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The Cochrane Database of Systematic... Oct 2012Ulcerative colitis (UC) is a chronic inflammatory condition of the colon characterized by episodes of disease activity and symptom-free remission.There is paucity of... (Review)
Review
BACKGROUND
Ulcerative colitis (UC) is a chronic inflammatory condition of the colon characterized by episodes of disease activity and symptom-free remission.There is paucity of evidence regarding the efficacy and safety of complementary or alternative medicines for the management of UC. Curcumin, an anti-inflammatory agent, has been used in many chronic inflammatory conditions such as rheumatoid arthritis, esophagitis and post-surgical inflammation. The efficacy of this agent for maintenance of remission in patients with UC has not been systematically evaluated.
OBJECTIVES
The primary objective was to systematically review the efficacy and safety of curcumin for maintenance of remission in UC.
SEARCH METHODS
A computer-assisted literature search of MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials, and the Cochrane Inflammatory Bowel Disease Specialized Trial Register was performed on July 11, 2012 to identify relevant publications. Proceedings from major gastroenterology meetings and references from published articles were also searched to identify additional studies.
SELECTION CRITERIA
Randomized placebo-controlled trials (RCT) of curcumin for maintenance of remission in UC were included. Studies included patients (of any age) who were in remission at the time of recruitment. Co-interventions were allowed.
DATA COLLECTION AND ANALYSIS
Two authors independently extracted data and assessed the methodological quality of the included studies using the Cochrane risk of bias tool. Data were analyzed using Review Manager (RevMan 5.1). We calculated the relative risk (RR) and 95% confidence interval (95% CI) for each dichotomous outcome. For continuous outcomes we calculated the mean difference (MD) and 95% CI.
MAIN RESULTS
Only one trial (89 patients) fulfilled the inclusion criteria. This trial randomized 45 patients to curcumin and 44 patients to placebo. All patients received treatment with sulfasalazine or mesalamine. The study was rated as low risk of bias. Curcumin was administered orally in a dose of 2 g/day for six months. Fewer patients relapsed in the curcumin group than the placebo group at six months. Four per cent of patients in the curcumin group relapsed at six months compared to 18% of patients in the placebo group (RR 0.24, 95% CI 0.05 to 1.09; P = 0.06). There was no statistically significant difference in relapse rates at 12 months. Twenty-two per cent of curcumin patients relapsed at 12 months compared to 32% of placebo patients (RR 0.70, 95% CI 0.35 to 1.40; P = 0.31). A total of nine adverse events were reported in seven patients. These adverse events included sensation of abdominal bulging, nausea, transient hypertension, and transient increase in the number of stools. The authors did not report which treatment group the patients who experienced adverse events belonged to. The clinical activity index (CAI) at six months was significantly lower in the curcumin group compared to the placebo group (1.0 + 2.0 versus 2.2 + 2.3; MD -1.20, 95% CI -2.14 to -0.26). The endoscopic index (EI) at six months was significantly lower in the curcumin group than in the placebo group (0.8 + 0.6 versus 1.6 + 1.6; MD -0.80, 95% CI -1.33 to -0.27).
AUTHORS' CONCLUSIONS
Curcumin may be a safe and effective therapy for maintenance of remission in quiescent UC when given as adjunctive therapy along with mesalamine or sulfasalazine. However, further research in the form of a large scale methodologically rigorous randomized controlled trial is needed to confirm any possible benefit of curcumin in quiescent UC.
Topics: Anti-Inflammatory Agents, Non-Steroidal; Colitis, Ulcerative; Curcumin; Drug Therapy, Combination; Humans; Maintenance Chemotherapy; Mesalamine; Randomized Controlled Trials as Topic; Recurrence; Sulfasalazine
PubMed: 23076948
DOI: 10.1002/14651858.CD008424.pub2 -
Alimentary Pharmacology & Therapeutics Aug 2003Previously, clinicians have had few choices in treating mild to moderate Crohn's disease. They currently treat these Crohn's disease patients with oral mesalamine and... (Meta-Analysis)
Meta-Analysis Review
Previously, clinicians have had few choices in treating mild to moderate Crohn's disease. They currently treat these Crohn's disease patients with oral mesalamine and antibiotics. This treatment approach is based on the safety of these agents, and the perception that they are effective. This perception regarding efficacy may be influenced by publication bias. This review examines the efficacy and safety data of the conventional corticosteroids, mesalamine, sulfasalazine, budesonide and antibiotics for inducing the remission of mild to moderate Crohn's disease from randomized controlled trials, and proposes an evidence-based treatment approach. Sulfasalazine has demonstrated modest efficacy when Crohn's disease is confined to the colon. Mesalamine has no clear benefit over placebo in treating active Crohn's disease. Conventional corticosteroids effectively induce remission but are associated with unwanted adverse effects. Budesonide has similar efficacy to conventional steroids with far fewer adverse effects. Antibiotics have not consistently demonstrated efficacy. We propose a new evidence-based approach which suggests inducing remission of mild to moderate Crohn's disease with budesonide 9 mg/day for patients with ileal and/or right colonic involvement; sulfasalazine for those with disease limited to the colon; and conventional steroids for high disease activity, those who failed budesonide and those with left-sided disease who are allergic or intolerant to sulfasalazine.
