwise healthy subjects. We distinguish between the primary vasospastic syndrome and secondary vasospasm. The term "vasospastic syndrome" summarizes the symptoms of patients having such a diathesis as responding with spasm to stimuli like cold or emotional stress. Secondary vasospasm can occur in a number of autoimmune diseases, such as multiple sclerosis, lupus erythematosus, antiphospholipid syndrome, rheumatoid polyarthritis, giant cell arteritis, Behcet's disease, Buerger's disease and preeclampsia, and also in infectious diseases such as AIDS. Other potential causes for vasospasm are hemorrhages, homocysteinemia, head injury, acute intermittent porphyria, sickle cell disease, anorexia nervosa, Susac syndrome, mitochondriopathies, tumors, colitis ulcerosa, Crohn's disease, arteriosclerosis and drugs. Patients with primary vasospastic syndrome tend to suffer from cold hands, low blood pressure, and even migraine and silent myocardial ischemia. Valuable diagnostic tools for vasospastic diathesis are nailfold capillary microscopy and angiography, but probably the best indicator is an increased plasma level of endothelin-1. The eye is frequently involved in the vasospastic syndrome, and ocular manifestations of vasospasm include alteration of conjunctival vessels, corneal edema, retinal arterial and venous occlusions, choroidal ischemia, amaurosis fugax, AION, and glaucoma. Since the clinical impact of vascular dysregulation has only really been appreciated in the last few years, there has been little research in the according therapeutic field. The role of calcium channel blockers, magnesium, endothelin and glutamate antagonists, and gene therapy are discussed.
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PMID:Vasospasm, its role in the pathogenesis of diseases with particular reference to the eye. 1128 96

Although rheumatological diagnosis often includes an assessment of antiphospholipid (aPL) antibodies, the significance of other prothrombotic factors has not been established in thrombotic patients who are not afflicted with either arteriosclerosis or vasculitis syndrome. We have observed both the presence of antiphospholipid antibodies and a reduction of factor XII in such patients. Our results identified both lupus anticoagulant-positive (50%) and anticardiolipin antibody-positive (58%) patients. In addition, 83% of patients showed factor XII antigen level reduction. Furthermore, 70% of aPL-positive thrombotic patients showed factor XII antigen level reduction. Only two cases had antiphospholipid antibody alone, and 4/12 showed just factor XII antigen reduction. Recently, it has been reported that the presence of antiphospholipid antibodies induces factor XII reduction, and that anti-factor XII autoantibody can be detected in thrombotic patients. However, our results indicate that there are smaller factor XII reductions in non-thrombotic controls who are positive for antiphospholipid antibodies. Furthermore, anti-factor XII autoantibody was not detected in patients with decreased factor XII levels. Kindred research suggested that in two patients there was a genetic component to factor XII reduction. We concluded that the presence of both antiphospholipid antibodies and reduced serum factor XII was observed in most thrombotic patients from our rheumatology clinic. It is therefore possible to consider that the coexistence of these prothrombotic factors can contribute to the onset of thrombosis.
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PMID:Reduction of factor XII in antiphospholipid antibody-positive patients with thrombotic events in the rheumatology clinic. 1260 17

Antiphospholipid syndrome is considered to be a cause of an acquired hypercoagulable state leading to stroke and transient ischemic attack. Antiphospholipid antibodies (aPL) comprise a heterogeneous group of autoantibodies. Among them, lupus anticoagulant (LA) and beta 2-glycoprotein I dependent anticardiolipin antibody (beta 2-GPI aCL) are important and commonly measured. Recently, LA has been considered to be closely related to phosphatidylserine anti-prothrombin antibody. APL is an independent risk factor for first-ever ischemic stroke and a prognostic marker of recurrent stroke. The precipitating factors for the occurrence of stroke are the presence of beta 2-GPI-dependent aCL, a GPL aCL level of more than 40, and the simultaneous presence of lupus anticoagulant. Several mechanisms are believed to be involved in the thrombotic process in patients with antiphospholipid antibodies. Human activated protein C functions as a potent anticoagulant in human plasma by inhibiting the activity of coagulation cofactors Va and VIIIa. Activation of protein C is impaired in patients with aPL. Recently, the presence of aPL has been considered to be contributory factor for the development of atherosclerotic lesions. Transgenic mouse lacking the LDL receptor develop accelerated arteriosclerosis upon immunization with beta 2-GPL Several therapeutic options are available for the prevention of ischemic stroke in patients with aPL, such as antiplatelet, anticoagulant, and immunosuppressive therapy. The rate of recurrence in patients undergoing antiplatelet and anticoagulation combination therapy was found to be lower than that in patients receiving other forms of therapy. The WARSS-APASS collaborative study showed that there was no difference in the recurrence rate between aPL patients receiving antiplatelet or anticoagulation therapy alone. APL has been investigated in other neurological disorders such as multiple sclerosis, chorea, migraine and convulsion. The association of aPL with multiple sclerosis remains debatable. APL could be a contributory factor for the development of convulsion, but not for migraine.
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PMID:[Neurological aspects in antiphospholipid syndrome]. 1515 54


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