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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In patients with rheumatoid arthritis high levels of prostaglandin E1 have been found in the joint fluid, and its increased production by adherent synovial cells and macrophages clearly supports the notion that this arachidonic acid metabolite is involved in the pathology of the disease. Besides its known inflammatory qualities and the suppressive effects on various lymphocyte functions prostaglandin E2 has proved to be an essential cofactor in the secretion of the lymphokine osteoclast activating factor. In this study we have discovered an enhanced release of prostaglandin E1 and thromboxane B2 from a subpopulation of blood monocytes from patients with rheumatoid arthritis and active systemic lupus erythematosus. No correlation between prostanoid release from monocytes and inflammatory activity of the disease was found. However, even monocytes from patients with early stage or mild inflammatory activity displayed a 'stimulated' arachidonic acid metabolism. In contrast only patients with active systemic lupus erythematosus showed in this respect comparable secretory activity or monocytes. Our findings may point to a possible pathogenic role of prostanoids in rheumatoid arthritis, which may also have some implication for the early diagnosis of this disease and for its differentiation from other chronic inflammatory rheumatic conditions.
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PMID:Enhanced prostanoid release from monocytes of patients with rheumatoid arthritis and active systemic lupus erythematosus. 402 5

The effect of pharmacologic quantities of prostaglandin E1 (PGE) was investigated in three strains of mice (NZB X NZW, MRL/1, and BXSB) that spontaneously develop lupus-like glomerulonephritis. PGE-treatment prolonged survival and retarded the glomerular deposition of immune complex (IC) and the development of glomerulonephritis in NZB X NZW and MRL/1 mice, but did not similarly protect BXSB mice. Changes in the responsive strains correlated well with reduced amounts of circulating gp70 complexed with anti-gp70 antibodies compared with untreated controls, although total concentrations of gp70 (free and complexed) detectable in sera were similar in both groups of mice. The results strongly suggest that: (a) PGE selectively suppressed the immune response to retroviral gp70, (b) PGe had little effect on the quantity or quality of anti-DNA antibodies but did reduce the deposition of anti-DNA containing IC in the kidneys, and (c) gp70 IC appear to play an important role in the pathogenesis of glomerulonephritis in murine systemic lupus erythematosus.
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PMID:Selective suppression of retroviral gp70-anti-gp70 immune complex formation by prostaglandin E1 in murine systemic lupus erythematosus. 696 75

The F1 hybrid of New Zealand black and New Zealand white mice--the NZB/W mouse--spontaneously develops a disease similar to human systemic lupus erythematosus. Male NZB/W mice with established disease were treated with a stable derivative of prostaglandin E1, 15(S)-15 methyl PGE1 (4 micrograms twice daily) from 7 months of age. The pge analog prolonged survival of these mice: At 14 months 7 of 10 control mice had died, whereas 9 of 10 15(S)-15 methyl PGE1 treated mice remained alive. Thus a dose of 200 micrograms/Kg/day 14(S)-15 methyl PGE1 retards progression of murine lupus.
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PMID:Treatment of NZB/W ("lupus") mice with 15(S)-15 methyl PGE1. 739 67

The physiologic role of the prostaglandins is complex and not yet defined precisely. Nevertheless, these ubiquitous compounds do appear important to regulation of cell function and host defenses. The therapeutic potential of the prostaglandins seems to be immense, and their use in a wide variety of clinical conditions is just beginning. Whether they will also prove helpful clinically as modulators of the immune response is not clear. It is likely that an appropriate balance of prostaglandin endoperoxides, thromboxanes, prostacyclins, and probably the stable prostaglandins themselves is important to physiologic regulation of many organ systems and of immunologic reactions. Thus, development of drugs that selectively inhibit one or another of the prostaglandins and their allied compounds may prove fruitful in treatment of many diseases, including those associated with disordered immunity and tissue injury. Prostaglandin therapy in such diseases must proceed with caution. In recent studies addition of amantadine to prostaglandin E (PGE) treatment of NZB/W mice not only increased survival of these animals, but prevented development of circulating antibodies to nuclear constituents including native DNA. The results are encouraging, but must be balanced against the observation that deprivation of prostaglandin precursors also prevented nephritis and markedly increased surival of lupus mice. However, prostaglandins might be useful in a disorder whose course is more easily monitored than that of systemic lupus erythematosus: cutaneous vasculitis. The studies in which even oral administration of a PGE1 derivative suppressed immune complex-induced vasculitis (reversed passive Arthus reaction in rat skin) suggest that a trial of PGE1 treatment of cutaneous vasculitis would not be unreasonable.
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PMID:Prostaglandins. Their potential in clinical medicine. 743 93

