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Ocular toxicity is exceedingly rare, occurring in only 1 out of 40, patients treated at the doses recommended. Patients with underlying retinopathies or risks may not be good candidates for antimalarial drugs. Baseline ophthalmologic examination and a follow-up examination every 12 months are recommended during the period of treatment.

Its effectiveness overall is somewhat less than that methotrexate, but it has been shown to reduce signs and symptoms and slow radiographic damage. Sulfasalazine is also used in the treatment of inflammatory bowel disease and spondyloarthropathies. Its mechanism of action in RA is unknown. Some of its effects may be due to folate depletion.

The usual dose is grams per day in a twice daily dosing regimen. The dose may be initiated at 1 gram per day and increased as tolerated. Sulfasalazine may cause hypersensitivity and allergic reactions in patients who have experienced reactions to sulfa medications.

Mild gastrointestinal complaints are commonly seen and these can be decreased by using enteric coated formulations or administration of the medication with meals. Occasionally, mild cytopenias are seen. Patients may be screened before the use of sulfasalazine for a deficiency of the enzyme glucosephosphate dehydrogenase G6PD which may predispose patients to red blood cell hemolysis and anemia.

Blood monitoring is typically every months depending on dose.

Hydroxychloroquine (Plaquenil) - Overview

Though sulfasalazine may cause increases in liver function tests, it is generally considered a preferable agent to methotrexate in patients with liver disease or in patients who have hepatitis B or C. Its efficacy is similar to methotrexate in terms of signs and symptoms, and is a viable alternative to patients who have failed or are intolerant to methotrexate. Leflunomide has been demonstrated to slow radiographic progression. Studies have demonstrated that it can also be carefully combined with methotrexate in patients with no preexisting liver disease, as long as the liver function tests are carefully monitored.

Leflunomide has also been studied in psoriatic arthritis with some efficacy demonstrated. The mechanism of action of leflunomide is not fully understood but may be related to its ability to inhibit de novo pyrimidine biosynthesis through the inhibition of the enzyme dihydroorotate dehydrogenase. Laboratory studies have demonstrated that it also has effects on stimulated T cells.

The half-life of the active metabolite of leflunomide is very long. Leflunomide and its metabolites are extensively protein bound and undergo further metabolism before excretion. When initially approved, the medication was given using a loading dose of mg daily for three days then followed by 20 mg daily.

The dose may be reduced to 10mg daily if not tolerated at the 20 mg dose. The onset of action is relatively rapid within weeks. The onset of action of Arava may be seen earlier than methotrexate when using a loading dose. Leflunomide has been associated with liver transaminase elevations that reversed with cessation of the drug in clinical trials. Routine monitoring should include complete blood count and hepatic panel more frequently at the beginning of therapy then on a regular basis at least every 2 months.

Other toxicities that are common include mild diarrhea, GI upset and alopecia and hair thinning sometimes of sufficient severity to cause cessation of the drug.

Because leflunomide and its metabolites are a teratogen , extreme care must be taken for treatment of women of child bearing potential. Women must be warned about the possible risk to the fetus and cautioned to use adequate birth control. Women wishing to become pregnant must take cholestyramine 8gm 3 times daily for 11 days and then have two leflunomide metabolite levels drawn 14 days apart to document serum concentration less than 0.

Leflunomide treatment does not appear to be associated with an increased risk for infection. Tumor necrosis factor alpha TNF is a pro-inflammatory cytokine produced by macrophages and lymphocytes. It is found in large quantities in the rheumatoid joint and is produced locally in the joint by synovial macrophages and lymphocytes infiltrating the joint synovium. TNF is one of the critical cytokines that mediate joint damage and destruction due to its activities on many cells in the joint as well as effects on other organs and body systems.

These drugs began to enter the market for rheumatoid arthritis in and are now considered a part the ACR recommendations for treatment of RA. Etanercept is a soluble TNF receptor-Fc immunoglobulin fusion construct; infliximab, adalimumab, and golimumab are monoclonal antibodies; and certolizumab pegol is an anti-TNF antigen binding domain-polyethylene glycol construct.

While differing in structure, the efficacy and safety of the drugs is similar across the class in reducing the signs and symptoms of RA, as well as in slowing or halting radiographic damage, when used either as monotherapy or in combination with methotrexate. Usual Time to Effect : TNF inhibitors have a rapid onset of action sometimes with improvements seen within 2 to 4 weeks.

However, additional improvements can be seen over months. Side Effects : With all TNF antagonists, there is an increased risk of infection both mild and severe. The most common are upper respiratory infections, pneumonia, urinary tract infections, and skin infections. Studies are currently ongoing regarding the practice of temporarily holding the administration of any biologic DMARD in the presence of infection and use of antibiotics.

However, many rheumatology practices are following that practice. In addition to routine infections, opportunistic infections have been seen. Disseminated tuberculosis due to reactivation of latent disease has been seen with all TNF inhibitors; therefore, screening for latent TB is prudent before treatment with any TNF inhibitor. Invasive fungal infections, including histoplasmosis, coccidioidomycosis, candidiasis, aspergillosis, blastomycosis, and pneumocystosis have all been seen in patients receiving TNF inhibitors. Patients with histoplasmosis or other invasive fungal infections may present with disseminated, rather than localized, disease.

Antigen and antibody testing for histoplasmosis may be negative in some patients with active infection. Empiric anti-fungal therapy should be considered in patients at risk for invasive fungal infections who develop severe systemic illness. In some clinical trials of TNF antagonists, lymphomas were more commonly observed in patients treated with TNF inhibitors compared to placebo controls but the incidence rates do not appear, at this time, to exceed those reported in the RA population prior to the availability of TNF inhibitors.

It is important to note that RA itself is a risk factor for Non-Hodgkins lymphomas. Other malignancies have been seen in patients taking TNF inhibitors. There does appear to be an increase in nonmelanoma skin cancer basal and squamous cell in patients receiving these agents.

Regular dermatologic assessment is recommended with any suspicious lesions promptly evaluated. The administration of TNF inhibitors in patients with a prior malignancy should be discussed with the patient and their oncologist to assess potential risk and benefit. TNF inhibitors are not recommended in patients with demyelinating disease or with congestive heart failure. Transient neutropenia lowering of white blood cell counts or other blood dyscrasias have been reported with TNF inhibitors. Some patients develop positive antinuclear antibodies ANA , and cases of clinical lupus are reported but rare.

The new onset of psoriasis has also been seen.

Abatacept is the first of a class of agents known as T-cell costimulatory blockers. T lymphocytes become activated due to an unknown stimulus but likely involving the interaction between antigen presented in the context of the Class II Major Histocompatability Complex molecule on the surface of antigen presenting cells. T cells recognize antigens as foreign and if they receive a second stimulus, will become active, proliferate, traffic to inflamed sites, and secrete proinflammatory cytokines including TNF.

One of the important second signals for T cell activation is mediated by the molecules CD80 and CD86 found on antigen presenting cells and the CD28 molecule on the T cell surface. When abatacept binds to CD28 on the T cell surface, it prevents the second signal from being delivered, thus turning down the T cell response. Additional effects are decreasing the production of T cell derived cytokines including TNF. Abatacept is administered either via IV or subcutaneously. When given by intravenous infusion it is used once per month after initial doses at baseline, 2 weeks, and 4 weeks.

The medication is administered over a period of approximately 30 minutes to one hour.

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Responses are typically seen within 3 months. In clinical trials, patients with initial responses continued to show improvements through the first year. These have ranged from mild to severe. Respiratory infections including pneumonia were more common in clinical trials in patients with underlying COPD, thus extreme caution is suggested in this population.