Your first injection must be given under the supervision of a health care professional. Make sure you have been shown how to inject HUMIRA before you do it yourself. If your doctor determines that it’s ok, HUMIRA can be taken at home. Check out patient stories to learn how other patients taking HUMIRA approach their injection routines.
Proper injection technique is important. Watch this demonstration video for step-by-step instructions on how to inject HUMIRA.
If you have any questions about injection, you can speak to a registered nurse about your HUMIRA treatment and request in-person injection training. Just call 1.800.4HUMIRA (1.800.448.6472).
Common side effects of HUMIRA include injection site reactions such as pain, redness, rash, swelling, itching, or bruising around the injection site. Call your doctor if these symptoms do not go away within a few days or get worse.
If you experience any adverse reactions or discomfort when taking HUMIRA, discuss them with your doctor right away.
TUESDAY, April 12, 2011 (HealthDay News) — In a new study, close to a third of patients taking the arthritis drug Humira developed an immune system reaction to it that rendered it ineffective.
Researchers say the finding helps to explain why some people get relief from their rheumatoid arthritis symptoms while on Humira (adalimumab), which is made by Abbott Laboratories, while others gain little or no benefit. Humira belongs to a class of drugs known as biologics.
In those people for whom the drug is ineffective, the immune system realizes the drug is a foreign substance and develops antibodies to it, researchers explained. Those antibodies bind to the drug and prevent it from working.
“What the publication shows is that Humira, like many other biologic agents, may induce an immunological response against the drug,” said senior study author Dr. Gerrit Jan Wolbink, a rheumatologist at Jan van Breemen Research Institute in the Netherlands. “The immunological response works against the drug. This is one of the explanations why some patients do not respond the way we hope they will.”
Patients who were also taking methotrexate, another arthritis drug and an immunosuppressant, were less likely to develop the antibodies, according to the study in the April 13 issue of the Journal of the American Medical Association.
Researchers followed 272 patients taking Humira for about three years.
About 28 percent developed immune system antibodies against the drug. The reaction tended to happen within the first few months of starting treatment: About 67 percent of those who developed antibodies did so during the first 28 weeks.
Patients without antibodies had more of the drug circulating in their blood. Lower levels of the drug are a sign that the body’s immune system is fighting the drug and it’s being removed from the body, Jan Wolbink explained.
Whether or not patients developed antibodies was also linked to whether they got relief from their rheumatoid arthritis while on Humira.
Nearly half — 48 percent — of those without antibodies experienced a significant reduction of their arthritis symptoms while taking the drug, while only 13 percent of those who developed antidrug antibodies got similar relief.
And while 34 percent of patients without antibodies experienced remission, only 4 percent of those who developed antibodies did.
Patients who developed antibodies were also more likely to drop out of the study because of “treatment failure.”
Humira is a tumor necrosis factor (TNF) inhibitor, which works by blocking the action of TNF, a substance known as a cytokine that contributes to the inflammation of rheumatoid arthritis and other conditions.
“If you make antibodies, then Humira doesn’t block the action of TNF, and it doesn’t work,” Jan Wolbink said.
Dr. Olga Belostotsky, a rheumatologist and chief of allergy and immunology at Lennox Hill Hospital in New York City, said the research helps explain why some patients don’t respond to Humira, and yet they do respond when switched to another drug in the same class of TNF inhibitors.
“It’s because they don’t have antibodies to the other drugs, even when it’s another drug in the same group of medications,” she said.
Belostotsky said the research suggests it’s very important that patients start methotrexate to suppress the immune system before starting Humira.
What isn’t known is why those 28 percent of patients developed antidrug antibodies while the rest didn’t.
“Why antibodies develop in some people more than the others is unclear, and why people react more to some drugs than others is unclear,” Belostotsky said.
The Arthritis Foundation has more on rheumatoid arthritis.
In both studies, patients were assessed for improvements in signs and symptoms of the disease, such as joint pain, swelling and stiffness, as well as physical function and achievement of clinical remission. Following up to 10 years of HUMIRA therapy, patients in the studies continued to maintain improvements in disease activity. In both DE019 and DE020, a DAS28 (CRP) <2.6, a measure of clinical remission, was observed in more than half of patients who continued on HUMIRA for up to 10 years (59.6 percent and 57.2 percent, respectively). A DAS28 score of <2.6 as a measure of clinical remission is supported by both EULAR and the American College of Rheumatology (ACR).
DE019 also assessed the ability of HUMIRA to inhibit radiographic progression. Patients who completed 10 years of treatment and also had X-rays available at baseline and year 10 demonstrated an average change of 2.8 in modified total Sharp score (mTSS), a measure of radiographic inhibition. In this study, patients who were initially treated with HUMIRA plus methotrexate (MTX) for the first year had less radiographic progression (measured as mean change in mTSS) at year 10 compared with patients who initially received placebo plus MTX. This result was driven by the change in mTSS during the one year randomized controlled trial.
“Managing RA is more than just treating the signs and symptoms, but also inhibiting joint damage, and improving physical function,” said Dr. Edward Keystone, Professor of Medicine, University of Toronto, Canada. “The results of these long-term studies add to the vast arsenal of evidence that rheumatologists can reference when treating their patients with RA, a disease with irreversible effects.”
