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Azulfidine

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.

Description

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.

Dosage

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.

Overdose

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

Storage

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.

Contraindications

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.

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Four principal factors were obtained from the analysis results of the 18 symptoms. The factors could represent the symptoms related to joints, cold-syndrome, deficiency syndrome and heat-syndrome in traditional Chinese medicine (TCM), respectively. The effect of WM therapy was better than CM therapy. After 12 weeks of treatment, the effect of CM on patients without deficiency-syndrome was better than the patients with deficiency-syndrome. After 24 weeks of treatment, WM therapy showed better effect on patients with cold syndrome than patients without cold syndrome.

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We identified silent liver fibrosis in patients with rheumatoid arthritis (RA) using transient elastography, and investigated medication that correlated with abnormal liver stiffness measurement (LSM) values.

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Three case reports.

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To evaluate the long-term frequency of disease remissions and the progression of joint damage in patients with early rheumatoid arthritis (RA) who were initially randomized to 2 years of treatment with either a combination of 3 disease-modifying antirheumatic drugs (DMARDs) or a single DMARD.

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Inflammation in the TNBS model was assessed by measuring the tissue myeloperoxidase activity, leukotriene B4 concentration, inducible nitric oxide protein expression, the ex-vivo production of tumour necrosis factor alpha (TNFalpha), macroscopic damage score, plasma corticosterone levels and by a qualitative histological evolution. The effect of nicotine on TNFalpha production in LPS stimulated THP-1 monocyte cells in-vitro was also determined. Statistical comparisons were made using the Mann-Whitney U-test for the macroscopic damage score and an ANOVA for all other parameters.

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Outcome data were available for only 62 patients at 24 weeks. In a mixed-model analysis that imputed data for patients who dropped out, 65.0% (95% CI, 51.6% to 76.9%) of the TwHF group and 32.8% (CI, 21.3% to 46.0%) of the sulfasalazine group met the ACR 20 response criteria (P=0.001). Patients receiving TwHF also had significantly higher response rates for ACR 50 and ACR 70 in mixed-model analyses. Analyses of only completers showed similar significant differences between the treatment groups. Significant improvement was demonstrated in all individual components of the ACR response, including the Health Assessment Questionnaire disability score. Interleukin-6 levels rapidly and significantly decreased in the TwHF group. Although not statistically significant, radiographic progression was lower in the TwHF group. The frequency of adverse events was similar in both groups.

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The patient cohort comprised 397 consecutive axial SpA patients who had never been treated with tumor necrosis factor (TNF) blockers. Clinical and laboratory outcome assessments were performed at baseline, and at week 24. The following parameters were evaluated: BASDAI, ASDAS-CRP, ASDAS-ESR, and SASDAS. Construct convergent validity was evaluated by correlating SASDAS with ASDAS CRP/ESR, BASDAI, Bath Ankylosing Spondylitis Functional Index (BASFI) and EuroQol five-dimensional (EQ-5D) questionnaire. One hundred and fifty-six patients were observed longitudinally for 6 months. Responsiveness was assessed after six months of treatment with sulfasalazine (SSZ) or biologics. Internal responsiveness was evaluated by using the effect size (ES) and standardized response mean (SRM). External responsiveness was investigated by receiver operating characteristic (ROC) analysis. Change scores were compared by calculating paired t-test statistic for the difference.

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We measured the ability of lactic acid bacteria (LAB) to inhibit lipid peroxidation in vitro and to inhibit colitis outcomes, colon shortening, and myeloperoxidase activity in TNBS-induced colitis in C3H/HeN and C3H/HeJ mice. We also measured levels of the inflammatory markers interleukin (IL)-1 beta and tumor necrosis factor (TNF)-alpha and their transcription factor, NF-kappaB, in the colon by enzyme-linked immunosorbent assay and immunoblot analysis.

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The production of superoxide by the peripheral blood neutrophils of 19 patients with active rheumatoid arthritis was measured during treatment with sulphasalazine (SASP). The response to drug treatment was determined by change in plasma viscosity, CRP, early morning stiffness and articular index over a 10-point scale. Of the 19 patients studied, eight were considered to have responded well to SASP and seven to have responded poorly or not at all. Over the treatment period, plateau levels of superoxide production fell in seven of the eight responders (P = 0.028) compared with a non-significant fall in 3/7 of the non-responder groups. The initial rate of superoxide production also fell in the responder group, but this was not statistically significant. Initial values in both the responder and non-responder groups were comparable with those seen for normal controls. Analysis of drug levels showed all patients to be compliant with drug treatment; however, drug levels and neutrophil activity were not correlated. Studies of the effect of SASP and sulphapyridine on superoxide production in vitro showed no difference between good and poor responders. These results suggest that there is no inherent difference between good and poor responders regarding the susceptibility of their neutrophils to SASP. SASP's action on neutrophils, therefore, appears not to be its main mechanism of disease-modifying activity in RA.

