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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection of the manubriosternal joint is an exceedingly rare event. We report a case of a 38-year-old patient with systemic lupus erythematosus who developed staphylococcal septic arthritis of this joint after bacteremia. Pathogenic factors are discussed. Physicians should be aware of this unusual complication of staphylococcal bacteremia.
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PMID:Septic arthritis involving the manubriosternal joint. 405 6

Candida vertebral osteomyelitis was diagnosed in a patient with systemic lupus erythematodes following X-ray evidence of osteomyelitis and the repeated culturing of Candida albicans from material obtained by needle biopsies from the third lumbar vertebra. The patient had been on glucocorticosteroids and parenteral nutrition six months previously. At that time, a yeast was cultured from the blood and the tip of the subclavian catheter which had been removed. After candida vertebral osteomyelitis was diagnosed, she was treated with ketoconazole for seven months. Recovery was impressive, as judged by the clinical and radiographic findings. At the time of writing this paper--12 months after the withdrawal of ketoconazole--the patient showed no signs of recurrence.
Infection
PMID:Hematogenous Candida vertebral osteomyelitis treated with ketoconazole. 629 75

Inherited deficiencies of the complement proteins are rare in unselected populations. Examination of patients with the clinical correlates of complement deficiency (autoimmune disease and certain bacterial infections) shows the frequency of inherited complement deficiency to rise enormously (5.9% of patients with systemic lupus erythematosus, 10 to 25% of adults with sporadic meningococcal disease). Autoimmune diseases of all types, but especially systemic lupus erythematosus, discoid lupus and glomerulonephritis, are seen in all categories of complement deficiency, most typically in those of the early classical pathway (C1, C4, C2). Pneumococcal infections are characteristic of deficiencies of the early classical pathway, as well. Deficiencies of C3 are associated with severe disease including autoimmune phenomena, pneumococcal and neisserial infections. C3-deficient patients become ill substantially earlier in life. Infections with N. meningitidis and N. gonorrhoeae are most typical of the late component deficiencies, with over 40% of homozygotes affected. Despite the presence of this deficiency from birth and the peak age-specific incidence of meningococcal disease in the general population at ages 3-8 months, the median age of first infection in the late component-deficient patients is 17 years. Relapse of infection is ten times more common in these patients, and discrete recurrences are seen in 45% of affected individuals. An unusual and unexplained predilection for infection with serogroup Y N. meningitidis exists. Despite an immune deficiency, and problems with ascertainment bias, it appears that persons with late component complement deficiency enjoy less mortality than normals who contract meningococcal disease. Attempts to explain the pathogenesis of neisserial infection in late component deficiencies have focused on the concept that normally non-pathogenic serum-sensitive bacteria are etiologic in the absence of serum bactericidal activity. Data to support this concept remain to be developed and contrary data exist. A separate mechanism may predispose properdin-deficient patients to meningococcal infection, since they appear to develop fulminant infections with high mortality.
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PMID:Complement deficiency states and infection: epidemiology, pathogenesis and consequences of neisserial and other infections in an immune deficiency. 643 45

Nephritis developed in 230 of 609 private patients with systemic lupus erythematosus (SLE) (38 percent) followed up from 1950 to 1980. Eighty-seven percent of patients with nephritis were female; 71 percent were Caucasian. They were observed a mean of 10 years. Five- and 10-year survival rates were 80 percent and 65 percent, with improvement to 86 percent and 76 percent in the last decade. Normalization of urinary sediment and protein levels, blood pressure and serum albumin levels correlated with improved survival and tended to occur during the first year. Life-threatening complications of SLE were more common after the onset of nephritis but decreased as renal function worsened. Infection was the most frequent cause of death in the last decade. Forty-four patients received nitrogen mustard; 55 percent of the courses were followed by significant improvement in renal function and reduced steroid dosage. Control of the disease was associated with improved long-term survival of patients with SLE.
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PMID:Lupus nephritis. Experience with 230 patients in a private practice from 1950 to 1980. 705 33

