**Background:** Pregnancy is an immune-tolerant state that can influence the course of inflammatory bowel disease (IBD), with 30%–40% of pregnant women with IBD experiencing worsening disease during pregnancy. Both pregnancy and IBD are independent risk factors for venous thromboembolism (VTE), and pregnant women with IBD have a 2-fold higher risk of VTE compared to pregnant women without IBD. Antiphospholipid antibody syndrome (APLS) is an autoantibody-induced thrombophilia that can be triggered by acute stressors such as pregnancy. This case is the first reported instance of IBD and APLS manifesting acutely after pregnancy.
**Methods:** This is a single case report of a 16-year-old gravida 1 para 1 female with no prior medical history. She presented 8 days postpartum with sudden right-sided weakness and aphasia. Diagnostic workup included head CT and angiography, hematologic evaluation (LA/APS panel repeated 4 times within 3 months), rheumatologic autoantibody and complement testing, colonoscopy with histopathology, video capsule endoscopy, abdominal CT angiography, and stool pathogen testing. Laboratory assessments included fibrinogen, platelet count, D-dimer, INR, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), fecal calprotectin, complete blood count, and albumin.
**Key Results:** Initial presentation revealed left cerebral vein thrombosis with hemorrhagic stroke, severe cerebral edema leading to transtentorial herniation, and disseminated intravascular coagulation (DIC) with fibrinogen <30 mg/dL, platelet count 55/nL, D-dimer >20 μg/mL, and INR 3.5. On hospital day 5, bilateral lower extremity deep vein thromboses developed. LA/APS panel showed evidence of lupus anticoagulant without anticardiolipin or anti-β2 glycoprotein antibodies, confirming APLS. Repeat panels over 3 months confirmed this result. Rheumatologic evaluation was negative for systemic lupus erythematosus. Two weeks after discharge, she presented with hypovolemic shock, Pseudomonas aeruginosa urosepsis, and voluminous bloody diarrhea with INR 4.9. Colonoscopy with histopathology showed diffuse moderate-to-severely active pancolitis with evidence of chronicity (crypt branching, lymphoplasmacytic infiltrate, crypt abscesses). Video capsule endoscopy showed a normal small bowel. Abdominal CT angiography indicated an inflammatory process without mesenteric ischemia. Laboratory findings: CRP 190 mg/L, ESR 66 mm/h, fecal calprotectin >1000 μg/g, WBC 11.3/nL, hemoglobin 9.3 g/dL, albumin 2.0 g/dL. Stool tests for pathogens including Clostridium difficile were negative. She was treated with intravenous methylprednisolone, then transitioned to adalimumab and methotrexate for ulcerative colitis. After 7 months, fecal calprotectin decreased to 244 μg/g and follow-up colonoscopy showed mildly active pancolitis. She achieved clinical remission and continues prophylactic enoxaparin for APLS.
**Clinical Implications:** This case demonstrates that pregnancy can precipitate both IBD and APLS in a previously healthy adolescent, leading to catastrophic thrombotic and inflammatory complications. The patient's severe DIC and VTE raise suspicion for catastrophic antiphospholipid syndrome (CAPS), but colonic biopsies showed no small vessel thrombosis and were consistent with IBD, not ischemic colitis. The case underscores the importance of suspecting IBD in postpartum patients with rectal bleeding and thrombosis, and considering APLS in IBD patients with extensive thrombosis. It also highlights the need for heightened VTE prophylaxis and monitoring in pregnant women with IBD, as they have a 2-fold increased VTE risk compared to pregnant women without IBD, and IBD itself confers a 3-fold higher VTE risk than the general population.