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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:

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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.

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Aminosalicylates have a wide range of anti-inflammatory and immunomodulatory effects. Oral salazosulfapyridine (SASP) and 5-aminosalicylic acid (5-ASA) are the 'first-line' therapy for induction of remission in mild to moderate active ulcerative colitis (UC). SASP, which is consisted of 5-ASA and sulfapyridine, has greater incidence of side effects. 5-ASA is a therapeutically active compound, while sulfapyridine is related to adverse effects. For this reason, 5-ASA formulas exclusive of sulfapyridine were developed and they enabled higher dose of 5-ASA administration without adverse effects. Topical treatment by 5-ASA enema or SASP suppository should be considered for the treatment of proctitis or distal type of UC. Oral aminosalicylate therapy is also effective for the maintenance of remission in UC. Therefore, aminosalicylates are key drugs for the treatment of UC.

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Ulcerative colitis is an inflammatory disorder characterized by neutrophils infiltration, oxidative stress, upregulation of pro-inflammatory mediators and cytokines. Cavidine possesses anti-inflammatory activity and has been used to treat various inflammatory diseases but its effect on ulcerative colitis has not been previously explored. The present study aims to evaluate the effect of cavidine on acetic acid-induced ulcerative colitis in mice. Colitis mice induced by intra-rectal acetic acid (5%, v/v) administration received cavidine (1, 5 and 10mg/kg, i.g) or sulfasalazine (500mg/kg, i.g) for seven consecutive days. After euthanized by cervical dislocation, colonic segments of mice were excised for clinical, macroscopic, biochemical and histopathological examinations. Results suggested treatment with cavidine significantly decreased mortality rate, body weight loss, disease activity index (DAI), wet colon weight, macroscopic and histological score when compared with that of acetic acid-induced controls. In addition, administration of cavidine effectively modulated expressions of MPO, GSH, SOD and MDA. Furthermore cavidine inhibited the level of TNF-α and IL-6 in the serum and colon tissue in response to the regulation of p65 NF-κB protein expression. All these results indicated cavidine exerts marked protective effect in experimental colitis, possibly by regulating the expression of oxygen metabolites, NF-κB and subsequent pro-inflammatory cytokines production.

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NF-kappaB promotes cell survival against external stress such as radiation. We examined whether NF-kappaB decoy transfection enhances the antiproliferative effects of radiation on vascular smooth muscle cells (VSMCs) in vitro. The irradiation induced activation or nuclear translocation of NF-kappaB p65 in VSMCs was confirmed by immunofluorescence. NF-kappaB decoy transfection resulted in inhibition of the radiation-induced NF-kappaB activation in VSMCs and the subsequent reduction of transcription and translocation of ICAM, iNOS, and TNF-alpha, downstream molecules under the control of NF-kappaB. By using MTT assay, NF-kappaB decoy augmented the antiproliferative effects of radiation, where the effect of low dose radiation (2 and 8-Gy) of the cells transfected with NF-kappaB decoy was equivalent to the high dose (16-Gy) irradiated non-transfected cells at 48 h after irradiation: 1.06+/-0.16, 1.11+/-0.22, 1.20+/-0.25, respectively. The decrease in proliferation and survival of the radiation treated cells by flow cytometry analysis showed that NF-kappaB inhibition did not show any additive effects on the cell cycle of the irradiated VSMCs, while apoptosis was significantly increased after NF-kappaB decoy transfection in the irradiated VSMCs (apoptosis fraction: 13.33+/-2.08% vs. 26.29+/-7.43%, for radiation only vs. radiation+NF-kappaB decoy transfection, P < 0.05). In addition, at 48 h, NF-kappaB decoy transfection dose dependently (10 microM vs. 20 microM) inhibited proliferation of 16Gy-irradiated VSMCs, and showed greater antiproliferative efficacy than 100 microM sulfasalazine, a specific NF-kappaB inhibitor. These results indicate that NF-kappaB inhibition reduces proliferation and survival of irradiated VSMCs, likely by increased apoptosis rather than additive cell cycle arrest and suggest the possibility of adjunctive gene therapy using NF-kappaB decoy to improve efficacy and to decrease the adverse effects of intracoronary radiation therapy.

