A drug that is used in the management of inflammatory bowel diseases. Its activity is generally considered to lie in its metabolic breakdown product, 5-aminosalicylic acid (see MESALAMINE) released in the colon. (From Martindale, The Extra Pharmacopoeia, 30th ed, p907)
Antibacterial, potentially toxic, used to treat certain skin diseases.
An anti-inflammatory agent, structurally related to the SALICYLATES, which is active in INFLAMMATORY BOWEL DISEASE. It is considered to be the active moiety of SULPHASALAZINE. (From Martindale, The Extra Pharmacopoeia, 30th ed)
A group of 2-hydroxybenzoic acids that can be substituted by amino groups at any of the 3-, 4-, 5-, or 6-positions.
Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions.They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects.
Drugs that are used to treat RHEUMATOID ARTHRITIS.
A chemotherapeutic agent that acts against erythrocytic forms of malarial parasites. Hydroxychloroquine appears to concentrate in food vacuoles of affected protozoa. It inhibits plasmodial heme polymerase. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p970)
Drugs used for their effects on the gastrointestinal system, as to control gastric acidity, regulate gastrointestinal motility and water flow, and improve digestion.
'Amino Acid Transport System y+', also known as System Y+, is a sodium-independent cationic amino acid transporter that mediates the uptake of primarily basic amino acids, such as arginine and lysine, into cells through a facilitated diffusion process.
Diazo derivatives of aniline, used as a reagent for sugars, ketones, and aldehydes. (Dorland, 28th ed)
A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.
An antineoplastic antimetabolite with immunosuppressant properties. It is an inhibitor of TETRAHYDROFOLATE DEHYDROGENASE and prevents the formation of tetrahydrofolate, necessary for synthesis of thymidylate, an essential component of DNA.
A bile salt formed in the liver from chenodeoxycholate and glycine, usually as the sodium salt. It acts as a detergent to solubilize fats for absorption and is itself absorbed. It is a cholagogue and choleretic.
Azoles with an OXYGEN and a NITROGEN next to each other at the 1,2 positions, in contrast to OXAZOLES that have nitrogens at the 1,3 positions.
Inflammation of the COLON that is predominantly confined to the MUCOSA. Its major symptoms include DIARRHEA, rectal BLEEDING, the passage of MUCUS, and ABDOMINAL PAIN.
Therapy with two or more separate preparations given for a combined effect.
A plant genus of the family CELASTRACEAE that is a source of triterpenoids and diterpene epoxides such as triptolide.
Ubiquitous, inducible, nuclear transcriptional activator that binds to enhancer elements in many different cell types and is activated by pathogenic stimuli. The NF-kappa B complex is a heterodimer composed of two DNA-binding subunits: NF-kappa B1 and relA.
Earlier than planned termination of clinical trials.
Inflammation of the joints of the SPINE, the intervertebral articulations.
The salts or esters of salicylic acids, or salicylate esters of an organic acid. Some of these have analgesic, antipyretic, and anti-inflammatory activities by inhibiting prostaglandin synthesis.
Chronic, non-specific inflammation of the GASTROINTESTINAL TRACT. Etiology may be genetic or environmental. This term includes CROHN DISEASE and ULCERATIVE COLITIS.
A method of studying a drug or procedure in which both the subjects and investigators are kept unaware of who is actually getting which specific treatment.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.

Is maintenance therapy always necessary for patients with ulcerative colitis in remission? (1/466)

BACKGROUND: The efficacy of sulphasalazine and mesalazine in preventing relapse in patients with ulcerative colitis is well known. It is less clear how long such maintenance should be continued, and if the duration of disease remission is a factor that affects the risk of recurrence. AIM: To determine whether the duration of disease remission affects the relapse rate, by comparing the efficacy of a delayed-release mesalazine (Asacol, Bracco S.p.A., Milan, Italy) against placebo in patients with ulcerative colitis with short- and long-duration of disease remission. METHODS: 112 patients (66 male, 46 female, mean age 35 years), with intermittent chronic ulcerative colitis in clinical, endoscopic and histological remission with sulphasalazine or mesalazine for at least 1 year, were included in the study. Assuming that a lower duration of remission might be associated with a higher relapse rate, the patients were stratified according to the length of their disease remission, prior to randomization into Group A (Asacol 26, placebo 35) in remission from 1 to 2 years, or Group B (Asacol 28, placebo 23) in remission for over 2 years, median 4 years. Patients were treated daily with oral Asacol 1.2 g vs. placebo, for a follow-up period of 1 year. RESULTS: We employed an intention-to-treat analysis. In Group A, whilst no difference was found between the two treatments after 6 months, mesalazine was significantly more effective than placebo in preventing relapse at 12 months [Asacol 6/26 (23%), placebo 17/35 (49%), P = 0.035, 95% Cl: 48-2.3%]. In contrast, in Group B no statistically significant difference was observed between the two treatments, either at 6 or 12 months [Asacol 5/28 (18%), placebo 6/23 (26%), P = 0.35, 95% Cl: 31-14%] of follow-up. Patients in group B were older, and had the disease and remission duration for longer, than those in Group A. CONCLUSIONS: Mesalazine prophylaxis is necessary for the prevention of relapse by patients with ulcerative colitis in remission for less than 2 years, but this study casts doubt over whether continuous maintenance treatment is necessary in patients with prolonged clinical, endoscopic and histological remission, who are at very low risk of relapse.  (+info)

Evaluation of 5-aminosalicylic acid (5-ASA) for cancer chemoprevention: lack of efficacy against nascent adenomatous polyps in the Apc(Min) mouse. (2/466)

Recent experimental and epidemiological evidence suggests that nonsteroidal anti-inflammatory drugs (NSAIDs) are effective in the prevention of colorectal cancer. However, the toxicity associated with the long-term use of most classical NSAIDs has limited their usefulness for the purpose of cancer chemoprevention. Inflammatory bowel disease (IBD) patients, in particular, are sensitive to the adverse side effects of NSAIDs, and these patients also have an increased risk for the development of intestinal cancer. 5-Aminosalicylic acid (5-ASA) is an anti-inflammatory drug commonly used in the treatment of IBD and may provide protection against the development of colorectal cancer in these patients. To directly evaluate the ability of 5-ASA to suppress intestinal tumors, we studied several formulations of 5-ASA (free acid, sulfasalazine, and Pentasa) at multiple oral dosage levels [500, 2400, 4800, and 9600 parts/million (ppm)] in the adenomatous polyposis coli (Apc) mouse model of multiple intestinal neoplasia (Min). Although the ApcMin mouse is not a model of colitis-associated neoplasia, it is, nonetheless, a useful model for assessing the ability of anti-inflammatory agents to prevent tumor formation in a genetically preinitiated population of cells. We used a study design in which drug was provided ad libitum through the diet beginning at the time of weaning (28 days of age) until 100 days of age. We included 200 ppm of piroxicam and 160 ppm of sulindac as positive controls, and the negative control was AIN-93G diet alone. Treatment with either piroxicam or sulindac produced statistically significant reductions in intestinal tumor multiplicity (95% and 83% reductions in tumor number, respectively; P < 0.001 versus controls). By contrast, none of the 5-ASA drug formulations or dosage levels produced consistent dose-progressive changes in polyp number, distribution, or size, despite high luminal and serum concentrations of 5-ASA and its primary metabolite N-acetyl-5-ASA. Thus, 5-ASA does not seem to possess direct chemosuppressive activity against the development of nascent intestinal adenomas in the ApcMin mouse. However, because intestinal tumor development in the ApcMin mouse is driven by a germline mutation in the Apc gene rather than by chronic inflammation, we caution that these findings do not definitively exclude the possibility that 5-ASA may exert a chemopreventive effect in human IBD patients.  (+info)

