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

A case of systemic lupus erythematosus (SLE) with subarachnoid hemorrhage due to a ruptured intracranial aneurysm is reported. A 31-year-old woman who had been treated with steroid for SLE was admitted to our department with severe headache, and nausea. CT scan showed subarachnoid hemorrhage and the left carotid angiogram revealed a small aneurysm at the supraclinoid portion of the left internal carotid artery. She had no neurological deficit. Hematological examination on admission showed disseminated intravascular coagulation (DIC), therefore, we decided to perform an intentionally delayed operation. In the meantime we treated the patient for DIC with FOY and methylprednisolone. The operation was performed after two weeks, when DIC had been eliminated completely. Postoperative hematological examination showed severe thrombocytopenia. We considered that SLE had come to the fore again, so we used Danazol in company with FOY and steroid. It seemed that Danazol was very effective for her. She was discharged about two months after admission with no problem. Cerebral apoplexy, such as cerebral infarction and cerebral hemorrhage, has often been seen in SLE, but subarachnoid hemorrhage due to a ruptured aneurysm is very rare. We could find only five reports of this phenomenon. Their prognoses were all, unfortunately, poor. It should be born in mind for therapy that a patient in SLE has a tendency to bleed. It seems that repeated hematological examinations and quick and proper management are important. We think that the aneurysmal formation in SLE is due to lupus vasculitis or the fragility of blood vessels due to a long use of Steroid.
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PMID:[A case of systemic lupus erythematosus with subarachnoid hemorrhage due to ruptured aneurysm]. 220 86

We investigated the clinical and pathologic characteristics of stroke in 234 patients with systemic lupus erythematosus. Thirteen patients (5.6%) developed cerebrovascular disease. Cerebral infarction was noted in eight, cerebral hemorrhage in two, and subarachnoid hemorrhage in three. In seven (54%) of these 13 patients, stroke occurred less than or equal to 5 years after systemic lupus erythematosus was diagnosed. Among the predisposing risk factors for stroke, hypertension was the most important. Lupus anticoagulant was detected in three (38%) and anticardiolipin antibody in three (43% of seven investigated) of the patients with infarction. Evaluation of the clinical manifestations and autoantibodies indicated that renal involvement and high titers of anti-deoxyribonucleic acid antibody were more frequent in the stroke group than in the non-stroke group. Autopsy studies on six of the patients with stroke revealed small infarcts and hemorrhages in all, but in no case was true angiitis observed. Libman-Sacks endocarditis was found in two of the three patients with infarction. In conclusion, the important contributory factor to the development of stroke in patients with systemic lupus erythematosus is considered to be hypertension mediated by immunologic abnormalities. Antiphospholipid antibodies and Libman-Sacks endocarditis are closely associated with occlusive cerebrovascular disease.
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PMID:Stroke in systemic lupus erythematosus. 223 45

We describe a patient with established systemic lupus erythematosus (SLE) in whom an intracerebral hemorrhage developed secondary to a ruptured aneurysm of the lenticulostriate artery (LSA). A 24-year-old woman with a four-year history of SLE was admitted to the department of internal medicine of Iwate Medical University for the treatment of lupus nephritis in 1985. She suddenly complained of severe headache and nausea, and soon lost consciousness. The computed tomographic scan revealed intracerebral hemorrhage in the left front-temporal region and subarachnoid hemorrhage. Left common carotid angiography demonstrated a 3 X 3 mm aneurysm of the LSA and displacement of other LSAs and anterior cerebral artery. The incidence of intracerebral hemorrhage in SLE was about ten percent in the reported central nervous system SLE, and it seemed that the prognosis of SLE with intracerebral hemorrhage was poor. The mechanisms of the intracerebral hemorrhage and the aneurysmal formation in SLE seemed to be due to lupus angiitis, but without clinical, radiologic and pathologic correlation. In operation, a ruptured aneurysm without neck was found in LSA and extirpated. In the pathological study, there was transmural angiitis, which fibrinoid necrosis, elastic tissue disruption and infiltration of inflammatory cells were found. Inflammatory cells were chiefly lymphohistiocytic with some polymorphonuclear leukocytes. It seemed that pathologic studies confirmed transmural angiitis with secondary aneurysm formation.
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PMID:[A case of systemic lupus erythematosus associated with an aneurysm of the lenticulostriate artery]. 332 45