Infections in systemic lupus erythematosus are frequent. However, osteoarticular Salmonella infections are rarely reported. We report a case of systemic lupus erythematosus diagnosed in a 15 year-old girl. Seven months later, she presented with fever and a localized collection of the upper extremity of the left tibia related to a Salmonella enteritidis acute osteomyelitis (sub periosteal abscess). The out-come was chronic and led to death. The authors emphasize the severity of non typhoidal salmonellosis in systemic lupus erythematosus.
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PMID:[Systemic lupus erythematosus and Salmonella enteritidis osteomyelitis]. 748 Nov 56

To determine the clinical characteristics and long-term prognosis of 11 Japanese systemic lupus erythematosus (SLE) patients who were starting dialysis, we studied the clinicopathological findings before dialysis and during the clinical course after dialysis. Patients were divided into three groups: Group A consisting of temporary dialysis patients (n = 5); Group B consisting of early-death patient (n = 1); and Group C consisting of maintenance dialysis patients (n = 6). At the start of dialysis, the progression pattern of renal failure in all Group A patients was either acute exacerbation of chronic renal failure (CRF) or rapidly progressive glomerulonephritis (RPGN). The pattern in Group C was mostly CRF (83%). Three patients from Group A and three from Group C were still alive at the latest follow-up (mean follow-up period was 11.0 years, ranging from 1.8 to 16.2 years) and they showed no signs of clinical or serological activity. Infection was the cause of death in 3 of the 5 patients who died. We suggest that dialysis can be discontinued in patients with SLE who receive dialysis for acute exacerbation of CRF or RPGN. After the initiation of dialysis, patients tend to show diminished SLE activity. Infection is the major contributor to the poor prognosis of SLE patients receiving dialysis.
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PMID:Clinicopathological study of dialysis patients with lupus nephritis. 756 54

Specific but ubiquitous cytoplasmic proteins are the targets of autoantibodies such as anti-Ro/SS-A, anti-La/SS-B, and anti-calreticulin. These antibodies may be pathogenic in systemic lupus erythematosus (SLE) and Sjogren's syndrome (SS). Tissue localization of the pathogenic process could be best explained by an abnormal expression of these cytoplasmic proteins. Several factors could likely displace the host proteins to the cell surface. This study was designed to use cytomegalovirus (CMV) infected human fibroblasts (MRC-5) as a model, to test whether a viral infection would induce the expression of the human autoantigen(s). Expression of Ro/SS-A, calreticulin, and MHC class I antigens, both in the cytoplasm and on the cell surface, was examined by a fixed cell ELISA, immunofluorescence, and immunoblotting. Infection of fibroblasts with CMV was found to increase the cell surface expression of calreticulin (p = 0.0314), but not the 60KD Ro/SS-A. Cytoplasmic expression of both the autoantigens tested increased following CMV infection. Enhanced expression of class I MHC was detected on the cell surface in response to the virus infection. The expression of the autoantigens and MHC class I polypeptides, as well as the virally induced elevated mitotic rate, diminished after 24 h of infection. Viral infection was found to alter the distribution of host cell proteins, including autoantigens. Cell surface expression of calreticulin could provide a target for circulating autoantibody and contribute to the autoimmune process.
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PMID:Viral induction of the human autoantigen calreticulin. 792 96

A review of 1,069 total admissions of 537 systemic lupus erythematosus (SLE) patients during a 10-yr period at Ramathibodi Hospital showed that 220 episodes which occurred in 137 patients (25.5%) were motivated by infection. Skin was the most common site (23%) with Herpes zoster being the most common organism (15.5%) found in our lupus patients. However, if we considered only major infections, pulmonary tuberculosis, salmonella septicemia and urinary tract infection by E. coli would be the most frequent complications respectively. In the absence of immunosuppressive therapy, infections coincided with the initial manifestation of SLE in 25 patients and were associated with exacerbation of the disease in 20 patients. Mean SLEDAI score in these patients was 8.8, suggesting that active lupus link together with infection. Steroid therapy influenced the rate of opportunistic infections (p = 0.006). Infections were determined to be the cause of death in 23 of 77 patients (29.9%). Opportunistic pathogens played an equal role as other common bacterial organisms in these fatal cases. SLE patients who died from infections were treated with cyclophosphamide in higher proportion than those with no infectious complication (p = 0.025). Our study demonstrated the rate, nature and predisposing factors of infection in SLE which may lead to better anticipation and diminution of morbidity and mortality related to infection in hospitalized patients with SLE.
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PMID:Infection in systemic lupus erythematosus. 796 23