Abbott’s global clinical trial database for HUMIRA is extensive and includes more than 14,000 RA patients representing more than 23,000 patient years of exposure to the medication.
“Many patients with RA are not diagnosed early in the disease process and then may not be treated as quickly as they should, which can result in long-term, and sometimes irreversible, effects of the disease,” said John Medich, Ph.D., divisional vice president, Clinical Development, Immunology, Abbott. “These long-term results on clinical response and radiographic inhibition provide additional data about the use of HUMIRA in long-standing RA and further demonstrate Abbott’s continued commitment to improving the standards of care for patients with the disease.”
Clinical outcomes were assessed by Disease Activity Score 28 (DAS28), which is a composite index that includes variables such as the number of tender and swollen joints and either erythrocyte sedimentation rate or C-reactive protein (CRP), both of which are measures of inflammation.
DE019 was a Phase 3, randomized, controlled trial in which patients with long-standing RA and an inadequate response to MTX were randomized to one year of HUMIRA 40 mg every other week (ADA-40), HUMIRA 20 mg weekly (ADA-20) or placebo (PBO) injections; all received concomitant MTX. The 52-week controlled portion of the trial demonstrated the clinical and radiographic superiority of HUMIRA plus MTX over placebo plus MTX. Of the 619 patients initially randomized, a total of 202 patients (32.6 percent) continued on open-label HUMIRA plus MTX through year 10. This post-hoc analysis evaluated the radiographic data available at baseline and year 10 for patients who had data available for both time periods.
Clinical and functional outcomes were assessed using the DAS28 and the Health Assessment Questionnaire Disability Index (HAQ-DI), which is a measure of a patient’s physical function. Radiographic damage was assessed at baseline and years one, eight and 10 using the modified total Sharp score (mTSS), which records both bone and cartilage damage (joint erosion score and joint space narrowing score, respectively) on X-ray.
After ten years in the study, patients had a mean DAS28 (CRP) of 2.6, mean HAQ-DI of 0.7 and a mean change in mTSS of 2.8. DAS28 (CRP) <2.6 was observed in more than half of patients who continued on HUMIRA for up to 10 years (59.6 percent). In the DE019 study, no new safety signals were identified following up to 10 years of HUMIRA exposure.
DE020 was a long-term, open-label, follow-up trial enrolling patients from four previous studies (including the ARMADA and STAR studies, as well as two smaller studies) in the early development program of HUMIRA. All four studies included patients with active RA and an inadequate response to MTX and/or other disease-modifying antirheumatic drugs (DMARDs). Patients could receive supplemental DMARD therapy at the investigator’s discretion after inclusion in DE020. A total of 846 patients were enrolled in this follow-up study.
Clinical and functional responses were assessed as the percentage of patients observed to achieve ACR criteria 20/50/70 responses, DAS28 <3.2 (a measure of low disease activity), DAS28 <2.6 and HAQ-DI <0.5 at year 10. ACR response criteria measure the percent improvement in tender and swollen joints, as well as patient and physician global assessment, pain, disability and inflammatory markers.
A total of 286 patients (33.8 percent) completed 10 years of treatment with HUMIRA. DAS28 (CRP) <2.6 was observed in more than half of patients (57.2 percent) at year 10. A composite of both DAS28 (CRP) <3.2 and HAQ-DI <0.5 was observed in more than one-third (37.3 percent) of patients at year 10. At baseline, the patient population showed a mean DAS28 score of 5.7, indicating high disease activity.
- 78.6 percent of patients achieved at least 20 percent improvement in the ACR criteria (ACR20)
- 55.5 percent achieved at least 50 percent improvement in the ACR criteria (ACR50)
- 32.8 percent achieved at least 70 percent improvement in the ACR criteria (ACR70)
- 71.2 percent achieved a Disease Activity Score 28
- 42.4 percent achieved a Health Assessment Questionnaire Disability Index (HAQ-DI) <0.5
No new safety signals were identified in this study following more than 10 years of HUMIRA exposure and rates of adverse events (AE) were consistent with the known safety profile of HUMIRA.
About HUMIRA® (adalimumab)
HUMIRA (adalimumab) is a prescription medicine used alone, with methotrexate, or with certain other medicines to reduce the signs and symptoms of moderate to severe rheumatoid arthritis in adults. It may prevent future damage to bones and joints and may help with the ability to perform daily activities.
Important Safety Information
HUMIRA is a TNF blocker medicine that affects the immune system and can lower the ability to fight infections. Serious infections have happened in people taking HUMIRA. These serious infections include tuberculosis (TB) and infections caused by viruses, fungi, or bacteria that have spread throughout the body. Some people have died from these infections. People should be tested for TB before HUMIRA use and monitored for signs and symptoms of TB during therapy. People at risk of TB may be treated with medicine for TB.
Treatment with HUMIRA should not be started in a person with an active infection, unless approved by a doctor. HUMIRA should be stopped if a person develops a serious infection.