We have previously described (Medicine 56:493, 1977) 12 patients with diffuse lupus glomerulonephritis who had no clinical or laboratory evidence of renal involvement at the time of the initial biopsy. In this article we report the course of 10 of these patients followed for 5-11 yr (mean 83 mo). One patient died in renal failure and two others of related causes (septicemia and subarachnoid hemorrhage). Seven patients (Group I) had a benign course from a renal standpoint, with stable renal function and mild or no urinary abnormalities. Repeat biopsy in four patients in this group revealed near complete resolution of the original lesion in two and considerable improvement in two others, who now have primarily mesangial hypercellularity and a focal lesion, respectively. Renal function deteriorated in three patients (Group II), resulting in loss of congruent to 50% of GFR in two and renal death in the third. Repeat biopsy in one of these patients showed a more severe, albeit focal, glomerulonephritis. Prognosis for renal function appears better in patients with silent nephropathy, but larger numbers are required to substantiate this impression. Until definitive answers become available, we believe it prudent to biopsy SLE patients even in the absence of overt renal involvement and to treat those with diffuse proliferative glomerulonephritis.
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PMID:Silent diffuse lupus nephritis: long-term follow-up. 704 6

The purpose of this study was to measure plasma platelet-activating factor (PAF) concentration, PAF-acetylhydrolase activities, anti-phospholipid antibody (aPLs) titers, and platelet function in patients with subarachnoid haemorrhage (SAH) and to assess the association of these variables with the development of cerebral vasospasm. Thirty-two patients with SAH due to ruptured cerebral aneurysm were studied. Plasma PAF concentration, PAF-acetylhydrolase activity, platelet count and aggregability, and plasma factor 4 (PF4) concentrations were measured regularly until approximately 2 weeks after SAH. aPLs, including lupus anticoagulant and anti-cardiolipin IgG and IgM were measured within 3 days after SAH. Plasma PAF concentration in patients with SAH showed the highest value on the occasion during 5 to 9 days after SAH. The concentrations were higher in patients with infarction due to vasospasm than in patients without cerebral infarction on any occasions after SAH. Plasma PAF-acetylhydrolase activities did not change in patients, regardless of the presence of cerebral infarction after SAH. Increased platelet consumption and aggregability and higher concentrations of PF 4 were detected in patients with cerebral infarction and not in patients without cerebral infarction. The patients with cerebral infarction due to cerebral vasospasm had aPLs more frequently than the control volunteers. Our findings indicate that increased plasma PAF and aPLs may contribute to the pathogenesis of cerebral vasospasm after SAH.
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PMID:Platelet-activating factor and antiphospholipid antibodies in subarachnoid haemorrhage. 784 32

Delayed ischaemic deficits due to cerebral vasospasm contribute to the high morbidity and mortality rates associated with subarachnoid haemorrhage. We evaluated the usefulness of measuring anti-phospholipid antibodies (aPLs) for prediction of the occurrence of symptomatic vasospasm and the outcome after subarachnoid haemorrhage. 32 consecutive patients with subarachnoid haemorrhage due to ruptured cerebral aneurysms were studied. They were admitted and operated on within 72 hours after the onset of subarachnoid haemorrhage. aPLs such as lupus anticoagulants, anti-cardiolipin IgG and anti-cardiolipin IgM were measured repeatedly after admission. Furthermore, platelet count, platelet aggregability and plasma platelet factor 4 were also measured. Eleven among the 32 patients (34.4%) showed positive in the examination for aPLs. Although aPLs could not predict symptomatic vasospasm, once symptomatic vasospasm occurred, patients with aPLs frequently demonstrated cerebral infarction and therefore their outcome was worse. aPLs were associated with a severe initial clinical grade and SAH grade on CT scan. Therefore it may explain the association of aPLs with worse outcome. aPLs were detected between 1 and 7 days. Four of 6 patients (67%) with aPLs became negative between 7 and 13 days after subarachnoid haemorrhage. The mechanism of transient aPLs is unclear but it is more likely to occur in the severer grade patients. The reduction in platelet count, the increased platelet aggregability, and the increased plasma platelet factor 4 concentration were also observed in aPLs-positive patients with symptomatic vasospasm.
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PMID:Anti-phospholipid antibodies and cerebral vasospasm following subarachnoid haemorrhage. 874 13