Does sulphasalazine cause drug induced systemic lupus erythematosus? No effect evident in a prospective randomised trial of 200 rheumatoid patients treated with sulphasalazine or auranofin over five years. (3/466)

BACKGROUND: Sulphasalazine (SSZ) has been reported to cause drug induced systemic lupus erythematosus (SLE), but diagnosis of this complication in the context of rheumatoid arthritis (RA) is difficult. OBJECTIVE: To determine prospectively: (1) if patients become seropositive for antinuclear antibodies (ANA) during prolonged treatment with SSZ without clinical evidence of SLE; (2) if ANA positive patients develop more adverse reactions than ANA negative patients; (3) if drug induced SLE was identified in this cohort. METHODS: 200 patients enrolled in a randomised prospective trial of SSZ and auranofin (AUR) were followed up for five years. Baseline and annual ANA results were collected along with information on drug toxicity and reasons for discontinuation of treatment. RESULTS: Over five years 24 patients stopped taking SSZ and 49 AUR because of side effects. Of the features common to SLE, rash developed in nine SSZ patients and 11 AUR treated patients and mouth ulcers in three and four patients respectively. Six SSZ treated patients and three treated with AUR developed leucopenia, which promptly resolved with drug withdrawal. No adverse event was ascribed to drug induced SLE. Of the 72 SSZ treated patients who were ANA negative or weakly positive at outset, 14 (19%) became strongly ANA positive compared with 11 (14%) of 80 AUR patients. Patients ANA positive at baseline or who became ANA positive were not more likely to develop drug toxicity or to withdraw from treatment than those ANA negative throughout. CONCLUSION: ANA positivity is common in patients with RA, but the presence or development of ANA did not increase the likelihood of withdrawing from treatment. No case of drug induced SLE was seen over five years in this study.  (+info)

Colonic ulceration caused by administration of loxoprofen sodium. (4/466)

A 54-year-old female with chronic headache was admitted to our hospital because of hematochezia. She had routinely taken loxoprofen sodium because of severe headache. Emergent colonoscopic examination revealed ulceration of the cecum. After administration of loxoprofen sodium was discontinued and administration of sulfasalazine was initiated, her intestinal bleeding subsided. Two months after discontinuation of loxoprofen sodium, the colonoscopic examination revealed scar formation at the site of cecal ulceration. In this case, it was conceivable that the administration of loxoprofen sodium might have induced colonic ulceration.  (+info)

Salicylates and sulfasalazine, but not glucocorticoids, inhibit leukocyte accumulation by an adenosine-dependent mechanism that is independent of inhibition of prostaglandin synthesis and p105 of NFkappaB. (5/466)

The antiinflammatory action of aspirin generally has been attributed to direct inhibition of cyclooxygenases (COX-1 and COX-2), but additional mechanisms are likely at work. These include aspirin's inhibition of NFkappaB translocation to the nucleus as well as the capacity of salicylates to uncouple oxidative phosphorylation (i.e., deplete ATP). At clinically relevant doses, salicylates cause cells to release micromolar concentrations of adenosine, which serves as an endogenous ligand for at least four different types of well-characterized receptors. Previously, we have shown that adenosine mediates the antiinflammatory effects of other potent and widely used antiinflammatory agents, methotrexate and sulfasalazine, both in vitro and in vivo. To determine in vivo whether clinically relevant levels of salicylate act via adenosine, via NFkappaB, or via the "inflammatory" cyclooxygenase COX-2, we studied acute inflammation in the generic murine air-pouch model by using wild-type mice and mice rendered deficient in either COX-2 or p105, the precursor of p50, one of the components of the multimeric transcription factor NFkappaB. Here, we show that the antiinflammatory effects of aspirin and sodium salicylate, but not glucocorticoids, are largely mediated by the antiinflammatory autacoid adenosine independently of inhibition of prostaglandin synthesis by COX-1 or COX-2 or of the presence of p105. Indeed, both inflammation and the antiinflammatory effects of aspirin and sodium salicylate were independent of the levels of prostaglandins at the inflammatory site. These experiments also provide in vivo confirmation that the antiinflammatory effects of glucocorticoids depend, in part, on the p105 component of NFkappaB.  (+info)

Influence of sulphasalazine, methotrexate, and the combination of both on plasma homocysteine concentrations in patients with rheumatoid arthritis. (6/466)

OBJECTIVE: To study the influence of sulphasalazine (SSZ), methotrexate (MTX), and the combination (COMBI) of both on plasma homocysteine and to study the relation between plasma homocysteine and their clinical effects. METHODS: 105 patients with early rheumatoid arthritis (RA) were randomised between SSZ (2-3 g/day), MTX (7.5-15 mg/week), and the COMBI (same dose range) and evaluated double blindly during 52 weeks. Plasma homocysteine, serum folate concentrations, and vitamin B12 were measured. The influence of the C677T mutation of the enzyme methyl-enetetrahydrofolatereductase (MTHFR) gene was analysed. RESULTS: A slight trend towards increased efficacy and an increased occurrence of minor gastrointestinal toxicity was present in the COMBI group, no differences existed clinically between SSZ and MTX. Only a slight and temporary increase in plasma homocysteine was found in the SSZ group, in contrast with the persistent rise in the MTX group and the even greater increase in the COMBI patients. Patients homozygous for the mutation in the MTHFR gene had significantly higher baseline homocysteine, heterozygous MTHFR genotype induced a significantly higher plasma homoeysteine at week 52 compared with no mutation. No correlation was found between clinical efficacy variables and homocysteine. Patients with gastrointestinal toxicity had a significantly greater increase in homocysteine. CONCLUSION: A persistent increase in plasma homocysteine concentrations was observed in patients treated with MTX alone and more pronounced in combination with SSZ, in contrast with SSZ alone. An increase in plasma homocysteine is related to the C677T mutation in MTHFR. A relation in the change in homocysteine concentrations with (gastrointestinal) toxicity was found, no relation with clinical efficacy existed.  (+info)

Combination therapy in early rheumatoid arthritis: a randomised, controlled, double blind 52 week clinical trial of sulphasalazine and methotrexate compared with the single components. (7/466)