People should tell their doctor if they live in or have been to a region where certain fungal infections are common, have had TB, hepatitis B, are prone to infections, or have symptoms such as fever, fatigue, cough, or sores.
For people taking TNF blockers, including HUMIRA, the chance of getting lymphoma or other cancers may increase. Some people have developed a rare type of cancer called hepatosplenic T-cell lymphoma. This type of cancer often results in death. If using TNF blockers including HUMIRA, the chance of getting two types of skin cancer (basal cell and squamous cell) may increase. These types are generally not life-threatening if treated.
Other possible serious side effects with HUMIRA include hepatitis B infection in carriers of the virus, allergic reactions, nervous system problems, blood problems, certain immune reactions, including a lupus-like syndrome, liver problems, and new or worsening heart failure or psoriasis. The use of HUMIRA with anakinra or abatacept is not recommended. People using HUMIRA should not receive live vaccines.
Common side effects of HUMIRA include injection site reactions (redness, rash, swelling, itching, or bruising), upper respiratory infections (including sinus infections), headaches, rash, and nausea.
HUMIRA is given by injection under the skin.
The benefits and risks of HUMIRA should be carefully considered before starting therapy.
Abbott is a global, broad-based health care company devoted to the discovery, development, manufacture and marketing of pharmaceuticals and medical products, including nutritionals, devices and diagnostics. The company employs approximately 91,000 people and markets its products in more than 130 countries.
Abbott’s news releases and other information are available on the company’s Web site at www.abbott.com.
Therapy with anti-tumor necrosis factor (anti-TNF) is highly effective in people with ankylosing spondylitis. But researchers suggest that patients whose treatment lost its effectiveness or resulted in adverse events can benefit from switching anti-TNF therapies.
These are the conclusions of a review study, “Ankylosing Spondylitis Treatment after First Anti-TNF Drug Failure,” published in the Israel Medical Association Journal.
Anti-TNF therapies have brought new relief to those with spondyloarthritis (SpA), but 20-30% of patients eventually stop responding properly and discontinue treatment, while 10-20% of patients stop taking their medication because their anti-TNF therapy has stopped working or from adverse effects.
These agents differ in their chemical structure and mechanism of action, which means that if one therapy no longer works for a patient, that patient can still respond to a different anti-TNF therapy.
Researchers gathered data from studies (randomized control trial, systematic review, and observational studies) conducted from 1999 to 2016, to characterize patients and treatment outcomes after the first anti-TNF failure among people with ankylosing spondylitis.
The National Danish (DANBIO) database included 432 patients, and the Norwegian database (NOR-DMARD; NCT01581294) included 77 patients, all of whom switched to a second anti-TNF drug.
Both registries revealed that most patients who switched were female, had a shorter duration of disease and symptoms, and a higher disease activity.
In addition, among those who switched, the effects of the first and second anti-TNF drug on disease activity were similar during the first year follow-up. But these registries included a higher proportion of patients achieving lower disease activity than other reports.
An earlier review study found that 30% of patients who start an anti-TNF therapy switch to a second one. However, the time between treatment initiation and discontinuation was not different between the first, second, and third anti-TNF drug.
Patients may stop responding to one anti-TNF agent because they start producing antibodies against this agent, an effect that seems to be dependent on the anti-TNF agent used.
Remicade, an antibody combining mouse and human proteins, induces the production of anti-drug antibodies more strongly than Humira/Symponi and Enbrel, both consisting of humanized proteins only.
Previous results indicate that 25.9% of spondyloarthritis patients produce anti-drug antibodies, mostly those treated with Remicade.
Because the presence of antibodies against anti-TNF therapies can worsen patients’ response to therapy, evaluating anti-drug antibody levels in ankylosing spondylitis patients may help when deciding to switch therapies.
And, the effect of anti-drug antibodies on anti-TNF responses is stronger in ankylosing spondylitis patients than in those with other inflammatory diseases.
A study involving 1,159 patients with ankylosing spondylitis found that by the end of a 12-week treatment period with Humira, 57.2% of participants had reduced disease activity, and 27.7% had reached partial remission. Among the predictors for a positive outcome was no previous treatment with anti-TNF therapies.
Another study confirmed the effectiveness of Humira, Enbrel, or Remicade in ankylosing spondylitis either as a first or second anti-TNF therapy, but found that partial remission was less likely in patients with enthesitis (inflammation at tendon, ligament or joint capsule insertions), psoriasis, or low C-reactive protein levels, an indicator of inflammation.
Data from the National Swedish Biologics Registry showed that patients with ankylosing spondylitis stayed on their first anti-TNF drug longer if they were also treated with conventional disease-modifying rheumatic drugs (DMARDs).
Additional research indicates that 30.5% of spondyloarthritis patients remain on a first-line anti-TNF drug after 10 years, but more patients stay longer on Enbril than on Remicade and Humira.
Researchers conclude that although some studies are conflicting, they suggest that switching anti-TNF therapies has become common practice in patients who fail their initial treatment. This trend is observed even though there are no published guidelines concerning the best strategy after a first anti-TNF failure.
