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What is Humira (adalimumab)?
- rheumatoid arthritis,
- psoriatic arthritis,
- ankylosing spondylitis, and
- Crohn's disease of the intestine.
Common side effects of Humira include
- stomach upset, and
- injection site reactions (swelling, redness, pain and itching).
Serious side effects of Humira include
- serious infections such as tuberculosis,
- sepsis (bacteria in the blood) and fungal infections;
- hypersensitivity reactions (including anaphylaxis), and
- reduced levels of platelets and red blood cells (aplastic anemia).
- Drugs that may cause harmful interactions when taken with Humira include
- other biologic DMARDS (e.g., anakinra and abatacept),
- other TNF blockers,
- live vaccines,
- cyclosporine, and
Tell your doctor if you are pregnant or plan to become pregnant before using Humira; it is unknown how it would affect a fetus. It is unknown if this drug passes into breast milk. Similar drugs pass into breast milk. Consult your doctor before breastfeeding.
What are the important side effects of Humira (adalimumab)?
Individuals with active infections should not be treated with adalimumab. Adalimumab also may worsen the symptoms of diseases of the nervous system. In studies some patients who used adalimumab or other TNF blocking drugs developed cancer. Since patients with rheumatoid arthritis have a higher rate of cancers than the general population, the connection between cancer and use of adalimumab is unclear.
Common side effects
The most common side effects are:
Adalimumab may cause swelling, redness, pain and itching at the site of injection. Adalimumab suppresses the immune system and is therefore associated with minor infections of the urinary tract, respiratory tract, and sinuses.
Other side effects of adalimumab include:
- hypersensitivity reactions (including anaphylaxis) and
- reduced levels in the blood of platelets and red cells (aplastic anemia).
Adalimumab may increase the risk of reactivating hepatitis B virus in chronic carriers of the virus.
Humira (adalimumab) side effects list for healthcare professionals
The most serious adverse reactions described elsewhere in the labeling include the following:
- Serious Infections
Clinical Trials Experience
Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice.
The most common adverse reaction with Humira was injection site reactions. In placebocontrolled trials, 20% of patients treated with Humira developed injection site reactions (erythema and/or itching, hemorrhage, pain or swelling), compared to 14% of patients receiving placebo. Most injection site reactions were described as mild and generally did not necessitate drug discontinuation.
The proportion of patients who discontinued treatment due to adverse reactions during the double-blind, placebo-controlled portion of studies in patients with RA (i.e., Studies RA-I, RAII, RA-III and RA-IV) was 7% for patients taking Humira and 4% for placebo-treated patients. The most common adverse reactions leading to discontinuation of Humira in these RA studies were clinical flare reaction (0.7%), rash (0.3%) and pneumonia (0.3%).
In the controlled portions of the 39 global Humira clinical trials in adult patients with RA, PsA, AS, CD, UC, Ps, HS and UV, the rate of serious infections was 4.3 per 100 patient-years in 7973 Humira-treated patients versus a rate of 2.9 per 100 patient-years in 4848 control-treated patients. Serious infections observed included pneumonia, septic arthritis, prosthetic and postsurgical infections, erysipelas, cellulitis, diverticulitis, and pyelonephritis.
Tuberculosis And Opportunistic Infections
In 52 global controlled and uncontrolled clinical trials in RA, PsA, AS, CD, UC, Ps, HS and UV that included 24,605 Humira-treated patients, the rate of reported active tuberculosis was 0.20 per 100 patient-years and the rate of positive PPD conversion was 0.09 per 100 patient-years. In a subgroup of 10,113 U.S. and Canadian Humira-treated patients, the rate of reported active TB was 0.05 per 100 patient-years and the rate of positive PPD conversion was 0.07 per 100 patient-years. These trials included reports of miliary, lymphatic, peritoneal, and pulmonary TB. Most of the TB cases occurred within the first eight months after initiation of therapy and may reflect recrudescence of latent disease. In these global clinical trials, cases of serious opportunistic infections have been reported at an overall rate of 0.05 per 100 patient-years. Some cases of serious opportunistic infections and TB have been fatal.
