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

Cryptococcal meningitis is a rare but well recognized complication of systemic lupus erythematosus (SLE). Since in all previously reported cases in the medical literature the patients developed this opportunistic infection as the result of immunosuppressive therapies, whether the intrinsic immunological abnormalities of SLE per se contribute to the susceptibility remains controversial. We report on a patient who presented concurrently with cryptococcal meningitis and cryptococcaemia at the time of her diagnosis of active SLE. This highlights the possibility that intrinsic immunological defects of SLE may be directly responsible for the predisposition to fungal infections. In addition, when SLE patients present with neurological symptoms, the possible presence of central nervous system (CNS) infection must be checked for, even if immunosuppressive treatment is not being considered.
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PMID:Cryptococcal meningitis presenting concurrently with systemic lupus erythematosus. 953 94

An opportunistic infection is a known, although under-diagnosed, complication of systemic lupus erythematosus (SLE). A 48-year-old woman with a recent diagnosis of SLE was admitted to the hospital because of a fever, confused state, and convulsive episode. Her symptoms were interpreted as being compatible with lupus cerebritis. Treatment with methylprednisolone resulted in a temporary improvement in the patient's condition. Nevertheless, during the next few weeks, her physical and mental condition deteriorated, and she died of massive pulmonary emboli. An autopsy revealed no signs of lupus cerebritis; however, disseminated cerebral toxoplasmosis was found. Cerebral toxoplasmosis is a rare complication of SLE that may be misdiagnosed as lupus cerebritis.
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PMID:Toxoplasma infection in systemic lupus erythematosus mimicking lupus cerebritis. 1037 32

The authors report the case of a 43-year-old woman suffering from severe systemic lupus erythematosus treated with long-term prednisone, who developed Nocardia nova infection on a hip prosthesis. Sepsis occurred about two years after an episode of pulmonary nocardiosis with the same Nocardia species, that was successfully treated by 12 months of antibiotics. A good outcome of the joint infection was observed in response to antibiotics and removal of the prosthesis. Nocardiosis is a rare infection, acting as an opportunistic infection, facilitated in the present case by systemic lupus erythematosus and chronic corticosteroid therapy. Nocardia infections mainly affect the lungs, skin and central nervous system; these last two sites are mostly due to haematogenous spread, a frequent event. Treatment is based on antibiotics, usually continued for 3-12 months, especially because of the risk of relapse. The imipenem-amikacin combination appears to be more effective than trimethoprim sulfamethoxazole. To our knowledge, this is the first case report of Nocardia nova joint prosthesis infection also presenting as late septic spread of pulmonary nocardiosis, complicating corticosteroid-treated systemic lupus erythematosus.
Lupus 2000
PMID:Nocardia infection of a joint prosthesis complicating systemic lupus erythematosus. 1086 3

Patients with systemic lupus erythematosus (SLE) who present with skin disease pose the clinician with diagnostic challenges. The skin disease can reflect an increase in systemic disease activity suggested by other features of active lupus and, as such, usually responds well to more aggressive immunosuppressive therapy. Other possibilities of skin disease include drug eruptions, skin disease unrelated to SLE and, more rarely, opportunistic skin infection. In patients who show a poor response to more aggressive immunosuppressive therapy, consideration must be given to the possibility of opportunistic infection. A high index of suspicion will allow prompt treatment. We describe two patients with SLE who developed cutaneous atypical mycobacterial infection during immunosuppressive therapy. The diagnosis of cutaneous vasculitis was considered in both cases, but subsequent skin biopsy revealed the correct diagnosis. This report illustrates the importance of skin biopsy in patients with suspected cutaneous lupus who are not responding to immunosuppressive therapy.
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PMID:When typical is atypical: mycobacterial infection mimicking cutaneous vasculitis. 1204 97