“The most frequent reason for discontinuing is lack of efficacy but, regardless of the reason and the sequence of drugs administered, disease activity is reduced after switching,” researchers wrote, adding that “ankylosing spondylitis patients can be successfully treated with a second TNF antagonist.”
- Author Details
Ana is a molecular biologist enthusiastic about innovation and communication. In her role as a science writer she wishes to bring the advances in medical science and technology closer to the public, particularly to those most in need of them. Ana holds a PhD in Biomedical Sciences from the University of Lisbon, Portugal, during which she focused her research on molecular biology, epigenetics and infectious diseases. ×Ana is a molecular biologist enthusiastic about innovation and communication. In her role as a science writer she wishes to bring the advances in medical science and technology closer to the public, particularly to those most in need of them. Ana holds a PhD in Biomedical Sciences from the University of Lisbon, Portugal, during which she focused her research on molecular biology, epigenetics and infectious diseases. Latest Posts
- Anti-TNF-alpha drugs for treating ankylosing spondylitis
- Humira (Adalimumab)
- What are the ingredients in Humira?
- How does Humira work?
- What are the possible side effects of Humira?
- Things to note about Humira
- Dosing information
- Adalimumab in ulcerative colitis: real-life data
- Remicade vs Humira: Main Differences and Similarities
- Remicade vs Humira Side by Side Comparison
Anti-TNF-alpha drugs for treating ankylosing spondylitis
We included twenty-one, short-term (24 weeks or less) RCTs with a total of 3308 participants; 18 contributed data to the MTC analysis: adalimumab (4 studies), etanercept (8 studies), golimumab (2 studies), infliximab (3 studies), and one head-to-head study (etanercept versus infliximab) which was unblinded and considered at a higher risk of bias. The risk of selection and detection bias was low or unclear for most of the studies. The risk of selective outcome reporting was low for most studies as they reported on outcomes recommended by the Assessment of SpondyloArthritis international Society. We found little heterogeneity and no significant inconsistency in the MTC analyses. The majority of the studies were funded by pharmaceutical companies. Most studies permitted concomitant therapy of stable doses of disease-modifying anti-rheumatic drugs, non-steroidal anti-inflammatory drugs, or corticosteroids, but allowances varied across studies.
Compared with placebo, there was high quality evidence that patients on an anti-TNF agent were three to four times more likely to achieve an ASAS40 response (assessing spinal pain, function, and inflammation, as measured by the mean of intensity and duration of morning stiffness, and patient global assessment) by six months (adalimumab: risk ratio (RR) 3.53, 95% credible interval (Crl) 2.49 to 4.91; etanercept: RR 3.31, 95% Crl 2.38 to 4.53; golimumab: RR 2.90, 95% Crl 1.90 to 4.23; infliximab: RR 4.07, 95% Crl 2.80 to 5.74, with a 25% to 40% absolute difference between treatment and placebo groups. The number needed to treat (NNT) to achieve an ASAS 40 response ranged from 3 to 5.
Compared with placebo, there was moderate quality evidence (downgraded for imprecision) that patients on an anti-TNF agent were more likely to achieve an ASAS partial remission by six months (adalimumab: RR 6.28, 95% Crl 3.13 to 12.78; etanercept: RR 4.24, 95% Crl 2.31 to 8.09; golimumab: RR 5.18, 95% Crl 1.90 to 14.79; infliximab: RR 15.41, 95% Crl 5.09 to 47.98 with a 10% to 44% absolute difference between treatment and placebo groups. The NNT to achieve an ASAS partial remission response ranged from 3 to 11.
Radiographic progression was measured in one trial (N = 60) of etanercept versus placebo and it found that radiologic changes were similar in both groups (detailed data not provided).
There were few events of withdrawals due to adverse events leading to imprecision around the estimates. When all the anti-TNF agents were combined against placebo, there was moderate quality evidence from 16 studies of an increased risk of withdrawals due to adverse events in the anti-TNF group (Peto odds ratio (OR) 2.44, 95% CI 1.26 to 4.72; total events: 38/1637 in biologic group; 7/986 in placebo) though the absolute increase in harm was small (1%; 95% CI 0% to 2%).
Due to low event rates, evidence of the effect of individual TNF-inhibitors against placebo or for all four biologics pooled together versus placebo on serious adverse events is inconclusive (moderate quality; downgraded for imprecision). For all anti-TNF pooled versus placebo based on 16 studies: Peto OR 1.45, 95% CI 0.85 to 2.48; 51/1530 in biologic group; 18/878 in placebo; absolute difference: 1% (95% CI 0% to 2%).
Using indirect comparison methodology, and one head-to-head study of etanercept versus infliximab, wide confidence intervals meant that results were inconclusive for evidence of differences in the major outcomes between different anti-TNF agents. Regulatory agencies have published warnings about rare adverse events of serious infections, including tuberculosis, malignancies and lymphoma.