In the rheumatoid arthritis controlled trials, 12% of patients treated with Humira and 7% of placebo-treated patients that had negative baseline ANA titers developed positive titers at week 24. Two patients out of 3046 treated with Humira developed clinical signs suggestive of newonset lupus-like syndrome. The patients improved following discontinuation of therapy. No patients developed lupus nephritis or central nervous system symptoms. The impact of long-term treatment with Humira on the development of autoimmune diseases is unknown.
Liver Enzyme Elevations
There have been reports of severe hepatic reactions including acute liver failure in patients receiving TNF-blockers. In controlled Phase 3 trials of Humira (40 mg SC every other week) in patients with RA, PsA, and AS with control period duration ranging from 4 to 104 weeks, ALT elevations ≥ 3 x ULN occurred in 3.5% of Humira-treated patients and 1.5% of controltreated patients. Since many of these patients in these trials were also taking medications that cause liver enzyme elevations (e.g., NSAIDS, MTX), the relationship between Humira and the liver enzyme elevations is not clear. In a controlled Phase 3 trial of Humira in patients with polyarticular JIA who were 4 to 17 years, ALT elevations ≥ 3 x ULN occurred in 4.4% of Humira-treated patients and 1.5% of control-treated patients (ALT more common than AST); liver enzyme test elevations were more frequent among those treated with the combination of Humira and MTX than those treated with Humira alone. In general, these elevations did not lead to discontinuation of Humira treatment. No ALT elevations ≥ 3 x ULN occurred in the open-label study of Humira in patients with polyarticular JIA who were 2 to <4 years.
In controlled Phase 3 trials of Humira (initial doses of 160 mg and 80 mg, or 80 mg and 40 mg on Days 1 and 15, respectively, followed by 40 mg every other week) in adult patients with CD with a control period duration ranging from 4 to 52 weeks, ALT elevations ≥ 3 x ULN occurred in 0.9% of Humira-treated patients and 0.9% of control-treated patients. In the Phase 3 trial of Humira in pediatric patients with Crohn's disease which evaluated efficacy and safety of two body weight based maintenance dose regimens following body weight based induction therapy up to 52 weeks of treatment, ALT elevations ≥ 3 x ULN occurred in 2.6% (5/192) of patients, of whom 4 were receiving concomitant immunosuppressants at baseline; none of these patients discontinued due to abnormalities in ALT tests. In controlled Phase 3 trials of Humira (initial doses of 160 mg and 80 mg on Days 1 and 15 respectively, followed by 40 mg every other week) in patients with UC with control period duration ranging from 1 to 52 weeks, ALT elevations ≥3 x ULN occurred in 1.5% of Humira-treated patients and 1.0% of control-treated patients. In controlled Phase 3 trials of Humira (initial dose of 80 mg then 40 mg every other week) in patients with Ps with control period duration ranging from 12 to 24 weeks, ALT elevations ≥ 3 x ULN occurred in 1.8% of Humira-treated patients and 1.8% of control-treated patients. In controlled trials of Humira (initial doses of 160 mg at Week 0 and 80 mg at Week 2, followed by 40 mg every week starting at Week 4), in subjects with HS with a control period duration ranging from 12 to 16 weeks, ALT elevations ≥ 3 x ULN occurred in 0.3% of Humira-treated subjects and 0.6% of control-treated subjects. In controlled trials of Humira (initial doses of 80 mg at Week 0 followed by 40 mg every other week starting at Week 1) in adult patients with uveitis with an exposure of 165.4 PYs and 119.8 PYs in Humira-treated and control-treated patients, respectively, ALT elevations ≥ 3 x ULN occurred in 2.4% of Humira-treated patients and 2.4% of control-treated patients.
