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)

Since immunological events were found to be pathogenetically involved in various forms of glomerulonephritis, corticosteroids and immunosuppressive drugs were introduced in the treatment of nephritis. However, as opposed to the findings in the paediatric nephrotic syndrome, controlled and multicentric trials with immunosuppressive therapy revealed disappointing results in the management of renal disease in adults. Significantly better results under immunosuppressive therapy, were seen only in the nephrotic syndrome based on the so-called "no changes" or "minimal changes" nephritis. In chronic membranous and proliferative glomerulonephritis the clinical course in the treated group was not statistically different from that of the untreated group. In some disorders of connective tissues, such as systemic lupus erythematosus, polyarteritis nodosa and Wegener's granulomatosis, corticosteroids and immunosuppressive agents seem to exert a favourable effect on the course of renal disease. Encouraging results concerning the combined use of immunosuppressive drugs, anticoagulants and platelet aggregation inhibitors in mesangiocapillary (membrano-proliferative) glomerulonephritis and rapidly progressive nephritis have also been presented. Several factors such as incomplete immunosuppression, druginduced antigen tolerance and increased immune complex formation as a consequence of inhibited antibody production may contribute to the fact that many patients with different forms of nephritis do not benefit from long-term immunosuppressive therapy.
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PMID:[Immunosuppressive therapy in renal disease (author's transl)]. 0 14

Extensive serologic changes occur in systemic lupus erythematosus (SLE) which are probably secondary to unknow primary cause(s). The New Zealand hybrid mouse model most likely has a viral-induced disease and does not show many of the clinical features of the human disease. The best example of human SLE which provides a clue to etiology is the drug-induced type, particularly that due to procainamide. In these patients it is possible to study the development of serologic changes prior to the onset of clinical manifestations, and then observe regression of the clinical and serological changes on withdrawal of the medication. Although there is a rough correlation between the many serologic abnormalities and the clinical picture, enough exceptions exist, so that single tests such as serum complement, anti-DNA antibodies, per cent DNA binding, and others, cannot be used as a sine qua non for management. Care of the patient still remains a clinical problem guided by various laboratory procedures but not dependent on any one. Alkyating agents have a limited role in the treatment of lupus nephropathy and cutaneous vasculitis but azathioprine is probably of no value in SLE.
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PMID:Serologic abnormalities in spontaneous and drug-induced systemic lupus erythematosus. 5 Apr 52

A 125I-DNA preparation for the detection of human anti-DNA antibodies (ADA) was evaluated as a diagnostic test for systemic lupus erythematosus (SLE). A normal range of 0-25 U/ml was established. Serum ADA level greater than 110 U/ml were diagnostic in clinically active SLE and levels greater than 45 U/ml were found in 75% of patients with inactive disease. This value was significantly greater than that found in rheumatoid arthritis, renal disease caused by non-immune mechanisms, post-streptococcal glomerulonephritis and a miscellaneous group of disorders comprising connective tissue diseases, auto-immune disorders and chronic active hepatitis. Anti-nuclear factor (ANF) titres greater than 1/160 and LE cells were found in 85% of these patients. In inactive disease the ADA levels ranged between 25 and 98 U/ml, ANF titres varied from 1/40 to 1/640, and LE cells were detected in only 20% of the cases. In 3 patients investigated during the course of the disease, the ADA levels correlated best with clinical improvement. Two patients with apparent active lupus nephritis showed intermediate ADA levels, which were probably caused by antigen-antibody formation and immune complex deposition in the kidneys.
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PMID:Evaluation of 125I-DNA for detecting anti-DNA antibodies in the diagnosis of systemic lupus erythematosus. 6 46

Main components of kinin system, the arginine-esterase activity and proteinase inhibitors were estimated in blood serum of patients with nephrotic syndrome of various etiology (glomerulonephritis, amyloidosis, systemic lupus erythematous) and also in patients with latent nephritis and in healthy donors. Content of all the kinin system components (kallikreinogen, kininogen and kininase 1) proved to be increased in all the forms of nephropathy studied. Free kallikrein was found in blood serum of patients with nephrotic syndrome as distinct from healthy persons and patients with latent nephritis. The arginine-esterase activity, which shows the level of trypsin-like proteinases, was altered dissimilarly, depending on the nephrotic syndrome etiology: it was maximally increased in nephrotic syndrome of amyloid genesis and decreased in patient with systemic lupus erythematosus. High content of kallikrein and kininase I with simultaneous decrease in kininogen was typical for patients with severe form of nephrotic syndrome. Impairment of kidney in nephrotic syndrome was also characterized by an increase in alpha1-antitrypsin and in the total antitryptic activity, which reached the maximal value in nephrotic syndrome of the I degree and decreased at the II degree of the disease. In nephrotic syndrome content of alpha2-macroglobulin was maximally increased at the II degree of nephrotic syndrome and decreased in severe form of the disease. The primary alteration in content of proteinase inhibitors and high level of kinin system components were assumed to determine the conditions for activation of kinin system in blood serum and to impair the nephrotic syndrome pathogenesis, which was complicated by systemic manifestations. High content of kinin system components was apparently determined by the increased synthesis in liver tissue in response to inflammation and massive proteinuria; kininase I and alpha2-macrolgobulin, as proteins with high molecular weight, were likely to be selectively retained in blood circulation when the capillary penetration was increased.
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PMID:[State of the kinin system and level of serum proteinase inhibitors in latent nephritis and the nephrotic syndrome of different etiology]. 7 Jan 11

