Patients starting methotrexate should be carefully evaluated for renal insufficiency, acute or chronic liver disease, significant alcohol intake or alcohol abuse, leukopenia low white blood cell counts , thrombocytopenia low platelet counts , or untreated folate deficiency. Obesity, diabetes and history of hepatitis B or C are factors that have been suggested but not confirmed to increase methotrexate hepatotoxicity liver injury.
If alternatives exist, concomitant use of methotrexate and trimethoprim is to be avoided. The coadministration of NSAIDS with methotrexate is routine in patients with rheumatoid arthritis and is considered safe by rheumatologists as long as liver function tests and blood counts are closely monitored. The onset of action is seen in as early as 4 to 6 weeks. However the dose required to achieve a response is variable in individual patients and may require weeks after a dose increase to determine if the drug is working.
A trial of 3 to 6 months at an increased dose e. In patients with partial responses to methotrexate, additional medications are usually added to rather than substituted for methotrexate to achieve combination therapies. Fortunately the most serious complications of methotrexate therapy: hepatic cirrhosis, interstitial pneumonitis, and severe myelosuppression are quite rare, especially with proper monitoring.
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Stomatitis and oral ulcers, mild alopecia and hair thinning, and GI upset may occur and are related to folic acid antagonism. These side effects can be improved with folic acid supplementation. Folic acid given at a dose of 1mg daily does not diminish the efficacy of methotrexate and is routinely given with methotrexate to decrease these side effects.
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Some patients complain of GI upset nausea or diarrhea with oral methotrexate. This may be lessened when methotrexate is taken at night. In most cases this is completely eliminated when methotrexate is given by subcutaneous administration. Before starting methotrexate, baseline studies should include complete blood count, liver chemistries, serum creatinine, hepatitis B and C serologies, and chest X-ray. Routine toxicity monitoring should include a CBC, liver profile, serum albumin and serum creatinine every weeks.
In all clinical trials combining methotrexate with one of these DMARDs, no unexpected toxicities or synergistic toxicities were observed with the exception of higher liver toxicity with leflunomide which is also metabolized by the liver. Hepatotoxicity liver injury has not been significant if patients with pre-existing liver disease, alcohol abuse, or hepatic dysfunction are excluded from treatment with methotrexate. Patients are instructed to limit alcohol containing beverages to no more than one-two per week. Baseline or surveillance liver biopsies are not indicated unless pre-existing liver disease is suspected.
Elevated liver enzymes do not directly correlate with toxicity but therapy should be stopped and doses of methotrexate reduced if transaminases are elevated to 2 times the upper limit of normal. Liver biopsy should be done if elevated liver enzymes persist or if methotrexate therapy is to be continued. Methotrexate pneumonitis may occur at any time during therapy and is not dose related.
A baseline chest x-ray is useful for comparison. Patients with poor pulmonary reserve from other causes may be excluded from therapy over concerns of increased morbidity if methotrexate pneumonitis occurs. A more chronic form of interstitial lung disease and fibrosis is also seen in patients with rheumatoid arthritis. This may be increased with methotrexate.
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Myelosuppression lowering of blood counts is also rare at the low doses of methotrexate utilized for rheumatoid arthritis. In the absence of leukopenia lowered white blood cell counts , there has not been conclusive information to link methotrexate use in rheumatoid arthritis with increased risk of infection. The exception is a slight increased risk of localized herpes zoster infection shingles.
Cancer risk with methotrexate. Although there are case reports of lymphoma associated with methotrexate therapy including cases where the lymphoma resolved after cessation of therapy, increased occurrence of malignancy has not been found in large population-based studies. It is important to recognize that patient with rheumatoid arthritis have an increased risk of developing lymphoma as a consequence of their autoimmune disease, independently from any potential medication effects.
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Pregnancy and Conception with methotrexate. There have not been any notable effects on sperm production or ovarian function after the prolonged administration of methotrexate. However, methotrexate is considered a teratogen ; therefore, women of childbearing potential or men with partners of childbearing potential must practice effective birth control. Women should discontinue methotrexate for at least one ovulatory cycle prior to attempting conception, while men should wait 3 months.
Hydroxychloroquine is an antimalarial drug which is relatively safe and well-tolerated agent for the treatment of rheumatoid arthritis.
Chloroquine is another antimalarial agent that is also sometimes used. The mechanism of action of antimalarials in the treatment of patients with rheumatoid arthritis is unknown but is thought to involve changes in antigen presentation or effects on the innate immune system. Chloroquine is not commonly used because of greater toxicity on the eye. It may be prescribed as a single daily dose or in divided doses twice per day.
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A period of 2 to 4 months is usual. The most important toxicities are on the eyes: corneal deposits, extraocular muscular weakness, loss of accommodation and sensitivity to light , and a retinopathy that may progress to irreversible visual loss. 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.
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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. 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.
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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.