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)

The F1 hybrid of New Zealand black and New Zealand white mice--the NZB/NZW mouse--spontaneously develops a disease similar to human systemic lupus erythematous, characterized by impaired cell-mediated and enhanced humoral immune responses, development of antibodies to nuclear antigens, and immune complex glomerulonephritis. Because there is experimental evidence that prostaglandin E1 (PGE1) can enhance T-cell function and cell-mediated responses and suppress B-cell activity, NZB/NZW mice were treated with 200 microgram PGE1 subcutaneously once or twice daily from 6 weeks of age. PGE1 treatment of female and male mice prevents giomerular deposition of immunoglobulins and complement (monitored by immunofluorescence), and development of the proliferative glomerulonephritis (determined by light and electron microscopy) characteristic of untreated NZB/NZW mice. After 1 year of treatment, 18 of 19 female mice survived, whereas only 2 of 19 untreated control mice were alive. Male mice treated with 200 microgram PGE1 daily were also protected: 9 of 11 versus 2 of 9 untreated mice were alive at 65 weeks. PGE1 treatment did not prevent development of antibodies to nuclear material in any of the treated groups.
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PMID:Prostaglandin E1 treatment of NZB/NZW F1 hybrid mice. II. Prevention of glomerulonephritis. 14 6

We studied the effect of prostaglandins in vitro on an immune reaction mediated by T cells; adherence of lymphocytes to measles-virus-infected human epithelial cells. Normal human lymphocytes adhered to a mean +/- S.D. 20.1 +/- 5.2 per cent of these HEp-2 cells. The percentage positive cells increased to 50.3 +/- 5.7 when lymphocytes were incubated with 10(-6) M prostaglandin E1 (P less than 0.01 vs. untreated lymphocytes); 10(-8) M and 10(-10) M were as effective. Prostaglandin F2alpha had no effect on lymphocyte adherence. Prostaglandin E1 increased lymphocyte cyclic AMP five to 10 times whereas prostagladin F2alpha did not affect cellular levels of this nucleotide. Dibutyryl cyclic AMP (10(-8) M) increased lymphocyte adherence: positive human epithelial cells increased from 16.0 +/- 2.4 to 38.7 +/- 1.1 per cent (P less than 0.01). Prostagladin E1 also increased adherence of lymphocytes from patients with systemic lupus erythematosus from 21.8 +/- 5.8 to 52.5 +/- 9.2 per cent (P less than 0.01). These results indicate that prostagladin E1 and cyclic AMP may serve to stimulate T-cell function and cell-mediated immunity.
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PMID:Adherence of human peripheral blood lymphycytes to measles-infected cells. Enhancement by prostaglandin E1. 19 53

The responses of 3 patients with systemic lupus erythematosus (SLE) and progressive digital ischemia to intravenous prostaglandin E1 (PGE1) were studied prospectively in an open 3-day trial. All patients were unresponsive to corticosteroids, one had vasculitis proven by biopsy. Digital ischemia diminished in all 3 patients. In one patient, angiograms documented reappearance of a previously obstructed deep palmar arch. Vasospasm plays a role in the outcome of SLE vasculitis even in the absence of Raynaud's phenomenon. As suggested by animal models of necrotizing and leukocytoclastic vasculitis, and by case reports, intravenous PGE1 may be a relatively nontoxic, adjunctive treatment for vasculitis.
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PMID:Reversal of the vasospastic component of lupus vasculopathy by infusion of prostaglandin E1. 178 1

Prostaglandin E1 (PGE1) was administered to 4 patients with collagen diseases presenting with high levels of circulating immune complexes (CIC) in sera. Our study patients had progressive systemic sclerosis, systemic lupus erythematosus, polyarteritis nodosa, and rheumatoid arthritis. In all 4 patients, CIC levels significantly decreased after administration of PGE1 by continuous infusion at 10/ng/kg/min via central venous catheter for 72 h. In addition, the skin ulcer in a patient with PSS healed completely, and the finger necrosis in a patient with RA improved. These results suggest that PGE1 given by continuous venous infusion is effective in reducing CIC, in addition to improving peripheral vascular disorders.
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PMID:Effects of prostaglandin E1 on collagen diseases with high levels of circulating immune complexes. 227 93

We describe here a 28-years-male with AIHA and SLE who had lipid and lipoprotein abnormalities during cholestasis induced by PGE1 administration. High free cholesterol level, 792 mg/dl was found in his serum, and markedly elevated, phospholipid level 1,614 mg/dl. But, LCAT activity was within normal range in this case. An agarose gel electrophoresis of lipoproteins showed abnormal bands which were located in slow alpha 2, pre beta and slow beta, and between beta and origin point. Moreover, it was detected formation of Lp-X from serum of the patient. Serum levels of apoprotein B, C-II, C-III, and E were higher, while apoprotein A-I, A-II were very lower than reference value. From these results, it was suspected that the patient might occur transient abnormal lipid metabolism according to the drug induced hepatic injury.
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PMID:[A case of systemic lupus erythematosus showing abnormal lipoproteins due to accompanied drug induced hepatitis]. 232 24