Analysis is carried out of the clinical, pathomorphological and immunological characteristic of lupus nephropathy in 62 patients, 56 females and 6 males. A series of new investigation methods were used for that purpose. An early tendency towards kidney involvement in the course of LED is established and in 22 of the patients (36%) the renal symptoms have been the first clinical manifestations of the basic illness. Lupus nephropathy progresses most often with a nephrosis syndrome (in 66.1% of the patients), rarely pure and not combined with hypertension and/or with renal insufficiency. The pathomorphological changes are rather multiform but in the majority of the cases almost all structural elements of glomerules and the rest of the renal tissue are affected. The clinical picture severity, histopathological changes and nephropathy evolution course were established to be distinctly dependent on the course acuteness of the basic morbid process. The importance of the detailed study of the clinico-morphological and immune characteristic of lupus nephropathy upon the timely diagnosis. Proper treatment and the prognosis assessment of the illness is stressed upon.
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PMID:[Clinical morphological and immunological characteristics of lupus nephropathy]. 7 Aug 87

The levels of C3, C4 and CH50 in patients with lupus erythematosus disseminatus (LED) were lower than in the controls. However, although in many patients these levels were below the normal values, there was no statistically significant difference between the two group. The levels are reduced during the acute phases and in some patients they remain high. On the whole, C3 was lower in patients with nephropathy (p less than 0,025) than in patients presenting with clinical activity (p less than 0,02). The positive relationship existing between C3 and C4 (r = 0,641, p less than 0,01) suggests activation of the complement system in LED via the classic route. In cases with concurrent lupus nephropathy a relationship between C3 and C3PA was seen, suggesting that in this case the alternative route is involved.
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PMID:[Complement system in disseminated lupus erythematosus]. 7 30

In the course of a prospective study of 165 patients with SLE a subgroup of eight patients with active SLE yet with persistently negative tests for ANF and LE cells was identified. These patients were characterized by a photosensitive skin rash with a negative lupus band test, a high incidence of arthritis, mild form of renal disease, and a positive family history for connective tissue disease. Antibodies to DNA and cytoplasmic antigens were detected in a few.
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PMID:Systemic lupus erythematosus with negative LE cells and antinuclear factor. 7 82

In healthy subjects with normal renal function beta2-microglobulin (beta2m) is constantly produced in the body. It is eliminated almost exclusively by the kidneys, predominantly by glomerular filtration but possibly also by some direct uptake from the blood. After glomerular filtration more than 99,9% of excreted protein is reabsorbed in the kidney tubules where it is catabolized. The main factor, influencing on the serum level of beta2m is the GFR. Determination of S-beta2m appears to be more effective than analysis of S-creatinine for the detection of a slightly reduced GFR. A relatively high S-beta2m, in comparison with the GFR, may be seen in e.g. malignant proliferative disorders and SLE. This indicates an increased production of the protein. An entirely free passage over the glomerular membranes is not likely for beta2m in healthy subjects but the sieving coefficient might approach 1,0 in renal disease. The increased glomerular elimination of the protein could then possibly be counterbalanced by an increased synthesis, which should explain the pronounced relationship at a log/log scale between S-beta2m and the GFR. An increased excretion of beta2m in the urine is a sensitive indicator of proximal tubular dysfunction in many clinical conditions. In marked renal insufficiency there is, however, an obligatory 100-1 000-fold increase of the normal excretion, not related to the kind of renal disorder. In studies of the protein precautions are necessary to avoid degradation of the protein, in urine with a low pH.
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PMID:The serum level and urinary excretion of beta2-microglobulin in health and renal disease. 8 68

Circulating antibodies against certain nuclear acidic protein antigens have been shown to have diagnostic and prognostic importance in connective tissue disease. We describe a new precipitin system found in the sera of patients with systemic lupus erythematosus. The antigen, called MA, was prepared from calf thymus nuclei, and was shown to be distinct from other nuclear acidic protein antigens by physicochemical and immunologic techniques. MA antibodies were detected in the serum of 12 of 66 lupus patients and in none of 554 sera from normal controls or patients with other rheumatic diseases. Lupus patients having MA antibodies had more severe disease than did lupus patients with Sm or native DNA antibodies, manifested by recalcitrant skin rashes and a significantly greater incidence of hypocomplementemia, serious renal disease, hypertension, hepatosplenomegaly, lymphadenopathy, and neurological disease (P values range from 0.025 to 0.005). The presence of circulating MA antigen was demonstrated in three lupus patients immediately before a flare of nephritis. These data suggest that MA is a nuclear acidic protein antigen that may identify a subset of lupus patients with very severe disease. The presence of the antigen in the circulation before clinical flares suggests a possible biologic role for the MA system in an immune complex nephritis.
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PMID:Characterization of a distinct nuclear acidic protein antigen (MA) and clinical findings in systemic lupus erythematosus patients with MA antibodies. 8 19

A 61-year-old man developed clinical lupus syndrome with positive antinuclear antibody, positive lupus erythematosus (LE) cell preparation, and diffuse proliferative glomerulonephritis following 26 months of procainamide therapy. He was treated sequentially with prednisone and azathioprine (2 weeks), decreasing doses of prednisone alone (21 months), and no immunosuppressive drugs (10 months). Coincidental with this treatment, the immunopathology of the glomerulonephritis improved dramatically, dramatically, renal function returned almost to normal, and both antinuclear antibody and LE cell preparation became negative. The course of this patient's renal disease contrasts sharply with diffuse proliferative glomerulonephritis of idiopathic systemic lupus, and suggests that this rare complication of procainamide therapy may have a favorable course.
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PMID:Glomerulonephritis in procainamide induced lupus erythematosus: report of a case and review of the literature. 9 11


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