A 54-year-old Caucasian female from an underserved rural community (roughly 375 miles from our institution) presented to her primary care physician with a 12-week history of progressive anorexia, 20-pound unintentional weight loss, lower quadrant abdominal pain, urgency, and up to 15 bloody bowel movements daily. She denied recent travel, sick contacts, antibiotic use, and any tobacco, alcohol, or illicit drug use. On examination, she was reportedly afebrile and nontoxic-appearing, but with signs of dehydration and mild lower abdominal quadrant tenderness without rebound or guarding. Her past medical history included Graves’ disease treated with radioactive iodine therapy and PsA diagnosed 2 years earlier. Family history revealed AS without a history of IBD or PsO, and the patient previously tested negative for HLA-B27.

Over the course of the 3 years preceding her acute presentation, the patient had numerous visits with her primary care physician for persistent joint pains involving her hands, feet, knees, and lower back, accompanied by nail ridging affecting both fingernails and toenails. Throughout this period, she consistently denied gastrointestinal symptoms, including abdominal pain, diarrhea, urgency, rectal bleeding, rectal pain, or perianal drainage. She also denied fever, fatigue, unintentional weight loss, ocular symptoms, or painful skin lesions. Vital signs during these visits were consistently within normal limits aside from chronic hypertension, and physical examinations revealed no evidence of ocular inflammation, oral (PO) ulcers, abdominal tenderness, or dermatological findings consistent with erythema nodosum or pyoderma gangrenosum. Baseline laboratory values obtained during this 3-year period were unremarkable, with hemoglobin (HGB) ranging from 13.3 to 14.1 g/dL (reference 12.0–16.0), albumin (ALB) from 4.1 to 4.4 g/dL (reference 3.5–5.2), white blood cell (WBC) count from 6.4 to 8.9 × 10³/µL (reference 4.5–11), and platelet (PLT) count from 237 to 324 × 10³/µL (reference 155–369). Vitamin B12, folate, and iron studies were consistently within normal limits. Her only medication was levothyroxine for secondary hypothyroidism. Additionally, a colonoscopy performed at age 52 for colorectal cancer screening reported a normal terminal ileum and colonic mucosa, without evidence of colorectal cancer, polyps, or inflammation.

Two years prior to the index presentation, the patient was referred to podiatry for evaluation of a left hallux nail abnormality and was diagnosed with onychocryptosis. During this podiatric evaluation, the patient described persistent finger and toe joint pains, alongside nail abnormalities characterized by ridging, brittleness, cuticle fissures, and erythematous periungual skin. Her podiatrist raised concerns for possible PsA, prompting referral to dermatology. Per review of the outside records, dermatologic assessment revealed irregular, moderately irritated, psoriasiform skin lesions primarily involving her fingers and fingernails, and the patient was diagnosed with psoriasiform dermatitis. Initial management was with topical clobetasol therapy. Due to ongoing joint symptoms despite several months of topical treatment, hand radiographs were obtained and showed “degenerative changes consistent with osteoarthritis, without erosions typical of PsA”. At follow-up, the patient continued to report joint discomfort, and examination revealed evolving psoriasiform lesions on her fingers, described as papules coalescing into plaques. Based on these persistent symptoms and cutaneous findings, her dermatologist initiated a “therapeutic trial” of adalimumab for what was described as PsA.

Following 7 months of adalimumab therapy without improvement in joint pain or nail changes, the patient was referred to rheumatology. Per review of the records, initial rheumatologic physical examination revealed Heberden’s and Bouchard’s nodes and persistent nail ridging, but no classic psoriatic skin lesions or signs of inflammatory joint swelling. The patient continued to report significant joint pain despite adalimumab treatment, and the rheumatologist elected to change therapy from adalimumab to ustekinumab based on the working diagnosis of PsA.

