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A case of systemic lupus erythematosus (SLE) was complicated by ruptured chordae tendineae. The mechanisms responsible for severe cardiac dysfunction in SLE are discussed.
A patient with systemic lupus erythematosus who developed reactive amyloidosis associated with high levels of serum amyloid-A protein (SAA) is reported. The possible relevance of elevated SAA levels in the aetiology of amyloidosis is discussed.
Although clinical manifestations of myocarditis in systemic lupus erythematosus are uncommon, noninvasive cardiac testing may detect subclinical cases. The pathogenesis of myocarditis in systemic lupus erythematosus has been ascribed to many factors, including autoimmunity, medications, and coexisting diseases. Lupus myocarditis merits urgent clinical attention because of the likely progression to arrhythmias, conduction disturbances and heart block, dilated cardiomyopathy, and heart failure. Endomyocardial biopsy can be used to identify the underlying inflammatory histopathology. Usual therapy includes high-dose corticosteroids, in addition to standard cardiac medications.
When systemic lupus erythematosus (SLE) is first suspected during pregnancy, though rare, the diagnostic criteria are not different from those for nonpregnant women. The pregnancy outcome is good if treatment with adequate immunosuppressive agents starts as soon as the diagnosis is made. There are 4 cases in this report who had SLE onset during pregnancy. Although 2 of them suffered from preeclampsia, all 4 pregnancies resulted in favorable outcomes after the lupus was controlled by medical treatment.
Tuberculosis associated with systemic lupus erythematosus (SLE) was studied in a cohort of 311 patients seen between 1963 to 1979. There were 16 such patients, giving rise to a prevalence rate of 5%. The characteristics of SLE-associated tuberculosis include a high incidence of miliary and far-advanced pulmonary disease, delay in establishing diagnosis, especially the extrapulmonary form, and tendency to attribute symptoms like fever, malaise, and weight loss to the lupus process. Treatment was successful in 9 patients. Of the 7 death 5 were attributed directly to the mycobacterial infection and 2 to complications of SLE.
A patient with systemic lupus erythematosus who developed osteonecrosis in 13 sites is presented. Most lesions occurred while corticosteroid dose was increased during disease exacerbations. Pathogenetic mechanisms are reviewed and possible simulation of polysynovitis is discussed.
PURPOSE: To review 1) advances in the pathogenesis, diagnosis, and management of dermatologic and joint disease and the antiphospholipid antibody syndrome in patients with systemic lupus erythematosus; 2) controversies related to pregnancy and hormonal therapy and to morbidity and mortality in these patients; and 3) current views on the pathogenesis of systemic lupus erythematosus. DATA SOURCES AND STUDY SELECTION: Review of the English-language medical literature with emphasis on articles published within the last 5 years. More than 400 articles were reviewed. DATA SYNTHESIS: Despite considerable overlap, cutaneous lesions specific to lupus erythematosus may be divided into subsets with distinct clinical, histologic, and immunofluorescent features. A recent short-term, prospective, uncontrolled trial found hydroxychloroquine and retinoids to be of similar efficacy in the treatment of cutaneous lupus erythematosus. Optimal treatment for patients with lupus and the anticardiolipin antibody syndrome remains to be defined; uncontrolled, retrospective, and treatment-withdrawal studies suggest that warfarin may be more protective than aspirin. Whether pregnancy induces lupus flares has not yet been established; existing data suggest both that it does and that it does not. Oral contraceptive use and postmenopausal estrogen replacement therapy appear not to cause clinical deterioration in patients with lupus. Recent studies have documented a substantial improvement in the survival of patients with systemic lupus erythematosus; they found 5-year survival rates of 90% or more and 10-year survival rates of more than 80%. Most data suggest that systemic lupus erythematosus results from the activation of self-reactive T cells and B cells by genetic or environmental factors. CONCLUSIONS: The optimal treatment for dermatologic disease and the antiphospholipid antibody syndrome in patients with systemic lupus erythematosus remains unknown. Although mortality has decreased substantially, the morbidity related to the disease itself and to complications of therapy is still considerable. More studies are needed to further elucidate the effects of pregnancy on this condition and the pathogenetic mechanisms responsible for the development of this disease.