OBJECTIVES: To investigate the potential clinical benefit of a combination therapy. METHODS: 205 patients fulfilling the ACR criteria for rheumatoid arthritis (RA), not treated with disease modifying antirheumatoid drugs previously, with an early (< or = 1 year duration), active (Disease Activity Score (DAS) > 3.0), rheumatoid factor and/or HLA DR 1/4 positive disease were randomised between sulphasalazine (SASP) 2000 (maximum 3000) mg daily (n = 68), or methotrexate (MTX) 7.5 (maximum 15) mg weekly (n = 69) or the combination (SASP + MTX) of both (n = 68). RESULTS: The mean changes in the DAS during the one year follow up of the study was -1.15, -0.87, -1.26 in the SASP, MTX, and SASP + MTX group respectively (p = 0.019). However, there was no statistically significant difference in terms of either EULAR good responders 34%, 38%, 38% or ACR criteria responders 59%, 59%, 65% in the SASP, MTX, and SASP + MTX group respectively. Radiological progression evaluated by the modified Sharp score was very modest in the three groups: mean changes in erosion score: +2.4, +2.4, +1.9, in narrowing score: +2.3, +2.1, +1.6 and in total damage score: +4.6, +4.5, +3.5, in the SASP, MTX, and SASP + MTX groups respectively. Adverse events occurred more frequently in the SASP + MTX group 91% versus 75% in the SASP and MTX group (p = 0.025). Nausea was the most frequent side effect: 32%, 23%, 49% in the SASP, MTX, and SASP + MTX groups respectively (p = 0.007). CONCLUSION: This study suggests that an early initiation therapy of disease modifying drug seems to be of benefit. However, this study was unable to demonstrate a clinically relevant superiority of the combination therapy although several outcomes were in favour of this observation. The tolerability of the three treatment modalities seems acceptable.  (+info)

Giant cell arteritis associated with rheumatoid arthritis monitored by magnetic resonance angiography. (8/466)

A 57-year-old Japanese woman with well controlled rheumatoid arthritis visited our hospital with a severe bitemporal headache and marked fatigue. Based on the classification criteria by the American College of Rheumatology, she was diagnosed as having giant cell arteritis. Magnetic resonance (MR) angiography was performed, from which stenotic changes in the bilateral superficial temporal arteries were strongly suspected. Corticosteroid therapy was quickly started. The patient followed an uneventful course with no complications. Therapeutic effect was confirmed by MR angiographic findings obtained 4 weeks after the initiation of therapy.  (+info)

Sulfasalazine is defined as a medication that is commonly used to treat inflammatory bowel disease (IBD), such as ulcerative colitis and Crohn's disease. It is also used in the treatment of rheumatoid arthritis. Sulfasalazine has an anti-inflammatory effect, which helps to reduce inflammation in the gut or joints.

The medication contains two components: sulfapyridine and 5-aminosalicylic acid (5-ASA). The sulfapyridine component is an antibiotic that may help to reduce the number of harmful bacteria in the gut, while the 5-ASA component is responsible for the anti-inflammatory effect.

Sulfasalazine works by being broken down into its two components after it is ingested. The 5-ASA component then acts directly on the lining of the gut to reduce inflammation, while the sulfapyridine component is absorbed into the bloodstream and excreted in the urine.

Common side effects of sulfasalazine include nausea, vomiting, heartburn, headache, and loss of appetite. Less common but more serious side effects may include allergic reactions, liver or kidney problems, and blood disorders. It is important to take sulfasalazine exactly as directed by a healthcare provider and to report any concerning symptoms promptly.

Sulfapyridine is an antibiotic drug that belongs to the class of medications known as sulfonamides or "sulfa drugs." It is used to treat various bacterial infections by interfering with the bacteria's ability to synthesize essential proteins. Sulfapyridine may be used to treat a variety of infections, including urinary tract infections, bronchitis, and traveler's diarrhea.

The medical definition of Sulfapyridine is:

A sulfonamide antibacterial drug with a prolonged action, primarily used for its antimicrobial properties in treating various bacterial infections. It works by inhibiting the bacterial synthesis of folic acid, an essential component for bacterial growth and survival. Sulfapyridine is often combined with other medications, such as pyrimethamine, to enhance its antibacterial effect in specific therapeutic applications.

It's important to note that sulfonamides can cause side effects, including rashes, allergic reactions, and gastrointestinal symptoms. In some cases, more severe adverse reactions may occur, particularly in individuals with a known hypersensitivity to sulfa drugs or those with specific genetic factors. Always consult with a healthcare professional for appropriate use, dosage, and potential side effects of Sulfapyridine or any other medication.

Mesalamine is an anti-inflammatory drug that is primarily used to treat inflammatory bowel diseases (IBD), such as ulcerative colitis and Crohn's disease. It works by reducing inflammation in the intestines, which can help alleviate symptoms like diarrhea, abdominal pain, and rectal bleeding.

Mesalamine is available in various forms, including oral tablets, capsules, suppositories, and enemas. The specific formulation and dosage may vary depending on the severity and location of the inflammation in the gut.

The drug's anti-inflammatory effects are thought to be mediated by its ability to inhibit the activity of certain enzymes involved in the inflammatory response, such as cyclooxygenase and lipoxygenase. By reducing inflammation, mesalamine can help promote healing and prevent recurrences of IBD symptoms.

It's important to note that mesalamine may cause side effects, including headache, nausea, vomiting, and abdominal pain. In rare cases, it may also cause more serious side effects like kidney damage or allergic reactions. Patients should talk to their healthcare provider about the potential risks and benefits of taking mesalamine.

Aminosalicylic acids are a group of medications that contain a chemical structure related to salicylic acid, which is the active ingredient in aspirin. These medications are primarily used to treat inflammatory bowel diseases (IBD), such as Crohn's disease and ulcerative colitis. The most common aminosalicylates used for IBD include mesalamine, sulfasalazine, and olsalazine.

These drugs work by reducing the production of chemicals in the body that cause inflammation in the lining of the intestines. By decreasing inflammation, they can help alleviate symptoms such as diarrhea, abdominal pain, and rectal bleeding associated with IBD. Additionally, aminosalicylates may also have a protective effect on the lining of the intestines, helping to prevent further damage.

Aminosalicylates are available in various forms, including tablets, capsules, suppositories, and enemas, depending on the specific medication and the location of the inflammation within the digestive tract. While these medications are generally well-tolerated, they can cause side effects such as headache, nausea, vomiting, and abdominal pain in some individuals. It is essential to follow the prescribing physician's instructions carefully when taking aminosalicylates to ensure their safe and effective use.

Non-steroidal anti-inflammatory agents (NSAIDs) are a class of medications that reduce pain, inflammation, and fever. They work by inhibiting the activity of cyclooxygenase (COX) enzymes, which are involved in the production of prostaglandins, chemicals that contribute to inflammation and cause blood vessels to dilate and become more permeable, leading to symptoms such as pain, redness, warmth, and swelling.

NSAIDs are commonly used to treat a variety of conditions, including arthritis, muscle strains and sprains, menstrual cramps, headaches, and fever. Some examples of NSAIDs include aspirin, ibuprofen, naproxen, and celecoxib.

While NSAIDs are generally safe and effective when used as directed, they can have side effects, particularly when taken in large doses or for long periods of time. Common side effects include stomach ulcers, gastrointestinal bleeding, and increased risk of heart attack and stroke. It is important to follow the recommended dosage and consult with a healthcare provider if you have any concerns about using NSAIDs.

Antirheumatic agents are a class of drugs used to treat rheumatoid arthritis, other inflammatory types of arthritis, and related conditions. These medications work by reducing inflammation in the body, relieving symptoms such as pain, swelling, and stiffness in the joints. They can also help slow down or prevent joint damage and disability caused by the disease.