Patients in Studies RA-I, RA-II, and RA-III were tested at multiple time points for antibodies to adalimumab during the 6- to 12-month period. Approximately 5% (58 of 1062) of adult RA patients receiving Humira developed low-titer antibodies to adalimumab at least once during treatment, which were neutralizing in vitro. Patients treated with concomitant methotrexate (MTX) had a lower rate of antibody development than patients on Humira monotherapy (1% versus 12%). No apparent correlation of antibody development to adverse reactions was observed. With monotherapy, patients receiving every other week dosing may develop antibodies more frequently than those receiving weekly dosing. In patients receiving the recommended dosage of 40 mg every other week as monotherapy, the ACR 20 response was lower among antibody-positive patients than among antibody-negative patients. The long-term immunogenicity of Humira is unknown.
In patients with polyarticular JIA who were 4 to 17 years of age, adalimumab antibodies were identified in 16% of Humira-treated patients. In patients receiving concomitant MTX, the incidence was 6% compared to 26% with Humira monotherapy. In patients with polyarticular JIA who were 2 to <4 years of age or 4 years of age and older weighing <15 kg, adalimumab antibodies were identified in 7% (1 of 15) of Humira-treated patients, and the one patient was receiving concomitant MTX.
In patients with AS, the rate of development of antibodies to adalimumab in Humira-treated patients was comparable to patients with RA.
In patients with PsA, the rate of antibody development in patients receiving Humira monotherapy was comparable to patients with RA; however, in patients receiving concomitant MTX the rate was 7% compared to 1% in RA.
In adult patients with CD, the rate of antibody development was 3%.
In pediatric patients with Crohn's disease, the rate of antibody development in patients receiving Humira was 3%. However, due to the limitation of the assay conditions, antibodies to adalimumab could be detected only when serum adalimumab levels were < 2 mcg/mL. Among the patients whose serum adalimumab levels were < 2 mcg/mL (approximately 32% of total patients studied), the immunogenicity rate was 10%.
In patients with moderately to severely active UC, the rate of antibody development in patients receiving Humira was 5%. However, due to the limitation of the assay conditions, antibodies to adalimumab could be detected only when serum adalimumab levels were < 2 mcg/mL. Among the patients whose serum adalimumab levels were < 2 mcg/mL (approximately 25% of total patients studied), the immunogenicity rate was 20.7%.
In patients with Ps, the rate of antibody development with Humira monotherapy was 8%. However, due to the limitation of the assay conditions, antibodies to adalimumab could be detected only when serum adalimumab levels were < 2 mcg/mL. Among the patients whose serum adalimumab levels were < 2 mcg/mL (approximately 40% of total patients studied), the immunogenicity rate was 20.7%. In Ps patients who were on Humira monotherapy and subsequently withdrawn from the treatment, the rate of antibodies to adalimumab after retreatment was similar to the rate observed prior to withdrawal.
Anti-adalimumab antibodies were measured in clinical trials of subjects with moderate to severe HS with two assays (an original assay capable of detecting antibodies when serum adalimumab concentrations declined to < 2 mcg/mL and a new assay that is capable of detecting antiadalimumab antibody titers in all subjects, independent of adalimumab concentration). Using the original assay, the rate of anti-adalimumab antibody development in subjects treated with Humira was 6.5%. Among subjects who stopped Humira treatment for up to 24 weeks and in whom adalimumab serum levels subsequently declined to < 2 mcg/mL (approximately 22% of total subjects studied), the immunogenicity rate was 28%. Using the new titer-based assay, antiadalimumab antibody titers were measurable in 61% of HS subjects treated with Humira. Antibodies to adalimumab were associated with reduced serum adalimumab concentrations. In general, the extent of reduction in serum adalimumab concentrations is greater with increasing titers of antibodies to adalimumab. No apparent association between antibody development and safety was observed.
In adult patients with non-infectious uveitis, anti-adalimumab antibodies were identified in 4.8% (12/249) of patients treated with adalimumab. However, due to the limitation of the assay conditions, antibodies to adalimumab could be detected only when serum adalimumab levels were < 2 mcg/mL. Among the patients whose serum adalimumab levels were < 2 mcg/Ml (approximately 23% of total patients studied), the immunogenicity rate was 21.1%. Using an assay which could measure an anti-adalimumab antibody titer in all patients, titers were measured in 39.8% (99/249) of non-infectious uveitis adult patients treated with adalimumab. No correlation of antibody development to safety or efficacy outcomes was observed.