Topics: Administration, Topical; Algorithms; Anti-Bacterial Agents; Anti-Inflammatory Agents; Anti-Inflammatory Agents, Non-Steroidal; Budesonide; Controlled Clinical Trials as Topic; Crohn Disease; Gastrointestinal Agents; Glucocorticoids; Humans; Mesalamine; Sulfasalazine
PubMed: 12895211
DOI: 10.1046/j.1365-2036.2003.01661.x -
Experimental Animals Nov 2018The aim of this study, was to determine the effect of sulfasalazine for different periods of time reduces disseminated intravascular coagulation, inflammation and organ...
The aim of this study, was to determine the effect of sulfasalazine for different periods of time reduces disseminated intravascular coagulation, inflammation and organ damages by inhibiting the nuclear factor kappa beta pathway. The study was performed with 30 Wistar albino rats and the groups were established as Control group, LPS group; endotoxemia was induced with LPS, SL5 group: sulfasalazine (300 mg/kg, single dose daily) was administered for 5 days before the LPS-induced endotoxemia, and LS group: sulfasalazine (300 mg/kg, single dose) was administered similtenously with LPS. Hemogram, biochemical, cytokine (IL-1β, IL-6, IL-10, TNF-α) and acute phase proteins (HPT, SAA, PGE2) analyzes and oxidative status values were measured from blood samples at 3 and 6 h after the last applications in the all groups. The rats were euthanized at 6 h and mRNA levels of BCL2 and BAX genes were examined from liver and brain tissues. Sulfasalazine reduced the increased IL-1β, IL-6, TNF-α and PGE levels and significantly increased anti-inflammatory cytokine IL-10 levels. In addition, decreasing of ATIII level was prevented in the SL5 group, and decreasing of fibrinogen levels were prevented in the LS and SL5 groups within first 3 h. In LPS group, leukocyte and thrombocyte levels were decreased, however sulfasalazine application inhibited decreases of leukocyte levels in LS and SL5 groups. In addition, sulfasalazine inhibited the decrease of total antioxidant capacity and unchanged apoptosis in brain and liver. In conclusion, the use of sulfasalazine in different durations reduce the excessive inflammation of endotoxemia cases.
Topics: Acute-Phase Proteins; Animals; Anti-Inflammatory Agents, Non-Steroidal; Cytokines; Endotoxemia; Inflammation Mediators; Lipopolysaccharides; Male; NF-kappa B; Oxidative Stress; Rats; Rats, Wistar; Signal Transduction; Sulfasalazine
PubMed: 29731490
DOI: 10.1538/expanim.18-0029 -
Gut Oct 2002
Topics: Aminosalicylic Acids; Colitis, Ulcerative; Crohn Disease; Enema; Humans; Inflammatory Bowel Diseases; Mesalamine; Sulfasalazine; Suppositories
PubMed: 12235078
DOI: 10.1136/gut.51.4.548 -
Gut May 2003
Topics: Aminosalicylic Acids; Anti-Inflammatory Agents, Non-Steroidal; Colonic Diseases, Functional; Humans; Mesalamine; Sulfasalazine
PubMed: 12692073
DOI: 10.1136/gut.52.5.771 -
Postgraduate Medical Journal Jun 2007Sulfasalazine is a well established disease-modifying anti-rheumatic drug commonly used in the treatment of rheumatic disorders and inflammatory bowel disease....
Sulfasalazine is a well established disease-modifying anti-rheumatic drug commonly used in the treatment of rheumatic disorders and inflammatory bowel disease. Sulfasalazine was generally well tolerated in clinical trials, the most frequently reported adverse effects being adverse gastrointestinal effects, headache, dizziness and rash; myelosuppression can also occur. We are now reporting the first case of autoimmune thrombocytosis following sulfasalazine treatment.
Topics: Aged; Antirheumatic Agents; Arthritis, Psoriatic; Humans; Male; Purpura, Thrombocytopenic, Idiopathic; Sulfasalazine
PubMed: 17551063
DOI: 10.1136/pgmj.2006.055194 -
Toxicological Sciences : An Official... Feb 2022An emerging clinical issue associated with immune-oncology agents is the collateral effects on the tolerability of concomitant medications. One report of this phenomenon...
