Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spontaneous bacterial peritonitis (SBP), a fascinating disease that had been reported perhaps 50 times in varying guises over the preceding century, suddenly burst forth in the 1960s and was recognized in clusters of cases almost simultaneously in Paris, London, and West Haven, Connecticut. The spectrum of the disease has broadened. Initially, it was associated almost exclusively with alcoholic cirrhosis, but it has now been found in association with posthepatitic cirrhosis, cryptogenic cirrhosis, chronic active liver disease, and, occasionally, in biliary cirrhosis and cardiac cirrhosis. Recently, it has been reported in alcoholic hepatitis and acute viral hepatitis. It occurs occasionally in malignant ascites and in pancreatitis in the absence of cirrhosis. It is surprisingly common in disseminated lupus, in which it occurs relatively more commonly than in alcoholic cirrhosis. A similar syndrome, primary peritonitis, occurs frequently in children with nephrotic ascites. The clinical pattern of SBP has broadened. Initially it consisted of abdominal pain, fever, rebound tenderness, hypoactive bowel sounds, hypotension, encephalopathy, and cloudy ascites with large numbers of polymorphonuclear leukocytes in ascitic fluid. Each and every symptom, sign, and laboratory abnormality may be absent; indeed, the syndrome can be completely silent. Initially, the causative bacteria appeared to be almost exclusively enteric, but now the list of bacteria isolated in cases of SBP looks like a bacteriology textbook. Anaerobes are rare. Multiple organisms usually suggest nonspontaneous origin such as perforation or vasopressin induction. The differentiation between spontaneous and nonspontaneous bacterial peritonitis is crucial in the differential diagnosis. The great majority of cases of SBP develop in the hospital, 80% more than one week after admission. It is therefore a nosocomial disease that may be precipitated by procedure-induced bacteremia, gastrointestinal bleeding, or diarrhea, and it tends to occur in patients with low ascitic fluid protein (complement) concentrations and severe portal-systemic shunting.
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PMID:Spontaneous bacterial peritonitis: variant syndromes. 368 33

The severity of renal disease in systemic lupus erythematosus is variable. Renal biopsy is important to guide the treatment. The World Health Organization classification define six different histological categories with possible transformations from one category to another. Histological signs of activity or chronicity are important with respect to prognosis and treatment. Examination of renal biopsy allows predicting the reversibility of histological lesions following therapy. Apart from histological signs of severity, other factors may influence the prognosis: arterial hypertension, initial serum creatinine, the delay between onset of renal disease and treatment, the occurrence of exacerbations of the nephropathy, and the response to therapy by the end of the first year. The prognosis of severe forms of lupus nephritis, mainly diffuse proliferative glomerulonephritis, has improved during the last 20 years. The addition of immunosuppressive agents (cyclophosphamide, azathioprine) to corticosteroids is responsible for this improvement. Methylprednisolone pulses are as effective as oral high doses of prednisone during initial treatment and have fewer side effects. Many authors advocate monthly cyclophosphamide pulses over six months, sometimes followed by quarterly pulse cyclophosphamide. However, such an approach has not been proven to be more effective than an oral course of cyclophosphamide and/or azathioprine. On follow-up, steroid therapy should be slowly tapered, and close monitoring of lupus serological parameters (anti-DNA antibodies, complement), urinary protein excretion rate, urinary sediment and renal function allow one to detect exacerbations of the disease, which may require adapted therapy. While such protocols have improved the outcome, they have potential side effects. In addition to the deleterious effect of steroids on physical appearance, often badly tolerated by adolescents, immunosuppressive treatments increase the risks of severe infectious complications and the risks of cardiovascular complications in young adults.
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PMID:[Treatment of lupus nephritis in children]. 1062 4

