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Azulfidine (Sulfasalazine)

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Generic Azulfidine is used for the treatment of mild to moderate ulcerative colitis, as adjunctive therapy (with other medications) in the treatment of severe ulcerative colitis, for the treatment of Crohn's disease, for the treatment of rheumatoid arthritis or ankylosing spondylitis.

Other names for this medication:
Azulfidina, Salazopyrin, Sulazine, Sulfazine

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Also known as:  Sulfasalazine.


Generic Azulfidine is used for the treatment of mild to moderate ulcerative colitis, as adjunctive therapy (with other medications) in the treatment of severe ulcerative colitis, for the treatment of Crohn's disease, for the treatment of rheumatoid arthritis or ankylosing spondylitis.

Generic Azulfidine is a sulfonamide that decreases inflammation and help regulate the immune system in various areas of the body.

Azulfidine is also known as Sulfasalazine.

Generic name of Generic Azulfidine is Sulfasalazine.

Brand name of Generic Azulfidine is Azulfidine.


Doses range: from 500 mg to 2000 mg, and dosing intervals range: from every 6 hours to every 12 hours, depending on the clinical condition of the patient.

Generic Azulfidine should be taken with a full glass of water after meals or with food to minimize stomach upset.

Patients with kidney diseases may need to use lower doses of Generic Azulfidine.

If you want to achieve most effective results do not stop taking Generic Azulfidine suddenly.


If you overdose Generic Azulfidine and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Azulfidine are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Generic Azulfidine if you are allergic to Generic Azulfidine components or to a salicylate (eg, aspirin) or a sulfonamide (eg, sulfisoxazole).

Be veru careful with Generic Azulfidine if you are pregnant, planning to become pregnant or breast-feeding.

Do not take Generic Azulfidine if you have the blood disease porphyria or a blockage of the intestine or urinary tract.

Some medical conditions may interact with Generic Azulfidine.

Be veru careful with Generic Azulfidine if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be veru careful with Generic Azulfidine if you have allergies to medicines, foods, or other substances.

Be veru careful with Generic Azulfidine if you have kidney or liver problems, a blood disorder, a gastrointestinal infection, glucose-6-phosphate dehydrogenase deficiency, or asthma.

Some medicines may interact with Generic Azulfidine.

Be veru careful with Generic Azulfidine if you are taking anticoagulants (eg, warfarin) or methotrexate because the actions and side effects of these medicines may be increased; anticoagulants (eg, warfarin) or beta-blockers (eg, propranolol) because their effectiveness may be decreased by Generic Azulfidine; methenamine because the risk of crystals in the urine is increased.

Do not share this medicine with others for whom it was not prescribed.

Do not use this medicine for other health conditions.

If using this medicine for an extended period of time, obtain refills before your supply runs out.

It can be dangerous to stop Generic Azulfidine taking suddenly.

azulfidine drug class

Nineteen patients (12 children and 7 adults) with severe Crohn's disease, all of whom were dependent on corticosteroids, were treated with 6-mercaptopurine. All patients received a daily dose of 6-mercaptopurine of 50 mg; in two pediatric patients with a poor response after 2 months, the dosage was increased to 75 mg/day. A complete or partial response to 6-mercaptopurine therapy was noted in 47% of patients, and therapy failed in 53%. The age of the patients, prior resection, or initial symptoms did not influence the response. The clinical response was better in male than in female patients and in patients with involvement of both the small intestine and the colon than in those with only enteritis. 6-Mercaptopurine is a possible alternative to long-term corticosteroid therapy or surgical treatment in selected patients with severe Crohn's disease.

