FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2066879424> ?p ?o ?g. }

• W2066879424 endingPage "225" @default.
• W2066879424 startingPage "223" @default.
• W2066879424 abstract "Adalimumab is a fully humanized anti-tumor necrosis factor alpha (TNF-α) monoclonal antibody approved for the treatment of moderately to severely active Crohn disease (CD) in adults. Although not yet approved by the US Food and Drug Administration (FDA) for the treatment of pediatric CD, it is often used when pediatric patients with CD lose responsiveness or develop an allergy to infliximab. The clinical efficacy of infliximab and adalimumab appear to be similar; however, there are no head-to-head trials directly comparing them (1,2). Common adverse effects of adalimumab include injection site reactions (20%), upper respiratory infections (17%), sinusitis (11%), headache (12%), rash (12%), nausea (9%), urinary tract infections (8%), and abdominal pain (7%). Edema is an uncommon adverse effect of adalimumab, occurring in 5% of patients. In the present study, we report 3 pediatric patients with CD who developed angioedema while being treated with adalimumab. The edema resolved in the 2 patients who discontinued adalimumab. CASE 1 A 17½-year-old girl with colonic CD of 3 years duration was given adalimumab after developing severe fatigue while receiving infliximab. She had previously failed a 6-month trial of 6-mercaptopurine and had been subsequently maintained with infliximab. She clearly associated her fatigue with infliximab infusions and did not wish to continue this therapy. Anti-infliximab antibodies were undetectable. She was given adalimumab, her fatigue resolved, and she continued to have no gastrointestinal symptoms. During the next 2 years, she developed nonpitting edema of the face and lower extremities and gained 4.7 kg in body mass (Fig. 1A). Her hemoglobin, erythrocyte sedimentation rate (ESR), creatinine, and albumin were normal. Because the edema and weight gain were associated with the initiation of adalimumab, the medication was discontinued and certolizumab was given. On certolizumab, the angioedema resolved and she diuresed 3.4 kg during the next 4 months (Fig. 1B). Follow-up after 6 months of therapy reveals no recurrence of edema, and her disease is in remission.FIGURE 1: Patient 1: (A) After receiving adalimumab for 2 years. Note the full face; (B) 4 months after adalimumab was replaced with certolizumab. Note resolution of facial edema.CASE 2 A 16-year-old girl with trisomy 21, hypothyroidism, insulin-dependent diabetes, and celiac disease was diagnosed with ileocolonic CD with perineal fistulae and anorectal stenosis. Her CD was treated with infliximab and periodic rectal dilatation using Haggar dilators. She developed an infusion reaction to infliximab and was switched to adalimumab. Three months after giving adalimumab, she developed angioedema of both hands and feet. At that time her ESR was 44 mm/h, albumin 3.5 g/dL, white blood cell count 5.4 K/μL (71.7% neutrophils, 23.8% lymphocytes, 3% monocytes, 1.2% eosinophils, and 0.3% basophils), hemoglobin 12.3 g/dL, and platelets 459 K/μL. She was changed to certolizumab, with resolution of the angioedema within several weeks. Her luminal CD remained in remission, and minimal disease activity was noted during an upper endoscopy and colonoscopy after 5 months of therapy with certulizumab. She continues to have anorectal dilitations periodically and an elevated ESR and hypoalbuminemia. CASE 3 An 11-year-old girl was diagnosed with ileocolonic CD in March 2001. She failed treatment with azathioprine and methotrexate. Three years after diagnosis she underwent resection of 50 cm of distal small bowel because of multiple strictures. Her postoperative course was complicated by an abdominal abscess and concern for fistulizing disease. Postoperatively she was treated with infliximab. Her disease remained in remission for 2 years 9 months, when she was transitioned to adalumab for ease of administration. She remained in clinical remission on adalimumab for 2 years. At the age of 19 years, she developed bilateral nonpitting pedal edema. She had gained 4.5 kg during the previous 1 year but was otherwise in clinical remission. She has microcytic anemia, but normal ESR, creatinine, and albumin. A change in therapy to certolizumab was offered, but she elected to continue on adalimumab. The edema did not resolve during the subsequent 6 months. DISCUSSION Adalimumab is a fully humanized recombinant immunoglobulin (Ig)G1 monoclonal antibody that binds specifically to TNF-α, a proinflammatory cytokine known to be elevated in patients with CD. The CLASSIC I & II and CHARM trials evaluated the efficacy and safety of adalimumab. These 3 randomized, double-blind, placebo-controlled trials support the use of adalimumab in the induction and maintenance of moderately to severely active CD in adults (3–5). Adalimumab received FDA approval for the treatment of adults with moderate to severe CD in February 2007. Although not yet FDA approved for the treatment of pediatric CD, it is used successfully in children with CD who have lost