Atypical presentations, such as peripheral edema, ascites, or systemic inflammatory syndromes, are less commonly recognized but may precede or entirely replace classic GI symptoms. Ascites, hypoalbuminemia, and unexplained systemic inflammation in young adults should prompt consideration of IBD as a differential diagnóstico, particularly when accompanied by suggestive serological markers [1] [5] . Extraintestinal manifestations (EIMs), including dermatological, ocular, and joint disorders, are reported in up to 30% of CD cases and may represent the initial presentation in some patients [3] .

In this patient, the presence of ascites, hypoalbuminemia, and peripheral edema initially directed diagnostic efforts toward hepatic or nephrotic syndromes. These were excluded via cytological, microbiological, and electrophoretic analyses. Elevated fecal calprotectin and ASCA positivity ultimately shifted diagnostic focus to IBD [6] .

Fecal calprotectin has emerged as a reliable, non-invasive marker of intestinal inflammation. Elevated levels, as observed in this case, are highly sensitive for active mucosal inflammation and correlate with endoscopic findings [7] . ASCA, while lacking diagnostic specificity, remains a valuable adjunct in differentiating CD from ulcerative colitis. Advances in serological profiling, including the use of anti-glycan antibodies, further enhance diagnostic accuracy [7] .

The combination of imaging modalities, such as contrast-enhanced MRI and CT, with endoscopy provides a robust framework for diagnosing atypical CD. Cross-sectional imaging delineates bowel wall inflammation and evaluates complications such as strictures, fistulas, and abscesses. Endoscopy remains the gold standard, offering visual and histological confirmation [2] . The Montreal Classification used here (L3 + L4) enables precise disease characterization, guiding therapeutic decisions [7] .

Infliximab, a monoclonal antibody targeting tumor necrosis factor-alpha (TNF-α), is one of the most established biological therapies for Crohn’s Disease (CD). TNF-α is a central cytokine in the inflammatory cascade of CD, promoting immune cell infiltration, tissue damage, and mucosal remodeling. By neutralizing this cytokine, infliximab reduces inflammation, promotes mucosal healing, and alleviates clinical symptoms [4] [5] .

In this case, the patient presented with moderate-to-severe CD characterized by significant nutritional impairment and active inflammation, as evidenced by elevated fecal calprotectin levels and positive ASCA. These features justified the initiation of infliximab to induce remission and control inflammatory activity. Treatment with infliximab led to notable clinical improvement, including resolution of peripheral edema, reduction in abdominal distension, and progressive normalization of laboratory markers such as albumin and hemoglobin.

Infliximab is administered intravenously, typically following an induction schedule (doses at weeks 0, 2, and 6) and maintenance therapy every 8 weeks thereafter. The standard dose is 5 mg/kg, though it may be escalated to 10 mg/kg in refractory cases [7] . Adherence to the therapeutic schedule and careful monitoring are essential to prevent complications such as immunogenicity and loss of response.

Assessing the effectiveness of infliximab requires a multidimensional approach involving clinical, laboratory, endoscopic, and imaging parameters. Biomarkers play a key role in this process:

1) Fecal Calprotectin

2) C-reactive Protein (CRP)

3) Serum Infliximab Levels and Antidrug Antibodies (ADA)

4) Endoscopic Evaluation

5) Emerging Biomarkers

While infliximab is highly effective, it is associated with potential adverse effects, including infusion reactions, opportunistic infections (such as reactivated tuberculosis), and, in rare cases, lymphoma. Rigorous monitoring is essential, particularly for patients with predisposing factors such as malnutrition, as seen in this patient.

In this case, the rapid clinical and laboratory improvement following infliximab initiation highlights the effectiveness of this treatment for atypical CD presentations. Continued monitoring with biomarkers such as fecal calprotectin and CRP, combined with scheduled endoscopic evaluations, will be crucial to confirm sustained remission and adapt therapy as needed.