There are several types of antirheumatic agents, including:

1. Nonsteroidal anti-inflammatory drugs (NSAIDs): These medications, such as ibuprofen and naproxen, reduce inflammation and relieve pain. They are often used to treat mild to moderate symptoms of arthritis.
2. Corticosteroids: These powerful anti-inflammatory drugs, such as prednisone and cortisone, can quickly reduce inflammation and suppress the immune system. They are usually used for short-term relief of severe symptoms or in combination with other antirheumatic agents.
3. Disease-modifying antirheumatic drugs (DMARDs): These medications, such as methotrexate and hydroxychloroquine, work by slowing down the progression of rheumatoid arthritis and preventing joint damage. They can take several weeks or months to become fully effective.
4. Biologic response modifiers (biologics): These are a newer class of DMARDs that target specific molecules involved in the immune response. They include drugs such as adalimumab, etanercept, and infliximab. Biologics are usually used in combination with other antirheumatic agents for patients who have not responded to traditional DMARD therapy.
5. Janus kinase (JAK) inhibitors: These medications, such as tofacitinib and baricitinib, work by blocking the action of enzymes called JAKs that are involved in the immune response. They are used to treat moderate to severe rheumatoid arthritis and can be used in combination with other antirheumatic agents.

It is important to note that antirheumatic agents can have significant side effects and should only be prescribed by a healthcare provider who is experienced in the management of rheumatoid arthritis. Regular monitoring and follow-up are essential to ensure safe and effective treatment.

Hydroxychloroquine is an antimalarial and autoimmune disease medication. It's primarily used to prevent or treat malaria, a disease caused by parasites that enter the body through the bites of infected mosquitoes. It works by killing the malaria parasite in the red blood cells of the human body.

In addition, hydroxychloroquine is also used to treat autoimmune diseases such as rheumatoid arthritis and lupus. In these conditions, the body's immune system mistakenly attacks healthy tissues, causing inflammation and damage. Hydroxychloroquine helps to regulate the immune system and reduce inflammation.

It is important to note that while hydroxychloroquine has been studied as a potential treatment for COVID-19, current evidence does not support its use outside of a clinical trial setting due to lack of efficacy and potential for harm.

Gastrointestinal agents are a class of pharmaceutical drugs that affect the gastrointestinal (GI) tract, which includes the organs involved in digestion such as the mouth, esophagus, stomach, small intestine, large intestine, and anus. These agents can have various effects on the GI tract, including:

1. Increasing gastric motility (promoting bowel movements) - laxatives, prokinetics
2. Decreasing gastric motility (reducing bowel movements) - antidiarrheal agents
3. Neutralizing gastric acid - antacids
4. Reducing gastric acid secretion - H2-blockers, proton pump inhibitors
5. Protecting the mucosal lining of the GI tract - sucralfate, misoprostol
6. Relieving symptoms associated with GI disorders such as bloating, abdominal pain, and nausea - antispasmodics, antiemetics

Examples of gastrointestinal agents include:

* Laxatives (e.g., psyllium, docusate)
* Prokinetics (e.g., metoclopramide)
* Antacids (e.g., calcium carbonate, aluminum hydroxide)
* H2-blockers (e.g., ranitidine, famotidine)
* Proton pump inhibitors (e.g., omeprazole, lansoprazole)
* Sucralfate
* Misoprostol
* Antispasmodics (e.g., hyoscyamine, dicyclomine)
* Antiemetics (e.g., ondansetron, promethazine)

It is important to note that gastrointestinal agents can have both therapeutic and adverse effects, and their use should be based on a careful evaluation of the patient's condition and medical history.

The amino acid transport system y+ is a type of sodium-independent cationic amino acid transporter that is responsible for the uptake of positively charged amino acids, such as arginine and lysine, into cells. It is a part of a larger family of amino acid transporters that are involved in the transport of various types of amino acids across cell membranes.

The y+ system is composed of several different transporter proteins, including rBAT/4F2hc heteromeric amino acid transporter (Cat1), and light chains such as y+LAT1, y+LAT2, and y+LAT3. These transporters are widely expressed in various tissues, including the small intestine, kidney, liver, and brain.

The y+ system plays important roles in various physiological processes, including protein synthesis, immune function, and neurotransmitter metabolism. Dysregulation of this transport system has been implicated in several diseases, such as cancer, neurological disorders, and kidney disease.

Phenylhydrazines are organic compounds that contain a phenyl group (a benzene ring with a hydrogen atom substituted by a hydroxy group) and a hydrazine group (-NH-NH2). They are aromatic amines that have been used in various chemical reactions, including the formation of azos and hydrazones. In medicine, phenylhydrazines were once used as vasodilators to treat angina pectoris, but their use has largely been discontinued due to their toxicity and potential carcinogenicity.

Rheumatoid arthritis (RA) is a systemic autoimmune disease that primarily affects the joints. It is characterized by persistent inflammation, synovial hyperplasia, and subsequent damage to the articular cartilage and bone. The immune system mistakenly attacks the body's own tissues, specifically targeting the synovial membrane lining the joint capsule. This results in swelling, pain, warmth, and stiffness in affected joints, often most severely in the hands and feet.

RA can also have extra-articular manifestations, affecting other organs such as the lungs, heart, skin, eyes, and blood vessels. The exact cause of RA remains unknown, but it is believed to involve a complex interplay between genetic susceptibility and environmental triggers. Early diagnosis and treatment are crucial in managing rheumatoid arthritis to prevent joint damage, disability, and systemic complications.

Methotrexate is a medication used in the treatment of certain types of cancer and autoimmune diseases. It is an antimetabolite that inhibits the enzyme dihydrofolate reductase, which is necessary for the synthesis of purines and pyrimidines, essential components of DNA and RNA. By blocking this enzyme, methotrexate interferes with cell division and growth, making it effective in treating rapidly dividing cells such as cancer cells.

In addition to its use in cancer treatment, methotrexate is also used to manage autoimmune diseases such as rheumatoid arthritis, psoriasis, and inflammatory bowel disease. In these conditions, methotrexate modulates the immune system and reduces inflammation.

It's important to note that methotrexate can have significant side effects and should be used under the close supervision of a healthcare provider. Regular monitoring of blood counts, liver function, and kidney function is necessary during treatment with methotrexate.

Glycochenodeoxycholic acid (GCDCA) is a type of bile acid that is produced in the liver and then conjugated with glycine. Bile acids are formed from cholesterol and play an important role in the digestion and absorption of fats and fat-soluble vitamins in the small intestine.

GCDCA is a secondary bile acid, which means that it is produced by bacterial metabolism of primary bile acids (such as cholic acid and chenodeoxycholic acid) in the colon. Once formed, GCDCA is then reabsorbed into the bloodstream and transported back to the liver, where it can be conjugated with glycine or taurine and excreted into bile again.

Abnormal levels of GCDCA and other bile acids have been associated with various health conditions, including cholestatic liver diseases, gallstones, and colon cancer. Therefore, measuring the levels of these acids in blood, urine, or feces can provide valuable diagnostic information for these conditions.

Isoxazoles are not a medical term, but a chemical compound. They are organic compounds containing a five-membered ring consisting of one nitrogen atom, one oxygen atom, and three carbon atoms. Isoxazoles have various applications in the pharmaceutical industry as they can be used to synthesize different drugs. Some isoxazole derivatives have been studied for their potential medicinal properties, such as anti-inflammatory, analgesic, and antipyretic effects. However, isoxazoles themselves are not a medical diagnosis or treatment.