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Since the discovery of the NF-kappaB transcription factor in 1986 and the cloning of the genes coding for NF-kappaB and IkappaB proteins, many studies demonstrated that this transcription factor can, in most cases, protect transformed cells from apoptosis and therefore participate in the onset or progression of many human cancers. Molecular studies demonstrated that ancient widely used drugs, known for their chemopreventive or therapeutic activities against human cancers, inhibit NF-kappaB, usually among other biological effects. It is therefore considered that the anti-cancer activities of NSAIDs (non-steroidal anti-inflammatory drugs) or glucocorticoids are probably partially related to the inhibition of NF-kappaB and new clinical trials are being initiated with old compounds such as sulfasalazine. In parallel, many companies have developed novel agents acting on the NF-kappaB pathway: some of these agents are supposed to be NF-kappaB specific (i.e. IKK inhibitors) while others have wide-range biological activities (i.e. proteasome inhibitors). Today, the most significant clinical data have been obtained with bortezomib, a proteasome inhibitor, for the treatment of multiple myeloma. This review discusses the preclinical and clinical data obtained with these various drugs and their putative future developments.

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Sulfasalazine is effective in decreasing clinically acute gastrointestinal toxicities. Long-term follow-up with the subjects will help to determine the net effect of sulfasalazine on the radiation-induced gastrointestinal injuries.

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Novel carrier-linked azo prodrugs of 4 and 5-aminosalicylic acids (4-ASA and 5-ASA respectively) using the same drugs as carriers in different permutations and combinations were designed for targeting colon affected with inflammatory bowel disease (IBD). Improved hydrophilic nature of the prodrugs assisted in minimizing their absorption in upper GIT and efficient delivery of the active drugs to colon as evidenced from their stability in aqueous buffers (pH 1.2 and 7.4) and upper GIT homogenates with 68-91% release on incubation with rat cecal matter. Amongst the series, 4A4AAZ (prodrug of 4-ASA with 4-ASA) at a dose of 53 mg/Kg was found to be the most promising candidate as it substantially alleviated the quantifying markers of colonic inflammation in TNBS-induced experimental colitis in Wistar rats. Moreover it displayed significantly lower GI toxicity (at ten times higher dose). 5-ASA- induced pancreatitis and sulfapyridine-induced adverse effects on liver that are characteristic of sulfasalazine were not observed with 4A4AAZ. It could be explored further as a potential candidate for IBD patients intolerant to pancreatitis induced by oral administration of 5-ASA.

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We have conducted a meta-analysis of 16 placebo-controlled trials of single drug therapy in ulcerative colitis (UC) for both induction (11 trials) and maintenance of remission (five trials). A total of 468 and 343 patients, respectively, was studied. Various clinical criteria of success were analyzed. The Dersimonian-Laird method for meta-analysis was used to calculate the risk difference. Therapeutic advantage, defined as the difference between drug and placebo response, was also determined. Using various criteria of success, single drug therapy for the induction of remission conferred a therapeutic advantage of 37-48% over placebo. In trials for maintenance of remission, the therapeutic advantage at 6 months was 21%, whereas at 12 months the therapeutic advantage rose to 46% because of a decline in placebo responders with time. In conclusion, meta-analysis has established a standard of reference against which future drug trials can be compared. This standard of reference for drug and placebo rates, as well as the corresponding therapeutic advantages, can help determine the relative value of newer agents in the therapy of UC.