An emerging clinical issue associated with immune-oncology agents is the collateral effects on the tolerability of concomitant medications. One report of this phenomenon was the increased incidence of hypersensitivity reactions observed in patients receiving concurrent immune checkpoint inhibitors (ICIs) and sulfasalazine (SLZ). Thus, the aim of this study was to characterize the T cells involved in the pathogenesis of such reactions, and recapitulate the effects of inhibitory checkpoint blockade on de-novo priming responses to compounds within in vitro platforms. A regulatory competent human dendritic cell/T-cell coculture assay was used to model the effects of ICIs on de novo nitroso sulfamethoxazole- and sulfapyridine (SP) (the sulfonamide component of SLZ) hydroxylamine-specific priming responses. The role of T cells in the pathogenesis of the observed reactions was explored in 3 patients through phenotypic characterization of SP/sulfapyridine hydroxylamine (SPHA)-responsive T-cell clones (TCC), and assessment of cross-reactivity and pathways of T-cell activation. Augmentation of the frequency of responding drug-specific T cells and intensity of the T-cell response was observed with PD-1/PD-L1 blockade. Monoclonal populations of SP- and SPHA-responsive T cells were isolated from all 3 patients. A core secretory effector molecule profile (IFN-γ, IL-13, granzyme B, and perforin) was identified for SP and SPHA-responsive TCC, which proceeded through Pi and hapten mechanisms, respectively. Data presented herein provides evidence that drug-responsive T cells are effectors of hypersensitivity reactions observed in oncology patients administered ICIs and SLZ. Perturbation of drug-specific T-cell priming is a plausible explanation for clinical observations of how an increased incidence of these adverse events is occurring.
Topics: Drug Hypersensitivity; Humans; Incidence; Lymphocyte Activation; Sulfasalazine; Sulfonamides
PubMed: 34850240
DOI: 10.1093/toxsci/kfab144 -
Journal of Neurochemistry Sep 2012
Topics: Amyotrophic Lateral Sclerosis; Animals; Anti-Inflammatory Agents, Non-Steroidal; Dinoprostone; Free Radicals; Humans; Sulfasalazine
PubMed: 22730915
DOI: 10.1111/j.1471-4159.2012.07843.x -
Theranostics 2020Loss of iron-sulfur cluster function predisposes cancer cells to ferroptosis by upregulating iron-starvation response, but the role of glutaredoxin 5 (GLRX5) silencing...
Loss of iron-sulfur cluster function predisposes cancer cells to ferroptosis by upregulating iron-starvation response, but the role of glutaredoxin 5 (GLRX5) silencing in ferroptosis remains unknown. We examined the role of GLRX5 functional loss in promoting ferroptosis in cisplatin-resistant head and neck cancer (HNC) cells. The effects of sulfasalazine treatment and GLRX5 gene silencing were tested on HNC cell lines and mouse tumor xenograft models. These effects were analyzed concerning cell viability and death, lipid reactive oxygen species (ROS) and mitochondrial iron production, labile iron pool, mRNA/protein expression, and malondialdehyde assays. Cyst(e)ine deprivation, erastin, or sulfasalazine induced ferroptosis in HNC cells, which was relatively less sensitive in cisplatin-resistant HNC cells. Sulfasalazine or cyst(e)ine deprivation-induced ferroptosis resulted from increased lipid peroxidation and intracellular free iron, which were significantly promoted by short-interfering RNA or short hairpin RNA (shRNA) targeting GLRX5 (<0.05). GLRX5 silencing activated iron-starvation response and boosted up intracellular free iron through the iron-responsive element-binding activity of increased iron regulatory protein (increased transferrin receptor and decreased ferritin). These effects were rescued by resistant GLRX5 cDNA but not by catalytically inactive mutant GLRX5 K101Q. The same results were noted in an mouse model transplanted with vector or shGLRX5-transduced HNC cells and treated with sulfasalazine. Our data suggest that inhibition of GLRX5 predisposes therapy-resistant HNC cells to ferroptosis.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Cell Line, Tumor; Cisplatin; Drug Resistance, Neoplasm; Ferroptosis; Glutaredoxins; Head and Neck Neoplasms; Humans; Iron; Male; Mice; Mitochondria; Mutation; RNA Interference; Sulfasalazine; Xenograft Model Antitumor Assays
PubMed: 32685019
DOI: 10.7150/thno.46903 -
Cleveland Clinic Journal of Medicine Mar 2004Diagnosing the spondyloarthropathies--chronic inflammatory diseases of the spine and peripheral joints that share several distinctive features--is challenging and... (Review)
Review
Diagnosing the spondyloarthropathies--chronic inflammatory diseases of the spine and peripheral joints that share several distinctive features--is challenging and depends on careful evaluation of the history, physical examination, and radiographs. The recent use of tumor necrosis factor inhibitors is exciting and may represent true disease-modifying drugs for these conditions.
Topics: Antirheumatic Agents; Back Pain; Blood Sedimentation; C-Reactive Protein; Diagnosis, Differential; Humans; Spondylarthropathies; Sulfasalazine
PubMed: 15055243
DOI: 10.3949/ccjm.71.3.184