Ulcerative colitis is a type of inflammatory bowel disease (IBD) that affects the lining of the large intestine (colon) and rectum. In ulcerative colitis, the lining of the colon becomes inflamed and develops ulcers or open sores that produce pus and mucous. The symptoms of ulcerative colitis include diarrhea, abdominal pain, and rectal bleeding.

The exact cause of ulcerative colitis is not known, but it is thought to be related to an abnormal immune response in which the body's immune system attacks the cells in the digestive tract. The inflammation can be triggered by environmental factors such as diet, stress, and infections.

Ulcerative colitis is a chronic condition that can cause symptoms ranging from mild to severe. It can also lead to complications such as anemia, malnutrition, and colon cancer. There is no cure for ulcerative colitis, but treatment options such as medications, lifestyle changes, and surgery can help manage the symptoms and prevent complications.

Combination drug therapy is a treatment approach that involves the use of multiple medications with different mechanisms of action to achieve better therapeutic outcomes. This approach is often used in the management of complex medical conditions such as cancer, HIV/AIDS, and cardiovascular diseases. The goal of combination drug therapy is to improve efficacy, reduce the risk of drug resistance, decrease the likelihood of adverse effects, and enhance the overall quality of life for patients.

In combining drugs, healthcare providers aim to target various pathways involved in the disease process, which may help to:

1. Increase the effectiveness of treatment by attacking the disease from multiple angles.
2. Decrease the dosage of individual medications, reducing the risk and severity of side effects.
3. Slow down or prevent the development of drug resistance, a common problem in chronic diseases like HIV/AIDS and cancer.
4. Improve patient compliance by simplifying dosing schedules and reducing pill burden.

Examples of combination drug therapy include:

1. Antiretroviral therapy (ART) for HIV treatment, which typically involves three or more drugs from different classes to suppress viral replication and prevent the development of drug resistance.
2. Chemotherapy regimens for cancer treatment, where multiple cytotoxic agents are used to target various stages of the cell cycle and reduce the likelihood of tumor cells developing resistance.
3. Cardiovascular disease management, which may involve combining medications such as angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, diuretics, and statins to control blood pressure, heart rate, fluid balance, and cholesterol levels.
4. Treatment of tuberculosis, which often involves a combination of several antibiotics to target different aspects of the bacterial life cycle and prevent the development of drug-resistant strains.

When prescribing combination drug therapy, healthcare providers must carefully consider factors such as potential drug interactions, dosing schedules, adverse effects, and contraindications to ensure safe and effective treatment. Regular monitoring of patients is essential to assess treatment response, manage side effects, and adjust the treatment plan as needed.

Tripterygium is not a medical term itself, but it refers to a genus of plants also known as thunder god vine. The root and bark extracts of this plant have been used in traditional Chinese medicine for various inflammatory and autoimmune conditions. Some compounds derived from Tripterygium species, such as triptolide and celastrol, have attracted interest in modern medical research due to their potential immunosuppressive and anti-inflammatory properties. However, the use of Tripterygium extracts is associated with several side effects, and further studies are required to establish their safety and efficacy for therapeutic purposes.

NF-κB (Nuclear Factor kappa-light-chain-enhancer of activated B cells) is a protein complex that plays a crucial role in regulating the immune response to infection and inflammation, as well as in cell survival, differentiation, and proliferation. It is composed of several subunits, including p50, p52, p65 (RelA), c-Rel, and RelB, which can form homodimers or heterodimers that bind to specific DNA sequences called κB sites in the promoter regions of target genes.

Under normal conditions, NF-κB is sequestered in the cytoplasm by inhibitory proteins known as IκBs (inhibitors of κB). However, upon stimulation by various signals such as cytokines, bacterial or viral products, and stress, IκBs are phosphorylated, ubiquitinated, and degraded, leading to the release and activation of NF-κB. Activated NF-κB then translocates to the nucleus, where it binds to κB sites and regulates the expression of target genes involved in inflammation, immunity, cell survival, and proliferation.

Dysregulation of NF-κB signaling has been implicated in various pathological conditions such as cancer, chronic inflammation, autoimmune diseases, and neurodegenerative disorders. Therefore, targeting NF-κB signaling has emerged as a potential therapeutic strategy for the treatment of these diseases.

Early termination of clinical trials refers to the discontinuation of a medical research study before its planned end date. This can occur for several reasons, including:

1. Safety concerns: If the experimental treatment is found to be harmful or poses significant risks to the participants, the trial may be stopped early to protect their well-being.
2. Efficacy demonstrated: If the experimental treatment shows promising results and is significantly better than the current standard of care, an independent data monitoring committee may recommend stopping the trial early so that the treatment can be made available to all patients as soon as possible.
3. Futility: If it becomes clear that the experimental treatment is unlikely to provide any meaningful benefit compared to the current standard of care, the trial may be stopped early to avoid exposing more participants to unnecessary risks and to allocate resources more efficiently.
4. Insufficient recruitment or funding: If there are not enough participants enrolled in the study or if funding for the trial is withdrawn, it may need to be terminated prematurely.
5. Violation of ethical guidelines or regulations: If the trial is found to be non-compliant with regulatory requirements or ethical standards, it may be stopped early by the sponsor, investigator, or regulatory authorities.

When a clinical trial is terminated early, the data collected up until that point are still analyzed and reported, but the results should be interpreted with caution due to the limited sample size and potential biases introduced by the early termination.

Spondylarthritis is a term used to describe a group of interrelated inflammatory diseases that primarily affect the spine and sacroiliac joints (where the spine connects to the pelvis), but can also involve other joints, ligaments, tendons, and entheses (sites where tendons or ligaments attach to bones). These conditions share common genetic, clinical, and imaging features.

The most common forms of spondylarthritis include:

1. Ankylosing spondylitis - a chronic inflammatory disease that primarily affects the spine and sacroiliac joints, causing pain and stiffness. In some cases, it can lead to fusion of the spine's vertebrae.
2. Psoriatic arthritis - a form of arthritis that occurs in people with psoriasis, an autoimmune skin condition. It can cause inflammation in the joints, tendons, and entheses.
3. Reactive arthritis - a type of arthritis that develops as a reaction to an infection in another part of the body, often the urinary or gastrointestinal tract.
4. Enteropathic arthritis - a form of arthritis associated with inflammatory bowel diseases like Crohn's disease and ulcerative colitis.
5. Undifferentiated spondylarthritis - when a patient presents with features of spondylarthritis but does not meet the criteria for any specific subtype.

Common symptoms of spondylarthritis include:

- Back pain and stiffness, often worse in the morning or after periods of inactivity
- Peripheral joint pain and swelling
- Enthesitis (inflammation at tendon or ligament insertion points)
- Dactylitis (swelling of an entire finger or toe)
- Fatigue
- Uveitis (inflammation of the eye)
- Skin rashes, such as psoriasis
- Inflammatory bowel disease symptoms

Diagnosis typically involves a combination of medical history, physical examination, laboratory tests, and imaging studies. Treatment often includes nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying antirheumatic drugs (DMARDs), biologic agents, and lifestyle modifications to manage symptoms and prevent joint damage.

Salicylates are a group of chemicals found naturally in certain fruits, vegetables, and herbs, as well as in some medications like aspirin. They are named after willow bark's active ingredient, salicin, from which they were derived. Salicylates have anti-inflammatory, analgesic (pain-relieving), and antipyretic (fever-reducing) properties.

