Disease relevance of Colo-Pleon

• Sulfasalazine-induced exacerbation of ulcerative colitis [1].
• Our investigations show that 5-aminosalicylic acid is the active moiety of sulfasalazine and that this effective metabolite may be an alternative to sulfasalazine in inflammatory bowel disease [2].
• Suppression of experimental autoimmune encephalitis by sulfasalazine [3].
• Sulfasalazine toxic reactions. Hepatitis, fever, and skin rash with hypocomplementemia and immune complexes [4].
• Infertility from sulfasalazine seems only temporary [5].

Psychiatry related information on Colo-Pleon

• Thus, two periods for sulfasalazine-induced amnesia were found in coincidence with the two phases of NF-kappaB activation previously described (immediately and 6 h after training) [6].
• After correction for hypertension, diabetes and hypercholesterolemia, 'MTX or SSZ ever' and 'MTX, SSZ and HCQ ever' showed significant CVD risk reduction [7].

High impact information on Colo-Pleon

• Therapeutic efficacy of sulfasalazine and its metabolites in patients with ulcerative colitis and Crohn's disease [2].
• When blocking proteasome-mediated degradation of IkappaBalpha, we could demonstrate that sulfasalazine interfered with IkappaBalpha phosphorylation, suggesting a direct effect on an IkappaBalpha kinase or on an upstream signal [8].
• Methotrexate and sulfasalazine promote adenosine release by a mechanism that requires ecto-5'-nucleotidase-mediated conversion of adenine nucleotides [9].
• Treatment of SW620 colon cells with sulfasalazine inhibited TNFalpha-, LPS-, or phorbol ester- induced NF-kappaB activation [8].
• These data describe a defect in RA lymphocytic GTase, with associated abnormal G(0) changes, which is corrected by sulphasalazine [10].

Chemical compound and disease context of Colo-Pleon

• In this study we demonstrate the sulfasalazine, at concentrations found in the stool of patients being treated for ulcerative colitis, blocks the synthesis of both 5-HETE and 5,12 diHETE by human neutrophils [11].
• The data suggest that olsalazine is effective for the treatment of ulcerative colitis and is well tolerated among patients intolerant to sulfasalazine [12].
• There was no appreciable change in this effect when models were fit to adjust for sulfasalazine dose, duration of disease, age at symptom onset, prednisone dose, sulfa allergy, sex, race, or family history of colon cancer [13].
• Perianal abscess appeared to respond to sulfasalazine and anal fissure to prednisone or azathioprine [14].
• Radiographic disease progression was significantly slower with leflunomide and sulphasalazine than with placebo (p<0.01) [15].

Biological context of Colo-Pleon

• RESULTS: Treatment of hepatic stellate cells with sulfasalazine (0.5-2.0 mmol/L) induced apoptosis of activated rat and human hepatic stellate cells [16].
• Findings on semen analyses rapidly improved in all patients on withdrawal of sulphasalazine, which resulted in four pregnancies in three of the wives [17].
• METHODS: The effects of sulfasalazine and its moieties on NF-kappaB signaling were evaluated using electromobility shift, transfection, and immune complex kinase assays [18].
• Antibiotic resistance in Escherichia coli from patients on sulphasalazine [19].
• Sulfasalazine (also as a representative of the salicylates) inhibited the diabetes-induced upregulation of several inflammatory gene products, which are regulated by NF-kappaB, including vascular cell adhesion molecule, intracellular adhesion molecule-1, inducible nitric oxide synthase, and cyclooxygenase-2 in whole-retinal lysate [20].

Anatomical context of Colo-Pleon

• Sulfasalazine inhibits the synthesis of chemotactic lipids by neutrophils [11].
• Sulfasalazine inhibited tumor necrosis factor alpha-induced activation of endogenous IKK in Jurkat T cells and SW620 colon cells, as well as the catalytic activity of purified IKK-alpha and IKK-beta in vitro [18].
• Reintroduction of sulphasalazine was followed by rapid deterioration in the semen of two patients [17].
• Effect of disodium azodisalicylate on electrolyte transport in rabbit ileum and colon in vitro. Comparison with sulfasalazine and 5-aminosalicylic acid [21].
• Actions of sulfasalazine and 5-aminosalicylic acid as reactive oxygen scavengers in the suppression of bile acid-induced increases in colonic epithelial cell loss and proliferative activity [22].

Associations of Colo-Pleon with other chemical compounds

• We compared the in vitro effects of azodisalicylate, sulfasalazine, and 5-aminosalicylic acid on rabbit intestinal electrolyte transport [21].
• Randomised comparison of combined step-down prednisolone, methotrexate and sulphasalazine with sulphasalazine alone in early rheumatoid arthritis [23].
• X-rays of the hands and feet at the start and after 24 and 48 weeks of treatment were available for 28 patients treated with hydroxychloroquine and 22 treated with sulphasalazine [24].
• This double-blind randomised trial compared leflunomide with placebo and sulphasalazine in active rheumatoid arthritis [15].
• The plasma concentration of orosomucoid increased significantly among the patients in the sulfasalazine group but not in the metronidazole group [25].

Gene context of Colo-Pleon

• The known IKK inhibitor sulfasalazine did not compromise TRAF1 expression [26].
• NF-kappaB-independent actions of sulfasalazine dissociate the CD95L- and Apo2L/TRAIL-dependent death signaling pathways in human malignant glioma cells [27].
• Low-dose sulfasalazine also prevented morphologically evident tight junction disruption induced by TNF-alpha [28].
• However, at doses below those needed for nuclear factor-kappaB inhibition, sulfasalazine was able to prevent TNF-alpha-induced barrier dysfunction, MLCK up-regulation, and MLC phosphorylation [28].
• Importantly, the specific removal of Pneumocystis from the preparation, or the pretreatment of AECs with sulfasalazine, a potent and specific inhibitor of NF-kappaB, nearly completely abrogated the chemokine response to Pneumocystis [29].

Analytical, diagnostic and therapeutic context of Colo-Pleon

• Drug therapy: Sulfasalazine [30].
• Here we provide evidence that the transcription factor NF-kappaB is a target of sulfasalazine-mediated immunosuppression [8].
• A multicenter double-blind study of the effectiveness of sulfasalazine and 6-methylprednisolone, alone and in combination, was conducted on 452 patients with Crohn's disease [31].
• Pending a larger case-control study, folate supplementation during sulfasalazine administration is recommended to possibly prevent the complication of dysplasia or cancer in ulcerative colitis [13].
• Prior therapy with sulfasalazine in 14, adrenocorticosteroids in 12, inpatient total parenteral nutrition in 7, and/or surgical resections in 6 failed to suppress disease activity [32].

References