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)

Serum C-reactive protein (CRP) concentration was determined by a radial immunodiffusion method in serum samples collected over a mean period of 19 months from a group of 17 patients with systemic lupus erythematosus (SLE). Thirty-two episodes of CRP elevation were detected. Twenty of these were associated with active SLE, and 9 with proven or possible infection or bone fracture. In 3 cases no explanation for CRP elevation was readily apparent. There were 8 instances of onset or exacerbation of lupus activity without accompanying CRP elevation. These data indicate that CRP elevation in the course of SLE is frequently associated with activation of lupus, and that detection of such elevation does not differentiate between lupus activity and infection.
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PMID:Significance of serum C-reactive protein elevation in patients with systemic lupus erythematosus. 10 59

Fifteen women with pseudo-LE syndrome were studied. The dissease is characterized by recurrent attacks of fever, myalgia, arthralgia, visceral manifestations (pericarditis, myocarditis, pleurisy, pleural effusion and lung involvement). A prominent feature was an abnormal liver function with elevated GOT and GPT levels in serum, and impaired bromsuophalein elimination. The incidence of varicosities and thrombophlebitis was markedly increased. There was a correlation between complement-fixing antimitochondrial antibody (AMA) titres and the degree of activity of the disease. A reverse correlation was observed between antimitochondrial antibody titres and the absolute lymphocyte count in peripheral blood. In all instances the antimitochondrial antibodies were of polyclonal origin, belonging mainly to immunoglobulin class IgG and, in a few patients, IgM, IgA, or IgD. AMA titres, lymphocyte counts in peripheral blood, sedimentation rate, serum iron level and alpha1- and alpha2-globulins proved to be valuable in following the course of the disease. Other values (C-reactive protein, alpha1-acid glycoprotein, immunoglobulin and beta1c-globulin in serum) were not helpful.
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PMID:[Clinical and serological aspects of the pseudo-LE syndrome (author's transl)]. 112 30

In vitro models have shown that interleukin-6 (IL-6) is the main dominator of the stimulation of the full spectrum of acute phase proteins. This study describes IL-6 levels in relation to levels of acute phase proteins in 15 systemic lupus erythematosus (SLE) patients, with special attention given to those patients with increased serum levels of IL-6. Three episodes with elevated levels of IL-6 were observed in a period shortly after a flare-up of SLE, in three of the 15 patients. In one of these three patients a clear increase in the C-reactive protein (CRP) level, preceded by an IL-6 increase, was observed. In the other two patients, CRP levels remained unchanged. It is speculated that, next to IL-6, another signal is operative or needed for the start of an acute phase reaction. However, influences of the disease itself or of the administered therapy cannot be excluded as the cause of the described discrepancy between IL-6 and acute phase protein profiles in these two SLE patients.
Lupus 1992 May
PMID:Observations on the interleukin-6 and acute phase protein profiles in the disease course of patients with lupus erythematosus. 128 44

Gastrointestinal manifestations in a lupus patient may be due to different aetiologies such as vasculitis or a surgical condition. Problems of diagnosis are frequently encountered because the clinical presentations may mimic each other. We analysed ten lupus patients with acute surgical abdomen to identify the clinical, laboratory and radiological features that may aid in early diagnosis and management. Three patients with surgical abdomen had concomitant active lupus. Intra-abdominal sepsis and bleeding peptic ulcer disease constituted two major causes of laparotomies. Overt signs of peritonitis might not be present due to steroid masking effect. There were no specific clinical features, laboratory or radiological tests that could distinguish gastrointestinal vasculitis from acute surgical abdomen. Blood cultures, C-reactive protein and CT abdomen were useful adjuncts in the management of abdominal sepsis. No correlation was found between the timing of surgery, mortality, steroid dosage and wound complication.
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PMID:Acute surgical abdomen in systemic lupus erythematosus--an analysis of 10 cases. 129 28