Prior to follow-up evaluation after 8 months of ustekinumab, lower body radiographs were obtained and demonstrated multilevel lumbar spondylosis, mild bilateral sacroiliac joint and femoroacetabular osteoarthritis, bilateral plantar fascia insertional enthesopathy, mild left-sided Achilles tendon insertional enthesopathy, and mild bilateral osteoarthritis of the feet. Laboratory studies prior to rheumatology follow-up revealed negative rheumatoid factor, WBC 6.14 × 10³/µL, HGB 13.7 g/dL, PLT 248 × 10³/µL, ALB 4.1 g/dL, vitamin B12 823 pg/mL, and 25-hydroxyvitamin D 71.2 ng/mL, all within normal limits. During the follow-up visit, review of systems from a gastrointestinal perspective was negative. Repeat physical examination again noted Heberden’s and Bouchard’s nodes and ongoing nail ridging, without evidence of inflammatory joint swelling, ocular inflammation, abdominal tenderness, or new cutaneous lesions. According to the medical records, due to ongoing patient-reported “morning stiffness, diffuse joint and muscle pain, and persistent nail changes” despite ustekinumab therapy, her rheumatologist elected to discontinue ustekinumab and initiate IXE to treat refractory joint pain. IXE was initiated with an induction dose of 160 mg subcutaneously, followed by 4 maintenance doses of 80 mg administered every 4 weeks. The patient developed her initial gastrointestinal symptoms approximately 16 weeks after the initial induction dose, marking the onset of the acute presentation described in this case report.

Initial laboratory studies obtained by her primary care physician at the time of her index presentation, 28 weeks after the initial IXE induction dose (and 12 weeks after the onset of gastrointestinal symptoms), revealed markedly elevated inflammatory markers, including C-reactive protein (CRP) 5.83 mg/dL (reference 0.00–0.50), erythrocyte sedimentation rate (ESR) 69 mm/hr (reference ≤ 30), and fecal calprotectin (FC) 3,650 mcg/g (reference 0–120). Based on the record review, basic serum labs were not obtained. Stool testing, including gastrointestinal PCR panel and ova and parasites, was negative. The patient was urgently referred to general surgery for a colonoscopy due to the lack of local gastroenterology subspecialty care, with the nearest major metropolitan city located more than 350 miles away. Unable to reach the patient’s rheumatologist, the primary care physician initiated PO prednisone 40 mg to manage symptoms of presumed colitis and serve as a bridge until further evaluation.

Due to limited access to general surgery care, the patient’s colonoscopy was delayed until 6.5 weeks after the initial presentation (34.5 weeks after IXE induction and 18.5 weeks after the onset of gastrointestinal symptoms), during which she experienced an additional 30-pound weight loss. Periprocedural labs revealed CRP 17.26 mg/dL and ESR 75 mm/hr. Once performed, the ileocolonoscopy report states the terminal ileum appeared normal, but the right colon displayed severe colitis, marked by pronounced erythema, friability, serpiginous ulcerations, and spontaneous bleeding. The sigmoid colon and rectum were reported as “relatively spared” (Figure 1). Histopathological examination of segmental biopsies obtained reported mild focal active ileitis and colitis without evidence of chronicity. Immunohistochemical staining for cytomegalovirus (CMV) was negative. IXE was discontinued, with the last dose administered 4 weeks prior to ileocolonoscopy.

Seven days after the endoscopy, the patient presented to her local emergency department with progressively worsening symptoms. Upon presentation, the patient was tachycardic (heart rate 105 bpm), dehydrated, and exhibited mild lower abdominal tenderness. Laboratory tests revealed ALB 2.9 g/dL, HGB 9.8 g/dL, and a negative Clostridioides difficile PCR. Abdominal and pelvic computed tomography (CT) in the emergency department demonstrated fluid-filled small bowel loops with mild circumferential wall thickening involving the splenic flexure and descending colon (Figure 2). She was admitted to general surgery with internal medicine consultation and was started on intravenous (IV) methylprednisolone 125 mg daily, along with PO budesonide 9 mg daily and PO mesalamine 4 g daily. After a negative infectious workup, PO loperamide was started for diarrhea. The patient’s abdominal pain worsened, and IV morphine and PO ibuprofen were ordered.