The frequency, clinical profile, treatment and outcome of subarachnoid hemorrhage (SAH) in patients with systemic lupus erythematosus (SLE) were assessed retrospectively, based on the case records of SLE of the Jichi Medical School Hospital over a 20 year period. Clinically defined SAH was found in 10 (3.9%) out of 258 SLE patients, which represented a frequency higher than previously assumed. Five patients had active SLE and lacked an apparent cause of SAH, other than SLE. A high mortality rate (5/5), no visible aneurysm on angiogram (3/4), and an onset during intractable SLE or after discontinued or no steroid therapy because of medical noncompliance (4/5) were characteristic of patients with active SLE, and thus an earlier successful suppression of SLE, if possible, might have prevented their SAH. In contrast, in the 5 patients with inactive SLE, 2 out of 3 saccular aneurysms were successfully clipped and small bleeding of one patient without aneurysms remitted spontaneously without the need for additional steroid therapy. When one death, which occurred outside of medical care, was excluded, the survival ratio of the hospitalized SAH patients with inactive SLE was significantly better than that with active SLE (3/4 versus 0/5, P=0.0476). In conclusion, the relatively common occurrence of SAH in SLE patients, and a significantly different clinical impact of SAH in respect to active and inactive SLE, were suggested from the results.
Lupus 2000
PMID:Subarachnoid hemorrhage and systemic lupus erythematosus. 1103 18

A 43-year-old female, who had been treated for systemic lupus erythematosus (SLE), presented with a subarachnoid hemorrhage (SAH) induced by rupture of cortical venous thrombosis, and be followed by medial medullary infarction during the acute stage of the SAH. The patient initially manifested a SAH. Angiography demonstrated no evidence of any aneurysms or arteriovenous malformations, but revealed cortical venous thrombosis. She suddenly developed left hemiplegia caused by medial medullary infarction on the 6th day. An active anticoagulant therapy was thought to be inappropriate because of initial symptoms as a hemorrhage. Since she had been accompanied by the medullary infarction, then, initially started by antiplatelet therapy. After the confirmation of no saccular or dissecting aneurysms with 2nd angiography, her treatment could be changed to anticoagulant therapy. Because of the sustained negative reactions of anti-cardiolipin beta 2 glycoprotein I antibody and lupus anticoagulant during the course of SLE, the definite diagnosis of antiphospholipid syndrome (APS) could not be made. However, this case is pathogenically thought to be cerebrovascular disease based upon APS, considering that this syndrome may be related to various antigen/antibody systems.
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PMID:[Systemic lupus erythematosus manifesting as subarachnoid hemorrhage induced by cortical venous thrombosis and followed by medial medullary infarction]. 1457 41

We examined a group of 83 patients (81 females and two males) diagnosed as systemic lupus erythenatosus (SLE) aged 19-77, with the mean duration of the disease of seven years. All patients had neurological examination and electroencephalography (EEG) complemented with magnetic resonance image (MRI) and single photon emission computed tomography (SPECT) in same cases. Among 83 patients we found the group of five (females) showing acute, stroke-like symptoms. Subarachnoid haemorrhage from a vascular malformation was diagnosed in one case. In four cases ischemical syndromes were observed mainly without strong clinical expression, with tendency to recede. In one patient the stroke was the first symptom of SLE. All these patients revealed abnormalities both in neurological examination and in neuroimaging techniques--as small, hyperintensive foci in MRI and multiple, diffused areas of decreased cerebral blood flow found in all but one cases in SPECT which seems to be the most sensitive method. In conclusions we want to stress that observed ischemic syndromes in patients with SLE were acute but of moderate intensity, with tendency to recede swiftly; transient ischemic attacks (TIA) were comparatively frequent. Acute stroke-like episodes might be the first symptom of SLE.
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PMID:[Cerebral strokes in patients with systemic lupus erythematosus]. 1467 47

Central nervous system symptoms occur in a substantial portion of patients with systemic lupus erythematosus. However, coma is a rare presentation and is usually secondary to complications such as subarachnoid hemorrhage, seizure, or ischemia. Here, we present a 49-year-old woman with lupus erythematosus and a history of recurrent aseptic meningitis and mild subarachnoid hemorrhage who presented with altered mental status and lethargy that progressed rapidly over hours to the herniation syndrome of coma, extensor posturing, and unilateral pupillary dilation. Spinal fluid showed massive protein elevation (>1600), and head computed tomography revealed global cerebral edema. The clinical and radiologic findings rapidly reversed with intravenous corticosteroids and mannitol within 24 hours, and her mental status improved to baseline. Her course was complicated by 2 episodes of recurrent encephalopathy when corticosteroids were tapered; these resolved after resuming high dosing. Because of ongoing pancytopenia, chemotherapy immunosuppression was delayed, and instead she received intravenous immunoglobulin with improvement in the pancytopenia. She remained cognitively intact during subsequent corticosteroid tapering. Rapid development of coma in lupus patients may be due to a primary process of the disease impacting blood brain barrier integrity. Although rare, this potentially fatal complication may be reversible with acute corticosteroid administration.
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PMID:Transient life-threatening cerebral edema in a patient with systemic lupus erythematosus. 1945 59


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