Humira is an engineered biologic medication that is approved for use against rheumatoid arthritis. In clinical studies, Humira helped reduce the signs and symptoms of RA for adults with moderate to severely active disease, including by slowing joint damage, improving physical functioning, increasing the quality of life in patients with RA.1,2 This medication can be used alone or in combination with methotrexate or other disease-modifying anti-rheumatic drugs (DMARDs), glucocorticoids, nonsteroidal anti-inflammatory drugs (NSAIDs), and/or analgesics.1,2
Humira is also approved for use in other autoimmune diseases, including juvenile idiopathic arthritis, psoriatic arthritis, ankylosing spondylitis, Crohn’s disease, ulcerative colitis, and plaque psoriasis.1
Humira is not available in generic forms.
What are the ingredients in Humira?
The active ingredient in Humira is adalimumab.
How does Humira work?
Humira is one of several monoclonal antibodies used to treat RA. Our bodies naturally produce antibodies, which are immune factors that act against bacteria, viruses, and other foreign organisms that invade and pose a threat to our health. Drug makers have engineered a variety of antibodies to target the mechanisms that cause certain diseases, including RA.
Humira blocks the action of tumor necrosis factor- α (TNF-α). TNF-α is an important immune system signaling factor (called a cytokine) that plays a key role in swelling and inflammation. It is found in higher levels in the synovial fluid in the joints of patients with RA, and it is connected to inflammation as well as bone and cartilage damage. Blocking TNF-α helps tamp down the damage caused by the dysfunction of the immune system that is characteristic of RA.2 It also causes cells that express TNF-α on their surface to rupture and die.1
What are the possible side effects of Humira?
Common side effects with Humira include :
- redness, itching, pain, or swelling at the site of injection
- back pain
- upper respiratory infection
In some patients, Humira can cause more harmful side effects. Patients who take Humira are at increased risk for serious infections, including tuberculosis, invasive fungal infections, viral infections, bacterial infections, and other opportunistic infections (infection caused by a microorganism that does not normally cause infection in humans, typically due to an abnormally functioning immune system).3
Children and adolescents as well as adults taking Humira are also at slightly higher risk for lymphoma and other cancers.iii Other rare but serious side effects include Hepatitis B reactivation, nerve diseases like multiple sclerosis, certain blood disorders, heart disease, and lupus-type symptoms.1
This is not an exhaustive list of all potential side effects of Humira. For more information, consult your doctor or healthcare provider. If you notice any new or worsening side effects, contact your doctor or healthcare provider immediately.
Things to note about Humira
Before taking Humira, tell your doctor if you1:
- Have a current infection or are prone to recurring infections, including open cuts
- Have HIV, diabetes, or a weakened immune system
- Have tested positive for TB or have been in close contact with someone who has TB
- Live in areas of the US where known for fungal infections, including the Ohio and Mississippi Valley and the southwest
- Have or have had Hepatitis B
- Have any nervous system problems like multiple sclerosis or Guillain-Barré syndrome
- Have or have had congestive heart failure
- Are scheduled to have surgery
- Are scheduled to receive a vaccine
- Are pregnant or plan to become pregnant or are breastfeeding
With Humira, there is an increased risk for serious infection. This is because Humira can decrease the ability of the immune system to fight infections. If an infection develops while you are taking this medication, or if you have a severe allergic reaction, contact your doctor immediately.3
Patients taking this medication should not receive live vaccines. Tell your doctor about any medications or supplements you are taking while on Humira, because it doesn’t mix well with certain medicines. It is important for doctors to test you for TB before you take Humira and to monitor for heart problems, infection, and nerve damage while you are on the medication.1
Humira comes in prefilled syringes and dosing pens and is usually administered by injection under the skin every other week. The recommended dose of Humira is 40 mg. In patients who are not taking methotrexate at the same time, there may be some benefit to increasing the frequency of Humira dosing to once every week. Your doctor will decide how often you should take this medicine.1
You will be given your first dose of Humira in a medical office, and after that, you may be able to administer it at home. Before injecting Humira, remove the syringe or pen from the refrigerator and place it on a flat surface without removing the cap. Allow it to come to room temperature for 15 to 30 minutes before you inject it. You can inject Humira anywhere on the front of your thighs or stomach except within 2 inches of your navel. Use a different site for each injection, to reduce soreness at the injection site.4
Make sure you have been instructed about how to give an injection of Humira before you do it yourself. If you have any questions about how to prepare and administer Humira, call your doctor.4
Adalimumab in ulcerative colitis: real-life data
Although adalimumab has been recently licensed, multiple lines of evidence from open-label and retrospective studies on adalimumab, administered for compassionate use in ulcerative colitis patients, have been available for several years (Table 1). Oussalah et al27 first presented data on 13 ulcerative colitis patients treated with adalimumab in 2008. All of the patients had been previously treated with infliximab, and most of them (90.31%) had been previously treated with thiopurines. Patients were treated with adalimumab, with an induction dose of 160/80 mg at weeks 0 and 2, and then maintained with 40 mg EOW. The primary endpoint was defined as the proportion of patients on adalimumab therapy during the study. After a median follow-up of 41 weeks, the percentage of patients remaining on adalimumab therapy was 32.5%. Eight patients discontinued adalimumab: six due to colectomy, one due to lack of response, and one due to an exacerbation of psoriasis. No significant differences were found in adalimumab withdrawal and colectomy rates between the patients who lost response to infliximab and those who became intolerant. From this small cohort of difficult-to-treat patients who had already been treated with all of the main available therapies, adalimumab treatment potentially avoided colectomy in about half of them.