By hospital day 4, her condition had not improved. According to a review of the medical records, the physical examination performed that day did not show any signs of systemic toxicity and only revealed mild abdominal tenderness without significant distension. Additionally, the patient exhibited no altered mental status, and no objective signs of dehydration were reported. Vital signs were stable (temperature 36.6°C, heart rate 61 bpm, respiratory rate 16 breaths per minute, blood pressure 128/66 mmHg, oxygen saturation 95% on room air). Laboratory results included WBC 6.72 × 10³/µL, HGB 9.4 g/dL, sodium 133 mmol/L, potassium 3.78 mmol/L, chloride 93 mmol/L, and corrected calcium 9.8 mg/dL. The record review indicates that the surgical team had low concern for toxic megacolon or the need for any urgent surgical intervention. Due to a persistent lack of improvement, the team contacted the nearest gastroenterology team, located approximately 375 miles away. Based on the clinical information provided, the specialist recommended discontinuing antidiarrheals, opioids, and nonsteroidal anti-inflammatory drugs (NSAIDs). With no immediate surgical indication identified by the surgical team, intensive infliximab therapy was initiated to manage presumed severe colitis medically.

An initial loading dose of IV infliximab 10 mg/kg was administered without any immediate issues. Later that evening, while ambulating to the restroom, the patient experienced severe left upper quadrant pain radiating to the left arm, accompanied by shortness of breath. A STAT abdominal radiograph showed significant intraperitoneal free air and marked colonic dilation with large air-fluid levels (Figure 3). She was immediately started on broad-spectrum antibiotics (IV piperacillin-tazobactam 3.375 g every 6 hours) and taken emergently to the operating room. Exploratory laparotomy revealed gross perforations at the splenic flexure, transverse colon, and ascending colon near the cecum, with pronounced inflammation in the left colon. An extended right hemicolectomy with end ileostomy was performed. Pathologic evaluation of the resected specimen showed severe acute colitis with ulceration, submucosal and subserosal abscesses, transmural inflammation, and non-caseating granuloma formation characterized by the presence of epithelioid cells, multinucleated giant cells, and lymphocytes, without necrosis (Figure 4).

Postoperatively, broad-spectrum antibiotics were continued, and IV methylprednisolone 50 mg daily was started due to intraoperative hypotension. Over several days, bowel function returned, abdominal drain output decreased, appetite improved, and abdominal pain lessened. At the outside hospital, enteral nutrition via tube feeding was not initiated, in part due to the patient’s strong aversion following a prior traumatic nasogastric tube placement earlier in her hospitalization. Additionally, the clinical team noted the absence of a prolonged postoperative ileus and opted to rely on PO intake as her gastrointestinal function appeared to recover, ultimately deferring tube feeding based on patient preference and observed clinical progress. Given the lack of severe malabsorption or sustained intolerance and the medical team’s desire to reduce risks associated with central venous access during the postoperative recovery period, total parenteral nutrition (TPN) was not initiated.

On postoperative day 6, she was transitioned to PO prednisone 40 mg daily. She completed 8 days of IV piperacillin-tazobactam 3.375 g every 6 hours, followed by PO ciprofloxacin 500 mg twice daily and PO metronidazole 500 mg four times daily for a total 14-day antibiotic course. During her 16-day hospitalization, she remained afebrile, and CRP decreased to 6.76 mg/dL. Other notable labs at the time of discharge included WBC 8.51 × 10³/µL, HGB 7.10 g/dL, and ALB 2.8 g/dL. She was discharged on postoperative day 10 with prescriptions for rectal mesalamine 1,000 mg, PO oxycodone 5 mg as needed, and a PO prednisone taper starting at 40 mg and decreasing by 10 mg weekly to 5 mg. Infliximab 10 mg/kg was resumed after discharge, with the second induction dose given 3 days post-discharge without issue.