responsiveness to infliximab (6,7). The clinical efficacy of infliximab and adalimumab appears to be similar; however, there are no head-to-head trials directly comparing them (1,2). Common adverse effects reported by patients treated with adalimumab include injection site reactions (20%), upper respiratory infections (17%), sinusitis (11%), headache (12%), rash (12%), nausea (9%), urinary tract infections (8%), and abdominal pain (7%). Rare but serious adverse effects including infections, tuberculosis, lymphoma, demyelinating disease, and drug-induced systemic lupus erythematosus have also been reported (3–5,8). Among the infrequent adverse reactions listed on the adalimumab package insert, occurring in fewer than 5% of patients, is peripheral edema (8). Angioedema is swelling of the deeper layers of the skin and/or mucous membranes and can result from multiple etiologies (9,10). It may or may not be associated with urticaria (swelling of the superficial skin layers). Urticaria is seen less frequently in association with angioedema that occurs as a result of angiotensin-converting enzyme inhibitors or from hereditary angioedema (HAE). Common causes of angioedema include allergic reactions, drugs (eg, angiotensin-converting enzyme inhibitors, salicylates, nonsteroidal anti-inflammatory drugs), C1 inhibitor deficiency (as seen in HAE type 1 and 2), and acquired angioedema. The pathophysiology of angioedema is not completely understood and varies depending on its cause (9,10). Histamine release during IgE-mediated reactions results in increased local blood flow and endothelial permeability, leading to edema. Other triggers via this mechanism include autoantibodies against the mast cell IgE receptor direct stimulation of mast cell degranulation by various agents (eg, anesthetics). Alternatively, bradykinin (BK) can mediate angioedema via the BK-2 receptor, causing increased vascular permeability. This mechanism is implicated in most forms of HAE. In these patients, deficiency (HAE type 1) or defective (HAE type 2) C1 inhibitor ultimately results in less negative regulation of the contact system and elevation of BK. In acquired angioedema, autoantibodies or immune complexes result in C1 inhibitor deficiency. This form is associated with lymphoproliferative disorders. In the case of salicylates and nonsteroidal anti-inflammatory drugs, inhibition of prostaglandins appears to result in excess leukotrienes. There are case reports of patients with the coincidental occurrence of both CD and HAE (11,12). There is also 1 case report of an adult patient with rheumatoid arthritis treated with adalimumab who developed an angioedema-like skin reaction and urticaria. This patient developed edema of the hands and lips, erythema of the face, and an urticaria-like skin reaction involving the trunk following her seventh dose of adalimumab 40 mg every 2 weeks (9). Our case series describes 3 girls who developed angioedema while receiving adalimumab for treatment of CD. In 2 patients, the angioedema developed shortly after giving adalimumab, although the diagnosis of angioedema and the association of the angioedema and adalimumab were delayed in the first patient. The third patient did not develop angioedema until 2 years after giving the adalimumab. In the 2 patients in whom adalimumab was replaced with certolizumab, the pegylated Fab′ fragment of the anti-TNF-α monoclonal antibody, the angioedema resolved and has not recurred. Because of this association between symptom resolution and discontinuation of adalimumab, we have not pursued additional workup for other causes of angioedema (Fig. 1). We cannot completely rule out the possibility that this represented an extraintestinal manifestation of CD (metastatic CD, or cheilitis granulomatosa (13), or vasculitis) because we did not request skin biopsies. None of the patients in our report exhibited other features associated with Melkersson-Rosenthal syndrome (facial paralysis, swelling of the face and lips, and folds or furrows in the tongue; OMIM: %155900), which has been reported in association with CD (14). All of the patients had involvement of extremities, which has not been reported in chelitis granulomatosa or Melkersson-Rosenthal syndrome. The fact that the symptoms resolved when the drug was withdrawn again suggests drug-induced angioedema. The mechanism by which adalimumab may cause angioedema is not known. The lack of urticaria in our patients would suggest that adalimumab does not involve histamine. The patient who remains on adalimumab is being closely monitored for progression of the angioedema and weight gain. Angioedema is described as a possible adverse effect of adalimumab on the package insert (8). On the basis of our 3 cases, angioedema may occur soon after the intake of adalimumab, but it may not be apparent until many years later. Although uncommon, it is important to recognize that unexplained weight gain and angioedema can be an adverse effect in patients with CD treated with adalimumab. The angioedema resolves after withdrawal of the medication and does not appear to preclude the use of other anti-TNF agents." @default.
