Variety Of Anti-inflammatory Agents Research Articles

COVID-19 and multisystem inflammatory syndrome in children: A systematic review and meta-analysis.

BackgroundMultisystem inflammatory syndrome in children (MIS‐C) associated with coronavirus disease 2019 has been increasingly recognized. However, the clinical features of MIS‐C and the differences from Kawasaki disease remain unknown. The study aims to investigate the epidemiology and clinical course of MIS‐C.MethodsPubMed and EMBASE were searched through August 30, 2020. Observational studies describing MIS‐C were included. Data regarding demographic features, clinical symptoms, laboratory, echocardiography and radiology findings, treatments, and outcomes were extracted. Study‐specific estimates were combined using one‐group meta‐analysis in a random‐effects model.ResultsA total of 27 studies were identified including 917 MIS‐C patients. The mean age was 9.3 (95% confidence interval [CI], 8.4–10.1). The pooled proportions of Hispanic and Black cases were 34.6% (95% CI, 28.3–40.9) and 31.5% (95% CI, 24.8–38.1), respectively. The common manifestations were gastrointestinal symptoms (87.3%; 95% CI, 82.9–91.6) and cardiovascular involvement such as myocardial dysfunction (55.3%; 95% CI, 42.4–68.2), coronary artery aneurysms (21.7%; 95% CI, 12.8–30.1) and shock (65.8%; 95% CI, 51.1–80.4), with marked elevated inflammatory and cardiac markers. The majority of patients received intravenous immunoglobulin (81.0%; 95% CI, 75.0–86.9), aspirin (67.3%; 95% CI, 48.8–85.7), and corticosteroids (63.6%; 95% CI, 53.4–73.8) with a variety of anti‐inflammatory agents. Although myocardial dysfunction improved in 55.1% (95% CI, 33.4–76.8) at discharge, the rate of extracorporeal membrane oxygenation use was 6.3% (95% CI, 2.8–9.8) and the mortality was 1.9% (95% CI, 1.0–2.8).ConclusionOur findings suggest that MIS‐C leads to multiple organ failure, including gastrointestinal manifestations, myocardial dysfunction and coronary abnormalities, and has distinct features from Kawasaki disease.

Synthesis of novel Naphthalene COX inhibitors for anti-inflammatory activity

Micropropagation and shoot regeneration of Cistus creticus ssp. CreticusPanagiotis Madesis, Elpiniki Konstantinidou, Athanasios Tsaftaris, Irini Nianiou-Obeidat

Suppressive effects of Lithospermum erythrorhizon extracts on lipopolysaccharide-induced activation of AP-1 and NF-κB via mitogen-activated protein kinase pathways in mouse macrophage cells

A variety of anti-inflammatory agents have been shown to exert chemopreventive activity via targeting of transcription factors such as NF-kappaB and AP-1. Lithospermum erythrorhizon (LE) has long been used in traditional oriental medicine. In this study, we demonstrated the inhibitory effects of LE extracts on lipopolysaccharide (LPS)-stimulated production of inflammatory cytokines. As an underlying mechanism of inhibition, LE extracts reduced LPS-induced transactivation of AP-1 as well as NF-kappaB in mouse macrophage cells. Electrophoretic mobility shift assays indicated that LE extracts inhibited the DNA binding activities of AP-1 and NF-kappaB. In addition, phosphorylation of IkappaB-alpha protein was suppressed by LE extracts. Moreover, LE extracts inhibited c-Jun N-terminal kinase and extracellular signal-regulated signaling pathways. Our results suggest that the anti-inflammatory activity of LE extracts may be mediated by the inhibition of signal transduction pathways that normally lead to the activation of AP-1and NF-kappaB. These inhibitory effects may be useful for chemoprevention of cancer or other chronic inflammatory diseases.