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We studied prospectively the efficacy of combination therapy with DMARDs. The study was designed as a randomized trial and a single DMARD or two or three DMARD combinations were administered to 180 consecutive, age- and sex-matched patients with active RA, each of whom was followed up for a period of 2 years under treatment. Patients were divided into 3 groups which did not differ with regard to demographic, clinical and laboratory parameters. Patients in group I were treated with a single DMARD [methotrexate (MTX) 7.5-15 mg/week or sulfasalazine (SSZ) 1-2 g/day or hydroxychloroquine (HCQ) 200 mg/day], group II with MTX + SSZ or MTX + HCQ, and group III with a combination of all three drugs. Patients were re-evaluated at regular intervals by means of clinical and biochemical tests designed to detect specific rheumatic activity. Radiological assessments were also performed and scored according to Larsen by the same radiologist who was blinded to the treatment groups.

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A total of 5,664 patients met selection criteria. The median time to discontinuation of index drug differed significantly across index medications (range, 98.5 days [sulfasalazine] to 177.5 days [Multi-Matrix System mesalamine], P  less than  0.0001). Patients on Multi-Matrix System mesalamine were less likely to discontinue (63.3% vs. ≥ 68.6%, P = 0.001) and more likely to adhere to their medication (MPR ≥ 0.8; 23.1% vs. ≤ 17.4%, P  less than  0.0001) than patients on other medications. Patients on mesalamine delayed-release (13.8%) or Multi-Matrix System mesalamine (14.3%) had lower switch rates than the patients on balsalazide (17.2%) or sulfasalazine (17.8%), P = 0.01. Significant predictors of nonpersistence included index medication versus Multi-Matrix System mesalamine (balsalazide disodium: HR = 1.21, 95% CI = 1.07-1.36; mesalamine delayed-release: HR = 1.21, CI = 1.11-1.32; sulfasalazine: HR = 1.40, CI = 1.25-1.57), female gender (HR = 1.16, CI = 1.09-1.23), never receiving specialist care (HR = 1.14, CI = 1.07-1.21), preferred provider organization (PPO) versus health maintenance organization (HR = 1.14, CI = 1.04-1.24), and Medicare fee for service or self-insured health plan versus commercial plan (HR = 1.29, CI = 1.10-1.52). Significant variables associated with nonadherence with 5-ASA treatment (PDC less than  0.8) included not switching medication (OR = 1.90, CI = 1.58-2.29), age less than  65 (OR = 1.90, CI = 1.56-2.31), index medication as compared with Multi-Matrix System mesalamine (balsalazide disodium: OR = 1.43, CI = 1.10-1.85; mesalamine delayed-release: OR = 1.41, CI = 1.19-1.68; sulfasalazine: OR = 1.66, CI = 1.30, 2.12), female gender (OR = 1.33, CI = 1.17-1.52), residing in different regions as compared with the Midwest region (the South [OR = 1.40, CI = 1.20-1.64] and Northeast [OR = 1.29, CI = 1.05-1.58]), no use of rectal forms during the post-index period (OR = 1.28, CI = 1.08-1.50), no use of immunosuppressive/biologic agents during the post-index period (OR = 1.70, CI = 1.35-2.14), never receiving specialist care (OR = 1.25, CI = 1.08-1.44), and Medicaid/Medicare versus commercial plan (OR = 1.48, CI = 1.03-2.13).

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B cells from patients with RA showed hyperactivity to stimulation by Staphylococcus aureus Cowan I. Sulfasalazine significantly inhibited this B cell hyperactivity in a dose dependent manner. The kinetic study and a decrease in 3H-thymidine incorporation on Day 3 indicate that sulfasalazine inhibited the early phase (0-48 h) of B cell proliferation in these patients. Sulfapyridine also inhibited B cell hyperactivity in these patients, but 5-aminosalicylic acid and N-acetylsulfapyridin had no significant effect.

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Contrary to traditional teaching, endoscopic and histological patchiness of inflammation and rectal sparing are common during the course of disease in treated UC and seem to be unrelated to specific therapy.

