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)

Patients with rheumatoid arthritis show increased levels of anti-influenza-A antibodies in their sera compared to healthy controls and patients with other inflammatory rheumatic diseases (systemic lupus erythematosus, ankylosing spondylitis and psoriatic arthritis). These antibody levels are dependent on the activity of rheumatoid arthritis.
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PMID:[Demonstration of increased influenza-A-antibody levels in the serum of patients with chronic polyarthritis]. 409 27

Kaposi's Syndrome (K. S.) was defined as a virus induced immunogenic tumour responding to interferon. It can be used as a guideline for therapeutical trials in A. I. D. S. K. S. mortality is 13%. K. S. + O. I. (opportunistic infections) mortality reaches 70% and O. I. mortality is approximately 50%. Therefore treating O. I. is a must but it is not mentioned in the paper. Attempts made to modify immunodepression, usual K. S. treatments, experimental treatments based upon similar pathogenicity (like systemic lupus erythematosus, Hansen's disease, preneoplasia dyskeratosis) were unsuccessful. Trials with alpha recombinant interferon realised at the Sloan Kettering Memorial for Cancer in New York are summarized for 74 patients and are in preliminary interpretation. Our study is based upon 13 cases studied for 14 to 4 months and comes up to the same conclusions using 18 to 36 million units/day for 6 months (6 cases) and 3 to 4 months (7 cases). For 6 full treatments the results are: 2 K. S. were cleaned up after 8 and 3 months follow up, 4 K. S. with O. I.: 3 remissions and then relapses and 1 stabilization, for 7 current treatments: 2 had to be discontinued because of bad tolerance, 1 stabilization and 4 remissions. For all treatments a decrease and a lesser gravity of O. I. can be noted during treatment. Besides flu-like syndromes, main clinical side effects, are: asthenia, general condition impairment, 2 fits were observed for which I.N.F. cannot be clearly incriminated. Daily treatment compelling and surveillance are real drawbacks. Different types of better used interferon will probably yield interesting results (40% regression or improvement).
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PMID:[Problems raised by the treatment of Kaposi's sarcoma in subjects with AIDS]. 621 Jan 62

Unfractionated mononuclear cells from patients with systemic lupus erythematosus (SLE) immunized with influenza vaccines do not produce a secondary in vitro anti-influenza antibody response when challenged with virus antigen. Irradiated T lymphocytes from normal, disease control and from SLE donors whether vaccinated or not, help allogeneic normal non-T cells to produce specific anti-influenza antibody in vitro. Irradiated normal T cells, however, do not help allogeneic non-T cells from SLE donors. Non-irradiated T cells from 40% of the SLE patients, irrespective of whether or not they had been vaccinated, also provide specific help for MLC incompatible normal non-T cells in the influenza antibody response. This non-restricted interaction was not seen using non-irradiated T cells from any normal or disease control donor. No anti-DNA antibodies were produced in virus stimulated cultures of non-irradiated or irradiated SLE T cells with allogeneic normal non-T cells.
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PMID:Specific allogeneic help by T lymphocytes from patients with systemic lupus erythematosus. 623 17

Antiviral activity was evaluated in sera from 65 patients with chronic glomerulonephritis (GN), 58 patients with SLE and 59 healthy controls. Antibodies to influenza A2 and B, and parainfluenza I-II-III viruses occurred much more frequently in GN than in healthy controls. Geometric mean antibody titers to measles, influenza A2 and B, and parainfluenza I-II-III were found to be elevated. The frequency of antiviral antibodies and their level in GN patients were similar to those in SLE patients. Detection of increased antiviral activity in sera of patients with chronic GN extends the range of diseases where persistent latent viral infection may be relevant.
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PMID:Antiviral immunity in chronic glomerulonephritis. 626 42

The effect of prednisone on serum levels of IgG antibodies to viral and bacterial antigens was measured and compared to its effect on IgG antibodies to nuclear antigens in 8 patients with systemic lupus erythematosus. Prednisone at 15-80 mg/day (mean 55 mg/day) for 14-30 days (mean 19 days) lowered the serum IgG by an average of 22% (p less than 0.005). An even greater reduction in IgG antinuclear antibodies occurred (mean 43%, p less than 0.001) including responses to double stranded DNA, single stranded DNA, and the nucleosides, adenosine, guanosine, cytidine and thymine riboside. In contrast, there was no alteration in serum IgG antibody levels to influenza virus vaccine and pneumococcal vaccine antigens. These results suggest that prednisone has a selective effect on the expression of autoimmunity which may, in part, be responsible for its clinical efficacy in systemic lupus erythematosus.
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PMID:Effect of corticosteroids on serum antinuclear antibodies in man. 633 72

The in vitro synthesis of specific anti-influenza virus antibody was measured in cultures of peripheral blood lymphocytes from 25 patients with systemic lupus erythematosus (SLE) and 23 control subjects. Whilst all cultures derived from normal individuals synthesized specific antibody, cultures from patients with SLE were consistently unable to produce anti-influenza antibody. This defect could not be corrected by manipulating the culture conditions or by in vivo immunization. Co-cultivation of separated SLE-B or control B cells, with SLE-T or control T cells showed that the immunodeficiency exhibited by the SLE peripheral blood lymphocytes resides in the B cells.
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PMID:Defective B cell function in systemic lupus erythematosus. 698 71