The lupus of NZB/NZW F1 female mice is associated with immune complex glomerulonephritis and premature death. Cyclophosphamide and 15(S)-15 methyl PGE1 therapy halt disease progression. Fluorescein conjugated antibodies were utilized to label specific leukocytes and the subsets were quantitated using a Fluorescence Activated Cell Sorter. Normal outbred CD-1 female mice showed a decrease in absolute T and B cell numbers with age, but the ratio of T and B cells remained essentially constant through 9 months of age. By contrast the NZB/W female mice showed decreased numbers of total lymphocytes relative to CD-1 controls at all ages. Moreover relative to CD-1s, there was a far greater decrease in T cell numbers (7 x for NZB/W versus 2 x for CD-1) and B cell numbers failed to decrease with age. The characteristic decline in T lymphocyte numbers and relative increase in B cell numbers in NZB/W mice were corrected with cyclophosphamide and PGE1 therapy. However, there was no selective modification of T cell subsets (L3T4+ or Ly2+) with therapy. Our investigation suggests correction of the abnormal T/B cell ratio may be a useful marker of therapeutic activity in NZB/W mice.
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PMID:Cyclophosphamide and 15(S)-15 methyl PGE1 correct the T/B lymphocyte ratios of NZB/NZW mice. 233 73

Cerebral ischemia is very rare in children and young adults. There can be a multitude of causes; in many cases etiology remains undetermined. We report here on 7 cases, 11 to 25 years of age. Pathogenetic factors (lupus erythematodes, endocarditis, fibromuscular dysplasia) and risk factors (cigarette smoking, oral contraceptives) were found in 5 patients whereas in 2 cases the etiology was not determinable. Three patients were treated with low weight dextrans, two patients received prostaglandin E1, and in 2 cases regional thrombolysis was performed. Three female patients died, two with occlusions of the rostral part of the basilar artery and one with an occlusion of the carotid artery and lupus erythematodes as the primary disease. Long-term observations of the surviving patients showed good recovery from neurological deficits. Prognosis quoad sanationem seems better in this age group than in elderly patients.
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PMID:Cerebral ischemia in children and young adults. 245 51

Autoimmune New Zealand (NZ) mice exhibit a broad spectrum of T and B cell disorders. These include abnormally high levels of terminal deoxynucleotidyl transferase-positive immature T cells in bone marrow and thymus. We have shown previously that prostaglandin E1 (PGE1) treatment of the NZB/NZW F1 hybrid, a murine model of systemic lupus erythematosus (SLE), reduces to normal the percentage of immature terminal deoxynucleotidyl transferase-positive cells in bone marrow and thymus, and prevents the immune complex-induced nephritis which kills these animals. We report here that short-term (1-5 days) treatment of NZB/W mice with PGE1 increases thymocyte responsiveness to mitogens and alloantigens. The majority (greater than 90%) of cortical thymocytes agglutinated by peanut lectin (PNA+) are depleted by PGE1 treatment. However, a small population of highly functional cells persists in the PNA+ fraction after PGE1 treatment. PGE1 appears to have little or no effect on the PNA-negative (medullary) fraction of thymocytes. Our data suggest that PGE1 may exert its therapeutic effect in NZ mice by increasing the functional maturity of immature T cells.
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PMID:Effect of PGE1 treatment on in vitro thymocyte function of normal and autoimmune mice. 297 49

Cyclophosphamide is a well established cytotoxic drug used in the treatment of lymphoproliferative disorders, certain solid tumors, and nonneoplastic disorders such as nephrotic syndrome, systemic lupus erythematosus and rheumatoid arthritis. Hemorrhagic cystitis can be a complication of this drug varying between two and 40 per cent. Misoprostol, which is a synthetic prostaglandin E1 analog, was found to significantly decrease the histological damage to the bladder from cyclophosphamide. Male rats receiving misoprostol in conjunction with cyclophosphamide were found to have a reduction in ulceration, inflammation and edema of the bladder walls as compared to those treated with cyclophosphamide alone.
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PMID:Evaluation of misoprostol cytoprotection of the bladder with cyclophosphamide (Cytoxan) therapy. 309 Feb 78

We measured the production of interleukin 1 (IL-1) and prostaglandin by adherent cells from patients with systemic lupus erythematosus (SLE). Compared to normal subjects, IL-1 production in the patients was lower but prostaglandin E1 production was higher. Furthermore, examination of monocyte subsets in patients with SLE using monoclonal anti-monocyte/granulocyte antibodies disclosed abnormal expression of membrane antigens on monocytes. It is speculated that aberration of monocyte function is related to impaired monokine production and that membrane antigens play a role in immunodysregulation in patients with SLE.
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PMID:Aberration of monokine production and monocyte subset in patients with systemic lupus erythematosus. 349 75


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