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A total of 3,724 ETN-MTX patients and 818 triple therapy patients were eligible. At 1 year, 27.9% who were taking ETN-MTX and 18.2% using triple therapy were adherent to all agents in their regimen (P < 0.0001), and 29.4% who were taking ETN-MTX and 23.2% using triple therapy were persistent (P < 0.001). After adjusting for confounders, ETN-MTX patients had significantly greater odds of being adherent (odds ratio [OR] 1.79, 95% confidence interval [95% CI] 1.47-2.17) and persistent (OR 1.45, 95% CI 1.20-1.72) compared with patients using triple therapy.

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One of the main characteristics of nonthyroidal illness (NTI) is a decrease in serum triiodothyronine, partly caused by a decrease in liver deiodinase type 1 (D1) mRNA and activity. Proinflammatory cytokines have been associated with NTI in view of their capability to decrease D1 and thyroid hormone receptor (TR)beta1 mRNA expression in hepatoma cells. Proinflammatory cytokine induction leads to activation of the inflammatory pathways nuclear factor (NF)kappaB and activator protein (AP)-1. The proinflammatory cytokine interleukin (IL)-1beta decreases thyroid hormone receptor (TR)beta1 mRNA in an NFkappaB-dependent way. The aim of this study was to unravel the effects of IL-1beta on endogenous TRalpha gene expression in an animal model and in a liver cell line. The TRalpha gene product is alternatively spliced in TRalpha1 and TRalpha2, TRalpha2 is capable of inhibiting TRalpha1-induced gene transcription. We showed that both TRalpha1 and TRalpha2 mRNA decreased not only after lipopolysaccharide administration in liver of mice, but also after IL-1beta stimulation of hepatoma cells (HepG2). Using the NFkappaB inhibitor sulfasalazine and the AP-1 inhibitor SP600125, it became clear that the IL-1beta-induced decrease in TRalpha mRNA expression in HepG2 cells can only be abolished by simultaneous inhibition of NFkappaB and AP-1. The IL-1beta-induced TRalpha1 and TRalpha2 mRNA decrease in HepG2 cells is the result of decreased TRalpha gene promoter activity, as evident from actinomycin D experiments. Cycloheximide experiments showed that the decreased promoter activity is independent of de novo protein synthesis and therefore most likely due to posttranslational modifications such as phosphorylation or subcellular relocalization.

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1. Chronic inflammatory diseases have been shown to be associated with NF-kappaB activation and impaired apoptosis of immune cells. The aim of the present study was to investigate if sulfasalazine and its colonic metabolites 5-aminosalicylic acid (5ASA) and sulfapyridine affect NF-kappaB/Rel activation and viability of T-lymphocytes. 2. Sulfasalazine inhibits NF-kappaB/Rel activation in the murine T-lymphocyte cell line RBL5 using electrophoretic mobility shift assays. In transfection assays sulfasalazine treatment for 4 h inhibits kappaB-dependent transcription with an IC50 value of approximately 0.625 mM. 3. Higher doses or prolonged treatment result in cell death of T-lymphocytes in a dose- and time-dependent manner. Cell death is caused by apoptosis as judged by DNA fragmentation, annexin V and Apo 2.7 staining. Induction of apoptosis is a fast event with 50% apoptotic cells after a 4 h incubation with 2.5 mM sulfasalazine. The ED50 value for apoptosis induction after 24 h treatment was approximately 0.625 mM. 4. In contrast, 5ASA and sulfapyridine neither inhibit NF-kappaB/Rel activation nor induce apoptosis in T-lymphocytes at doses up to 5.0 mM. 5. These results demonstrate that sulfasalazine, but not 5ASA or sulfapyridine, strongly inhibits NF-kappaB activation and potently induces apoptosis in T-lymphocytes. Inhibition of NF-kappaB/Rel activation and subsequent clearance of activated T-lymphocytes by apoptosis might thus explain the beneficial effects of sulfasalazine in the treatment of chronic inflammatory disorders.

