Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe three cases of cerebral vein thrombosis (CVT) in girls with systemic lupus erythematosus. Severe, persistent, unremitting headache was a common manifestation. In the first patient, although the clinical features were suggestive of CVT, the diagnosis was delayed and she had a significant cerebral infarct. In the other two patients the diagnosis was made earlier and led to more rapid treatment; the institution of early therapy may have prevented further sequelae. The CVT was diagnosed in all patients with a combination of computed tomography and magnetic resonance imaging studies without the need for angiography. All patients were treated for their underlying systemic lupus erythematosus and with anticoagulation. All are receiving long-term low doses of warfarin and have not had any recurrences.
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PMID:Cerebral vein thrombosis in childhood systemic lupus erythematosus. 775 95

Twenty-eight SLE patients (Arabs and Asians) in the UAE were studied in this report. The F:M ratio was markedly high; 27:1 in the group as a whole and 21:1 among Arabs. Local patients (Emirians) developed the disease at an earlier age compared to their expatriate Arab compatriots. Arthropathy occurred in 86% and nephropathy in 43% of cases. Next in frequency were leucopenia, mucocutaneous manifestations and serositis. Apart from lupus headache, the other neuro-psychiatric LE were uncommon or not encountered. Anti-cardiolipin syndrome, Sneddon's syndrome, shrunken lung syndrome, sicca complex, thyrotoxicosis and myasthenia gravis were also present in this small group of patients. Their presence reflects the marked heterogeneity displayed by the disease irrespective of the number of cases involved. An unusually high prevalence of anti ds (DNA) antibodies (92.5%) as compared to ANF (82.5%) was detected (P = NS). Anti-Sm antibody occurred in 30% of cases particularly in those patients with lymphadenopathy and fever. There was a relative paucity in the prevalence of anti RNP, Ro and La antibodies in this group. Differences with and similarities to previous reports concerning other populations are also presented.
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PMID:Characterization of systemic lupus erythematosus in patients in U.A.E. 778 58

Central nervous system compromise is a major cause of morbidity and mortality in SLE. The clinical picture of cerebral cryptococcosis is non-specific and can be mistaken for lupic activity. A retrospective study was undertaken with 10 patients with SLE and cryptococcal meningitis compiled in a 23-year period. The most common symptoms were fever and headache. Lymphocyte counts ranged from 169 to 912 cells/mm. An average delay of 13.6 days in diagnosis was observed in patients with cryptococcal meningitis with no complications and an average delay of 52.4 days in patients with complications. Low lymphocyte counts, observed in all patients, was considered a possible risk factor for cerebral cryptococcosis. To note the association between the delay in the correct diagnosis and complications derived from cerebral cryptococcosis.
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PMID:[Central nervous system cryptococcosis in 10 patients with systemic lupus erythematosus]. 787 60

The diagnosis of systemic lupus erythematosus (SLE) in a patient who presents with isolated central nervous system (CNS) abnormalities, is a difficult clinical challenge. The pathogenesis of such CNS involvement in SLE is unknown. Twelve patients with active SLE were examined for serum and cerebrospinal fluid (CSF) autoantibodies and compared with 21 patients with headache. Four of six patients with SLE and active CNS presentation had CSF autoantibodies while none of the other SLE patients and the controls had autoantibodies. We describe these four patients in whom immunological work-up revealed CSF antinuclear, anti-DNA, anti-SSA/Ro, anti-SSB/La and antineuronal autoantibodies. A newly devised antibody activity index provided means to demonstrate that the CSF autoantibodies in these patients were produced intrathecally. Beyond the importance of our finding of the potential role of autoantibodies in the pathogenesis of CNS damage in SLE, we propose that CSF analysis for autoantibodies should become an essential part of the diagnostic work-up in autoimmune diseases with CNS involvement.
Lupus 1994 Apr
PMID:Evidence for intrathecal synthesis of autoantibodies in systemic lupus erythematosus with neurological involvement. 792 Jun 11

We describe a 35-year-old woman with benign intracranial hypertension (BIH) secondary to systemic lupus erythematosus (SLE). She had low grade fever and skin eruptions, but neurological examination revealed no abnormal findings. Antinuclear and anti ds-DNA antibodies were positive, and complements were decreased. MRI demonstrated diffuse hyperintense white matter lesions on T2-weighted imaging. Mild bilateral papilledemas developed in the fundi, when her headache was exacerbated. The cerebrospinal fluid (CSF) pressure was 550 mmH2O. Cerebral angiography showed no cerebral sinus thrombosis. She was diagnosed as BIH secondary to SLE. Since RI cisternography revealed remarkably delayed absorption of the CSF, it was speculated that the CSF absorption by arachnoid villi would be probably disturbed in association with some autoimmune mechanisms by SLE. The subsequent rise of intraventricular pressure may result in retrograde transependymal flow of the CSF and the diffuse hyperintense white matter lesions on MRI.
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PMID:[A case of benign intracranial hypertension associated with systemic lupus erythematosus (SLE) showing diffuse white matter lesions on MRI]. 795 16