To assess the helper T cell dependence of B lymphocyte stimulator (BLyS) protein-driven autoantibody production in vivo, serum levels of BLyS protein, total IgG, and anti-IgG anti-phospholipid (aPhL) autoantibodies from HIV-infected patients (n = 105) with varying degrees of CD4+ cell depletion and healthy control donors at low risk for HIV (n = 64) were determined. Peripheral blood mononuclear cells from these subjects were stained for surface expression of BLyS protein. Monocyte surface expression and serum levels of BLyS protein were increased in HIV-infected patients as were serum total IgG and IgG aPhL autoantibody levels. No associations were detected between increased serum BLyS protein levels and patient age, sex, disease duration, history of opportunistic infection or malignancy, or serum total IgG levels. However, serum levels of IgG aPhL autoantibodies were greater in patients with high serum BLyS protein levels than in those with normal serum BLyS protein levels. Importantly, this association between serum levels of BLyS protein and IgG aPhL was appreciated only in patients who were not severely CD4+ cell-depleted and not in patients who were severely CD4+ cell-depleted (peripheral blood CD4+ cell counts <or= 200/mm(3)). Thus, BLyS protein may preferentially facilitate IgG autoantibody production in vivo in a helper T cell-dependent manner. This raises the possibility that the combination of a BLyS protein antagonist with an agent that targets (helper) T cells may have salutary synergistic effects on autoantibody production in diseases such as systemic lupus erythematosus.
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PMID:B lymphocyte stimulator protein-associated increase in circulating autoantibody levels may require CD4+ T cells: lessons from HIV-infected patients. 1216 72

A 41-year-old woman who had suffered from systemic lupus erythematosus (SLE) for 22 years presented with signs of neurological deficits. CT-scanning of the brain revealed hypodense lesions that suggested cerebral infarction due to vasculitis in SLE. However, in spite of intensified immunosuppressive therapy, she showed rapid neurological deterioration. After extensive, additional examinations and tests, the diagnosis was finally changed to progressive multifocal leukoencephalopathy, caused by an opportunistic infection by the JC polyomavirus. Neurological and psychiatric symptoms frequently occur in patients with SLE. The differential diagnosis of these symptoms in SLE is extensive and includes, on the one hand, primary neurological and psychiatric diseases related to direct involvement of the nervous system by SLE, and on the other hand, secondary syndromes arising as a result of complications of the SLE or the immunosuppressive treatment. Opportunistic infections are often an important secondary cause of neurological and psychiatric syndromes in patients with SLE. The clinical symptoms and radiological cerebral signs are non-specific and usually do not suffice to differentiate between the various syndromes. Since each syndrome requires its own specific clinical approach and treatment, extensive diagnostics are mandatory before the diagnosis 'cerebral lupus' can be made and immunosuppressive therapy can be started or intensified.
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PMID:[Progressive multifocal leukoencephalopathy in a patient following long-term immunosuppressive therapy for systemic lupus erythematosus]. 1652 99

Nocardiosis has become a significant opportunistic infection over the last two decades as the number of immunocompromised individuals has grown worldwide. We present two patients with nocardial brain abscess. The first patient was a 39-year-old woman with systemic lupus erythematosus. A left temporoparietal abscess was detected and aspirated through a burr-hole. Nocardia farcinica infection was diagnosed. The patient had an accompanying pulmonary infection and was thus treated with imipenem and amikacine for 3 weeks. She received oral minocycline for 1 year. The second patient was a 43-year-old man who was being treated with corticosteroids for glomerulonephritis. He was diagnosed with a ring-enhancing multiloculated abscess in the left cerebellar hemisphere, with an additional two small supratentorial lesions and triventricular hydrocephalus. Gross total excision of the cerebellar abscess was performed via a left suboccipital craniectomy. Culture revealed Nocardia asteroides, and the patient was successfully treated with intravenous ceftriaxone, then oral trimethoprime-sulfamethoxazole for 1 year. The clinical course, radiological findings, and management of nocardial brain abscess are discussed in light of the relevant literature, and current clinical management is reviewed through examination of the cases presented here.
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PMID:Nocardial brain abscess: review of clinical management. 1667 31

