INTRODUCTION: Evidence supports an association between CNS demyelination disorders and use of with Tumor Necrosis Factor-α (TNF-α) inhibitors. Here we present a case of optic neuritis onset after initiating therapy with infliximab-dyyb and describe subsequent treatment response. CASE DESCRIPTION/METHODS: A 31-year-old female with a history of Ulcerative Colitis, presented with new left periorbital heaviness 2 weeks after receiving the first dose of infliximab-dyyb. The pain eventually progressed to darkening and blurring of vision. The physical examination was positive for reduced visual acuity, color desaturation, and positive relative afferent pupillary reflex on the left eye only. CSF studies were remarkable for positive Oligoclonal bands and increased IgG Index. Orbital and brain MRI were suggestive of optic neuritis. Infliximab-dyyb was discontinued and she was treated with a course of IV Methylprednisolone and discharged home on Glatiramir acetate. On follow up visits, eye pain and blurry vision dramatically improved. In order to avoid extra-colonic side effects, she was switched to vedolizumab which she has tolerated well. DISCUSSION: It has been described that IBD patients can present with CNS demyelination, which can be explained by both conditions sharing epidemiological and immunological characteristics. However, this association can be confounded by the use of TNF-α inhibitors, which are commonly used in treating IBD and have been themselves associated with CNS demyelination. Though mechanism is unclear, blocking TNF-α receptors in the CNS has been found to result in neuroinflammation and long-term neural damage. The average time from exposure to the onset of symptoms has been described as seventeen months in one case series on infliximab. However, in our patient she started experiencing symptoms after the initial dose. This rapid reaction may be due to infliximab-dyyb being used. To our knowledge this is the first reported reaction related to a bio-similar. This demonstrates that further studies are needed to estimate the true incidence of demyelinating disorders in patients with IBD and to elucidate if bio-similar may be subject to stronger demyelinating reactions.
INTRODUCTION: Mantle cell lymphoma (MCL) is non-Hodgkin lymphoma that classically does not involve the gastrointestinal (GI) tract. Although in some cases MCL has been shown to spread to the GI tract, primary gastrointestinal MCL is exceedingly rare and has only been described anecdotally. Often, the diagnosis of MCL is made once the disease is metastatic given its largely nonspecific symptom profile. We present a case of diffuse MCL of the GI tract presenting as hematochezia, in a patient with ulcerative colitis. CASE DESCRIPTION/METHODS: An 80-year-old male with history of newly diagnosed ulcerative colitis (UC) presented with four weeks of worsening diarrhea and hematochezia associated with a 30-pound weight loss over five months. He had been on mesalamine for UC, but had not experienced symptomatic relief. On admission, the patient was anemic to a hemoglobin of 9.3 g/dL, white blood cell count of 21.6 × 103/L with 13% bands and 48% atypical lymphocytes, and an albumin of 1.7 g/dL with normal platelets and INR. Abdominal imaging showed diffuse mesenteric lymphadenopathy concerning for a lymphoproliferative process and circumferential gastric, rectal and sigmoid wall thickening and edema. Clostridium Difficile (C. Diff) stool PCR was positive, and he was started on oral vancomycin therapy. Colonoscopy showed diffuse inflammation and edema of the colon with poor mucosal integrity and a hypertrophic mass in the ascending colon. Upper endoscopy showed diffuse, hypertrophied, thickened folds within the stomach and duodenum along with ulcerations. Endoscopic ultrasound was performed to biopsy para-aortic and celiac lymph nodes. Given high suspicion for lymphoma, a bone marrow biopsy was also obtained. Histopathology from the multiple biopsies were all consistent with Stage 4 pleomorphic Mantle Cell Lymphoma. DISCUSSION: This case describes a rare presentation of MCL, complicated by C. Diff colitis in addition to UC. There has been little data to show that these unique clinical entities are significantly correlated. Although hematochezia is a rare presentation of MCL, clinicians should maintain a high index of suspicion for malignancy and pursue additional imaging and/or procedures, even in a patient that has other reasons to present with hematochezia. This case of advanced stage MCL of the GI tract adds to a small body of literature regarding primary gastrointestinal MCL and warrants further research in to this rare gastrointestinal malignancy.
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