The serum antihistone antibody (AHA) positivity of patients with various autoimmune diseases was compared with their positive reaction for antinuclear factor, rheumatoid factor, lupus erythematosus factor, cryoglobulin, immunocomplex, C-reactive protein, total protein, gamma globulin, IgG and IgM. In non-drug-induced SLE cases the predictive value of the AHA test was not higher than that of the other tests. It was striking that in 42% of patients with non-autoimmune disease aged over 70 the AHA test was positive. Elevated IgM values were recorded in about 70% of positive AHA samples.
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PMID:Relationship of serum antihistone antibody level to the patient's age. 129 90

We investigated so-called superoxide scavenging activity (SSA) of plasma in patients with several immunological disorders, such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), polymyo-dermatomyositis (PM), progressive systemic sclerosis (PSS), myasthenia gravis (MG) and autoimmune thyroid disease (AT), using the electron paramagnetic resonance/spin trapping technique. Since carboxyethylgermanium sesquioxide, Ge-132, has been reported to modulate both the immune response and leukocyte functions, we have studied in vivo effect of Ge-132 on plasma SSA and other laboratory parameters in these disorders. The plasma SSA was significantly lower in RA, SLE, PM and PSS, but not in MG and AT, as compared with that in healthy controls. An inverse correlation was observed between plasma SSA and parameters such as erythrocytes sedimentation rates, absolute number of leukocytes, C-reactive protein and serum globulin levels. Furthermore, plasma SSA was significantly decreased in rheumatoid factor-positive patients as compared to negative patients. No correlation was observed between plasma SSA and factors such as ages, sex of patients or the other laboratory parameters, such as serum albumin, triglyceride, cholesterol, hemoglobin and serum iron levels. Patients treated with prednisolone, especially ones with RA, showed an increase of plasma SSA. It appears that Ge-132 promotes prednisolone effects. Our results indicate that a decrease in plasma SSA is not disease specific, but inversely correlates with the severity and activity of inflammation. The methodology to measure plasma SSA presented in this work provides a helpful tool for determining the actual activity of the diseases as well as in vivo studies of antiinflammatory agents.
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PMID:Decreased plasma superoxide scavenging activity in immunological disorders--carboxyethylgermanium sesquioxide (Ge-132) as a promoter of prednisolone. 131 42

An inflammatory disease is sometimes suspected despite a normal erythrocyte sedimentation rate (ESR). When this dissociation is present, the reasons for the lack of ESR elevation, which concern the red cells, the plasma and the laboratory techniques, must be excluded, the reality of the inflammatory syndrome being then confirmed by assay of the inflammatory proteins. However, an inflammatory syndrome is missing in 5 to 10 percent of inflammatory diseases, more frequently in cases of polymyositis or scleroderma, less frequently in those of giant cell arteritis. Little information can be found in the literature, concerning the missing inflammatory syndrome. Does it confer peculiar semeiological or prognostic features? Is the dissociation related to the patient, as would appear in some special cases, or to the disease, as suggested by the small rise of the C-reactive protein in acute episodes of lupus erythematosus? The absence of inflammatory syndrome is a source of diagnostic problems when the symptoms are atypical or when there are no specific signs of the suspected disease. Differential diagnoses, especially non-inflammatory diseases, must then be carefully discussed. Improving our knowledge of the missing inflammatory syndrome would require the creation of this key-word.
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PMID:[The missing inflammatory syndrome]. 143 98