The data reflect the percentage of patients whose test results were considered positive for antibodies to adalimumab or titers, and are highly dependent on the assay. The observed incidence of antibody (including neutralizing antibody) positivity in an assay is highly dependent on several factors including assay sensitivity and specificity, assay methodology, sample handling, timing of sample collection, concomitant medications, and underlying disease. For these reasons, comparison of the incidence of antibodies to adalimumab with the incidence of antibodies to other products may be misleading.
Other Adverse Reactions
Rheumatoid Arthritis Clinical Studies
The data described below reflect exposure to Humira in 2468 patients, including 2073 exposed for 6 months, 1497 exposed for greater than one year and 1380 in adequate and well-controlled studies (Studies RA-I, RA-II, RA-III, and RA-IV). Humira was studied primarily in placebo- controlled trials and in long-term follow up studies for up to 36 months duration. The population had a mean age of 54 years, 77% were female, 91% were Caucasian and had moderately to severely active rheumatoid arthritis. Most patients received 40 mg Humira every other week.
Table 1 summarizes reactions reported at a rate of at least 5% in patients treated with Humira 40 mg every other week compared to placebo and with an incidence higher than placebo. In Study RA-III, the types and frequencies of adverse reactions in the second year open-label extension were similar to those observed in the one-year double-blind portion.
Table 1: Adverse Reactions Reported by ≥5% of
Patients Treated with Humira During Placebo-Controlled Period of Pooled RA
Studies (Studies RA-I, RA-II, RA-III, and RA-IV)
|Humira 40 mg subcutaneous Every Other Week
|Adverse Reaction (Preferred Term)|
|Upper respiratory infection||17%||13%|
|Laboratory test abnormal||8%||7%|
|Alkaline phosphatase increased||5%||3%|
|Injection site reaction **||8%||1%|
|Urinary tract infection||8%||5%|
|* Laboratory test abnormalities were reported as adverse
reactions in European trials
** Does not include injection site erythema, itching, hemorrhage, pain or swelling
Less Common Adverse Reactions In Rheumatoid Arthritis Clinical Studies
Other infrequent serious adverse reactions that do not appear in the Warnings and Precautions or Adverse Reaction sections that occurred at an incidence of less than 5% in Humira-treated patients in RA studies were:
Body As A Whole: Pain in extremity, pelvic pain, surgery, thorax pain
Cardiovascular System: Arrhythmia, atrial fibrillation, chest pain, coronary artery disorder, heart arrest, hypertensive encephalopathy, myocardial infarct, palpitation, pericardial effusion, pericarditis, syncope, tachycardia
Endocrine System: Parathyroid disorder
Hemic And Lymphatic System: Agranulocytosis, polycythemia
Special Senses: Cataract
Thrombosis: Thrombosis leg
Urogenital System: Cystitis, kidney calculus, menstrual disorder
Juvenile Idiopathic Arthritis Clinical Studies
In general, the adverse reactions in the Humira-treated patients in the polyarticular juvenile idiopathic arthritis (JIA) trials (Studies JIA-I and JIA-II) were similar in frequency and type to those seen in adult patients. Important findings and differences from adults are discussed in the following paragraphs.
In Study JIA-I, Humira was studied in 171 patients who were 4 to 17 years of age, with polyarticular JIA. Severe adverse reactions reported in the study included neutropenia, streptococcal pharyngitis, increased aminotransferases, herpes zoster, myositis, metrorrhagia, and appendicitis. Serious infections were observed in 4% of patients within approximately 2 years of initiation of treatment with Humira and included cases of herpes simplex, pneumonia, urinary tract infection, pharyngitis, and herpes zoster.