One year later, the Mayo Clinic Group published the results of an uncontrolled, open-label study on adalimumab in 20 patients with ulcerative colitis, of whom 35% were naïve to infliximab. All patients had active disease (defined as a Mayo score of 6–12 points, with an endoscopic subscore of at least 2) despite concurrent treatment (steroids, and/or thiopurines, and/or aminosalicylates). Patients were treated with adalimumab at an induction dose of 160/80 mg at weeks 0 and 2, respectively, and maintained with 40 mg EOW. The primary endpoint was defined as the proportion of patients achieving a clinical response at week 8. The percentages of patients who had a clinical remission or response were 5% and 25% at week 8, respectively and 25% and 50% at week 24, respectively. No significant differences were found between infliximab-naïve and infliximab-exposed patients. Among the patients who entered the trial on corticosteroids, 58% were able to withdraw by week 24, showing the potential effectiveness of adalimumab as a steroid-sparing agent.28
Hudis et al29 retrospectively reported data on nine patients, with active ulcerative colitis (mean Mayo score of 6 ± 1.66 at baseline) and secondary infliximab failure, who were treated with adalimumab (induction, 160/80 mg at weeks 0/2; maintenance, 40 mg EOW). During the follow-up, adalimumab was found to be effective at inducing a clinical response (mean Mayo score, 2.5 ± 1) (P < 0.0005), with a steroid-sparing effect (P < 0.003).
Gies et al,30 in 2010, also reported “real life” data, from a single referral center, involving 53 ulcerative colitis outpatients treated with biologic drugs, following a structured protocol for a “step-up” approach. All patients were intolerant and/or nonresponders to conventional therapy, including aminosalicylates, steroids, and thiopurines. Among them, 25 patients were treated with adalimumab (160/80 mg at weeks 0 and 2, then 40 mg EOW) and 28 with infliximab (5 mg/kg at weeks 0, 2, and 6, then every 8 weeks). Most of patients had extensive colitis (96% in the adalimumab group and 90% in the infliximab group). Concomitant immunosuppressive therapy (azathioprine or methotrexate) was taken by significantly fewer patients in the adalimumab group (20% vs 53.4%) (P = 0.0118). The primary endpoint was defined as the proportion of patients treated with adalimumab or infliximab achieving and maintaining a clinical response. At 14 weeks, 47 of the 53 (88.7%) patients had a clinical response to anti-TNF therapy, without a significant difference between the adalimumab (20/25 patients, 80%) and infliximab (27/28 patients, 96%) groups (P = 0.0889). Among the patients who entered the maintenance treatment phase, 14⁄20 adalimumab (70.0%) and 14⁄18 (77.8%) infliximab patients had a response up to the end of follow-up (P = 0.7190). The median duration for the maintenance phase was 54.5 weeks (range, 3–108 weeks) for the adalimumab group and 64.5 weeks (range, 8–180 weeks) for the infliximab group. Of the six adalimumab patients who lost response, two underwent colectomy, one switched to infliximab, and three were treated with another course of steroids. About 92% of the patients who were initially taking steroids were able to stop over the course of the maintenance period, with similar results observed in both groups. Thus, in this “real life” cohort, adalimumab seemed to be as effective as infliximab at achieving induction and maintenance responses in ulcerative colitis patients.
The effectiveness of adalimumab in a real-life setting has also been reported in a Spanish retrospective multicenter study that enrolled 30 ulcerative colitis patients after the failure of other therapies. All patients were infliximab experienced: 53.3% had lost responsiveness, 40% had become intolerant, and 6.7% were primary nonresponders. Adalimumab was administered to 26 patients because of moderate-to-severe, refractory ulcerative colitis, and four patients received adalimumab because of a severe attack that was refractory to intravenous corticosteroids. All patients received a loading dose of 160/80 mg of adalimumab at weeks 0 and 2, respectively and were maintained with 40 mg EOW. Patients were assessed at weeks 4 and 12, and then every 4 weeks in order to evaluate the short- and long-term outcomes. The primary endpoint was defined as the induction of a clinical response at week 12. Sixteen (53.3%) and 18 (60%) patients achieved a clinical response at week 4 and 12, respectively. Three (10%) and eight (26.7%) patients achieved a clinical remission at week 4 and 12, respectively. Fifteen (50%) patients discontinued adalimumab during the median follow-up of 48 weeks (interquartile range , 16–104), and 13 (86.6%) of them discontinued because of a lack or loss of response, including four inpatients with severe intravenous corticosteroid-refractory disease. All patients who were under corticosteroid treatment at baseline and entered the maintenance adalimumab treatment were able to discontinue the steroids. The rate of colectomy was 20%, with a median time to colectomy of 16 weeks (IQR, 5.2–40.5 weeks). A lack of response at week 12 was associated with an increased probability of withdrawal (P = 0.001) and a higher rate of colectomy (P = 0.001). Thus, adalimumab induced a durable clinical response in a good percentage of patients with medically refractory ulcerative colitis, especially in those who achieved short-term clinical response.31
The same issue was also addressed by McDermott et al,32 who collected data on 23 patients with ulcerative colitis treated with adalimumab (standard induction and maintenance treatment). Twenty-two of the patients (96%) had received prior immunomodulatory therapy and 20 (86%) had previously been treated with infliximab (three primary nonresponders, eleven secondary failures, and six who experienced side effects). The primary endpoint was defined as treatment failure. During a median follow-up period of 22 months (IQR, 8–32 months), 16 patients (69.5%) discontinued adalimumab. The reasons for discontinuation were primary nonresponse in six patients (37%), secondary nonresponse in eight (50%), and side effects in one (6%). Nine patients underwent colectomy, and three refused surgery; the colectomy-free survival was estimated to be 78% at 6 months, 70% at 12 months, and 59% at 2 years. No significant predictors of colectomy were identified, but 55% of patients who underwent surgery had failed adalimumab treatment within 3 months of starting treatment.32