Infection with gram-negative and gram-positive bacteria remains a leading cause of death in patients with systemic lupus erythematosis (SLE), even in the absence of immunosuppressive therapy. To elucidate the mechanisms that underly the increased risk of infection observed in patients with systemic autoimmunity, we have investigated host defense against bacterial infection in a murine model of autoimmunity, the MRL/Mp-lpr/lpr (MRL/lpr) mouse. Our previous study implicated transforming growth factor beta (TGF-beta) in a novel acquired defect in neutrophil function in MRL/lpr but not congenic MRL/Mp-+/+ (MRL/n) mice (Gresham, H.D., C.J. Ray, and F.K. O'Sullivan. 1991. J. Immunol. 146:3911). We hypothesized from these observations that MRL/lpr mice would have defects in host defense against bacterial infection and that they would have constitutively higher local and systemic levels of active TGF-beta which would be responsible, at least in part, for the defect in host defense. We show in this paper that spontaneous elaboration of active TGF-beta adversely affects host defense against both gram-negative and gram-positive bacterial infection in MRL/lpr mice. Our data indicate that MRL/lpr mice, as compared with congenic MRL/n mice, exhibit decreased survival in response to bacterial infection, that polymorphonuclear leukocytes (PMN) from MRl/lpr mice fail to migrate to the site of infection during the initial stages of infection, that MRL/lpr mice have a significantly increased bacterial burden at the site of infection and at other tissue sites, and that this increased bacterial growth occurs at a time (> 20 h after infection) when PMN influx is greatly enhanced in MRL/lpr mice. Most intriguingly, the alteration in PMN extravasation during the initial stages of infection and failure to restrict bacterial growth in vivo could be duplicated in MRL/n mice with a parenteral injection of active TGF-beta 1 at the time of bacterial challenge. Moreover, these alterations in host defense, including survival in response to lethal infection, could be ameliorated in MRL/lpr mice by the parenteral administration of a monoclonal antibody that neutralizes the activity of TGF-beta. These data indicate that elaboration of TGF-beta as a result of autoimmune phenomenon suppresses host defense against bacterial infection and that such a mechanism could be responsible for the increased risk of bacterial infection observed in patients with autoimmune diseases.
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PMID:Spontaneous elaboration of transforming growth factor beta suppresses host defense against bacterial infection in autoimmune MRL/lpr mice. 796 55

A 52-year-old woman was admitted to our hospital because of a skin rash, high fever and myalgia. She had been diagnosed ten years ago by a dermatologist as having MCTD (mixed connective tissue disease). At the time of admission a diagnosis of active SLE was made by fulfilling four of the 1982 ARA criteria together with increasing levels of anti-DNA antibody and low levels of complements. Prednisolone (PSL) given orally in an initial dosage of 60 mg/day was effective during the first 6 weeks. Then a high fever, skin rash and pancytopenia appeared without active findings of SLE. Infection caused by bacteria, fungus or virus was suspected, but no infectious agent was present in cultures derived from blood or other sources. Antimicrobic drugs used were not effective at all. The clinical picture was suggestive of a drug allergy, but no causative drug was found. A diagnosis of hemophagocytic syndrome (HPS) was made because of the increased number of unusual hemophagocytic cells in the bone marrow. High levels of serum ferritin and neopterin, which are known to reflect macrophage activation, supported the diagnosis of HPS. HPS is characterized by activated phagocytosis presumably induced by hypersecretion of cytokines. Malignant lymphoma and infection are the two representative diseases which may cause HPS. Recently, an acute lupus HPS was reported in patients with active SLE. Here we reported a case of reactive HPS observed in a patient with SLE who had been receiving high dose PSL. Symptoms and findings of the patient gradually disappeared in several weeks after rapid reduction of the PSL dose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemophagocytic syndrome observed in a patient with systemic lupus erythematosus]. 797 30


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