In Study JIA-I, 45% of patients experienced an infection while receiving Humira with or without concomitant MTX in the first 16 weeks of treatment. The types of infections reported in Humira-treated patients were generally similar to those commonly seen in polyarticular JIA patients who are not treated with TNF blockers. Upon initiation of treatment, the most common adverse reactions occurring in this patient population treated with Humira were injection site pain and injection site reaction (19% and 16%, respectively). A less commonly reported adverse event in patients receiving Humira was granuloma annulare which did not lead to discontinuation of Humira treatment.
In the first 48 weeks of treatment in Study JIA-I, non-serious hypersensitivity reactions were seen in approximately 6% of patients and included primarily localized allergic hypersensitivity reactions and allergic rash.
In Study JIA-I, 10% of patients treated with Humira who had negative baseline anti-dsDNA antibodies developed positive titers after 48 weeks of treatment. No patient developed clinical signs of autoimmunity during the clinical trial.
Approximately 15% of patients treated with Humira developed mild-to-moderate elevations of creatine phosphokinase (CPK) in Study JIA-I. Elevations exceeding 5 times the upper limit of normal were observed in several patients. CPK levels decreased or returned to normal in all patients. Most patients were able to continue Humira without interruption.
In Study JIA-II, Humira was studied in 32 patients who were 2 to <4 years of age or 4 years of age and older weighing <15 kg with polyarticular JIA. The safety profile for this patient population was similar to the safety profile seen in patients 4 to 17 years of age with polyarticular JIA.
In Study JIA-II, 78% of patients experienced an infection while receiving Humira. These included nasopharyngitis, bronchitis, upper respiratory tract infection, otitis media, and were mostly mild to moderate in severity. Serious infections were observed in 9% of patients receiving Humira in the study and included dental caries, rotavirus gastroenteritis, and varicella.
In Study JIA-II, non-serious allergic reactions were observed in 6% of patients and included intermittent urticaria and rash, which were all mild in severity.
Psoriatic Arthritis And Ankylosing Spondylitis Clinical Studies
Humira has been studied in 395 patients with psoriatic arthritis (PsA) in two placebocontrolled trials and in an open label study and in 393 patients with ankylosing spondylitis (AS) in two placebo-controlled studies. The safety profile for patients with PsA and AS treated with Humira 40 mg every other week was similar to the safety profile seen in patients with RA, Humira Studies RA-I through IV.
Adult Crohn's Disease Clinical Studies
Humira has been studied in 1478 adult patients with Crohn's disease (CD) in four placebocontrolled and two open-label extension studies. The safety profile for adult patients with CD treated with Humira was similar to the safety profile seen in patients with RA.
Pediatric Crohn's Disease Clinical Studies
Humira has been studied in 192 pediatric patients with Crohn's disease in one double-blind study (Study PCD-I) and one open-label extension study. The safety profile for pediatric patients with Crohn's disease treated with Humira was similar to the safety profile seen in adult patients with Crohn's disease.
During the 4-week open label induction phase of Study PCD-I, the most common adverse reactions occurring in the pediatric population treated with Humira were injection site pain and injection site reaction (6% and 5%, respectively).
A total of 67% of children experienced an infection while receiving Humira in Study PCD-I. These included upper respiratory tract infection and nasopharyngitis.
A total of 5% of children experienced a serious infection while receiving Humira in Study PCD-I. These included viral infection, device related sepsis (catheter), gastroenteritis, H1N1 influenza, and disseminated histoplasmosis.
In Study PCD-I, allergic reactions were observed in 5% of children which were all non-serious and were primarily localized reactions.
Ulcerative Colitis Clinical Studies
Humira has been studied in 1010 patients with ulcerative colitis (UC) in two placebocontrolled studies and one open-label extension study. The safety profile for patients with UC treated with Humira was similar to the safety profile seen in patients with RA.
Plaque Psoriasis Clinical Studies
Humira has been studied in 1696 subjects with plaque psoriasis (Ps) in placebo-controlled and open-label extension studies. The safety profile for subjects with Ps treated with Humira was similar to the safety profile seen in subjects with RA with the following exceptions. In the placebo-controlled portions of the clinical trials in Ps subjects, Humira-treated subjects had a higher incidence of arthralgia when compared to controls (3% vs. 1%).