Specific antibody responses to influenza viral antigens produced by cultured peripheral blood mononuclear leucocytes stimulated with influenza virus or pokeweed mitogen (PWM) have been measured in seven patients with systemic lupus erythematosus (SLE) before and at time intervals after influenza immunization. Cells from two patients stimulated with influenza virus in vitro produced high levels of specific antibody 7 days after immunization. Cells from a third patient produced small amounts of specific antibody at day 14. No antibody was produced by cells from the remaining four patients. Responses were of short duration and were not detectable 1 month after immunization. Specific anti-influenza antibody was induced by PWM only from cells of those patients who responded to virus antigen although absolute levels of antibody produced were not as high. In six patients serum haemagglutination inhibiting antibody to influenza virus was measured, and all six had a greater than four-fold increase. The disparity between in vitro antibody production by peripheral blood mononuclear leucocytes and changes in serum antibody suggests that in patients with systemic lupus erythematosus, in vitro functions of peripheral blood lymphocytes do not reflect the immune system as a whole.
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PMID:Kinetics of specific anti-influenza antibody production by cultured lymphocytes from patients with systemic lupus erythematosus following influenza immunization. 712 6

Since their initial description in 1957, the interferons (IFNs) have been increasingly used to treat a wide array of diseases. Acute adverse effects, i.e. 'flu-like' syndromes, hypo- or hypertension, tachycardia, headache, myalgias and gastrointestinal disorders, occur within the first hour or day after starting treatment. They are seldom treatment-limiting and are easily manageable. Sub-acute and chronic effects develop after several days, usually within 2 and 4 weeks of therapy. The most typical is neurological toxicity, including fatigue/asthenia, and behavioural and cognitive changes. Such symptoms may seriously impair quality of life and result in treatment discontinuation. Seizures have seldom been described. Other infrequent central nervous system adverse effects include vertigo, cramp and oculomotor nerve paralysis. Distal paraesthesias and peripheral neuropathy have been reported. IFN-associated autoimmunity is quite rare but a matter of concern. Biological or clinical manifestations usually require several months to become apparent. Autoantibodies have been shown to develop in most patients but have been inconsistently associated with clinical symptoms of systemic lupus erythematosus, rheumatoid-like arthritis and thyroiditis. Both hypo- and hyperthyroidism have been described but are usually reversible. Other infrequent autoimmune reactions include diabetes, pemphigus and worsening of multiple sclerosis. Although several patients present with a pre-existing autoimmune disorder, no predisposing factor has been clearly established. While hypotension and tachycardia are the most frequent acute cardiovascular complications, a few additional cases of cardiac arrhythmias and myocardial ischaemia have been reported after a short course or several weeks of treatment. These latter complications do not appear to be dose-dependent or age-related. Isolated cases of congestive heart failure have also been described. Mild proteinuria has been observed in 15 to 25% of patients, but acute renal toxicity is uncommon. A transient rise in serum aminotransferase levels is frequently noted during the first stage of therapy, especially in patients receiving the highest dosages. Direct hepatotoxicity is extremely rare. Autoimmune hepatitis, which is ill-diagnosed as chronic viral hepatitis, and de novo induction of autoimmune hepatitis, account for the majority of liver diseases. Haematotoxicity is relatively common but mild to moderate, and develops gradually during the first weeks of treatment. Neutropenia is the most common haematological toxicity, but is usually not dose-limiting and resolves rapidly upon drug discontinuation. Myelosuppression, autoimmune and immune allergic haemolytic anaemias and thrombocytopenias have seldom been described. Cutaneous adverse effects comprised nonspecific erythema and hair loss and, less frequently, vasculitis, local ulcerations at the site of injection and exacerbation of psoriasis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical toxicity of the interferons. 751 63

Parvoviruses are small single-strand DNA viruses. Human parvovirus (PV B19) was isolated in the 1970s and recognized as a pathogen in the 80s. Its role was first demonstrated in acute erythroblastopenia in patients with chronic haemolytic anaemia, then in epidemic megalerythema. More recently PVB19 has been shown to be the aetiologic agent in fetal loss and chronic infection in immunodepressed patients. Further attention has focused on rheumatologic manifestations, particularly in prolonged joint diseases raising the problem of differential diagnosis and a possible pathogenic relationship with rheumatoid arthritis and systemic lupus erythematosus. Clinically, subjects with parvovirus B19 infection have flu-like manifestations of joint pain and myalgia lasting for about 1 week. Generally, the joint pain is symmetrical, of inflammatory type usually involving proximal joints (phalangeal joints in two-thirds of the cases). Acute back pain or associated extra-articular signs are often absent. Signs regress spontaneously in 10 to 15 days although longer periods have been observed. Diagnosis can be confirmed by ELISA identification of specific IgM antibodies. Nonsteroid antiinflammatory drugs are generally effective.
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PMID:[Rheumatic manifestations of parvovirus B19 infection]. 789 71

CFIDS (chronic fatigue and immune disfunction syndrome) is also known as CFS (chronic fatigue syndrome), CEBV (chronic Epstein-Barr virus), M.E. (myalgic encephalomyelitis), yuppie flu and by other names. It is a complex illness characterized by incapacitating fatigue (experienced as exhaustion and extremely poor stamina), neurological problems and a constellation of symptoms that can resemble many disorders, including; mononucleosis, multiple sclerosis, fibromyalgia, AIDS-related complex (ARC) and autoimmune diseases such as lupus. These symptoms tend to wax and wane, but any often severely debilitating and may last for many months or years. All sections of the population (including children) are at risk, but women under 45 seem to be most susceptible. The investigators suggest that CFIDS results from dysfunction of the immune system. The exact nature of this dysfunction is not yet well defined, but it can generally be viewed as an unregulated or overactive state which is responsible for most of the symptoms. There is also evidence of some immune suppression in CFIDS. None of the treatments is consistently satisfactory, but some may be helpful: psychotherapy, physiotherapy, exercise programs, acupunctures, small doses of antidepressants, etc.
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PMID:[The chronic fatigue syndrome]. 790 Apr 53


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