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A placebo-controlled trial of sulfasalazine (SSZ) in patients with oligoarticular- and polyarticular-onset JIA yielded the data for this study. Data were obtained from 418 sets of radiographs of the clinically involved and contralateral joints (at study entry and at 6 months' followup) from 66 JIA patients. The Dijkstra score assesses the presence or absence of swelling, osteopenia, joint space narrowing, growth abnormalities, subchondral bone cysts, erosions, and malalignment. These signs were combined in the Dijkstra composite score, to assess inflammation (DI), growth (DG), and damage (DD). Progression was defined as an increase in either the DG or the DD score. Scores were evaluated among all radiographs, a standard set of films (hand, foot, and knee), and per patient. All scores were used to explore differences between the 2 treatment groups.

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Despite changing the drug's properties by crushing it for incrementally increasing administration, we successfully desensitized two patients on three occasions with 5-aminosalicylic acid.

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To examine how agents currently used to treat inflammatory bowel disease affect MAdCAM-1: induced by tnf-alpha in an in vitro model of inflammatory bowel disease.

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To describe radiologic features of patients with juvenile idiopathic arthritis (JIA) in a standardized manner, to test the reliability and feasibility of this description, and to correlate these features with clinical signs as a first step in the development of a standardized assessment method.

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Infertility and the outcome of pregnancy has been examined in 112 married women with Crohn's disease who were below the age of 45 years. Fifty four patients were available for study. The infertility rate (12%) was similar to that seen in the general population. Patients who had active disease at the time of conception continued to have symptoms and they mostly failed to go into satisfactory remission despite therapy. Furthermore, there was a high rate (35%) of spontaneous abortion in this group. In contrast, patients whose disease was in remission at the time of conception had a normal pregnancy and, in the majority, the Crohn's disease remained quiescent.

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Forty five patients with acute ulcerative colitis were randomly allocated to receive (a) sulphasalazine, (b) levamisole, or (c) a combination of sulphasalazine and levamisole. Each group contained 15 patients. The ulcerative colitis activity index (UCAI), the remission and relapse rates were compared at three monthly intervals for one year. The UCAI fell in each group. Detailed analysis of all clinical and biochemical parameters used for estimation of UCAI showed that the only difference was in patients receiving combined therapy who continued to have a raised ESR and platelet count. Fewer patients, however, went into remission on levamisole therapy (46.6%) compared with the other two groups (66.6%). The cumulative relapse rate was 20% for those receiving levamisole compared with 6.6% in the other groups. Side effects were observed in 20% of patients receiving levamisole, 26% receiving sulphasalazine, and 40% in those having combined therapy. The results indicate that levamisole is unlikely to have a major role in the management of patients with ulcerative colitis.

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The aim was to study the side-effect profile and the survival characteristics of leflunomide used in a regional patient population in New Zealand (NZ).

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A comparative assessment of the patterns of IBD in Accra from 1997 to 2011.

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Sulphasalazine (SASP), used in the treatment of inflammatory bowel disease, is split into sulphapyridine (SP) and 5-aminosalicylic acid (5-ASA) in the colon. Lower plasma levels of SASP and 5-ASA as compared to those of SP may be due to different absorption rates from the colon because of different pK values and pH dependent lipid-water partition coefficients. In this study we determined the pK values of 5-ASA and its major metabolite, N-acetyl amino-salicylic acid (AcASA), by 13C-NMR spectroscopy and compared the pH dependent apparent benzene-water partition coefficients (Papp) of SASP, SP and 5-ASA with respect to their different plasma levels. The COOH group of 5-ASA had a pK value of 3.0, the -NH3+ group had 6.0, the -OH group 13.9; the -COOH group of AcASA had 2.7 and the -OH group 12.9; The Papp of SASP (0.042 +/- 0.004) and 5-ASA (0.059 +/- 0.01) were significantly lower than that of SP (0.092 +/- 0.03) (at pH 5.5).

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Orocaecal transit time (OCTT) was assessed in six healthy beagles by means of the breath hydrogen test (BH2T) and the sulphasalazine/sulphapyridine method (SLZ) after the administration of a test meal of canned food mixed with sulphasalazine. Orocaecal transit time was defined as the time taken from the oral administration of the test meal to the time when the first portion of the meal reached the colon. In five of the dogs the OCTTs assessed by the BH2T were shorter than those measured by the SLZ method by 30, 15, 45, 30 and 45 minutes. However, the median OCTT assessed by the BH2T (135 minutes, range 120 to 195 minutes) was not significantly different from that measured by the SLZ (180 minutes, range 150 to 210 minutes) and was highly correlated with it (r = 0.94, P = 0.016). The sixth dog maintained baseline hydrogen and plasma sulphapyridine readings throughout the monitoring period and the OCTT could not be measured.