Hidradenitis Suppurativa Clinical Studies
Humira has been studied in 727 subjects with hidradenitis suppurativa (HS) in three placebocontrolled studies and one open-label extension study. The safety profile for subjects with HS treated with Humira weekly was consistent with the known safety profile of Humira.
Flare of HS, defined as ≥25% increase from baseline in abscesses and inflammatory nodule counts and with a minimum of 2 additional lesions, was documented in 22 (22%) of the 100 subjects who were withdrawn from Humira treatment following the primary efficacy timepoint in two studies.
Uveitis Clinical Studies
Humira has been studied in 464 adult patients with uveitis (UV) in placebo-controlled and open-label extension studies and in 90 pediatric patients with uveitis (Study PUV-I). The safety profile for patients with UV treated with Humira was similar to the safety profile seen in patients with RA.
The following adverse reactions have been identified during post-approval use of Humira. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to Humira exposure.
General disorders and administration site conditions: Pyrexia
Hepato-biliary disorders: Liver failure, hepatitis
Immune system disorders: Sarcoidosis
Vascular disorders: Systemic vasculitis, deep vein thrombosis
What drugs interact with Humira (adalimumab)?
Humira has been studied in rheumatoid arthritis (RA) patients taking concomitant methotrexate (MTX). Although MTX reduced the apparent adalimumab clearance, the data do not suggest the need for dose adjustment of either Humira or MTX.
In clinical studies in patients with RA, an increased risk of serious infections has been seen with the combination of TNF blockers with anakinra or abatacept, with no added benefit; therefore, use of Humira with abatacept or anakinra is not recommended in patients with RA. A higher rate of serious infections has also been observed in patients with RA treated with rituximab who received subsequent treatment with a TNF blocker. There is insufficient information regarding the concomitant use of Humira and other biologic products for the treatment of RA, PsA, AS, CD, UC, Ps, HS and UV. Concomitant administration of Humira with other biologic DMARDS (e.g., anakinra and abatacept) or other TNF blockers is not recommended based upon the possible increased risk for infections and other potential pharmacological interactions.
Avoid the use of live vaccines with Humira.
Cytochrome P450 Substrates
The formation of CYP450 enzymes may be suppressed by increased levels of cytokines (e.g., TNFα, IL-6) during chronic inflammation. It is possible for a molecule that antagonizes cytokine activity, such as adalimumab, to influence the formation of CYP450 enzymes. Upon initiation or discontinuation of Humira in patients being treated with CYP450 substrates with a narrow therapeutic index, monitoring of the effect (e.g., warfarin) or drug concentration (e.g., cyclosporine or theophylline) is recommended and the individual dose of the drug product may be adjusted as needed.
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Related Disease Conditions
Rheumatoid Arthritis (RA)
Rheumatoid arthritis (RA) is an autoimmune disease that causes chronic inflammation of the joints, the tissue around the joints, as well as other organs in the body. Because it can affect multiple other organs of the body, rheumatoid arthritis is referred to as a systemic illness and is sometimes called rheumatoid disease. The 16 characteristic early RA signs and symptoms include the following. Anemia Both sides of the body affected (symmetric) Depression Fatigue Fever Joint deformity Joint pain Joint redness Joint stiffness Joint swelling Joint tenderness Joint warmth Limping Loss of joint function Loss of joint range of motion Many joints affected (polyarthritis)
16 Early Rheumatoid Arthritis (RA) Symptoms and Signs
Early RA symptoms and signs vary differently from person to person. The most common body parts that are initially affected by RA include the small joints of the hands, wrists, and feet, and the knees and hip joints. Joint inflammation causes stiffness. Warmth, redness, and pain may vary in degree.
Crohn's disease is a chronic inflammatory disease, primarily involving the small and large intestine, but which can affect other parts of the digestive system as well. Abdominal pain, diarrhea, vomiting, fever, and weight loss are common symptoms.