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Current Controlled Trials ISRCTN45828668.

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azulfidine sulfasalazine dosage 2015-05-22

Rheumatoid arthritis is a common disease that causes substantial morbidity and mortality. The responses of patients with rheumatoid arthritis to treatment with a single so-called disease-modifying drug, such as methotrexate, are Serevent 25 Mg often suboptimal. Despite limited data, many patients are treated with combinations of these drugs.

azulfidine buy 2015-02-15

Non-responders to MTX had a significantly greater risk Lopressor Hct Cost of HBL than MTX-responders, despite the add-on therapies. Patients with HBL during the 12 months had greater risk of radiographic progression after 24 months. Evaluation of HBL may help to identify patients who are at risk of radiographic progression.

azulfidine tabs 2016-09-11

Alendronate treatment (25 or 75 mg kg(-1) day(-1)) resulted in a decrease in the colonic damage score and loss of body weight (at 25 mg kg(-1) day(-1) only). This was associated to a dramatic reduction in the mRNA levels of interleukin 1 beta (IL-1 beta), monocyte chemoattractant protein 1 (MCP-1) and interleukin 1 receptor antagonist (IL-1 ra). The magnitude of the beneficial effect was comparable to that of sulphasalazine (at a 6-20 fold higher dose). Thus sulphasalazine post-treatment reduced the mRNA levels of IL-1 beta/IL-1 ra and MCP-1 to the same extent as alendronate and additionally lowered Triphala 1000 Mg colonic alkaline phosphatase activity, but failed to affect body weight loss or colonic damage score. Alendronate failed to exert beneficial effects when administered intraperitoneally.

azulfidine tab 500mg 2017-11-20

Two hundred sixty-four patients with AS were recruited from Sporanox Pulse Reviews 15 clinics, randomized (double-blind) to SSZ or placebo treatment, and followed up for 36 weeks. Treatment response was based on morning stiffness, back pain, and physician and patient global assessments.

azulfidine en generic 2015-09-18

Twenty Zithromax Online patients were diagnosed in our department with LP of the skin and/or mucosa between 1985 and 2001 on the basis of clinical and histologic findings.

azulfidine buy online 2015-02-08

83 patients with severe ulcerative colitis were enrolled. Fifty patients who relapsed within two months on corticosteroid withdrawal were randomized into two groups. The azathioprine group received oral sulfasalazine (6-8 g/day), oral prednisolone (1 mg/Kg/day) and oral azathioprine (2 mg/Kg/day). The placebo group Detrol Er Dosage received oral sulfasalazine (6-8 g/day), oral prednisolone (1 mg/Kg/day) and placebo. Corticosteroids were tapered over 12-16 weeks.

azulfidine suspension 2016-07-16

Chronic urticaria is now recognized as an autoreactive disorder in a substantial fraction of patients. A serologic mediator of whealing has been demonstrated in 50-60% of patients with chronic urticaria, and autoantibodies against the high affinity IgE receptor or IgE have been detected in about half of these patients. The demonstration that chronic urticaria is frequently autoimmune has encouraged a more aggressive therapeutic approach, with the use of immunomodulatory drugs. Tofranil Online A step-by-step approach to the management of chronic urticaria is proposed, based on our personal experience and review of current medical literature, identified through Medline research and hand searching in medical journals. The non- or low-sedating H(1) receptor antagonists (antihistamines), such as cetirizine, fexofenadine, loratadine, mizolastine and, more recently, levocetirizine, desloratadine and ebastine, represent the basic therapy for all chronic urticaria patients. Older sedating antihistamines, such as hydroxyzine and diphenhydramine, may be indicated if symptoms are severe, are associated with angioedema, and if the patient is anxious and disturbed at night.Corticosteroid therapy with prednisone or methylprednisolone can be administered for a few days (7-14) if urticarial symptoms are not controlled by antihistamines and a rapid clinical response is needed. In cases of relapse after corticosteroid suspension, leukotriene receptor antagonists, such as montelukast and zafirlukast, should be tried. In our experience, remission of urticarial symptoms can be achieved in 20-50% of chronic urticaria patients unresponsive to antihistamines alone. When urticaria is unremitting and is not controlled by combined therapy with antihistamines and leukotriene receptor antagonists, prolonged corticosteroid therapy may be needed. Long-term corticosteroid therapy should be administered at the lowest dose able to control urticarial symptoms, in order to minimize adverse effects. In a few patients, however, high-dose corticosteroid therapy may have to be administered for long periods. In these patients, immunosuppressive treatment with low-dose cyclosporine can be started. This type of treatment has a corticosteroid-sparing effect and is also generally effective in patients with severe, unremitting urticaria, but requires careful monitoring of cyclosporine plasma concentration and possible adverse effects. Other immunomodulating drugs that have been tried in chronic urticaria patients include hydroxychloroquine, dapsone, sulfasalazine and methotrexate, but their efficacy has not been proven in large controlled studies. Warfarin therapy may also be considered in some patients with chronic urticaria and angioedema unresponsive to antihistamines.