Neuropsychiatric abnormalities frequently occur in patients with systemic lupus erythematosus, affecting as many as 14-75% of people with this disease. High-dose steroid with or without anticoagulation is the mainstay of treatment in neuropsychiatric systemic lupus erythematosus (NPSLE). Use of mycophenolate as a steroid sparing drug may be a potential alternative agent in the therapy of NPLE, but lack of randomized trials and cost prohibit its widespread use. Its safety profile is higher than that of cyclophosphamide and azathioprine. We report a successfully treated case of neuropsychiatric systemic lupus erythematosus, presenting as psychosis, whose long-term remission was maintained on treatment with mycophenolate mofetil.
Eight patients with systemic lupus erythematosus (S.L.E.) have been treated with plasmapheresis. In four patients in whom immunochemical studies indicated high levels of circulating immune complexes, the removal of 5-8 litres of plasma weekly produced a striking clinical and immunochemical improvement. The four other patients, with only minor complement disturbances and no direct evidence of circulating immune complexes, could not be shown to benefit from plasmapheresis and one patient in this group died of cerebral lupus despite intensive treatment with cytotoxic drugs. It is concluded that plasmapheresis may be of value as an adjuvant to the treatment of acute S.L.E.
The etiology of systemic lupus erythematosus (SLE) is unknown but genetic factors seem to play a role in the disease pathogenesis. The tumor necrosis factor alpha (TNFa) gene, encoded at the TNF locus in the MHC class III region, is now known to be an important candidate gene in SLE, due to the proinflammatory activities of the TNFa. The objectives of this study were to examine the role of the TNFa polymorphism for the susceptibility of Malaysian Chinese lupus patients to SLE and to determine its association with organ involvement. The allelic frequencies of the TNFa polymorphic variant (TNF2) of seventy lupus patients were determined during follow-up at the Medical Clinic of the National University Hospital Malaysia by PCR-RFLP technique. Sixty-four females and 6 males with a mean age of 33+/-12 years were included. Clinical data were obtained from case records. Autoantibody levels were measured by ELISA. Fifty-nine ethnically-matched blood donors were used as controls. The allelic frequency of the TNF2 variant was found to be significantly increased in the patients compared to the controls (52.8% vs 33.8%). SLE patients with the polymorphic TNF2 variant were found to be at increased risk of central nervous system involvement (p = 0.004, RR = 2.59) and to have an increased frequency of anti-La antibodies (p = 0.03). In view of these findings we suggest that TNF2 variant is playing a role in conferring susceptibility to SLE and in the disease pathogenesis.
Hypertrophic lupus erythematosus (HLE) is a distinct and rare subset of chronic cutaneous lupus erythematosus characterized by verrucous lesions which are chronic in course and resistant to treatment (1). We describe the successful use of acitretin in a patient with HLE who had multiple hyperkeratotic verrucous plaques over the dorsa of his hands, feet, and legs and who failed to respond to local steroids and antimalarials.
A patient with systemic lupus erythematosus had chills, fever, and headache on four separate occasions after ibuprofen ingestion. One such episode was accompanied by cerebrospinal fluid findings compatible with meningitis. Drug rechallenge under controlled conditions established the relationship between ibuprofen ingestion and meningitis.
Simultaneous occurrence of subacute cutaneous lupus erythematosus and malignancy has rarely been reported. We report the first case of subacute cutaneous lupus erythematosus associated with Hodgkin's disease. Although our case does not fulfill the criteria of paraneoplastic process, a relationship between the two disorders might be suggested by their simultaneous occurrence and in view of the cases of disseminated lupus erythematosus associated with lymphoma reported so far. The different hypotheses are discussed.
INTRODUCTION: Amongst the various causes of anemia in systemic lupus erythematosus, isolated and acquired erythrocyte dysplasia is rare and most often part of global dysmyelopoiesis. EXEGESIS: The authors report a case of acquired erythrocyte dysplastic syndrome that occurred in a 34-year-old woman in whom previous diagnosis had evidenced systemic lupus erythematosus of rather benign course. Other causes of dysmyelopoiesis were ruled out. Myeloid stem cell cultures showed selective inhibition of erythroid cells growing, with no particular effect of the patient's serum. While a corticosteroid treatment with prednisone (1 mg/kg/d) did not show any efficacy upon anemia, the patient's pregnancy was followed by prolonged correction of hemoglobin, making possible the tapering of prednisone down to 10 mg/d. CONCLUSION: Acquired erythrocyte dysplastic syndrome remains a rare cause of anemia in systemic lupus erythematosus. This case report suggests an immunological phenomenon, but the mechanisms underlying both the appearance and long-lasting remission after pregnancy remain unexplained.
