Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immune complex-induced vascular damage can be markedly suppressed by treatment of rats with either prostaglandin (PG)E1 or its stable derivative, 15-(S)-15-methyl PGE1, but not with PGF2 alpha. In addition, PGD2 and PGE2 also show suppressive effects. The PGE1 derivative is considerably more effective than PGE1 and shows potent anti-inflammatory activity even after oral administration. Suppression of the vasculitis reaction is reflected by a greatly diminished increase in vasopermeability, indicating little or no vascular damage. In suppressed animals, the infiltration of neutrophils is greatly reduced, and those leukocytes that have appeared at tissue sites fail to show phagocytic uptake of immune complexes. In suppressed animals, the skin sites nevertheless show deposits of immune complexes and C3 fixation in vascular walls. Neutrophils harvested from the blood of rats treated with PGE1 show depressed responsiveness in chemotaxis and in enzyme secretion after incubation with chemotactic peptide. These studies indicate that certain PG have potent anti-inflammatory activity, which may be related to their effects on leukocytes.
 ...
PMID:Suppression of immune complex vasculitis in rats by prostaglandin. 15 14

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.
 ...
PMID:Reversal of the vasospastic component of lupus vasculopathy by infusion of prostaglandin E1. 178 1

Prostaglandin E's (PGEs) are used therapeutically in newborn infants to maintain an open ductus arteriosus when there is obstruction to systemic or pulmonary arterial blood flow. These prostaglandins have been shown to have other systemic physiologic effects, such as vasodilation, inhibition of platelet aggregation, and enhancement of chemotactic-factor-mediated polymorphonuclear leukocyte infiltration, with resultant loss of lysosomal granules and possibly the generation of free radicals. We have recently seen previously unreported vascular lesions in 3 infants with hypoplastic left heart syndrome treated with usual therapeutic doses of PGE1 for prolonged periods. At autopsy, pulmonary vascular changes reflecting increased flow were present in each infant. One infant had a necrotizing vasculitis, sometimes associated with infarcts, in the lungs and in small muscular arteries in other organs. The form and severity of the vascular changes appear to be related to the duration of PGE1 administration.
 ...
PMID:Pulmonary vascular changes associated with prolonged prostaglandin E1 treatment. 365 41

Oral administration of a stable analog of prostaglandin E1 (PGE1) 15-(S)-15-methyl-prostaglandin E1, can suppress both chronic adjuvant-induced polyarthritis and acute immune complex-induced vasculitis in a dose dependent manner. Histopathologic studies of tibiotarsal joints from rats with adjuvant disease showed suppression of arthritis in animals treated with the PGE1 analog from time of adjuvant challenge. This study represents the first demonstration of suppressed experimental polyarthritis by an orally administered prostaglandin. Suppression of the acute immune complex-induced vasculitis was demonstrated using 15- methyl-PGE1 administered orally 12 hours prior to antigen-antibody challenge. Diminution of tissue injury resulting from immune complex-induced vasculitis is reflected by a decrease in vaso-permeability, indicating suppressed vascular damage in animals treated with prostaglandin. These studies demonstrate the potential use of orally active prostaglandins as an antiinflammatory agent.
 ...
PMID:Suppression of acute and chronic inflammation by orally administered prostaglandins. 645 4

Several auto-immune diseases have been described in human beings. Though the exact aetiological agent(s) is not known, clinical or subclinical viral infections and certain drugs are known to induce them. Hyperactivity of B-cells, possibly due to the loss of normal regulatory control by T-cells may account for the increased synthesis of auto-antibodies in these diseases. Prostaglandins (PGs) are known to regulate immune response and fibrous tissue formation. Deficiency of PGE1 and/or thromboxane A2 (TxA2) and excess PGE2 seem to activate B-cells and suppress T-Cell function and enhance fibrosis. Viruses are known to block the enzyme delta-6-desaturase necessary for PGE1 synthesis and thus depress cell-mediated immune response. Drugs known to cause autoimmune disorders also seem to block PGE1 and/or TxA2 synthesis and enhance PGE2 formation which may lead to excess auto-antibody formation. Drugs like colchicine known to enhance TxA2 formation and the biological actions of PGE1 were found to be of benefit in Behcet's syndrome, vasculitis, amyloidosis, scleroderma and in controlling the auto-immune disease in adjuvant arthritis in rats, the renal disease in NZB/W mice and passively transferred vasculitis. Thus altered PG function may play a major role in auto-immunity.
 ...
PMID:Auto-immunity and prostaglandins. 703 43

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.
 ...
PMID:Prostaglandins. Their potential in clinical medicine. 743 93

We recently encountered a patient with mitral insufficiency, accompanied by PN (polyarteritis nodosa), who developed a cardiac rupture immediately after a mitral valve replacement. The patient was a 60-year-old woman. After she was diagnosed as having mitral stenosis and insufficiency in 1968, the patient developed congestive heart failure and underwent repeated hospital admissions and discharges. In 1989, she was diagnosed as having PN and began to receive a high-dose steroid therapy (prednisolone; total dose 5245 mg). Because of transient brain ischemia and exacerbation of the symptoms of heart failure, the patient underwent mitral valve replacement on December 19, 1991. For anesthesia, oxygen, fentanyl, midazolam and vecuronium were administered. During surgery, catecholamine, nitroglycerin and prostaglandin E1 were continuously infused intravenously. The patient was weaned smoothly from the cardiopulmonary bypass. The operation was completed in about 6 hours. Her postoperative course was satisfactory until she suddenly developed left ventricular rupture and died 6 hours after surgery. The rupture seemed to be attributable to a weakening of the myocardial wall following long-term, high-dose steroid therapy, and to myocardial degeneration caused by PN-associated necrotizing vasculitis of myocardial arterioles.
 ...
PMID:[Anesthetic management of a patient with polyarteritis nodosa who suddenly developed cardiac rupture after valve replacement]. 790 39

"Lipo-PGE1", PGE1 incorporated into lipid microspheres (LM), has marked antiplatelet and vasodilatory actions. Since LM largely accumulate in inflamed vascular lesions, lipo-PGE1 shows a marked efficacy for treating vascular diseases such as atherosclerosis and vasculitis. Another recently developed drugs against intractable vasculitis are monoclonal antibodies to surface antigens of lymphocytes. Treatment with humanized anti-CDw52, and subsequent anti-CD4 monoclonal antibodies was reported to have brought remission up to 42 months.
 ...
PMID:[Development of new drugs for intractable vasculitis--lipo-PGE1 and monoclonal antibody]. 793 10

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.
 ...
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.
 ...
PMID:Systemic lupus erythematosus with ischemic peripheral neuropathy and lupus anticoagulant: response to intravenous prostaglandin E1. 897 Jul 75


1 2 Next >>