Further findings by Ferrante et al33 confirmed that adalimumab is effective in inducing a durable clinical remission in patients who have already been treated with infliximab. Fifty patients with moderate-to-severe ulcerative colitis received adalimumab induction treatment (160/80 mg at weeks 0 and 2, followed by 40 mg EOW). The primary endpoint was the long-term efficacy of adalimumab. At week 4, 68% patients showed a short-term clinical response. In particular, 22% of the patients achieved a complete clinical response, defined as the absence of diarrhea and bloody stools, and 46% of the patients achieved a partial response, defined as a marked clinical improvement, with persisting rectal blood loss. After a median follow-up of 23 months, 52% achieved a durable response to adalimumab, defined as a lasting clinical response. Colectomy was necessary in 20% of patients. Dose escalation was necessary in 76% of patients and was associated with significantly increased serum adalimumab levels (from 4.75 to 7.95 μg/mL) (P = 0.023). Short-term clinical response and response to dose escalation were associated with colectomy-free survival (P = 0.030 and P < 0.001, respectively).
Data from the Spanish ENEIDA (Estudio Nacional en Enfermedad Inflamatoria Intestinal sobre Determinantes genéticos y Ambientales) registry of 48 patients with ulcerative colitis treated with adalimumab (induction dose, 160/80 mg at weeks 0 and 2, in 93.7% of patients; maintenance dose, 40 mg EOW) have been recently reported.31 Among these patients, 39 (81.3%) had previously received infliximab and were categorized into one of three categories: remission, 51.3%; response, 33.3%; and primary nonresponse, 15.4%. The primary endpoint was defined as the proportion of patients achieving a clinical response during the follow-up period. The clinical response rates were assessed at weeks 12, 28, and 54 and were 70.8% (34/48), 43.2% (19/44), and 35% (14/40), respectively. A response to prior treatment with infliximab was the only factor predictive of a response to adalimumab at week 12, which was obtained in 90% of infliximab remitters, 53.8% of responders, and 33.3% of primary nonresponders (P = 0.01). Eleven patients (22.9%) needed colectomy after a mean time of 205 days. A lack of response to adalimumab at week 12 was shown to be an independent predictor of colectomy: five of the 34 (14.7%) responders and six of the 14 (42.9%) nonresponders (P = 0.035) required a colectomy, with a colectomy-free time that was significantly reduced among the nonresponding patients (P = 0.01).34
The last real-life experience comes from an Italian multicenter study that represents the largest case series of active ulcerative colitis treated with adalimumab. Eighty-eight patients were treated with adalimumab (induction dose of 160 mg/80 mg in 77 patients and 80 mg/40 mg in eleven patients , at weeks 0 and 2, respectively). After induction, the patients were maintained with adalimumab 40 mg EOW; a dose escalation was allowed at the physician’s discretion. All patients had active disease (medium partial Mayo score, 6) (IQR, 4–8), and 57 (64.8%) had extensive colitis. Sixty-nine patients (78.4%) had been previously treated with infliximab, and 65 (73.9%) had been exposed to immunomodulators (azathioprine, methotrexate, and cyclosporine). The indications for adalimumab treatment were corticosteroid dependence in 41 patients (46.6%), corticosteroid resistance in 23 patients (26.1%), extraintestinal manifestations in 14 patients (15.9%), and a combination of corticosteroid dependence and extraintestinal manifestations in ten patients (11.4%). The median duration of adalimumab therapy was 13 months (IQR, 6–21 months), with a median follow-up duration of 15.5 months (IQR, 12–24 months). The co-primary endpoints were defined as the proportion of patients achieving clinical remission (partial Mayo score ≤ 1) at 4, 12, 24, and 54 weeks. The clinical remission rates were 17%, 28.4%, 36.4%, and 43.2% at 4, 12, 24, and 54 weeks, respectively, with no significant differences between the infliximab-naïve and infliximab-exposed patients. Fifteen patients (17%) achieved sustained clinical remission, defined as a lasting clinical remission from week 12 up to 24 and 54 weeks. Among the 60 patients who were taking steroids at baseline, 56.7% were able to discontinue steroids, and a steroid-free remission was achieved in 24 of 60 patients (40.0%) at week 54. Fifty-seven patients underwent baseline and follow-up endoscopy after a median of 11 months (IQR, 5.1–13.2 months). An endoscopic remission was achieved in 28 (49.1%) of 57 patients, and 15 (26.3%) of the 57 achieved complete mucosal healing. Overall, 25% (22 of 88) of the patients required colectomy, with a median time to colectomy of 5.5 months (IQR, 3–13 months). The rate of colectomy was higher in the infliximab-exposed group than in the infliximab-naïve group (28.9% vs 10.5%), but this result did not achieve statistical significance, probably because of the small number of patients who ultimately required surgery and the small number of infliximab-naïve patients enrolled in the study. In conclusion, in this large, real-life cohort of refractory and difficult-to-treat ulcerative colitis patients, adalimumab was shown to be effective at inducing and maintaining a durable clinical remission and to have a steroid-sparing effect.35
Sept. 28, 2012 — The FDA has approved Abbott’s Humira for the treatment of moderate to severe ulcerative colitis.