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Dyslipidaemia in rheumatoid arthritis, is associated with accelerated atherosclerosis. A nonrandomised trial was conducted to find out the proportion of rheumatoid arthritis patients suffering from dyslipidaemia and change in lipid levels after an intervention with antirheumatic drugs in a tertiary care centre in Eastern India from April 2006 to July 2008. The trial was done on 161 diagnosed patients of rheumatoid arthritis (fulfilling the American College of Rheumatology criteria) on lipid levels. Lipids estimations were done enzymatically by semi-autoanalyser and dyslipidaemia was defined by taking the cut-off value of National Cholesterol Education Programme-Adult Treatment Panel III (NCEP-ATP III) guidelines. Patients with other comorbid illness and on statins were excluded. Disease activity score 28 (DAS-28) was also employed for evaluating disease activity. Patients were followed up to 10 -12 weeks for repeat lipid level estimation. Using the high cut-off values of NCEP-ATP III, 39.1% of the patients showed dyslipidaemia in initial visit. Low high density lipoprotein cholesterol (HDL-C) was the commonest abnormality seen in 37.2%. In the follow-up study after getting disease modifying antirheumatic drugs (methotrexate, sulfasalazine, hydroxychloroquine) therapy, 19.9% patients had dyslipidaemia again and there were increase in total cholesterol, low density lipoprotein cholesterol, HDL-C but triglyceride was reduced. Low HDL-C again became the commonest (17.9%) and rise in HDL-C level was statistically significant. DAS-28 showed a good reduction and significant negative correlation with HDL-C. Lipid abnormalities, common in Indian patients with rheumatoid arthritis, are also observed in Eastern India. Low HDL-C being the commonest abnormality. Disease activity in rheumatoid arthritis is inversely related to the lipid levels.

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All BS patients seen at the NYU Hospital for Joint Diseases in the US and the Kameda Medical Center and St. Luke's International Hospital in Japan between 2003 and 2010 were included. Diagnosis of BS was made on the basis of clinical manifestations and the clinical decisions of experienced specialists familiar with BS. We classified the patients into complete and incomplete types based on their symptoms; both complete or incomplete types were assumed to fulfil the Japanese criteria.

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Ninety-three cases who were definitely diagnosed as having ankylosing spondylitis at active stage were randomly divided into a medication group (n=46) and an observation group (n=47). The observation group were treated by needle-pricking the main points, Neck No. 2 nerve, Neck No. 5 nerve point, etc., combined with spinal rotation massage, and the medication group were treated with Azulfidine. Changes of cumulative score of arthralgia and arthroncus, function of joint, Keitel test, and ESR and CRP before and after treatment were observed.

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The influence of inflammatory bowel disease (IBD) and its therapy upon pregnancy is a frequent consideration before and after conception. We looked at the influence of disease activity and drug therapy during pregnancy on fetal outcome in 147 pregnancies in 124 women. Patients were divided into two groups; 46 (28 ulcerative colitis, 18 Crohn's disease) who received drug treatment during pregnancy, and 101 (42 ulcerative colitis, 59 Crohn's disease) who received no treatment. The frequency of fetal complications was higher than in the general population in the "treated" patients, but was not higher than in patients with IBD who received no drug treatment. Active IBD was present in 43% of the treated patients whose pregnancies resulted in fetal complications. Of patients with Crohn's disease whose pregnancies resulted in fetal complications, active IBD was present in 62.5%. Thus, our experience suggests that patients with IBD who receive therapy during pregnancy are at greater risk of fetal complications than the average population, but that disease activity is more likely to be responsible for this risk than drug treatment. This risk is much more evident in active Crohn's disease than in ulcerative colitis.

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We analyzed DMARD treatment data for 3,734 patients with rheumatoid arthritis (RA) from 1998 to 2009 at Juntendo Hospital in Tokyo, Japan. The DMARD usage rate per month was determined to evaluate RA treatment history in the last decade. We also evaluated continuation rates of nonbiologic DMARDs in single and combination therapies and number of nonbiologic DMARD combination therapies used in each patient.

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azulfidine dosage 2016-12-02

Crohn's disease (CD) is a chronic inflammatory disorder of the gastrointestinal tract. Evidence for treatment with 5-aminosalicylic acid (5- Nolvadex Cheap Uk ASA) drugs is conflicting. We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) to examine this issue.

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NF-kappaB activation of spermatogenic epithelium is related to apoptosis of spermatogenic cells. Sulfasalazine can prevent apoptosis in spermatogenic cells after the experimental testicular torsion through prevention of NF Celexa 300 Mg -kappaB activation.

azulfidine and alcohol 2016-07-26

Coated mesalazine (Mesasal) 1.5 g daily or sulphasalazine 3.0 g daily for Effexor 500 Mg eight weeks. Compliance monitored by pill counts.

