A 50-year-old male with CD diagnosed in 1992 developed ankylosing spondylitis and sacroiliitis in 2002. The sacroiliitis presented with edema in the lowest sacral segment and the highest coccyx segment (Fig. 1). Prior treatment consisted of infliximab from 2002 to 2014, prednisolone for 2 months between 2012 and 2013, and azathioprine from 2007 to 2014. Infliximab and azathioprine were discontinued in 2014 because of recurrent peritonsillar abscesses, infectious keratoconjunctivitis, acne causing skin abscesses, and failure to achieve symptomatic remission. The patient then initiated treatment with vedolizumab. At the time, the patient had 3–4 bowel movements per day with some mucus, a fecal calprotectin concentration of 722 mg/kg, and primary symptoms of back pain, stiffness, and joint pain. Five months after initiation of treatment with vedolizumab, these symptoms resolved, and the patient had 1 bowel movement per day without mucus and a fecal calprotectin concentration that had decreased to 33 mg/kg. Overall, CD symptoms improved and were well controlled throughout vedolizumab treatment. One year after resolution of symptoms, the patient experienced acne-like skin lesions on the face, which were diagnosed as rosacea that immediately resolved with tetracycline treatment.
A 44-year-old male with CD initially diagnosed in 2009 developed polyarthritis in 2010. He had also been experiencing back pain since 1991. Prior treatments included prednisolone for 2 months in 2009 and 1 month in 2010, budesonide for 1 month in 2009 and 2 months in 2015, methotrexate for 2 months in 2010 (discontinued because of diffuse skin rash), azathioprine for 1 week in 2009 (discontinued because of pancreatitis), adalimumab for 1 month in 2010 (discontinued because of swollen and painful joints), sulfasalazine for 1 month in 2011 (discontinued because of lack of response), and natalizumab from 2011 to 2014.
Natalizumab was effective in controlling both the luminal symptoms and the polyarthritis; however, it was discontinued for safety concerns because the patient was positive for antibodies to the John Cunningham (JC) virus. After discontinuation, the patient presented with back pain likely caused by degenerative changes and knee pain from arthritis. Intestinal symptoms included 4–5 bowel movements per day with a small amount of blood and mucus and moderate abdominal pain. Vedolizumab treatment was initiated in 2014, and 4 months later all of his arthritic complaints had resolved. Although some back pain returned 2 years after initiation of treatment, the patient’s knee pain remained resolved. Furthermore, the patient’s stool frequency had improved to 2 loose stools per day with no blood or abdominal pain. It is noteworthy that this patient developed a perianal abscess that was drained in 2015 and a perianal fistula that was resected in 2016. It is unclear whether a causal relationship exists between vedolizumab and these events.
A 34-year-old male with UC diagnosed in 2012 presented with joint and back pain in 2013. The pain mainly affected his back; however, he also had peripheral arthritis type 1 with severe pain in his hips, knees, and muscles. No diagnosis of sacroiliitis was confirmed despite MR imaging of the lumbosacral spine and pelvis. Prior treatments included prednisolone for 2 months in 2013, mesalamine for 1 week in 2013 (discontinued because of myocarditis), infliximab for 14 months between 2013 and 2014 (discontinued because of lack of efficacy and development of antidrug antibodies), and golimumab for 7 months between 2014 and 2015 (discontinued because of insomnia and migraine).
Vedolizumab treatment was initiated in 2015, and after 1 month the patient’s back and joint pain resolved. However, for the first 5 months he received vedolizumab, the patient experienced arthralgias in both his back and peripheral joints approximately 5 days before the vedolizumab infusions. One year after resolution of symptoms, the patient developed pityriasis rosea on his abdomen, which resolved spontaneously within 2 months without treatment. The patient continues to be in remission on vedolizumab therapy.
An 18-year-old female with UC diagnosed in 2014 had polyarticular arthropathy diagnosed in 2016. At the time of presentation, the patient was being treated with mesalamine and was naïve to corticosteroids.
Although a definitive diagnosis of UC was not made until 2016, the patient had been experiencing arthralgias in her hands and knees since her initial presentation. Colonoscopy showed no active disease, and her C-reactive protein (CRP) and fecal calprotectin concentrations were normal; however, random colon biopsies revealed mildly active histopathologic disease. Although the entire colon appeared to be normal on endoscopic examination, histological evaluation revealed mild-to-moderate active disease. Characteristics of mild-to-moderate chronic disease, including cryptitis, crypt abscesses, mild-to-moderate mucosal ulceration, and moderate crypt architectural distortion, were observed. The patient opted to initiate vedolizumab after being offered the options of treatment with corticosteroid, immunosuppressives, or TNF antagonists. The patient noted that the joint pains resolved completely after the third induction dose of vedolizumab.