In a medical context, salicylates are often used to relieve pain, reduce inflammation, and lower fever. High doses of salicylates can have blood thinning effects and may be used in the prevention of strokes or heart attacks. Commonly prescribed salicylate medications include aspirin, methylsalicylate, and sodium salicylate.

It is important to note that some people may have allergic reactions to salicylates, and overuse can lead to side effects such as stomach ulcers, ringing in the ears, and even kidney or liver damage.

Inflammatory Bowel Diseases (IBD) are a group of chronic inflammatory conditions primarily affecting the gastrointestinal tract. The two main types of IBD are Crohn's disease and ulcerative colitis.

Crohn's disease can cause inflammation in any part of the digestive system, from the mouth to the anus, but it most commonly affects the lower part of the small intestine (the ileum) and/or the colon. The inflammation caused by Crohn's disease often spreads deep into the layers of affected bowel tissue.

Ulcerative colitis, on the other hand, is limited to the colon, specifically the innermost lining of the colon. It causes long-lasting inflammation and sores (ulcers) in the lining of the large intestine (colon) and rectum.

Symptoms can vary depending on the severity and location of inflammation but often include abdominal pain, diarrhea, fatigue, weight loss, and reduced appetite. IBD is not the same as irritable bowel syndrome (IBS), which is a functional gastrointestinal disorder.

The exact cause of IBD remains unknown, but it's thought to be a combination of genetic factors, an abnormal immune response, and environmental triggers. There is no cure for IBD, but treatments can help manage symptoms and reduce inflammation, potentially leading to long-term remission.

The double-blind method is a study design commonly used in research, including clinical trials, to minimize bias and ensure the objectivity of results. In this approach, both the participants and the researchers are unaware of which group the participants are assigned to, whether it be the experimental group or the control group. This means that neither the participants nor the researchers know who is receiving a particular treatment or placebo, thus reducing the potential for bias in the evaluation of outcomes. The assignment of participants to groups is typically done by a third party not involved in the study, and the codes are only revealed after all data have been collected and analyzed.

Treatment outcome is a term used to describe the result or effect of medical treatment on a patient's health status. It can be measured in various ways, such as through symptoms improvement, disease remission, reduced disability, improved quality of life, or survival rates. The treatment outcome helps healthcare providers evaluate the effectiveness of a particular treatment plan and make informed decisions about future care. It is also used in clinical research to compare the efficacy of different treatments and improve patient care.

