Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A woman, aged 26 years, who died of progressively worsening demyelinating encephalomyelitis in the course of 4 years is reported. The neuropathological findings included large subcortical softenings in the cerebral hemispheres, tiny perivenous demyelinated foci in their neighborhood and scattered in the white matter. There was an acute vasculitis with fibrinoid exudation in the affected as well as unaffected areas. Focal perivenous mononuclear cell infiltrations are conspicuous in the white matter. The laboratory and postmortem examinations suggested a collagen disease like SLE. The abnormalities included marked increase of serum gamma-globulin, especially of IgG, and elevation of CRP, RA, and ANA titer, moderate thickening of the basement membranes of the renal glomeruli, onion skin-like periarteriolar fibrosis in the spleen, fibrous pericarditis and periadventitial fibrosis of myocardial arteries. Bilateral degeneration of the spinal posterior columns and dorsal roots was also observed. A probable relationship of the modified features in this example of demyelinating encephalomyelitis with abnormal immune mechanisms in the background is discussed.
 ...
PMID:A case of demyelinating encephalomyelitis with some resemblance to collagen disease. 7 51

A 40-yr-old Caucasian woman who had been suffering from systemic lupus erythematosus (SLE) since five years developed vague abdominal complaints whilst under treatment with a low dose of steroids. She had been admitted because of vomiting and abdominal tenderness. The ESR and CRP levels were rising and the C4 level had been persistently low in the preceding months. Normal non-invasive procedures did not allow a diagnosis to be made. Therefore exploratory laparotomy was performed and revealed a non-bacterial peritonitis and an oedematous jejunum. She responded well to a high dose of prednisone. Serositis of the peritoneum as well as bowel vasculitis may be a rare manifestation of SLE despite apparent control of other lupus manifestations. In this patient serositis flares were associated with a rise in CRP level.
 ...
PMID:Lupus peritonitis presented as vague abdominal complaints in a SLE patient. 143 59

Studying the gene polymorphism of serum amyloid P a common constituent of amyloid deposits two restriction fragment length polymorphism patterns were found among Hungarian rheumatoid arthritis (RA), juvenile rheumatoid arthritis (JRA), systemic lupus erythematosus (SLE) patients and healthy controls. Although no direct connection between DNA polymorphism and the frequency of amyloidosis in three patient groups was found, a marked predominance of the heterozygosity in all studied groups has been described. Authors found close correlation between the serum levels of SAP and CRP in juvenile rheumatoid arthritis, but failed to find the same correlation in SLE and healthy controls. Moreover, the serum level of CRP of heterozygous patients were significantly higher than that of homozygous patients within the juvenile rheumatoid arthritis patient groups.
 ...
PMID:[Molecular genetic, laboratory and clinical study of serum amyloid P]. 152 87

Over the last three years there has been a dramatic rise in the number of trials using monoclonal antibodies in the treatment of rheumatoid arthritis. So far, the numbers of patients treated in the individual studies have been small, and the study designs not comparable. All these trials have been conducted in a non-blinded, uncontrolled fashion. The patient populations tended to represent the severe end of the disease spectrum, being usually individuals for whom all other conventional and sometimes even unconventional experimental therapeutic approaches have failed. Clearly, therefore, larger controlled double blind studies in patients with less advanced stages of rheumatoid arthritis are needed. In the trials thus far, long-standing diseases afflicting the joints, usually with severe destruction, have frequently made clinical evaluation very difficult. Moreover, apparently with the exception of one or two reagents (16H5 and possibly B-F5) routine laboratory parameters which are helpful in determining disease activity such as CRP or the rheumatoid factor usually remain unaltered with anti-T cell therapy. In addition, in some individuals there was no clinical improvement despite sometimes severe CD4 cell depletion. The notion that the mere depletion of CD4+ cells is not sufficient to permanently suppress disease activity in autoimmune disease is further supported by studies carried out by Conolly and Wofsy in 1990. In a mouse lupus model, these investigators demonstrated that a small subpopulation of CD4+ T cells may be refractory to depletion by anti-CD4 and may be able to promote the full expression of the disease. Similar mechanisms could apply to certain individuals with human autoimmune disorders. Many additional questions remain open. The most important of these is which markers identify clinical responders to therapy. Attempts to correlate clinical response to the level of T cell depletion, modulation of the target antigens or in vitro functional assays so far have not yielded significant results. Other questions relate to the frequency of antibody administration and the amounts needed to permanently suppress disease activity. The initial hope based on animal experiments of inducing a permanent tolerance to certain antigens by anti-CD4 treatment has been clearly shown not to apply to rheumatoid arthritis. Even though there are individual variations, the efficacy of anti-T cell treatment tends to wear off after 3 or even 1 month, necessitating retreatment. Protocols will have to be designed for either longer treatment periods, repeated courses or more frequent single administrations.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Management of early inflammatory arthritis. Intervention with immunomodulatory agents: monoclonal antibody therapy. 152 46