Five days post-discharge, the patient returned to the general surgery clinic with purulent drainage from a right pelvic Jackson-Pratt drain and right flank pain and was sent directly to her local emergency department for further evaluation. Vitals revealed (temperature 37.3°C, heart rate 115 bpm, respiratory rate 18 breaths per minute, blood pressure 126/76 mmHg, oxygen saturation 98% on room air). Laboratory results included WBC 18.9 × 10³/µL, HGB 9.4 g/dL, PLT 490 × 10³/µL, ALB 3.0 g/dL, and CRP 13.98 mg/dL. A contrast-enhanced (IV, PO, and rectal) abdominal CT showed post-surgical changes but no small bowel obstruction or contrast extravasation. A 4.0 cm × 7.4 cm × 7.2 cm rim-enhancing fluid collection with multiple air foci was identified in the right hemiabdomen (Figure 5). Physical examination, once admitted to the general surgery service, revealed greenish discoloration on the surgical dressing. Upon removal, a wound gap with fascial separation was identified, along with fecal leakage into the wound from a separated stoma appliance. Exploratory laparotomy confirmed mid-abdominal fascial dehiscence and a peri-hepatic abscess. The abscess was evacuated, the right Jackson-Pratt drain was repositioned, and a new left upper quadrant drain was placed. Wound cultures were polymicrobial, including 1+ Candida albicans. The treating teams initiated IV ciprofloxacin, IV metronidazole, and IV fluconazole, while low-dose PO prednisone 20 mg was continued due to concerns for secondary adrenal insufficiency from the prior hospitalization. By hospital day 3 of readmission, she had remained afebrile and without leukocytosis for 24 hours. She was discharged on PO ciprofloxacin, PO metronidazole, and PO fluconazole to complete a 3-week course.

Initially, the patient’s abdominal pain improved with the PO antimicrobial regimen. However, 9 days post-discharge, she developed new left-sided abdominal pain, intermittent nausea, malaise, and subjective fevers, prompting her return to her local emergency department. Initial vital signs were within normal limits, and the patient was afebrile. Labs were notable for WBC 14.0 × 10³/µL, HGB 7.6 g/dL, PLT 584 × 10³/µL, ESR > 140 mm/hr, CRP 11.60 mg/dL, ALB 1.6 g/dL, and lactate 1.7 mmol/L (reference 0.5–2.0). Repeat contrast-enhanced (IV, PO, and rectal) CT imaging of the abdomen revealed no evidence of contrast extravasation from the gastrointestinal tract and resolution of right hemiabdomen fluid collection. However, findings now included long-segment small bowel wall thickening with surrounding fat stranding, a 2.0 cm × 1.3 cm superficial fluid collection located midline above the umbilicus, and a 9.0 cm × 1.2 cm left subdiaphragmatic fluid collection with peripheral enhancement (Figure 6). The patient was readmitted and started on IV ciprofloxacin and IV metronidazole. The surgical and internal medicine teams contacted our Gastroenterology service for transfer to our center, as they solely attributed the postsurgical complications, including recurrent abscess formation, to active severe penetrating CD.

Upon transfer, the patient was afebrile, with normal ileostomy output and appearance, and no evidence of stomal ulcerations. She denied rectal bleeding and discharge. The patient had lost more than 70 pounds since the onset of her initial symptoms, there was evidence of significant muscle wasting, and ALB 1.9 g/dL, consistent with severe protein-calorie malnutrition. Vitals revealed (temperature 37.3°C, heart rate 115 bpm, respiratory rate 18 breaths per minute, blood pressure 126/76 mmHg, oxygen saturation 98% on room air). Laboratory results were significant for WBC 15.6 × 10³/µL, HGB 9.2 g/dL, PLT 524 × 10³/µL, ESR > 140 mm/hr, CRP 14.80 mg/dL, ileostomy FC 61 mcg/g, and negative blood cultures.