MRL-lpr/lpr mice spontaneously develop an autoimmune disease with nephritis similar to human systemic lupus erythematosus. In these animals, treatment with E-series prostaglandins ameliorates renal disease and prolongs survival, perhaps by modulating production of cytokines or eicosanoids. To further define the mechanisms of action of E-series prostaglandins in established murine lupus nephritis, we administered the prostaglandin E1 (PGE1) analog misoprostol to 20-week-old MRL-lpr/lpr mice by twice-daily subcutaneous injection. After 2 days of treatment, misoprostol reduced renal cortical interleukin-1 beta (IL-1 beta) mRNA levels compared to vehicle-treated controls (0.19 +/- 0.06 (misoprostol) vs 0.50 +/- 0.04 (vehicle) densitometry units; P < 0.005). A similar reduction in cortical IL-1 beta mRNA levels was found in left kidneys harvested from MRL-lpr/lpr mice following 2 days of treatment with misoprostol compared to right kidneys harvested from the same animal prior to the first dose of PGE1 analog (0.12 +/- .05 (left) vs 0.39 +/- 0.18 (right) densitometry units; P < 0.05). This reduction in cortical IL-1 beta mRNA levels was not associated with alterations in renal production of thromboxane B2, PGE2, or leukotriene B4 or with significant changes in the severity of renal inflammatory cell infiltrates. Time-course studies indicated that IL-1 beta mRNA levels were decreased within 24 hr of initiating misoprostol therapy. This reduction in IL-1 beta mRNA levels was transient because levels were not reduced after 1 week of treatment with the PGE1 analog.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of short-term treatment with the prostaglandin E1 (PGE1) analog misoprostol on inflammatory mediator production in murine lupus nephritis. 770 69

An autopsied case of systemic lupus erythematosus with pulmonary hypertension is reported. A 29-year-old woman with a seven-year history of polyarthralgia, butterfly rash, nephrotic syndrome and Raynaud's phenomenon was admitted because of progressive dyspnea on exertion. Tests for antinuclear antibody, anti-cardiolipin antibody and lupus anticoagulant were positive. Echocardiographic examination revealed right ventricular hypertrophy and a moderate pericardial effusion. Estimated systolic pulmonary arterial pressure was 53 mmHg. Despite treatment with corticosteroids including pulse methylprednisolone therapy, lipo-PGE1 and warfarin, she died of progressive congestive heart failure. Postmortem examination of the pulmonary vasculature revealed findings consistent with plexogenic pulmonary arteriopathy, without evidence of vasculitis, fibrinoid necrosis, or thromboemboli.
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PMID:Pulmonary hypertension in systemic lupus erythematosus: a report of an autopsied case. 800 Jan 4

We report a case of systemic lupus erythematosus with cutaneous vasculitis and peripheral neuropathy. Results of laboratory examinations revealed lupus anticoagulant in the patient's serum. His lower limbs showed asymmetry. A sural nerve biopsy specimen showed modest degeneration of nerve fibers and incomplete obstruction of nutrient vessels. His cutaneous vasculitis responded to treatment with high-dose corticosteroid, but the lower limb neuropathy responded incompletely. Daily intravenous prostaglandin E1 treatment improved his neurologic and cutaneous symptoms markedly. Our case implied that nutritional vascular ischemia caused by lupus anticoagulant is involved in the pathogenesis of lupus neuropathy in addition to well-known peripheral nerve vasculitis. It also documented the effectiveness of intravenous prostaglandin E1 in the treatment of systemic lupus erythematosus.
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PMID:Systemic lupus erythematosus with ischemic peripheral neuropathy and lupus anticoagulant: response to intravenous prostaglandin E1. 897 Jul 75

Hemorrhagic cystitis is a potentially life-threatening complication in systemic lupus erythematosus (SLE). No safe, effective and conservative treatment exists for patients who fail to respond to standard therapy. We report a 17-year-old girl with SLE who suffered from severe hemorrhagic cystitis. Initially, she received frequent red blood cell and platelet transfusions, continuous bladder irrigation, and blood clots were evacuated. Numerous kinds of treatment were tried, including electrocoagulation of bleeding foci, prostaglandin E1 bladder instillation, and hyperbaric oxygen. However, she remained severely anemic and thrombocytopenic necessitating daily transfusions of blood products. After intravesical formalin instillation was performed twice, the hematuria ceased completely.
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PMID:Formalin treatment of refractory hemorrhagic cystitis in systemic lupus erythematosus. 987 30

Chronic leg ulcers have various causes and can be difficult to treat, although topical treatments, including basic fibroblast growth factor and PGE1, have been used. We applied an allogeneic cultured dermal substitute (CDS) to eight patients with intractable ulcers. The patients had various underlying diseases, including diabetes mellitus, systemic lupus erythematosus, antiphospholipid syndrome, necrobiosis lipoidica, stasis dermatitis, livedo vasculopathy, and rheumatoid arthritis. The CDS was prepared by seeding cultured human fibroblasts on a spongy matrix consisting of hyaluronic acid and atelocollagen. Good clinical results were achieved, as demonstrated by reepithelization, healthy granulation tissue formation, and a subsequent decrease in wound size. Daily dressing changes became unnecessary when the allogeneic CDS was used. Based on these results, we suggest that CDS may be useful for the treatment of intractable skin ulcers.
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PMID:Treatment of intractable skin ulcers caused by vascular insufficiency with allogeneic cultured dermal substitute: a report of eight cases. 2186 Oct 88

Some connective tissue diseases are associated with an increased risk of developing neoplastic disorders. Association of rheumatoid arthritis and systemic lupus erythematosus with lymphoma, and of dermatomyositis with different malignancies including ovarian and lung cancer has been reported in the literature. Here, we describe a 58 years old man with systemic sclerosis (SSc) for 15 years who developed severe lumbar pain when he was admitted for intravenous infusion of prostaglandin E1 for his fingertip ulcers. He was found to have abnormal skeletal imaging. Laboratory tests including bone marrow aspiration and biopsy determined multiple myeloma causing extensive bony infiltration. The patient expired after two cycles of VAD and Bortezomide chemotherapy.
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PMID:Visual problem and low back pain as initial manifestation of multiple myeloma complicating pre-existing systemic sclerosis. 2471 97


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