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  • In general, most patients can take sulfasalazine with few side effects. (rheumatology.org)
  • How do I take sulfasalazine? (familywize.org)
  • Drug interactions are reported among 37 people who take Sulfasalazine and Salagen. (ehealthme.com)
  • The phase IV clinical study analyzes what interactions people who take Sulfasalazine and Salagen have. (ehealthme.com)
  • 37 people who take Sulfasalazine and Salagen together, and have interactions are studied. (ehealthme.com)
  • Do you take Sulfasalazine and Salagen? (ehealthme.com)
  • should i take sulfasalazine if I have a cold. (asaliftco.com)
  • Sulfasalazine, sold under the brand name Azulfidine among others, is a medication used to treat rheumatoid arthritis, ulcerative colitis, and Crohn's disease. (wikipedia.org)
  • In people with rheumatoid arthritis, the cost-effectiveness of sulfasalazine is improved by combining it with other drugs. (wikipedia.org)
  • Sulfasalazine is used in the treatment of rheumatoid arthritis (RA), inflammatory bowel disease, and some other autoimmune conditions. (rheumatology.org)
  • Administration of sulfasalazine alone is not a complete treatment for rheumatoid arthritis. (drugs.com)
  • If your doctor has prescribed this medication to help ease the pain associated with ulcerative colitis or rheumatoid arthritis, save on the cost of your sulfasalazine prescription fills with coupons from FamilyWize. (familywize.org)
  • Sulfasalazine pet meds are also used to treat rheumatoid arthritis and other types of joint pain. (vetdepot.com)
  • We enrolled 102 patients with rheumatoid arthritis and poor responses to at least one disease-modifying drug in a two-year, double-blind, randomized study of treatment with methotrexate alone (7.5 to 17.5 mg per week), the combination of sulfasalazine (500 mg twice daily) and hydroxychloroquine (200 mg twice daily), or all three drugs. (nih.gov)
  • In patients with rheumatoid arthritis, combination therapy with methotrexate, sulfasalazine, and hydroxychloroquine is more effective than either methotrexate alone or a combination of sulfasalazine, and hydroxychloroquine. (nih.gov)
  • In addition, delayed-release tablets of sulfasalazine are used to treat rheumatoid arthritis. (hellohippo.com)
  • Early treatment of rheumatoid arthritis with sulfasalazine helps to reduce/prevent further joint damage so you can do more of your normal daily activities. (hellohippo.com)
  • Sulfasalazine treats pain and inflammation caused by rheumatoid arthritis and an intestinal disease called ulcerative colitis. (rxwiki.com)
  • Sulfasalazine delayed-release (enteric-coated) is also used to treat rheumatoid arthritis in adults and children when other medications have not worked. (rxwiki.com)
  • You may be prescribed Azulfidine EN-Tabs if you are anadult with rheumatoid arthritis and you have previously responded inadequately to salicylates orother non-steroidal anti-inflammatory medications (NSAIDs). (thecanadianpharmacy.com)
  • Pediatric patients withpolyarticular-course1 juvenile rheumatoid arthritis may also be prescribed Azulfidine EN Tabs ifprevious treatments with other salicylates and NSAIDs have not been therapeutic. (thecanadianpharmacy.com)
  • We report the case of a 60-year-old woman with rheumatoid arthritis being treated with sulfasalazine who developed linear IgA dermatosis and drug rash with eosinophilia and systemic symptoms (DRESS). (actasdermo.org)
  • Sulfasalazine metabolizes to sulfapyridine. (wikipedia.org)
  • citation needed] Around 90% of a dose of sulfasalazine reaches the colon, where most of it is metabolized by bacteria into sulfapyridine and mesalazine (also known as 5-aminosalicylic acid or 5-ASA). (wikipedia.org)
  • A mix of unchanged, hydroxylated, and glucuronidated sulfapyridine is eliminated in urine, as is acetylated mesalazine and unmetabolized sulfasalazine. (wikipedia.org)
  • Our objective was to examine whether the D. desulfuricans strains isolated from the human body are susceptible to sulfasalazine (SAS) and the products of its biotransformation, i.e. 5-aminosalicylic acid (5-ASA) and sulfapyridine (SP), in order to determine the relationship between the strains' susceptibility to SAS and their ability to reduce the azo bond within this drug. (medscimonit.com)
  • Sulfasalazine is created by bonding a sulfa antibiotic called sulfapyridine to a salt of salicylic acid ( aspirin ). (vin.com)
  • Other potential side effects stem from the sulfapyridine portion of the sulfasalazine compound. (vin.com)
  • Sulfasalazine is made up of two components, 5-aminosalicylic acid and a sulfa antibiotic, called sulfapyridine. (rheumatoidarthritis.net)
  • Sulfasalazine EP Impurity C (CAS No: 66030-25-9) Or 2-Hydroxy-5-[2-[4-(2-iminopyridin-1-(2H)-yl)phenyl]diazenyl]benzoic acid, it is an impurity of Sulfasalazine, Sulfasalazine is synthesized by the diazotization of sulfapyridine, which is a disease-modifying anti-rheumatic drug. (veeprho.com)
  • The cost of sulfasalazine is often about $40 for 120 tablets. (familywize.org)
  • Sulfasalazine 500 mg, 500 Tablets is a generic form of Azulfidine, which is used to treat IBD (inflammatory bowel disease) and colitis in cats and dogs. (vetdepot.com)
  • Sulfasalazine comes in regular or delayed-release tablets. (giforkids.com)
  • Sci-Hub, Liquid Chromatographic Determination of Sulfasalazine in Tablets and Bulk Powder, 10.1093/jaoac/68.4.803. (veeprho.com)
  • Sulfasalazine comes as regular and delayed-release tablets. (rxwiki.com)
  • You cannot take Azulfidine EN-Tabs tablets if you have folate deficiency anemia. (thecanadianpharmacy.com)
  • What are the possible side effects of taking sulfasalazine? (familywize.org)
  • The mechanism of action of mesalamine (and sulfasalazine) is not fully understood, but appears to be topical rather than systemic. (theodora.com)
  • Use of sulfasalazine is contraindicated in people with sulfa allergies and in those with urinary tract obstructions, intestinal obstructions, and severe liver or kidney problems. (wikipedia.org)
  • Sulfasalazine is a sulfa drug. (rheumatology.org)
  • A member of a class of drugs called sulfa drugs, sulfasalazine was first used in patients with RA about 70 years ago when the disease was thought to result from a bacterial infection. (rheumatoidarthritis.net)
  • Sulfasalazine is used in the treatment of inflammatory bowel disease, including ulcerative colitis and Crohn's disease. (wikipedia.org)
  • The active ingredient in Azulfidine EN-tabs is sulfasalazine, formulated in an enteric-coated, delayed-release tablet. (rheumatoidarthritis.net)
  • Order Azulfidine EN-Tabs 500mg Tablet (sulfasalazine) from Canada & Save! (thecanadianpharmacy.com)
  • What is Azulfidine EN-Tabs? (thecanadianpharmacy.com)
  • Azulfidine EN-Tabs is a medication that treats ulcerative colitis and also helps to increasethe time between attacks of ulcerative colitis. (thecanadianpharmacy.com)
  • Azulfidine EN-Tabs is a salicylate and works bydecreasing inflammation in your body. (thecanadianpharmacy.com)
  • Azulfidine EN-Tabs may also be prescribed for other reasons not listed in this medicationguide. (thecanadianpharmacy.com)
  • You should be cautious when administering Azulfidine EN-Tabs to the elderly, as this patientpopulation may be more sensitive to the side effects of this medication. (thecanadianpharmacy.com)
  • Azulfidine EN-Tabs should not be given to children younger than 2 years old. (thecanadianpharmacy.com)
  • Extreme cautionshould be taken when giving children younger than age 10 Azulfidine EN-Tabs if they are sufferingfrom diarrhea or an infection of the bowel or stomach. (thecanadianpharmacy.com)
  • Tell your doctor immediately if you experience stomach pain that is severe, cramping, bloodydiarrhea or a fever while taking Azulfidine EN-Tabs. (thecanadianpharmacy.com)
  • While you are taking Azulfidine EN-Tabs tell your doctor right away if you show signs ofjaundice, like a fever, unusually pale skin, dark urine, clay-colored stools, stomach pain,appetite loss, yellowing of your skin or eyes and unusual bruising or bleeding. (thecanadianpharmacy.com)
  • Some men who take Azulfidine EN-Tabs have developed a decreased number of sperm and issueswith infertility. (thecanadianpharmacy.com)
  • These side effects stopped after the discontinuation of Azulfidine EN-Tabs.Talk to your doctor if you are a man taking this medication and concerned about yourfertility. (thecanadianpharmacy.com)
  • Azulfidine EN-Tabs is in FDApregnancy category B. Azulfidine EN-Tabs is not known to harm your unborn baby. (thecanadianpharmacy.com)
  • Sulfasalazine is a drug that negates the effects of bodily substances that cause inflammation, tissue damage, and diarrhea in patients who suffer from ulcerative colitis. (familywize.org)
  • Sulfasalazine is used to treat bowel inflammation, diarrhea (stool frequency), rectal bleeding, and abdominal pain in patients with ulcerative colitis, a condition in which the bowel is inflamed. (asaliftco.com)
  • Sulfasalazine is used to treat a certain type of bowel disease called ulcerative colitis. (hellohippo.com)
  • Sulfasalazine is a drug that is used primarily for treating ulcerative colitis. (canpharm.com)
  • The active ingredient Sulfasalazine is used to treat ulcerative colitis (UC), and to decrease the frequency of UC attacks. (greencrosspharmacy.online)
  • Sulfasalazine is a prescription medication used to treat the symptoms of ulcerative colitis including bowel inflammation, diarrhea (stool frequency), rectal bleeding, and abdominal pain. (rxwiki.com)