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Male Wistar rats were used for the in-vivo and ex-vivo studies. In-vitro studies were performed using human leukemia peripheral blood monocyte cells (THP-1 cells) grown in Lanoxin Dosage Tablets continuous culture.

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Agranulocytosis is a Diamox Drug Interactions life-threatening disorder, often caused by drugs. Incidences or risks of drug-induced agranulocytosis are not well known, since it is rare.

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In testing for convergent validity a strong correlations (p < 0.0001) were observed between both SASDAS and ASDAS-ESR (r = 0.835), and ASDAS-CRP (r = 0.805). Strong correlations (p < 0.0001) were also found between SASDAS and BASDAI score (r = -0.886), SASDAS and BASFI scores (rho = 0.588) and SASDAS and EQ-5D scores (rho = -0.579). The cross-classification showed a significant overall agreement (defined as the percentage of observed exact agreements) for SASDAS vs ASDAS-ESR (weighted k = 0.704) and for SASDAS vs ASDAS-CRP (k = 0.661). The most efficient composite measure in detecting change was the ASDAS-CRP (ES 1.95 and SRM 0.97). The responsiveness of SASDAS was slightly higher to ASDAS Pamelor Normal Dosage -ESR with an ES of 1.62 and 1.33, and an SRM of 0.88 and 0.71, respectively. The BASDAI appear to be the less responsive (ES = 0.93 and SRM = 0.52). The area under ROC curve of the SASDAS gives similar results to those provided by ASDAS CRP/ESR. The score changes of all combinations were highly correlated (p < 0.0001).

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The chemopreventive and therapeutic efficacy of the cyclooxygenase (COX) inhibitor ibuprofen (IB) and of sulfasalazine (SASP), a drug that targets the antioxidant xc- system, were exploited in the experimental model of 3-methylcholantrene (3-MCA)-induced mouse sarcoma. The chemopreventive treatments gave unsatisfactory results because administration of IB one day after the 3-MCA injection only slightly delayed the tumor development, whereas SASP dispensed under the same conditions resulted in accelerated tumorigenesis. Similarly, the therapeutic treatment with either drug, administrated daily from the tumor detection, decreased the proliferation rate of tumor cells and increased the survival of treated mice only at a low extent. Remarkably, the combined chemopreventive treatment with IB and therapeutic treatment with SASP displayed a better efficacy, with strong delay of sarcoma growth, reduced tumor size and increased survival of treated mice. The two drugs target not only tumor cells but also tumor-associated macrophages that were dramatically decreased in the tumor infiltrate of mice subjected to the combined treatment. The synergistic effects of the association between a broad anti-inflammatory compound, such as IB, and a redox-directed drug, such as SASP, shed new light in the role of inflammation and of the redox response Pamelor Drug Class in chemical tumorigenesis and point to the combined chemopreventive plus therapeutic treatment with IB and SASP as a promising novel approach for antitumor therapy.

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Significant advances have occurred in Amoxil Capsules our understanding of the pathophysiology, diagnosis, and classification of the spondyloarthritides and effective treatments are available.

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At week 24 (beginning of the step-up period), subjects in the 2 immediate-treatment groups demonstrated a greater reduction in the DAS28-ESR compared with those in the 2 step-up groups (3.6 versus 4.2; P < 0.0001); no differences between the combination-therapy regimens were observed. Between week 48 and week 102, subjects randomized to the step-up arms had a DAS28-ESR clinical response that was not different from that of subjects who initially received combination therapy, regardless of the treatment arm. There was no significant difference in the DAS28-ESR between subjects randomized to oral triple therapy and those Aciphex Dosage Information randomized to receive MTX plus etanercept. By week 102, there was a statistically significant difference in the change in radiographic measurements from baseline between the group receiving MTX plus etanercept and the group receiving oral triple therapy (0.64 versus 1.69; P = 0.047).