azulfidine 500 mg 2015-07-21

To assess the effect of comedication with conventional synthetic disease modifying antirheumatic Cleocin Solution Dosage drugs (csDMARDs) on retention to tumour necrosis factor inhibitor (TNFi) therapy in patients with ankylosing spondylitis (AS) and undifferentiated spondyloarthritis (uSpA).

azulfidine tablets 2015-02-02

Four patients developed adrenal hemorrhage during treatment with intravenous adrenocorticotropic hormone (ACTH) for severe inflammatory bowel disease (IBD). This complication presented suddenly with upper abdominal and flank pain mimicking an acute surgical abdomen. In each patient the symptoms of the underlying bowel disease had subsided under the ACTH therapy. In our first patient the diagnosis was not made until laparotomy, but in the subsequent three patients the diagnosis was suspected by the strikingly similar clinical presentation. In each of these three latter patients the diagnosis was confirmed by sonography or computed tomography ( Combivir 300 Mg CT) scan, and surgery was avoided. All four of our patients are doing well at 1-58 months of follow-up. Signs of adrenal insufficiency occurred only in the one of our four patients, and in those six of 11 previously reported patients, who had bilateral adrenal hemorrhage. ACTH-induced adrenal hemorrhage requires stopping ACTH and maintaining corticosteroid support. The diagnosis of adrenal hemorrhage should be considered in the patient treated with ACTH who develops unexplained acute abdominal or flank pain. Failure to recognize this complication of ACTH therapy can lead to unnecessary surgery or the dangerous continuation of the offending agent.

azulfidine 1000 mg 2015-01-14

The effectiveness of the disease-modifying antirheumatic drugs (DMARDs) methotrexate (MTX), bucillamine (BUC), salazosulphapyridine (SASP) and gold sodium thiomalate (GST) over two courses of treatment with a follow-up period of at least 12 months was evaluated in 425 patients with rheumatoid arthritis.

azulfidine 10 mg 2015-06-17

189 patients were compliant with the protocol for 6 months or stopped receiving therapy because of relapse or adverse events. Of these 189 patients, 25 of the 63 patients (39.7%) in the placebo group had treatment success compared with 40 of the 68 patients (58.8% [95% CI, 46.4% to 71.3%]) in the group receiving mesalamine, 0.8 g/d (P = 0.036) and 38 of the 58 patients (65.5% [CI, 52.4% to 78.6%]) in the group receiving mesalamine, 1.6 g/d (P = 0.006). In the intention-to-treat analysis of all patients, 42 of the 87 patients (48.3%) in the placebo group had treatment success compared with 57 of the 90 patients (63.3% [CI, 52.8% to 73.8%]) in the group receiving mesalamine, 0.8 g/d (P = 0.050) and 61 of the 87 patients (70.1% [CI, 59.9% to 80.3%]) in the group receiving mesalamine, 1.6 g/d (P = 0.005). Age, sex, and race were not found to predict treatment success or failure. The mesalamine tablet was well tolerated, and no clinically significant changes were seen in hematologic, hepatic, or renal laboratory profiles.

azulfidine reviews 2017-10-13

Long-term effects of disease-modifying antirheumatic drugs are not at all satisfactory. Therefore combinations of different substances have long been studied. But no convincing recommendations could be derived from those results. Some combinations seem to be more effective than the single substances, but often have more side-effects. First of all, those types of rheumatoid arthritis must be defined which require an aggressive therapy. These may profit from combinations with sulfasalazine, methotrexate or azathioprine. But such questions may only be answered by long-term studies which can be statistically evaluated.

azulfidine brand 2017-06-29

The objective of this study is to explore the role of Traditional Chinese Medicine (TCM) pattern differentiation in identifying a subset of patients with rheumatoid arthritis (RA) who are more likely to respond to biomedical combination therapy.