• W2066879424 created "2016-06-24" @default.
• W2066879424 creator A5010534045 @default.
• W2066879424 creator A5080343755 @default.
• W2066879424 creator A5087885832 @default.
• W2066879424 date "2010-08-01" @default.
• W2066879424 modified "2023-10-09" @default.
• W2066879424 title "Angioedema Occurring in Pediatric Patients With Crohn Disease Treated With Adalimumab" @default.
• W2066879424 cites W1990696193 @default.
• W2066879424 cites W1991810959 @default.
• W2066879424 cites W2007289031 @default.
• W2066879424 cites W2020336502 @default.
• W2066879424 cites W2054131812 @default.
• W2066879424 cites W2081814720 @default.
• W2066879424 cites W20989772 @default.
• W2066879424 cites W2137775651 @default.
• W2066879424 cites W2151526724 @default.
• W2066879424 cites W2152026434 @default.
• W2066879424 cites W2165107045 @default.
• W2066879424 cites W92487011 @default.
• W2066879424 doi "https://doi.org/10.1097/mpg.0b013e3181c615e1" @default.
• W2066879424 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20410840" @default.
• W2066879424 hasPublicationYear "2010" @default.
• W2066879424 type Work @default.
• W2066879424 sameAs 2066879424 @default.
• W2066879424 citedByCount "2" @default.
• W2066879424 countsByYear W20668794242022 @default.
• W2066879424 crossrefType "journal-article" @default.
• W2066879424 hasAuthorship W2066879424A5010534045 @default.
• W2066879424 hasAuthorship W2066879424A5080343755 @default.
• W2066879424 hasAuthorship W2066879424A5087885832 @default.
• W2066879424 hasConcept C126322002 @default.
• W2066879424 hasConcept C16005928 @default.
• W2066879424 hasConcept C2777995640 @default.
• W2066879424 hasConcept C2779134260 @default.
• W2066879424 hasConcept C2779280984 @default.
• W2066879424 hasConcept C2780132546 @default.
• W2066879424 hasConcept C2992200296 @default.
• W2066879424 hasConcept C71924100 @default.
• W2066879424 hasConceptScore W2066879424C126322002 @default.
• W2066879424 hasConceptScore W2066879424C16005928 @default.
• W2066879424 hasConceptScore W2066879424C2777995640 @default.
• W2066879424 hasConceptScore W2066879424C2779134260 @default.
• W2066879424 hasConceptScore W2066879424C2779280984 @default.
• W2066879424 hasConceptScore W2066879424C2780132546 @default.
• W2066879424 hasConceptScore W2066879424C2992200296 @default.
• W2066879424 hasConceptScore W2066879424C71924100 @default.
• W2066879424 hasIssue "2" @default.
• W2066879424 hasLocation W20668794241 @default.
• W2066879424 hasLocation W20668794242 @default.
• W2066879424 hasOpenAccess W2066879424 @default.
• W2066879424 hasPrimaryLocation W20668794241 @default.
• W2066879424 hasRelatedWork W1577352824 @default.
• W2066879424 hasRelatedWork W1986340848 @default.
• W2066879424 hasRelatedWork W1987189293 @default.
• W2066879424 hasRelatedWork W2006176929 @default.
• W2066879424 hasRelatedWork W2007611884 @default.
• W2066879424 hasRelatedWork W2085446880 @default.
• W2066879424 hasRelatedWork W2399201492 @default.
• W2066879424 hasRelatedWork W2434653209 @default.
• W2066879424 hasRelatedWork W2436073988 @default.
• W2066879424 hasRelatedWork W4281781548 @default.
• W2066879424 hasVolume "51" @default.
• W2066879424 isParatext "false" @default.
• W2066879424 isRetracted "false" @default.
• W2066879424 magId "2066879424" @default.
• W2066879424 workType "article" @default.