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A 10-year-old girl who complained of fatigue and debilitating pain in both hips and legs for >1 year had recurrent episodes of redness and discharge in both eyes with little response to different topical medications. The diagnosis of CRMO was confirmed with the help of magnetic resonance imaging, bone scan, and bone biopsy results. She had moderate hyperemia and multiple discrete salmon-colored lesions in both palpebral and fornical conjunctivae. Biopsy revealed chronic inflammatory infiltration composed predominantly of lymphocytes forming a follicular pattern. Conjunctival lesions worsened during relapses of skeletal symptoms, improved during remission, and resolved shortly after the initiation of oral prednisolone therapy. No recurrence was observed during 16 months of follow-up.

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A literature search for relevant studies (inception to January 20, 2012) was performed using MEDLINE, EMBASE and the Cochrane Library. Review articles and conference proceedings were also searched to identify additional studies.

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Periostal new bone formation can be observed as a symptom secondary to numerous diseases. In gastrointestinal disease this hypertrophic osteoarthropathy occurs very rare. The present case report demonstrates an extensive periostal proliferation involving the long bones in a 14 years old girl with longstanding ulcerative colitis.

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To determine the effect of nicotine on colonic inflammation in the trinitrobenzenesulphonic acid (TNBS) model of inflammatory bowel disease in comparison with sulphasalazine.

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In this case report, a 58-year-old Malay woman with a 17-year history of ulcerative colitis had persistent left knee effusion and synovitis for seven years, despite remission of the primary disease. She had had multiple courses of systemic and intra-articular steroid that caused significant systemic side effects such as impaired fasting glucose, hypertension, cataract, and weight gain. She also had a total left knee replacement for secondary osteoarthritis. But the left knee synovitis and effusion recurred a month after the total knee replacement, and she was subjected to a total synovectomy the following year. In view of failure of remission despite multiple immunosuppressants (100 mg of azathioprine daily, 1 g of sulfasalazine twice a day, 10 mg of prednisolone daily, and 10 mg of methotrexate weekly), 25 mg of subcutaneous etanercept twice weekly was started. After 5 weeks of treatment, complete resolution of left knee effusion and normalization of the inflammatory markers were shown. This continued up to 12 months of follow-up while our patient was on etanercept and 10 mg of methotrexate weekly. No relapse or serious side effects were noted.

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An examination is needed of the potential adverse effects of the agents most commonly used to treat inflammatory bowel disease. Most of these therapies can be used safely to induce or maintain remissions, although some aspects of monitoring for toxicity are necessary. Aminosalicylates, including sulfasalazine and mesalamine delivery systems, are most commonly associated with sulfa-related effects (sulfasalazine) or intolerance, with rare instances of nephritis, pulmonitis, hepatitis, or worsening colitis. The immunomodulators are most commonly associated with bone marrow suppression, hepatitis, and the risk of opportunistic infections. Methotrexate is contraindicated in pregnancy. Antibiotics used for inflammatory bowel disease are generally safe and well tolerated, although metronidazole carries a long-term risk of peripheral neuropathy. The well-recognized multitude of adverse effects from corticosteroids are eliminated or minimized when rapidly metabolized steroids, such as budesonide, are used.

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To describe the treatment with DMARDs established for the first time in patients with rheumatoid arthritis (RA) or persistent arthritis (PA) in routine clinical practice in Spain.

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All patients were treated with sulfasalzine at initial doses of 1.5 g/day, increasing by 0.5 g/week to 3 g/day for 4-16 weeks. Some patients also received descendent doses for 2-12 months. Complete responses were observed in 13 patients and partial responses in seven patients. All patients reported an early resolution of the pruritus. No changes were detected in mucosal LP. Most of the patients tolerated the treatment well and only eight patients presented some minor side-effects.