A 46-year-old female with CD diagnosed in 2005 received multiple courses of corticosteroid therapy resulting in initiation of azathioprine. However, this agent was discontinued because pancreatitis developed within 2 weeks of treatment. Although infliximab monotherapy was started, it was not possible to provide continuous treatment for insurance reasons. In 2015, the patient experienced a rash and shortness of breath following re-initiation of infliximab and the medication was discontinued.
In 2016, the patient presented with right lower quadrant pain and increasingly frequent non-bloody stools. Physical examination revealed right lower quadrant tenderness and a questionable mass. Tender, raised red nodules of EN were present on the extensor surfaces of both tibias. Her white blood cell (WBC) count was 14.6 × 109/L, erythrocyte sedminentation rate (ESR) was 34 mm/h, and the serum CRP concentration was 6 mg/L. Stool calprotectin concentrations were elevated. Magnetic resonance enterography showed active inflammation of the terminal ileum. A colonoscopy to the terminal ileum revealed a normal colon examination, but multiple ulcers were present in the terminal ileum. Biopsies from the ileum were consistent with active CD, with a single non-caseating granuloma demonstrated.
Treatment with vedolizumab was initiated, and resolution of the skin lesions followed the third infusion of the drug. The abdominal pain resolved completely after the fifth dose. The CRP, ESR, and stool calprotectin values were also normal after the fifth dose. The patient continued treatment with vedolizumab, and mesalamine was discontinued. Repeat endoscopy revealed a normal colon and ileum; however, the ileocecal valve was noted to be deformed and mildly stenotic. Biopsies of the colon and valve were normal, and biopsies of the ileum revealed mild enteritis.
A 24-year-old male with comorbid osteoporosis and diabetes, who was diagnosed with UC in 1998, presented with PG in 2016. Prior treatments were 6-mercaptopurine, mesalamine, corticosteroids, and multiple TNF antagonists. The patient underwent a colectomy and permanent ileostomy in 2012.
In 2016, the patient presented with a peristomal ulceration. The lesion had irregular borders and was diagnosed by a dermatologist as PG. The patient was positive for anti-saccharomyces cerevisiae antibodies (ASCA) and anti-neutrophil cytoplasmic antibodies (ANCA). The patient deferred corticosteroid treatment because of his osteoporosis. Small bowel was normal by endoscopy and video capsule endoscopy. The patient began vedolizumab therapy in 2016, and the lesion resolved after the sixth dose. The patient remains on vedolizumab and has been lesion free for 1 year.
An 87-year-old patient with a history of CD underwent an end ileostomy in 1972, and in 2014, he developed peristomal PG. The patient was treatment naïve since surgery, CD symptoms were well controlled, and luminal disease was not present at the time of PG presentation. Treatment with infliximab and methotrexate was commenced in 2015, leading to improvement in PG. However, 6 months after initiation of treatment, the patient developed a diffuse rash and infliximab was discontinued. Subsequently, the peristomal ulcer worsened. After a period without any biologic therapy, the patient began treatment with vedolizumab and continued methotrexate. Six months later, the PG had improved but was not resolved. Although PG improved with maintenance infusions dosed every 8 weeks, it began to worsen 4–5 weeks after each infusion. In response, treatment was intensified to an infusion every 4 weeks, which led to complete healing of PG after 4 months.
Nine months into the adjusted vedolizumab infusion schedule, the patient began to experience recurrent PG. Three months later, PG worsened to the severity level exhibited before the initiation of vedolizumab. The patient discontinued vedolizumab and began treatment with ustekinumab in 2017 and achieved complete healing.
A 24-year-old male with UC diagnosed in 2014, following presentation with bloody diarrhea that required hospitalization, developed uveitis in 2016. After intravenous corticosteroid induction therapy, the patient received mesalamine for maintenance or remission, which was successful for 2 years. In 2016, the patient presented with headaches, bilateral ocular pain, and blurred vision without symptoms of bloody diarrhea or abdominal cramps. Although the stool fecal calprotectin concentration was within the normal range, the CRP concentration was 14 mg/L and ESR was 64 mm/h. An initial colonoscopy revealed moderately active pancolitis, and biopsies confirmed the endoscopic findings. The patient’s ophthalmologic assessment revealed anterior chamber uveitis. Treatment with oral prednisone 40 mg daily for 2 weeks was initiated with tapering by 5 mg weekly. The patient developed recurrent symptoms when the prednisone dose was reduced to 15 mg. At this time, a colonoscopy revealed mild disease of the rectum and sigmoid, which was confirmed by biopsies.
Subsequently, treatment with vedolizumab was initiated. Corticosteroid tapering was resumed after the third dose of vedolizumab. The patient had no recurrence of uveitis and was off prednisone 1 year later, when a repeat colonoscopy showed a normal mucosa. Biopsies confirmed the absence of active histopathologic inflammation.