In light of persistent intra-abdominal infection without source control, most consistent with bacterial seeding from the prior colonic perforation and compounded by profound iatrogenic immunosuppression, severe protein-calorie malnutrition, and postoperative wound dehiscence with contamination of the abdomen by stoma effluent, all immunosuppressive therapies were discontinued, and antimicrobial therapy was continued. A multidisciplinary team was assembled, including specialists from gastroenterology, general surgery, infectious disease, interventional radiology, nutrition, and physical therapy.

Interventional radiology determined that the left subdiaphragmatic fluid collection was not amendable to percutaneous drainage. Infectious disease recommended continuing antimicrobial therapy with short-interval repeat imaging. Follow-up CT imaging performed 7 days later revealed a left pleural effusion with a split pleura sign, raising concern for empyema. Additionally, midline rim-enhancing fluid collections were observed within the postsurgical midline incision, along with a reduction in the size of the perisplenic fluid collection (Figure 7). Antimicrobials were broadened to IV piperacillin-tazobactam and IV micafungin, guided by infectious disease specialist input.

Subsequently, appetite improved significantly, and the patient began consistently meeting her nutritional goals through PO intake, verified by daily inpatient assessments conducted by our registered dietitian. Enteral nutrition via tube feeding was considered but ultimately not initiated due to the patient’s demonstrated clinical improvement, absence of ileus or gastrointestinal dysfunction impairing PO intake, and a documented history of intolerance to nasogastric tube placement during an earlier hospitalization. After counseling, she also declined tube feeding. Given these factors, PO nutrition was favored due to its lower risk profile compared to tube feeding, including a reduced risk of aspiration, diarrhea, and device-related complications.

Over several days, she showed marked clinical improvement, with decreasing leukocytosis and thrombocytosis. She remained afebrile, and antimicrobials were transitioned to PO amoxicillin-clavulanate 875 mg/125 mg twice daily and PO fluconazole 400 mg once daily, with a planned 4-week outpatient course and follow-up imaging. She tolerated this regimen while admitted and was discharged home after a 12-day hospital course.

After completing 17 days of PO amoxicillin-clavulanate, the patient’s antibiotic regimen was adjusted by her primary care team due to reported antibiotic-related gastrointestinal upset. The new regimen included PO ciprofloxacin 500 mg twice daily and PO metronidazole 500 mg three times daily, while fluconazole 400 mg once daily was continued. Twenty-four days post-discharge, inflammatory markers improved significantly. Repeat labs revealed WBC 9.27 × 10³/µL, HGB 11.3 g/dL, PLT 469 × 10³/µL, ESR 56 mm/hr, ALB 3.5 g/dL, and CRP 0.49 mg/dL. To assess small-bowel involvement, CT enterography (CTE) was performed as magnetic resonance enterography was unavailable locally. Imaging demonstrated persistent mesenteric stranding near the colonic stump in the left upper quadrant but revealed otherwise normal stomach and bowel caliber, without evidence of obstruction, strictures, small bowel wall thickening, masses, or fistulas.

Approximately 4 months after discontinuing IXE and 3 months post-extended right hemicolectomy with end ileostomy, the patient underwent ileoscopy and flexible sigmoidoscopy with our team for disease surveillance. Ileoscopy revealed a normal-appearing ileum, with findings confirmed on histology (Figure 8). Flexible sigmoidoscopy showed normal descending and sigmoid colon and mild rectal changes, including faint erythema and punctate hemorrhages with air insufflation, endoscopically suggestive of mild diversion colitis (Figure 9). Sigmoid biopsies revealed focal active colitis without evidence of chronic changes, whereas rectal biopsies demonstrated mild chronic active colitis with non-necrotizing granulomata. Our team recommended a 3-month course of short-chain fatty acid enemas, followed by repeat flexible sigmoidoscopy and routine IBD surveillance labs to evaluate for resolution of mild colitis.