Psoriatic arthritis is a disease that causes skin and joint inflammation. Symptoms and signs include painful, stiff, and swollen joints, tendinitis, and organ inflammation. Treatment involves anti-inflammatory medications and exercise.
Crohn's Disease vs. Ulcerative Colitis (UC)
Crohn's disease and ulcerative colitis are diseases that cause inflammation of part of or the entire digestive tract (GI). Crohn's affects the entire GI tract (from the mouth to the anus), while ulcerative colitis or ulcerative colitis only affects the large and small intestine and ilium. Researchers do not know the exact cause of either disease. About 20% of people with Crohn's disease also have a family member with the disease. Researchers believe that certain factors may play a role in causing UC. Both Crohn's disease and ulcerative colitis are a type of inflammatory bowel disease, or IBD. Crohn's disease and ulcerative colitis both have similar symptoms and signs, for example, nausea, loss of appetite, fatigue, weight loss, episodic and/or persistent diarrhea, fever, abdominal pain and cramping, rectal bleeding, bloody stools, joint pain and soreness, eye redness, or pain. Symptoms unique to Crohn’s disease include anemia and skin changes. Symptoms of unique to ulcerative colitis include, certain rashes, an urgency to defecate (have a bowel movement). Doctors diagnose both diseases with similar tests and procedures. While there is no cure for either disease, doctors and other health care professionals can help you treat disease flares, and manage your Crohn's or ulcerative colitis with medication, diet, nutritional supplements, and/or surgery.
Polymyalgia rheumatica (PMR) is a disorder of the muscles and joints that causes pain and stiffness in the arms, neck, shoulders, and buttocks. Treatment for polymyalgia rheumatica aims to reduce inflammation with aspirin, ibuprofen, and low doses of cortisone medications.
Rheumatoid Arthritis vs. Fibromyalgia
Though rheumatoid arthritis (RA) and fibromyalgia have similar symptoms, RA is an autoimmune disease and fibromyalgia is a chronic pain syndrome. RA symptoms include joint redness, swelling, and pain that lasts more than six weeks. Fibromyalgia symptoms include widespread pain, tingling feet or hands, depression, and bowel irritability. Home remedies for both include stress reduction, exercise, and getting enough sleep.
Pain Management and Rheumatoid Arthritis
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Second Source WebMD Medical Reference
Second Source article from Government
Rheumatoid Arthritis vs. Arthritis
Arthritis is a general term used to describe joint disease. Rheumatoid arthritis (RA) is a type of arthritis in which the body’s immune system mistakenly attacks the joints, causing chronic inflammation.
Rheumatology is the study of rheumatic diseases and conditions. Rheumatologists are internal medicine physicians who treat these illnesses, in particular arthritis.
Juvenile Rheumatoid Arthritis (JRA)
Juvenile rheumatoid arthritis (JRA) annually affects one child in every thousand. There are six types of JRA. Treatment of juvenile arthritis depends upon the type the child has and should focus on treating the symptoms that manifest.
Is Crohn's Disease Contagious?
Crohn's disease, a form of inflammatory bowel disease (IBD), and is characterized by symptoms and signs that include diarrhea, fever, weight loss, vomiting, and abdominal pain. Though Crohn's disease is not contagious it can spread throughout a person's gastrointestinal tract. An increase in the above symptoms and signs warrants a visit to a doctor's office.
Osteoarthritis vs. Rheumatoid Arthritis
Osteoarthritis (OA) and rheumatoid arthritis (RA) are chronic joint disorders. RA is also an autoimmune disease. OA and RA symptoms and signs include joint pain, warmth, and tenderness. Over-the-counter pain relievers treat both diseases. There are several prescription medications that treat RA.
Treatment & Diagnosis
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Medications & Supplements
Prevention & Wellness
Report Problems to the Food and Drug Administration
You are encouraged to report negative side effects of prescription drugs to the FDA. Visit the FDA MedWatch website or call 1-800-FDA-1088.
Professional side effects and drug interactions sections courtesy of the U.S. Food and Drug Administration.