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azulfidine 10 mg 2015-03-15

PBL and LPL were isolated by Ficoll-Hypopaque gradient centrifugation and the EGTA-collagenase method, respectively. PBL/LPL were stimulated with FasL, 5-ASA, sulphapyridine, and sulphasalazine for 24/48 hours and apoptosis was quantified by buy azulfidine flow cytometry (annexin V- propidium iodide method) and immunofluorescence. The molecular mechanisms of drug induced apoptosis were analysed in wild-type and FADD-/- Jurkat T cells using western blots and caspase assays.

azulfidine y alcohol 2015-12-12

5-Aminosalicylic acid (5-ASA), the presumed active moiety of sulfasalazine, has shown clinical efficacy when administered per rectum as initial therapy to patients with distal ulcerative colitis. We report the results of a randomized double-blind trial comparing nightly retention of a 4-g 5-ASA enema with continued administration of hydrocortisone enemas in 18 patients with persistent active distal ulcerative colitis after at least a 3-wk course of treatment with 100-mg hydrocortisone enemas with or without oral sulfasalazine. Continuation of hydrocortisone enemas rather than placebo was used in the control group to reflect the realistic alternative therapy likely to be employed in current practice. Response to therapy was assessed after 3 wk by comparing pretreatment and posttreatment point scores of clinical, sigmoidoscopic, and histological severity. Improvement in clinical score was achieved in seven of nine 5-ASA enema-treated patients versus one of nine hydrocortisone enema-treated patients (p less than 0.05). Sigmoidoscopic and histological improvement generally paralleled clinical improvement. We conclude that in patients with distal ulcerative colitis unresponsive to standard therapy, treatment with 5-ASA enemas results in significant short-term clinical and sigmoidoscopic improvement in a majority of cases. Moreover, a significantly greater number of refractory patients improve when switched to 5-ASA enemas than when continued on buy azulfidine standard therapy.

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Initial remission targeted therapy with the FIN-RACo DMARD combination in early RA is safe for kidneys and does not induce more short- or long-term renal complications compared buy azulfidine to traditional therapy with a single DMARD.

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The proposed mechanism of angle closure glaucoma induced by sulphonamide medication involves an idiosyncratic reaction in the uveal tissues to these systemic drugs that is associated with expansion of the extracellular tissue of the ciliary body and choroid. Management identification of sulphonamide-derived medications and immediate cessation of suspected sulphonamide-derived medication, refraction and ultrasound B scan or buy azulfidine ultrasound biomicroscopy may aid in the proper diagnosis and can also be helpful for confirmation.

azulfidine buy 2016-12-07

ABCG2 is an efflux transporter conferring multidrug resistance (MDR) on cancer cells. However, the initial molecular events leading to its up-regulation in MDR tumor cells are poorly understood. Herein, we explored the impact of drug treatment on the methylation status of the ABCG2 promoter and consequent reactivation of ABCG2 gene expression in parental tumor cell lines and their MDR sublines. We demonstrate that ABCG2 promoter methylation is common in T-cell acute lymphoblastic leukemia (T-ALL) lines, also present in primary T-ALL lymphoblast specimens. Furthermore, drug selection with sulfasalazine and topotecan induced a complete demethylation of the ABCG2 promoter in the T-ALL and ovarian carcinoma model cell lines CCRF-CEM and IGROV1, respectively. This resulted in a dramatic induction of ABCG2 messenger RNA levels (235- and 743-fold, respectively) and consequent acquisition of an ABCG2-dependent MDR phenotype. Quantitative genomic polymerase chain buy azulfidine reaction and ABCG2 promoter-luciferase reporter assay did not reveal ABCG2 gene amplification or differential transcriptional trans-activation, which could account for ABCG2 up-regulation in these MDR cells. Remarkably, mimicking cytotoxic bolus drug treatment through 12- to 24-hour pulse exposure of ABCG2-silenced leukemia cells, to clinically relevant concentrations of the chemotherapeutic agents daunorubicin and mitoxantrone, resulted in a marked transcriptional up-regulation of ABCG2. Our findings establish that antitumor drug-induced epigenetic reactivation of ABCG2 gene expression in cancer cells is an early molecular event leading to MDR. These findings have important implications for the emergence, clonal selection, and expansion of malignant cells with the MDR phenotype during chemotherapy.