Immunosuppressive acidic protein (IAP) is evaluated to be a useful parameter for the observation of the clinical course of patients with cancer, who are frequently associated with an increment of serum IAP levels. And also, immune complex diseases such as rheumatoid arthritis (RA), SLE and so on, have been described to produce immune-complex and, consequently, to generate IAP in vivo. Our study focuses on correlations of the IAP values with acute phase reactants, chronic phase reactants and grading of bone stages in patients with RA. Serum IAP showed the positive relationships with grading of bone stages, erythrocyte sedimentation rate (ESR), CRP, RF, RAHA, beta 2-microglobulin (BMG) and IgA in RA. Serum IAP was influenced by deterioration of bone pathological change. The more progressed pathological change of bone, the more increased serum IAP levels. It seems likely that there exist the similar mechanisms with production of IAP and parts of acute and chronic phase reactants and also, serum IAP level may be a useful parameter to predict bone pathological change in patients with RA.
 ...
PMID:[Evaluation of immunosuppressive acid protein (IAP) in patients with rheumatoid arthritis]. 159 4

With the sandwich binding protein assay utilizing hyaluronic acid binding protein, we measured serum concentration of hyaluronic acid in 458 healthy persons, 71 patients with rheumatoid arthritis (RA) and 51 patients with various rheumatic diseases such as osteoarthritis (OA), progressive systemic sclerosis (PSS), systemic lupus erythematosus (SLE) and gout. The mean concentration +/- standard deviation (SD) of healthy persons whose age ranged 2 to 92 years old was 38.5 +/- 35.7ng/ml, and those with over 50 years old had apparently higher concentrations (51.9 +/- 40.5ng/ml) than those with below 50 of age (20.6 +/- 14.8ng/ml). When the upper limit of normal range was set up at 130 ng/ml, abnormal percentages were 62.0% (44/71) in RA, 0% (0/18) in OA, 6.3% (1/16) in PSS, 18.2% (2/11) in SLE and 0% (0/6) in gout. Patients who apparently had arthritis but not RA revealed normal or near to the upper limit in serum hyaluronic acid compared to RA patients having the mean +/- SD of 351.4 +/- 463.7ng/ml. When patients with RA were classified into stage I to IV with X ray of bone destruction, patients with more advanced X ray stage showed significantly higher serum concentrations of hyaluronic acid. Similarly, patients with lower activity of daily living revealed significantly higher serum concentrations of hyaluronic acid. In addition, serum hyaluronic acid level did correlate to concentration of serum CRP and sialic acid. Lansbury's index, strength of grip, joint score and erythrocyte sedimentation rate, but did not to duration of morning stiffness and titer of rheumatoid factor.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Serum concentration of hyaluronic acid in healthy populations and patients with rheumatoid arthritis--relationship to clinical disease activity of RA]. 194 54

Systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) are prototypes of autoimmune diseases. In order to assess the inflammatory status in these conditions, lactoferrin, stored in specific granules of neutrophils, was measured in serum samples of patients with SLE and RA. In RA, the mean serum lactoferrin level (1221.397 +/- 289.476 ng/ml) was significantly higher than that in normal individuals (753.364 +/- 124.063 ng/ml). Surprisingly, there were no significant differences between active SLE (672.682 +/- 356.154 mg/ml) and inactive SLE (642.267 +/- 270.456 ng/ml). Still, no differences were found between normal volunteers, active SLE and inactive SLE. Serum lactoferrin in SLE correlated significantly with CRP (Rs = 0.4089, p less than 0.01), but not with complement level and ANA titers. Thus in RA serum lactoferrin was highly elevated and this indicated that PMN in systemic circulation was activated. In SLE the correlation of CRP with lactoferrin reflected the role of later protein in inflammation.
 ...
PMID:Lactoferrin in rheumatoid arthritis and systemic lupus erythematous. 199 Jan 49

A 17-year-old female with a 5-year history of disseminated lupus erythematosus has remained without immunosuppressive therapy for the last 3 years. She was admitted to the hospital for acute abdominal pain, generalized edema, and rapidly developing dyspnea and somnolence. Although all symptoms were consistent with active SLE, septicemia was suspected because of leukocytosis (20,000/microliters), greatly elevated C-reactive protein (45 mg/dl), and normal complement values (C3 0.74 g/l, C4 0.21 g/l). Directly after bacterial blood cultures were prepared, a combined treatment was instituted consisting of plasmapheresis (3 x 2.1 l against fresh frozen plasma), antibiotics, prednisolone, and cyclophosphamide following the last plasmapheresis. Within three days cerebral function returned to normal, edema improved, and CRP fell to 0.5 mg/dl. The blood cultures and pericardial effusion displayed meningococcal colonies.
 ...
PMID:Successful therapy of meningococcal sepsis in acute disseminated lupus erythematosus with plasmapheresis, immunosuppression, and antibiotics. 223 29

One of the mediators responsible for the induction of the production of acute phase proteins by hepatocytes is interleukin-6 (IL-6), formally known as hybridoma growth factor (HGF). In a prospective study the biological significance of IL-6, but also the relationship with the acute phase response (C-reactive protein [CRP], alpha 1-antitrypsin and alpha 1-acid glycoprotein) during flare-ups in 12 systemic lupus erythematosus (SLE) patients was investigated. Only 2 SLE patients showed sustained elevated IL-6 levels, and in one of these patients a clear correlation was found between the increases in IL-6 and the acute phase response. In the other SLE patients hardly any response or change in the levels of IL-6, CRP, and/or alpha 1-antitrypsin was found. In contrast to the profiles of alpha 1-acid glycoprotein, in seven of the SLE patients a significant increase in the serum levels took place in the period preceding the exacerbation. This difference between the three acute phase proteins suggests that the regulatory mechanisms are different. Our results are in agreement with the findings that IL-6 might be responsible for the CRP response.
 ...
PMID:Interleukin-6 (IL-6) and acute phase proteins in the disease course of patients with systemic lupus erythematosus. 247 Dec 49

CRP levels in 194 serum samples from 43 SLE patients were measured. Patients with inactive disease have levels below 10 micrograms/ml; patients with active SLE have higher levels, but never over 50 micrograms/ml. In the presence of infection or inflammatory processes, regardless of the activity of SLE, the levels are significantly higher (p less than 0.05), and well over 50 micrograms/ml. Both active SLE patients and inactive SLE patients with local infections have levels between 10 micrograms/ml and 50 micrograms/ml. In this situation, the presence of anti-DNA antibodies strongly suggests disease activity (82% versus 9%, p less than 0.05). The clinical and physiopathological meaning of these findings is discussed.
 ...
PMID:C-reactive protein (CRP) levels in systemic lupus erythematosus (SLE). 348 99


1 2 3 4 5 6 7 8 9 10 Next >>