OBJECTIVE: Patients with systemic lupus erythematosus (SLE) are at increased risk for cardiovascular and cerebrovascular events, even after adjustment for traditional risk factors. We examined the association of traditional risk factors, novel markers of cardiovascular disease (C-reactive protein, homocysteine, lipoprotein(a), plasminogen activator inhibitor-1, fibrinogen), and markers indicative of SLE activity (including C3, C4, anti-dsDNA, and prednisone use) with the presence of significant plaque on carotid duplex imaging. METHODS: Six hundred five patients with SLE enrolled in the Hopkins Lupus Cohort Study (92% female, 38% African-American) underwent carotid duplex testing. Prospectively gathered clinical, laboratory, and serologic data from their quarterly followup visits in the Hopkins Lupus Cohort were used in the analyses. For predictors that varied over time, such as cholesterol, the mean values during cohort participation were calculated for the analysis. Informed consent was obtained from all patients. RESULTS: The presence of carotid plaque was strongly associated with age, ranging from 1% among those less than 30 years of age to 61% among those 60 years or older. After adjusting for age, there were moderate or strong associations of carotid plaque with male gender (age-adjusted risk 25% vs 13%; p = 0.051), hypertension (age-adjusted risk 18% vs 8%; p = 0.0001), diabetes mellitus (age-adjusted risk 19% vs 13%; p = 0.075), C3 > 120 mg/dl (age-adjusted risk 18% vs 11% and 14% for normal and low C3, respectively; p = 0.046), serum creatinine > 1.3 (age-adjusted risk 32% vs 13%; p = 0.039), and mean systolic blood pressure > 140 (age-adjusted risk 23% vs 13%; p = 0.028). There was no strong evidence of an association between plaque and SLE disease activity (age-adjusted risk 14% among those with adjusted mean SLEDAI > 3 vs 14% among those with lower SLEDAI) or with time since SLE diagnosis (age-adjusted risk 12%, 14%, and 16% among those with SLE for < 2, 2-8, and > 8 years, respectively; p = 0.49). CONCLUSION: Traditional cardiovascular risk factors were associated with carotid plaque in SLE. However, SLE disease activity and duration of SLE are not strongly associated with carotid plaque. A "lupus factor" separate from traditional risk factors remains unidentified.
The activity of systemic lupus erythematosus (SLE) was investigated in 18 recipients of 20 renal transplants by retrospective analysis of their medical records and by screening the ten patients with more than one year follow-up. Eight grafts were lost, all because of rejection occurring within the first year. From the 12 patients with functioning transplants, one was lost to follow-up at seven years and another had not completed one year. The remaining ten patients were studied, and no evidence of lupus nephritis was found despite serologically active SLE in four cases. Their follow-up was 4.5 +/- 1.3 years. Our study provides the relatively scarce literature on renal transplantation in patients with SLE with a series of 18 recipients of 20 allografts, confirms that the recurrence of lupus nephritis in the allografts is very rare, as previously suggested, and discloses that graft and patient survivals are comparable with those of the general nondiabetic transplant population.
Patients with systemic lupus erythematosus require adequate information (sun avoidance, fair compliance, smoking discontinuation, adequate contraception and diet, pregnancy planning). Nonsteroidal antiinflammatory drugs and antimalarials are effective in patients presenting with skin and articular involvement. Visceral lesions and hemocytopenias require the use of steroids, alone or in association with immunosuppressive agents. Long-term anticoagulation with an INR of 3-3.5 achieves the prevention of recurrent thrombotic events. Experimental data suggest that more specific treatments and even regimens aimed at eradication of human lupus might soon arise.
Systemic lupus erythematosus and Sjögren syndrome remain elusive in the description of their underlying etiologic causes and pathogenic mechanisms. Although underlying genetic predisposition appears to contribute to both diseases based on twin and other genetic studies, additional factors must play a role. Over the decades additional factors, such as hormonal influence, UV light, environmental exposures (e.g., silica, solvents), and infectious agents have been postulated to play a role. Over the past few years additional information has been published concerning roles of various infectious agents in both lupus and Sjögren syndrome. Although the understanding of this field is still incomplete, significant advances are being made.