We have investigated the individual role of FcgammaR and CR, as well as their cooperation, in mediating the oxidative burst and degranulation of neutrophils of Brazilian systemic lupus erythematosus (SLE) patients. Neutrophils were stimulated with the immune complexes (IC)-IgG or -F(ab')2, opsonized or not with normal or SLE human serum. The oxidative burst was decreased in neutrophils of active SLE patients compared to healthy controls when this response was mediated by FcgammaR and/or CR, while the degranulation was unaffected. The SLE hypocomplementemia did not affect the oxidative burst mediated only by CR. FcgammaRII and CR1 expression on neutrophils of active SLE patients was reduced, while the expression of FcgammaRIII and CR3 was unaffected. These results suggest that the different FcgammaR and CR may be involved or cooperate in different ways in the mediation of the oxidative burst and the degranulation. Moreover, the decreased oxidative burst of neutrophils of active SLE patients may not depend only on SLE hypocomplementemia for IC opsonization. These observations are directed at the understanding of how each of these immune system components (FcgammaR, CR and complement) influences the precise biological neutrophil responses both in physiological and pathological conditions. Since the Brazilian population comprises many races, these results are important because they are directed at a specific population of SLE patients.
Lupus 2002
PMID:Fcgamma and complement receptors: expression, role and co-operation in mediating the oxidative burst and degranulation of neutrophils of Brazilian systemic lupus erythematosus patients. 1204 88

The term Pulmonary-renal syndrome refers to the combination of diffuse alveolar haemorrhage and rapidly progressive glomerulonephritis. A variety of mechanisms such as those involving antiglomerular basement membrane antibodies, antineutrophil cytoplasm antibodies or immunocomplexes and thrombotic microangiopathy are implicated in the pathogenesis of this syndrome. The underlying pulmonary pathology is small-vessel vasculitis involving arterioles, venules and, frequently, alveolar capillaries. The underlying renal pathology is a form of focal proliferative glomerulonephritis. Immunofluorescence helps to distinguish between antiglomerular basement membrane disease (linear deposition of IgG), lupus and postinfectious glomerulonephritis (granular deposition of immunoglobulin and complement) and necrotizing vasculitis (pauci-immune glomerulonephritis). Patients may present with severe respiratory and/or renal failure and require admission to the intensive care unit. Since the syndrome is characterized by a fulminant course if left untreated, early diagnosis, exclusion of infection, close monitoring of the patient and timely initiation of treatment are crucial for the patient's outcome. Treatment consists of corticosteroids in high doses, and cytotoxic agents coupled with plasma exchange in certain cases. Renal transplantation is the only alternative in end-stage renal disease. Newer immunomodulatory agents such as those causing TNF blockade, B-cell depletion and mycophenolate mofetil could be used in patients with refractory disease.
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PMID:Bench-to-bedside review: pulmonary-renal syndromes--an update for the intensivist. 1749 92

Systemic lupus erythematosus (SLE) can be a severe and potentially life-threatening disease that often represents a therapeutic challenge because of its heterogeneous organ manifestations. Only glucocorticoids, hydroxychloroquine, mycophenolate mofetil, azathioprine, cyclophosphamide, and very recently belimumab have been approved for SLE therapy. Dependence on glucocorticoids and resistance to the approved therapeutic agents, as well as substantial toxicity, are frequent. B-cells abnormalities leading to autoantibody production play a central role in Systemic Lupus Erythematosus (SLE) pathogenesis. The targets of these biological therapies are directed toward the B cell depletion, interference in the co-stimulation signals and the blockade of cytokines. Biologic agents targeting specific pathways (i.e. T-B lymphocyte interaction, cytokines and complement) have been also proposed as new tools for SLE treatment. B-cell targeted therapies, including anti-B lymphocyte stimulator (BLyS) and anti-CD20 monoclonal antibodies are at forefront of new SLE treatment. Results from randomized trials in systemic lupus erythematosus (SLE) have been very disappointing, with lack of efficacy for some drugs and development of severe side-effects such as infections for others. Fortunately, as more and more trials of biologics in the treatment of lupus are being performed, the first promising results have been achieved. Today, belimumab is expected to become the first approved drug for use in lupus in several decades. In this review we will focus on biological drugs whose potential efficacy have been evaluated in open-label and randomized clinical trials. Biologics provide encouraging results that represent a possible option in the treatment of refractory lupus. Thus we review recent clinical trials in patients with systemic lupus erythematosus (SLE), with emphasis on outcomes and on mechanisms by which the biological agents suppress autoimmunity.
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PMID:Biologics in SLE: the current status. 2448 65