  • Azulfidine (Sulfasalazine) is an anti-inflammatory medicine, is prescribed for the treatment of mild to moderate ulcerative colitis (a long-term, progressive bowel disease) and as an added treatment in severe ulcerative colitis (chronic inflammation and ulceration of the lining of large bowel and rectum, the main symptom of which is bloody diarrhea). (paulmischellab.org)
  • Sulfasalazine has been used in the treatment of ulcerative colitis for over 55 years. (theodora.com)
  • Background: Sulfasalazine is well established in the treatment of active ulcerative colitis. (ncl.ac.uk)
  • Aim: To compare the safety and efficacy of balsalazide, 6.75 g daily, with sulfasalazine, 3 g daily, in the treatment of active ulcerative colitis of all grades of severity. (ncl.ac.uk)
  • Conclusions: This study confirms the better tolerability of balsalazide compared to sulfasalazine, and supports the use of balsalazide in ulcerative colitis of all grades of severity. (ncl.ac.uk)
  • sulfasalazine and methotrexate in rahow to sulfasalazine and methotrexate in ra for Can't stand up straight without wincing in pain? (asaliftco.com)
  • These include corticosteroids, methotrexate, and sulfasalazine. (webmd.com)
  • Patients who receive sulfasalazine should have complete blood count and liver function tests before starting treatment, every 1 to 2 weeks during the first 3 months of therapy, every 2 to 4 weeks during the second 3 months of therapy, and then every 3 months once you establish a regular dose. (rheumatoidarthritis.net)
  • Results: Fifty-seven patients were randomized: 28 to receive balsalazide and 29 to receive sulfasalazine. (ncl.ac.uk)
  • Sulfasalazine can cause an allergic reaction that varies from mild (skin rash) to more severe (fevers, abnormal liver tests). (rheumatology.org)
  • Some patients experience life-threatening allergies to sulfasalazine, so sulfasalazine should be stopped at the first signs of an allergic reaction. (rheumatoidarthritis.net)
  • About this is sulfasalazine maximum dosage. (co.ke)
  • 0.001 for the comparison with the three-drug group), and 14 of 35 patients treated with sulfasalazine and hydroxychloroquine (40 percent), P = 0.003 for the comparison with the three-drug group). (nih.gov)
  • Sulfasalazine is in the disease-modifying antirheumatic drugs (DMARDs) family of medications. (wikipedia.org)
  • Sulfasalazine may interfere with warfarin (Coumadin), cyclosporine or digoxin, so dose adjustments may be needed if these medications are taken together. (rheumatology.org)
  • Sulfasalazine increases the risk for liver injury if given with the drug isoniazid (INH), a drug for tuberculosis and may increase the risk for low blood sugar in patients taking certain medications for diabetes such as glimepiride (Amaryl), glyburide (Diabeta, Micronase, Glynase) and glipizide (Glucotrol). (rheumatology.org)
  • Sulfasalazine comes in a 500 mg tablet and should be taken with food and a full glass of water to avoid an upset stomach. (rheumatology.org)
  • Each dark yellow to yellowish-brown, round, biconvex tablet, scored on one side and engraved with 'PMS' on the other side, contains sulfasalazine 500 mg. (rxhealthmed.ca)
  • Those on sulfasalazine should use sunscreen (SPF 15 or higher) when outdoors and avoid prolonged exposure to sunlight. (rheumatology.org)
  • It is important to avoid unnecessary or prolonged exposure to sunlight and to wear protective clothing, sunscreen, and sunglasses, as sulfasalazine may make your skin sensitive to the sun. (rheumatoidarthritis.net)
  • If you are taking sulfasalazine for an intestinal inflammatory disease, the night-time dose interval should not be longer than eight hours. (rxhealthmed.ca)
  • Sulfasalazine should be used with caution in patients who have liver or kidney damage, disorders of the blood, bronchial asthma, or those with intestinal or urinary blockages. (rheumatoidarthritis.net)
  • Sulfasalazine is available as a generic medication. (wikipedia.org)
  • Sulfasalazine can lower sperm counts but this effect is reversible when the medication is discontinued. (rheumatology.org)
  • For some patients, the cost of purchasing this medication may be difficult, so FamilyWize offers coupons for sulfasalazine that lower the cost of prescription fills at many pharmacies all over the country. (familywize.org)
  • How does the pms-Sulfasalazine medication work? (rxhealthmed.ca)
  • What form(s) does the pms-Sulfasalazine medication come in? (rxhealthmed.ca)
  • How should I use the pms-Sulfasalazine medication? (rxhealthmed.ca)
  • Who should NOT take the pms-Sulfasalazine medication? (rxhealthmed.ca)
  • Once the medication has been cleared from your blood, you may … You will need regular blood tests while taking sulfasalazine to check if it is causing problems with your liver, kidneys or blood. (asaliftco.com)
  • In the case of sulfasalazine, there are no specific foods that you must exclude from your diet when receiving this medication. (rxwiki.com)
  • These images are a random sampling from a Bing search on the term "Sulfasalazine. (fpnotebook.com)
  • The mechanism of action is not clear, but it appears that sulfasalazine and its metabolites have immunosuppressive, antibacterial, and anti-inflammatory effects. (wikipedia.org)
  • Those who have not received corticosteroids or have not undergone surgery may respond substantially better to sulfasalazine than to placebo. (drugs.com)
  • There is some evidence that concomitant therapy with sulfasalazine and corticosteroids may not be more effective than either drug alone, but some subgroups of patients may have a better response to combined therapy (e.g., those with disease localized in the colon). (drugs.com)
  • Describimos el caso de una mujer de 60 años con artritis reumatoide en tratamiento con sulfasalazina, que desarrolló un cuadro de dermatosis IgA lineal con clínica de DRESS (drug-rash with eosinophilia and systemic symptoms) el cual respondió al suspender el fármaco causal más tratamiento con corticoides sistémicos durante dos meses. (actasdermo.org)
  • Sulfasalazine (Azulfidine) is considered a disease-modifying anti-rheumatic drug (DMARD). (rheumatology.org)
  • The drug sulfasalazine helps to prevent the body's natural inflammatory response. (familywize.org)
  • Sulfasalazine is the generic name for the brand-name drug Azulfidine. (familywize.org)
  • Sulfasalazine is a disease-modifying anti-rheumatic drug (DMARD) used for the treatment of adults and children over 6 with RA who have not responded to non-steroidal anti-inflammatory drugs (NSAIDs). (rheumatoidarthritis.net)
  • This is not a complete list of sulfasalazine drug interactions. (rxwiki.com)
  • What if I forget to take a dose of sulfasalazine? (familywize.org)
  • The dose of sulfasalazine varies widely according to the condition being treated and the needs of the person. (rxhealthmed.ca)
  • It usually takes between 2 to 3 months to notice any improvement in RA symptoms after starting sulfasalazine. (rheumatology.org)
  • Doses of sulfasalazine should be taken at regular and even intervals over the 24 hour daily period. (rxhealthmed.ca)
  • Patients with kidney diseases may need to use lower doses of sulfasalazine. (canpharm.com)
  • Balsalazide has been designed to deliver 5-aminosalicylic acid to the colon without the poor tolerability of sulfasalazine. (ncl.ac.uk)
  • Methods: Balsalazide and sulfasalazine were compared in a multicentre, double-blind, parallel group study over 12 weeks. (ncl.ac.uk)
  • These data confirm that balsalazide is better tolerated than sulfasalazine. (ncl.ac.uk)
  • Sulfasalazine belongs to a group of drugs called aminosalicylates. (rxwiki.com)
  • The most common side effects of the use of sulfasalazine include nausea, vomiting, upset stomach, loss of appetite, headache, or low sperm count in men. (familywize.org)
  • Sulfasalazine should be taken with a full glass of water after meals or with food to minimize upset stomach. (canpharm.com)
  • In humans, approximately 30 percent of people taking sulfasalazine report some kind of GI side effect and it is felt this statistic can be extrapolated to animals. (vin.com)
  • Side-effects of sulfasalazine on the blood or liver may be picked up at an early stage by regular checks on your blood. (asaliftco.com)
  • These are not all the possible side effects of sulfasalazine. (rheumatoidarthritis.net)
  • This is not a complete list of sulfasalazine side effects. (rxwiki.com)
  • The simultaneous administration of sulfasalazine and folic acid is regular practice in the therapy of inflammatory bowel diseases in order to maintain sufficient folate concentration in patients. (mdpi.com)
  • Sulfasalazine is considered to be safe for pregnancy and breastfeeding. (rheumatology.org)
  • In some cases, sulfasalazine may reduce the number of blood cells, or may cause abnormal liver tests. (rheumatology.org)
  • Save on Sulfasalazine at your pharmacy with the free discount below. (familywize.org)
  • Buy Azulfidine (Sulfasalazine) from a Canadian Pharmacy. (canpharm.com)
  • Show your sulfasalazine coupons to your pharmacist, who will give you a discount worth up to 76% off the different prices of sulfasalazine. (familywize.org)
  • Sulfasalazine can cause kidney stones. (wikipedia.org)
  • While taking sulfasalazine, drink an adequate amount of fluids to minimize the risk of crystals in the urine and the forming of kidney stones. (rxhealthmed.ca)
  • Drink a full glass of water after taking sulfasalazine to protect the kidneys and to prevent kidney stones. (rxwiki.com)
  • Sulfasalazine has active ingredients of sulfasalazine . (ehealthme.com)
  • It is based on sulfasalazine and pilocarpine hydrochloride (the active ingredients of Sulfasalazine and Salagen, respectively), and Sulfasalazine and Salagen (the brand names). (ehealthme.com)
  • What are the ingredients in sulfasalazine? (rheumatoidarthritis.net)

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