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)

In the context of prospective trials of immunosuppressive drugs in systemic lupus erythematosus (SLE) nephritis, 83 patients were studied with regard to development of herpes zoster. Herpes zoster was found to occur with high frequency (21%) in patients with SLE nephritis treated with immunosuppressive agents. The course of herpes zoster was benign: no deaths occurred and only 2 of the 18 patients developed generalized disease, which resolved without sequelae. Specific antiviral therapy was not necessary and there appears to be no need to decrease immunosuppressive medications. Zoster occurred when the SLE was relatively inactive and did not exacerbate the SLE. No statistical difference in the incidence of zoster was found among the patient groups treated with different immunosuppressive regimens.
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PMID:Herpes zoster in patients with systemic lupus erythematosus. 69 50

Seventy unselected patients with systemic lupus erythematosus (SLE) were studied to determine the prevalence of cognitive impairment and the association with other clinical variables. Twenty-five patients with rheumatoid arthritis (RA) and 23 healthy subjects were used as controls. All patients were evaluated with a battery of standardized neuropsychological tests to determine ability in 8 areas of cognitive function. Clinically overt neuropsychiatric (NP) SLE, cumulative disease manifestations and concurrent medications were documented. In patients with SLE, generalized disease activity was expressed using the SLE disease activity index. Cognitive impairment was identified in 15/70 (21%) patients with SLE, 1/25 (4%) patients with RA and in 1/23 (4%) healthy subjects (p = 0.042). The prevalence was higher in patients with active NP-SLE at the time of assessment (2/5, 40%) compared to patients with inactive NP-SLE (2/10, 20%) but was also increased in those patients who had never had known clinical NP-SLE (11/55, 20%). A history of serositis (p = 0.015), active SLE (p = 0.064) and corticosteroid use (p = 0.027) at the time of assessment were more common in patients with cognitive impairment. The results suggest that cognitive impairment is increased in patients with SLE. It may occur independently of clinically overt NP-SLE and is more common in patients with active disease who are receiving corticosteroids.
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PMID:Cognitive impairment in patients with systemic lupus erythematosus. 159 78

Systemic lupus erythematosus (SLE) is an autoimmune disease affecting the connective tissue of the skin and the vascular system. In about 90% of the cases, the first diagnosis is made in women of child-bearing age. We report on 11 pregnancies in 5 patients with SLE. The incidence of SLE was found to be 1:2966 in relation to obstetric cases in our hospital. In one patient, an acute exacerbation of the disease led to preterm delivery in the 31st week of pregnancy. The affected patient died postpartum due to generalised disease and septic complications. In general, perinatal mortality was found to be 25% (excluding early abortion). The number of spontaneous abortions, premature deliveries and small for date babies was elevated in our group of patients, in comparison to the normal group. As a result of our own observations in serological controlled pregnancies and of an extensive review of the literature, we came to the following conclusions: Uncomplicated SLE is no contraindication for pregnancy. However, an SLE nephritis represents a relative or even absolute contraindication, depending on the clinical course. Recent prospective studies permit us to conclude, that a pregnancy will not lead to an aggravation of SLE. On the other hand, SLE can cause complications in pregnancy with a subsequent rise in maternal and foetal morbidity and mortality. Most frequent are preeclampsia, premature labour, foetal maldevelopment and flare-ups of the underlying disease. For monitoring the disease, frequent determinations of complement proteins C3/C4 are helpful. The measurement of the C3 turnover can be used to distinguish between the development of preeclampsia and exacerbation of the disorder.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Systemic lupus erythematosus and pregnancy. Clinical aspects, serology and management]. 239 Oct 23

Disorders of serum proteins, circulating antibodies, immune complexes to the dermo-epidermal junction, B- and T-cell markers from peripheral blood lymphocytes and the suppressor function of peripheral mononuclear cells have been investigated in 106 patients with histologically proven discoid lupus erythematosus (discoid LE). The results confirm that this condition is primarily a localized skin disease with low concentrations of autoantigens and circulating autoantibodies. By contrast, systemic lupus erythematosus (systemic LE) is a multifocal, generalized disease with high concentrations of autoantigens, autoantibodies and immune complexes. The transformation of discoid LE to systemic LE is discussed, and a possible two-hit mechanism is proposed.
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PMID:Immunological studies in patients with discoid lupus erythematosus. 702 Nov 13

Poor performance on cognitive testing is common in SLE but it is not progressive in the majority of patients and may fluctuate or resolve without specific treatment. Cognitive impairment in patients without overt CNS-SLE may result from generalised disease activity or psychiatric disorder which reduce speed, concentration and motivation. This emphasises once again the importance of recognising and treating psychiatric disorder in these patients. Although mean cognitive scores are lower in SLE patients with overt CNS involvement than those without, an individual's cognitive score is a poor predictor of the presence of CNS involvement because of considerable overlap between groups. It has been suggested that the pattern of cognitive impairment, rather than simply whether it is present or absent, may be more helpful in identifying patients with CNS involvement but this requires further investigation in prospective studies. Cognitive impairment at one point in time is not predictive of future CNS events during 1 or 2 years of follow-up. Routine cognitive testing in SLE does not therefore appear to be helpful either for identifying patients with current CNS involvement or for identifying those at future risk of this complication. In the absence of double-blind randomised controlled trials, treatment of neuropsychiatric SLE is based on clinical experience and anecdotal case reports. Aggressive immunosuppression with high-dose corticosteroids in conjunction with either azathioprine or cyclophosphamide may be indicated in patients with life-threatening CNS-SLE but, on the basis of current evidence, is not justified in those with lone subtle cognitive abnormalities.
Lupus 1994 Jun
PMID:Psychiatric disorder and cognitive impairment in SLE. 795 Dec 98

Neuropsychiatric events are common in patients with systemic lupus erythematosus (SLE), but less than one-third of these events can be directly attributed to SLE. Increased generalized SLE disease activity or damage, previous or concurrent major neuropsychiatric SLE (NPSLE) events, and persistently positive moderate-to-high antiphospholipid antibody titers are established risk factors, and their presence could facilitate proper attribution to the disease itself. Diagnostic evaluation is guided by the presenting manifestation; MRI is used to visualize brain or spinal pathologies. For neuropsychiatric events believed to reflect an immune or inflammatory process, or when these events occur in the context of active generalized disease, evidence (primarily from uncontrolled studies) supports the use of glucocorticoids alone or in combination with immunosuppressive therapy. Antiplatelet and/or anticoagulation therapy is recommended for NPSLE manifestations related to antiphospholipid antibodies, especially for thrombotic cerebrovascular disease. For the future, we anticipate that novel biomarkers and advanced neuroimaging tests will better define the underlying pathologic mechanisms of SLE-related neuropsychiatric disease, and help guide therapeutic decisions.
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PMID:Pathogenesis, diagnosis and management of neuropsychiatric SLE manifestations. 2045 32