We evaluated the occurrence of cytomegalovirus (CMV) infection and the background characteristics in twenty-three hospitalized patients with inflammatory connective tissue diseases including systemic lupus erythematosus, polymyositis/dermatomyositis, rheumatoid vasculitis, microscopic polyangitis, and Takayasu's arteritis. Cytomegalovirus antigenemia was demonstrated in 10 of 23 evaluable patients. Five of ten patients with CMV antigenemia developed symptomatic CMV disease (all cases of fever, two cases of liver involvement, two cases of interstitial pneumonia, and one case of unknown organ involvement), whereas the remaining five patients were asymptomatic. Most of CMV antigenemia-positive patients had been administered intravenous steroid pulse, or in combination with immunosuppressive agents intravenously or orally because of refractory disease activity. Particularly, in patients who received intravenous methylprednisolone pulse in combination with additional intravenous cyclophosphamide pulse, the incidence of CMV antigenemia was markedly higher (four out of four). Four of ten CMV antigenemia-positive patients simultaneously showed detection of Pneumocystis jiroveci in induced sputum by PCR, increase in level of serum beta-D-glucan and the finding of geographical ground-glass opacities on chest computed tomography. These findings suggested that patients with connective tissue diseases under intensive immunosuppressive therapies (intravenous steroid pulse in combination with additional intravenous cyclophosphamide pulse in particular) are highly susceptible to CMV infection and disease, and that patients complicated by CMV antigenemia are susceptible to combined opportunistic infection such as Pneumocystis pneumonia.
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PMID:Clinical evaluation of patients with inflammatory connective tissue diseases complicated by cytomegalovirus antigenemia. 1676 51

Cytomegalovirus (CMV) infection is an uncommon but potentially fatal opportunistic infection in patients with systemic lupus erythematosus (SLE). We report 2 patients with severe SLE with life-threatening, multisystemic involvement who were treated with intensive immunosuppressive therapy. SLE was successfully controlled, but the patients succumbed to fatal reactivation of CMV disease despite antiviral therapy. Both were seropositive for CMV. We therefore advocate that there should be more active CMV vigilance, and polymerase chain reaction (PCR)-based CMV prophylaxis should be considered in CMV PCR-positive patients with SLE/rheumatic disease undergoing intensive immunosuppressive therapy.
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PMID:Fatal cytomegalovirus infection in two patients with systemic lupus erythematosus undergoing intensive immunosuppressive therapy: role for cytomegalovirus vigilance and prophylaxis? 1704 67

As the demographics of human immunodeficiency virus (HIV) infection continue to include more African-American and Hispanic females, the prevalence of concomitant HIV infection and systemic lupus erythematosus (SLE) may increase. We describe a 36-year-old woman with a 19-year history of active SLE who, after acquiring HIV infection, developed quiescent SLE with advanced immunosuppression (CD4 cell count 10/2%). After presenting with an opportunistic infection, she began receiving highly active antiretroviral therapy. Throughout a 6-month period, highly active antiretroviral therapy resulted in suppression of her viremia, as well as a concomitant rise in her CD4 cell count. With recovery of her immune status, she presented with transverse myelitis caused by her SLE, which responded well to intravenous steroids. There have been several observations of quiescence of lupus disease activity with advanced immunosuppression in HIV patients. This is a report of the recurrence of rheumatic disease in an acquired immunodeficiency syndrome patient after the initiation of highly active antiretroviral therapy. We recommend careful observation of HIV patients for reactivation of rheumatic disease while initiating highly active antiretroviral therapy.
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PMID:Reactivation of systemic lupus erythematosus after initiation of highly active antiretroviral therapy for acquired immunodeficiency syndrome. 1704 54


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