Repeat flexible sigmoidoscopy performed 3 months after short-chain fatty acid enemas demonstrated an overall normal-appearing left colon (Figure 10). Histopathological examination of biopsies from the left colon and rectum showed no acute or chronic colitis, no granulomas, and minimal crypt architectural distortion (Figure 11). Overall, this reflected the complete resolution of disease activity, consistent with clinical, endoscopic, and histologic remission. There were notable improvements in HGB 13.1 g/dL, ESR 21 mm/hr, and CRP < 0.30 mg/dL. Because her PsA diagnosis was uncertain and the presentation favored CD induced by an IL-17i rather than primary severe, penetrating Crohn’s, we recommended conservative management without advanced therapy. We also advised referral to a new rheumatologist to re-evaluate the PsA diagnosis.

At her second-opinion visit, the patient reported that PsA had never been firmly established; the earlier label rested mainly on longstanding foot pain and nail ridging without documented synovitis. Prior dermatology notes described “psoriasiform lesions” on the fingers, but no biopsy was performed, and she denied any personal history of cutaneous PsO. A comprehensive assessment, including expert review of peripheral and axial imaging, showed no erosive or inflammatory changes, and inflammatory markers were normal; the joint exam again revealed no synovitis. Mild entheseal tenderness was present but judged non-specific and more compatible with degenerative or mechanical causes. Applying the CASPAR framework, the entry criterion of inflammatory articular disease was considered met by enthesitis, yet the score totaled only 2 points: nail pitting (+1) and rheumatoid factor negativity (+1), with no current, past, or family history of PsO, no dactylitis, and no juxta-articular new bone formation on hand or foot radiographs. Because at least 3 points are required, classification as PsA was not supported, and she was transitioned to conservative symptom management with acetaminophen and localized corticosteroid injections, which have provided effective relief.

Since her acute hospitalization, the patient has not required any pharmacologic treatment for IBD during the recovery period, including corticosteroids. Eight months after her initial presentation, she underwent ileostomy takedown with ileocolonic anastomosis. Four months following surgical reversal, repeat disease-staging colonoscopy demonstrated a normal-appearing neoterminal ileum and colonic mucosa. A small, isolated 1 mm ulceration was noted at the ileocolonic anastomosis, with no surrounding inflammation. Biopsies from the neoterminal ileum and colonic segments revealed no evidence of active inflammation, chronicity, or granulomas. This focal ulcer was interpreted as a nonspecific postoperative finding, commonly observed at anastomotic sites. The patient remained entirely asymptomatic, with normal laboratory markers, including CRP < 0.30 mg/dL and FC 18 mcg/g. At present, 18 months after initial acute hospitalization and 16 months following endoscopic confirmation of remission, the patient remains clinically stable, with recovered nutritional status, and sustained remission across clinical, laboratory, and endoscopic parameters (Figure 12).

This is a single-case report; it cannot establish causality and demonstrates only a temporal association between IL-17 inhibition and IBD. The findings should not be generalized to all IL-17i (e.g., BKZ, BRO, SEC), as agent- and patient-specific responses and adverse events may differ. Early clinical decisions were made by outside clinicians, and our reconstruction of their diagnostic rationale, therapeutic choices, and consent discussions relies solely on available records. Undocumented elements of history, labs, imaging, or procedures may have influenced management; therefore, some questions about the initial care remain unanswered. Feasibility may limit the application of our proposed framework in rural or resource-constrained settings, where colonoscopy or advanced imaging is not readily available. In such contexts, early telemedicine consultation with tertiary centers, use of validated simplified activity indices, selective basic laboratory markers, and expedited transfer are practical interim strategies. Finally, although the patient has sustained clinical, biochemical, and endoscopic remission for 16 months, the lack of multi-year follow-up precludes conclusions about long-term relapse risk or delayed complications.