Delayed neurological symptoms and signs following herpes zoster ophthalmicus (HZO) such as "Delayed contralateral hemiplegia with HZO" are supposed to be due to ipsilateral intracranial angiitis and ischemic disorder. We experienced a rare case with ipsilateral cerebral hemorrhage following HZO. Under the diagnosis of cerebral angiitis associated with HZO, we treated her conservatively and observed sequential change of angiography for four months. A 54-year-old female, who had been treated for systemic lupus erythematosus (SLE), developed HZO on left ophthalmic nerve area. Seven weeks after the onset of HZO, she complained of headache, mild right hemiparesis, and disturbance of consciousness. Computed tomography revealed subcortical hemorrhage at the left temporo-occipital lobe. Cerebral angiography showed vascular irregularities such as segmental narrowing and sausage-like dilation on proximal portion of the ipsilateral anterior, middle and posterior cerebral arteries. Same findings were seen on peripheral portions of the posterior cerebral artery on the same side. Moreover sequential angiograms showed appearance of an aneurysm in the left middle cerebral artery (M2 potion). Under the diagnosis of cerebral angiitis associated with HZO, she was treated with antiviral agents, antiplatelet drugs, steroid and stellate ganglion block. Those irregularities were found to diminish on the sequential angiograms, and the aneurysm disappeared four month later.
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PMID:[Sequential change of cerebral angiography in a case of cerebral angiitis following herpes zoster ophthalmicus]. 799 42

An examination has been carried out of 46 patients (33 females, 13 males, a mean age 40) with Sneddon's syndrome characterized by cerebrovascular disturbances and marked livedo. A clinical spectrum of the syndrome included miscarriage and intrauterine death of the fetus (20 cases), peripheral vein thromboses (12 cases), coronary heart disease (18 cases), thrombocytopenia (8 cases), arterial hypertension (27 cases), headache (39 cases), epileptic seizures (5 cases). Similar manifestations are usually seen in antiphospholipid syndrome (AFLS). Antibodies to phospholipids, those to cardiolipin, lupus anticoagulant were detectable in 78, 50 and 61% of the cases, respectively. Clinical and immunological signs of AFLS in the absence of SLE-typical symptoms provided grounds for considering them primary AFLS. Similar clinical patterns in 36 patients with cardiolipin antibodies and/or lupus anticoagulant and 10 patients without the antibodies and anticoagulant suggest these cases to be AFLS too.
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PMID:[Sneddon's syndrome and the primary antiphospholipid syndrome]. 805 89

We systematically investigated clinical, laboratory, radiologic, and pathologic features, including treatment and prognosis, of stroke syndromes in 30 patients, six from our institution and 24 from the literature, with systemic lupus erythematosus (SLE) and symptomatic large cerebral vessel occlusive disease, documented by angiography or autopsy. The average age at stroke onset was 35 years, and the diagnosis of SLE was made on average 4.4 years prior to that. At least 86% had active SLE at the time of their stroke. Headache was common at onset. We found major intracranial or extracranial vessel occlusive process by (1) thrombus, (2) dissection, (3) fibromuscular dysplasia or vasculitis, and (4) atherosclerosis. The presumed mechanisms were coagulopathy, cardiogenic embolism, large cerebral vessel vasculitis or occlusive vasculopathy, cervical arterial dissection, and premature atherosclerosis. The short-term death rate was 40% and the recurrent stroke rate was 13%. We conclude that symptomatic large cerebral vessel occlusive disease in SLE generally occurs several years after the diagnosis of SLE, usually during the active phase of the disease, is related to heterogeneous mechanisms, and carries a relatively poor short-term outcome.
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PMID:Large cerebral vessel occlusive disease in systemic lupus erythematosus. 814 3

A case of systemic lupus erythematosus (SLE) complicated with hypopituitarism after steroid pulse therapy is reported. A 46-years-old-female with a history of SLE starting in 1975 was admitted to our hospital in February 1991 for lupus nephritis. Steroid pulse therapy, 1000 mg methyl-prednisolone for 3 successive days as one therapy unit, was administered. Proteinuria improved remarkably, however, general fatigue and headache appeared 2 weeks after initiation of therapy. Endocrinological examination revealed hypopituitarism including the levels of TSH, FSH, GH and ACTH. The secretion of FSH and LH gradually improved after replacement therapy of dried thyroid. MRI examination of the brain revealed an empty sella. It is known that pituitary tumor, cerebrovascular accident and autoimmune lymphocytic hypophysitis cause hypopituitarism. In this case, it is unlikely that the pulse therapy may be responsible for the infarction of the anterior pituitary artery furthermore, there has been no articles describing such incidence after steroid pulse therapy. This case may be indicative of a very rare case in which the empty sella might have been exacerbated by the pulse therapy in the causation of hypopituitarism.
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PMID:[Hypopituitarism associated with empty sella after steroid pulse therapy in a patient with SLE]. 814 29

A 26-year old woman, who was diagnosed as having systemic lupus erythematosus at the age of 23 year old, presented diarrhea and headache. She showed severe hypoproteinemia (serum total protein 3.7 g/dl, serum albumin 1.4 g/dl) and hyperlipidemia. She revealed to have protein-losing enteropathy with the result of alpha-1-antitrypsin clearance test using stool. Increase of prednisolone improved the loss of albumin into the bowel and abnormal laboratory findings. She also showed watershed infarction in the area of middle cerebral artery and posterior cerebral artery. Protein-losing enteropathy is a rare complication of SLE, only 18 cases are available on literature. No case is found to have cerebral infarction in patients with protein-losing enteropathy associated with SLE. It is known that blood levels of anticoagulation factors decrease in protein-losing enteropathy due to the leakage of plasma protein into intestinal lumen. Serum antithrombin III was decreased in this case. Hyperlipidemia found in this case seems to be caused by same mechanism in nephrotic syndrome. Lupus anticoagulant was also positive in this patient. These factors seems to be related to the occurrence of cerebral infarction. This case suggests the possibility of cerebral infarction in patients with protein-losing enteropathy in SLE.
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PMID:[Protein-losing enteropathy and cerebral infarction associated with systemic lupus erythematosus]. 814 30


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