In order to study the role of interleukin-6 (IL-6) in inflammatory disease we monitored plasma levels of IL-6 and acute phase proteins such as C-reactive protein (CRP) and renin substrate (RS) in patients with reactive arthritis (ReA), rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE). Venous plasma samples were collected: (1) during the acute phase or exacerbation of the disease, and (2) several months latter during convalescence. Increased mean [95% confidence intervals (CI)] levels of plasma IL-6 were observed in patients with ReA both in the acute phase and later, 229 (177 to 280) ng/l and 197 (134 to 260) ng/l respectively (P less than 0.001 as compared to controls). The corresponding plasma IL-6 levels in RA patients were 283 (223 to 340) ng/l and 183 (151 to 226) ng/l, respectively (P less than 0.001 as compared to controls). Plasma IL-6 levels in SLE patients were not increased. Plasma RS levels were increased in all patient groups, but no significant correlation to IL-6 or CRP levels was observed, whereas plasma IL-6 and CRP levels showed a positive correlation in ReA and RA patients.
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PMID:Plasma interleukin-6 and renin substrate in reactive arthritis, rheumatoid arthritis, and systemic lupus erythematosus. 138 3

To investigate the possible role of IL-6 in the activation of the autoimmune process in systemic lupus erythematosus (SLE), we serially measured concentrations of IL-6, IgG, and anti-dsDNA antibodies before and during exacerbations in patients with SLE. In addition, we serially related the IL-6 response to the generation of the acute phase reactant C-reactive protein (CRP). Sixteen consecutive patients who developed an exacerbation were analysed in this study. Blood samples were drawn in EDTA monthly. At the time of maximal disease activity during exacerbation, IL-6 plasma concentrations were increased (greater than or equal to 6 pg/ml) in 12 out of the 16 cases. Concentrations of IL-6 correlated with the concentrations of CRP (P less than 0.01) and the score of the disease activity index (P less than 0.05). No correlation was found between IL-6 concentrations and concentrations of anti-dsDNA or IgG. The course of changes in IL-6 concentrations before the exacerbation was variable. Five out of the 16 exacerbations studied were characterized by a prominent rise of IL-6 at the time of maximum disease activity. In this subgroup serositis as well as elevated concentrations of CRP were observed more frequently (P less than 0.02). Seven exacerbations were not accompanied or preceded by changes in IL-6 concentrations and showed generally low IL-6 concentrations. In this latter subgroup cerebral involvement was seen more frequently (P less than 0.02). Our data do not suggest a pathogenic role for IL-6 in the generation of IgG and/or anti-dsDNA antibodies before exacerbations. Rises of IL-6 concentrations before exacerbations in SLE seem only to occur in a subgroup of patients with SLE characterized by the presence of serositis and elevated concentrations of CRP during exacerbation.
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PMID:Plasma concentration of IL-6 in systemic lupus erythematosus; an indicator of disease activity? 139 90

A 51-year-old woman had been suffering from blood-stained purulent sinusitis and antibiotic-resistant bouts of fever for 4 months. She had microhematuria and serological evidence of inflammation (erythrocyte sedimentation rate [ESR] 92/135 mm, C-reactive protein 5.0 mg/dl). When she was admitted to hospital suspected of having postinfectious glomerulonephritis she complained of spontaneous colic-like pains in the left flank. Within one day the haemoglobin concentration fell from 10 to 6.5 g/dl. Ultrasound and computed tomography demonstrated a large space-occupying lesion around the left kidney. At operation this was found to be a rupture of the kidney with perirenal bleeding which was treated without removing the kidney. No biopsy was taken, but serological tests showed antineutrophil cytoplasmatic antibodies (cANCA), indicating Wegener's granulomatosis as the cause of the compensated renal insufficiency and spontaneous renal rupture. Under immunosuppressive treatment the inflammatory signs (ESR 18/44 mm), fever, chronic maxillary sinusitis, raised serum creatinine concentration and the ANCA titre all regressed, while proteinuria of about 4 g/24 h persisted. There was no recurrence during a follow-up period of 15 months. Serological signs of marked inflammatory activity, urinary sediments of nephritis and spontaneous retroperitoneal bleeding should suggest that, in addition to lupus erythematodes and panarteritis nodosa, Wegener's granulomatosis be included in the differential diagnosis.
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PMID:[Spontaneous kidney rupture as an early complication of Wegener's granulomatosis]. 154 1


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