Humira (adalimumab) now is approved for both forms of inflammatory bowel disease (IBD): ulcerative colitis and Crohn’s disease.
It was already approved to treat Crohn’s disease, rheumatoid arthritis, psoriatic arthritis, plaque psoriasis, juvenile idiopathic arthritis, and ankylosing spondylitis.
For ulcerative colitis, Humira is approved when other drugs to suppress immune responses haven’t worked.
“Each patient with ulcerative colitis experiences the disease differently, and treatment must be adjusted to meet each individual’s needs,” says Donna Griebel, MD, director of the FDA’s gastroenterology division. “Today’s approval provides an important new treatment option for patients who have had an inadequate response to conventional therapy.”
Clinical studies tested Humira in treating ulcerative colitis patients with moderate to very severe disease. Clinical remission — defined as relatively mild disease — happened after eight weeks of Humira treatment in 16.5% to 18.5% of patients, compared to 9.2% to 9.3% of patients given an inactive placebo.
The FDA-approved dosing regimen for Humira for ulcerative colitis begins with an initial dose of 160 milligrams, a second dose two weeks later of 80 mg, and a maintenance dose of 40 mg every other week, thereafter. The drug is given by injection.
Ulcerative colitis patients who do not get clinical remission after eight weeks of treatment should stop taking Humira.
Common side effects of Humira include infections, reactions at the injection site, headache, and rash.
Remicade vs Humira: Main Differences and Similarities
Remicade (infliximab) and Humira (adalimumab) are two medications that can treat inflammatory conditions such as rheumatoid arthritis, Crohn’s disease, and ulcerative colitis. Both medications are classified as monoclonal antibodies that work by blocking specific immune responses. By blocking inflammatory processes, Remicade and Humira can provide valuable relief for certain conditions. Their similarities and differences will be reviewed here.
Remicade is the brand name for infliximab. It is approved to treat Crohn’s disease in both adults and children. It is also approved to treat inflammatory conditions such as rheumatoid arthritis, but only in combination with another drug called methotrexate.
Remicade is given as an intravenous infusion by a healthcare professional. This means that you will have to make a doctor’s visit for each infusion.
Remicade is dosed in different intervals when it is first started. For example, after the first dose, it is given after 2 weeks and then after 6 weeks. After that, it is given every other month when treating Crohn’s disease in adults.
Remicade is not recommended at certain doses in people with severe heart failure.
Humira is the brand name for adalimumab. It is approved to treat Crohn’s disease among other inflammatory conditions. It can also be used alone or with methotrexate to treat rheumatoid arthritis in adults and children.
Humira can be given as an injection under the skin at home. It is available as a 40 mg/0.4 mL, 40 mg/0.8 mL, and 80 mg/0.8 mL single-use prefilled pen. Prefilled syringes can also be used.
When treating Crohn’s disease in adults, the maintenance dose is given every other week.
Remicade vs Humira Side by Side Comparison
Remicade and Humira are two drugs that can be used to treat similar conditions. Despite their similarities, they also have some differences to review. Their features can be compared below.
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Remicade (infliximab) and Humira (adalimumab) are similar prescription medications that can treat inflammatory conditions. Both drugs work as monoclonal antibodies and, more specifically as TNF blockers, to treat inflammation.
Humira can be used to treat rheumatoid arthritis in adults and children aged 2 years and older. Unlike Humira, Remicade was not shown to be useful for children aged 2 years and older with rheumatoid arthritis. However, it can still be used in adults with rheumatoid arthritis.
Remicade is given as an intravenous infusion that must be administered by a healthcare professional. Humira, on the other hand, is administered as a single-use pen or syringe injection that can be given at home.
Both Remicade and Humira have similar side effects and drug interactions. For example, they both increase the risk of infections due to possible effects on the immune system. For the same reason, they should not be used with live vaccines or other drugs that may affect the immune system.
It is important to discuss these medications with your doctor. Due to some differences in how they are used, it is important to review your overall condition. The information presented here is meant to be an educational overview.