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Despite buy azulfidine reports published during the study period suggesting equivalent efficacy of triple therapy and biologic DMARDs for RA, the use of triple therapy was infrequent and did not increase over time in this large nationwide study.

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Since the etiology and cure for inflammatory bowel disease remain elusive, treatment is still largely empiric. The major goals of therapy include control of bowel inflammation and alleviation of symptoms. Careful attention must be directed toward special problems when appropriate, such as short bowel syndrome, perianal disease, extraintestinal disease manifestations, and cancer surveillance. Standard and new forms of medical therapy and the approach buy azulfidine to special problems will be discussed.

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Spirulina platensis (SP) is used as a source of protein and vitamin supplement in humans without any significant side-effects. Dunaliella salina (DS) is also regarded as one of the richest natural producers buy azulfidine of carotenoid, thus used as a source of antioxidants to protect cells from oxidative damage.

azulfidine dosage 2017-02-05

This study is designed to compare the efficacy and safety of traditional Chinese medicine (TCM) with western medicine (WM) in the management of rheumatoid arthritis (RA). This is a 24-week, randomized, multicenter, single-blind study comparing TCM with WM (as used in China) carried out between June 2002 and December 2004 in nine research centers in China, involving 489 patients. Patients were randomized to receive TCM (n = 247), MTX and SSZ (n = 242). MTX was started at a dose of 5 mg to a final dose of 7.5-15 mg weekly. The maintenance dose was 2.5-7.5 mg weekly. The starting dose of SSZ was 0.25 g bid, increasing by 0.25 g a day once a week to a final dose of 0.5-1 g qid. The maintenance dose was 0.5 g tid to qid. Primary end point was the proportion of patients with response according to the American College of Rheumatology 20 % improvement criteria (ACR20) at weeks 24. At 24 weeks, ACR20 responses were 53.0 % in TCM group and 66.5 % in WM group, (P < 0. buy azulfidine 001) at 24 weeks. ACR 50 responses were 31.6 % of TCM group and 42.6 % in WM group, (P = 0.01). ACR70 responses were 12.6 % in TCM group and 17.4 % in WM group, (P = 0.14). Side effects were observed more frequently in WM group. In this study, ACR20, ACR50 responses at 24 weeks were significantly better in the WM treated group, by intention to treat (ITT) and per protocol analysis. The ACR 70 response showed no significant difference between the two groups. TCM, while effective in treating RA, appears to be less effective than WM in controlling symptoms, but TCM is associated with fewer side effects.

azulfidine 500 mg 2016-04-03

EULAR response criteria were developed combining change from baseline and level of disease activity attained during follow up. In a trial comparing hydroxychloroquine and sulfasalazine, we studied construct (radiographic buy azulfidine progression), criterion (functional capacity), and discriminant validity.

buy azulfidine 2017-09-09

Patients on once-daily dosed Multi-Matrix System mesalamine had the lowest risk of discontinuation and the highest adherence rate buy azulfidine . Multiple factors were associated with either nonpersistence or nonadherence, including multiple-daily dosed index medication, younger age, female gender, residing in the South region, PPO plan, noncommercial payer, not using immunosuppressive/biologic agents, not using rectal 5-ASA, and never receiving specialist care.

azulfidine suspension 2015-07-12

Familial Mediterranean fever (FMF) is an autosomal recessive disease characterized by self-limited attacks of fever and polyserositis. Articular involvement in early-onset FMF is a common finding characterized by non-erosive, generally asymmetric monoarthritis in large joints. Protracted FMF arthritis was reported in 2.6% of Turkish patients. An 8-year-old female who has a buy azulfidine history of FMF for 5 years applied to our hospital with complaints of persistent swelling and pain of her left knee for 8 months. The patient had been tried to be managed with non-steroidal anti-inflammatory drugs as well as intra-articulary steroids and colchicine. However, arthritis and acute phase response persisted. With sulphasalazine, complete recovery was achieved. It is our belief that sulphasalazine can be a choice of medical treatment in protracted FMF arthritis.