New Therapies and Preventive Approaches for Necrotizing Enterocolitis: Report of a Research Planning Workshop

The National Institute of Child Health and Human Development and the Digestive Diseases Interagency Coordinating Committee held a workshop, chaired by Dr. W. Allan Walker, on July 10-11, 2006, to identify promising leads in necrotizing enterocolitis (NEC) research. The goals of the workshop were to identify new approaches to the prevention and treatment of NEC, to define basic and translational mechanisms of potential approaches to NEC, and to develop recommendations for clinical studies to reduce the incidence of NEC. Workshop participants implicated prematurity, introduction of enteral feedings, gastrointestinal bacterial colonization, gut motility, proinflammatory cytokines, impaired gut blood flow, and various neonatal complications in the pathogenesis of NEC. They concluded that a unifying hypothesis encompassing these pathogenetic factors is the uncontrolled exuberant inflammatory response to bacterial colonization that characterizes the intestine of premature infants. The inflammatory cascade appears to offer multiple targets for interventions with a variety of anti-inflammatory agents, including human milk and probiotics. Because of the rapidity with which the inflammatory response gets out of control in infants with NEC, workshop participants agreed that searching for ways to prevent NEC will be more rewarding than trying to identify ways to treat the condition once it has become established.

Mechanism-Oriented Therapy for Multiple Systems Organ Failure

Damage caused by systemic sepsis is only in part caused by the viable microbe and therefore treatable by antibiotics. Most damage is produced by host defenses. The rationale for anti-inflammatory therapy in severely septic patients is based on these concepts. A variety of anti-inflammatory agents are being studied that might help "tide the patient through" the initial phases of the septic event until antimicrobial therapy has had a chance to work. Antibiotics certainly help minimize the suppurative complications of bacteremia/septicemia. The initial approach to the septic patient should be rapid but thorough, permitting data to be gathered that will permit decisions ultimately to be made as to whether or not sepsis was actually present and what appropriate therapeutic agents are best for longer term treatment. The septic patient will continue to provide a challenge to the clinician. The better one understands the mechanisms involved in the pathophysiology of the development of severe sepsis, septic shock, and the syndrome of MSOF, the better will become the clinical management of such patients. Also, development of additional such insights will certainly permit important new therapeutic modalities to evolve.

Additional inhibitors of rat serum acute phase alpha 2-macroglobulin levels. Effect of 6-mercaptopurine and some lipoxygenase and cyclo-oxygenase inhibitors.

With the use of a previously described electroimmunoassay, 4 more compounds were found to depress acute phase alpha 2-macroglobulin levels in rat serum following the injection of turpentine. The compounds, meclofenamic acid, dextropropoxyphene, 5,8,11,14-eicosatetraynoic acid and 6-mercaptopurine are thus grouped with a variety of anti-inflammatory agents, cyclo-oxygenase inhibitors, hypolipidaemics and colchicine, all of which share the property of reducing the concentration of alpha 2-macroglobulin in rat serum. Compounds with immunosuppressant properties, namely amethopterin, azathioprine, cyclophosphamide and 5-fluorouracil, the steroids, betamethasone and dexamethasone, the lipoxygenase inhibitor, nordihydroguaiaretic acid, and MK477, a compound said to stimulate prostaglandin synthesis, did not reduce serum levels of the acute phase protein. 6-Mercaptopurine, a compound known to show anti-inflammatory properties in some systems, proved to be the strongest inhibitor found so far. The rat acute phase protein electroimmunoassay may thus be an effective screen for detecting a new class of anti-inflammatory agents. Knowledge of the mechanisms of action of drugs that depress rat serum alpha 2-macroglobulin concentrations may promote understanding of the control of acute phase protein production by the liver.

The Anti-Inflammatory Agents Used in Rheumatic Disorders

The objectives of nonspecific anti-inflammatory therapy are, for the most part, to relieve symptoms. In selected patients such therapy may also slow, prevent, or reverse the destructive effects of the inflammatory process. It is well to remember that none of the wide variety of anti-inflammatory agents is without some inherent toxicity, although some agents are obviously much more toxic than others. The physician prescribing these agents must keep in mind both the potential benefits and the potential risks attendant to their use. In this way he can balance potential benefit against potential risk and arrive at the most rational drug therapy for any given rheumatic disorder.