azulfidine drug 2015-04-04

Pyoderma gangrenosum is a rare ulcerative skin disorder mainly occurring in adults. It is seen less frequently in children. The cause is unknown buy azulfidine but it may occur in association with several disorders. Osteomyelitis is a very rare association. We report a case of pyoderma gangrenosum associated with osteomyelitis in a two-year-old girl.

azulfidine tab 2016-11-16

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Many patients with rheumatoid arthritis (RA) need continuous medication, bringing considerable costs for drugs and a Prograf 5 Mg need for monitoring adverse drug reactions. We studied drug exposure, drug costs, and adverse drug reactions in patients with RA in Sweden from 1987 to 1997.

cost of azulfidine 2015-03-08

97 RCTs (14 159 patients) were analysed for efficacy. The pooled analysis indicated that methotrexate (MTX) was more efficacious in reducing signs and symptoms, disability and radiographic Persantine Dose Calculation structural damage than other synthetic DMARDs pooled: ES for swollen joint count (SJC) versus pooled DMARDs=1.42 (95% CI 0.65 to 2.18). Leflunomide appeared to be as effective as MTX. Sulfasalazine and injectable gold were efficacious in reducing signs and symptoms and structural damage. Ciclosporin, minocycline, tacrolimus and hydroxychloroquine showed some efficacy in reducing SJC. Auranofin and D-penicillamine showed no significant superiority over placebo. The risks of cancer and of infection were increased with cyclophosphamide and azathioprine.

azulfidine drug interactions 2017-12-15

Change in JSW was determined by 5 measurement methods on 4 radiographs per patient from 107 patients included in the COBRA trial (comparing sulfasalazine alone or in combination with methotrexate and corticosteroids). For each method the number Topamax Alcohol Dependence of patients with sufficient available results was assessed (efficiency). An independent repeated measurement was carried out on a random sample of 30 patients' baseline and 1-year radiographs, to evaluate within-method reliability of change scores. Discriminatory ability (DA) of the measurement methods (between the 2 treatment arms) was compared with the DA of the Sharp-van der Heijde score (SHS) and its 2 components (erosion and JSW scores).

azulfidine tabs 2015-12-29

Cancer stem cells (CSCs) have enhanced mechanisms of protection from oxidative stress. A variant form of CD44 (CD44v), a major CSC marker, was shown to interact with xCT, a subunit of cystine-glutamate Glucovance Y Alcohol transporter, which maintains high levels of intracellular reduced glutathione (GSH) which defend the cell against oxidative stress. Sulfasalazine (SSZ) is an inhibitor of xCT and was shown to suppress the survival of CD44v-positive stem-like cancer cells both in vitro and in vivo. To find the dose of SSZ which can safely reduce the population of CD44v-positive cells in tumors, a dose-escalation study in patients with advanced gastric cancer was conducted.

azulfidine tablets 2017-06-03

We studied the Clomid Pct Dosage human teratogenic risk of sulfasalazine because this drug interferes with folate metabolism.

dosage of azulfidine 2016-09-19

MTX is still considered the anchor drug among the disease-modifying antirheumatic agents, and it is widely accepted as first line treatment in the management of rheumatoid arthritis (RA). The ultimate therapeutic goal in treatment of Lopid Cholesterol Medication RA is remission or at least low disease activity and this goal may not always be achieved with MTX monotherapy. Over the last two decades drug combinations based on MTX have been used increasingly to treat patients with RA. Combination DMARD therapy may be used initially or in a step-up strategy after MTX monotherapy in patients with persistently active disease on monotherapy. Many different MTX based combination regimens have been studied. Frequently used combinations on an MTX background include leflunomide, cyclosporine, azathioprine, sulfasalazine, gold and hydroxychloroquine. In conclusion, the use of MTX in combination with other DMARDs may still represent a valuable therapeutic option in patients who fail to DMARD monotherapy or in whom combination therapy is considered initially. However, in patients at risk for rapid radiographic progression, the early use of biologics has to be considered.

azulfidine generic 2015-04-23

Pyoderma gangrenosum (PG) is a neutrophilic dermatosis rarely seen in children. Its features have not been well characterized in children. We sought Amoxil 800 Mg to characterize the clinical features, etiologic associations, and treatment of PG in children younger than 18 years.