A “multidimensional” diagnostic mindset and individualized therapeutic armamentarium for inflammatory bowel disease

Inflammatory bowel disease (IBD) is characterized by complex etiology and highly heterogeneous manifestations, which poses significant challenges to precise diagnosis and individualized therapy due to difficulties in early differential diagnosis, incomplete standardization of endoscopic and imaging criteria, insufficient sensitivity and specificity of biomarkers, imperfect predictive systems for treatment response, and poor patient adherence. In recent years, the incidence of IBD has continued to rise both globally and in China, with diagnostic delay being common, necessitating the urgent development of systematic diagnostic and therapeutic strategies. The critical steps in diagnosis are as follows: ① screening high-risk populations (age at onset of 15 to 35 years or 60 to 75 years, family history in first-degree relatives, persistent diarrhea with hematochezia, perianal lesions, etc.), and initiating colonoscopy and imaging assessment as early as possible; ② elucidating the three core manifestations—diarrhea, abdominal pain, and wasting—while recognizing extraintestinal manifestations [arthritis, erythema nodosum, primary sclerosing cholangitis (PSC), etc.] and special presentations (anal fistulas, failure to improve after appendectomy, etc.); ③ establishing a logical chain of imaging assessment from 3 dimensions: the bowel wall, mesenteric marginal vessels, and mesenteric lymph nodes, with computed tomography enterography (CTE) and intestinal ultrasound each offering distinct advantages; ④ systematically excluding intestinal tuberculosis, ischemic bowel disease, drug-induced enteropathy, and rare inherited immune disorders in differential diagnosis, integrating information from epidemiology, serum biomarkers, dynamic endoscopic evolution, and precise histopathology. In terms of treatment: ① emphasizing the “treat-to-target” paradigm, with therapeutic goals shifting from symptom relief to mucosal healing and even to histological healing. Drug selection should be individualized based on disease phenotype, biomarkers, endoscopic activity, and patient characteristics. Mesalazine serves as first-line therapy for mild-to-moderate UC; corticosteroids are used only as a “bridge” in the acute phase; biologics (anti-TNF-α, anti-integrin, anti-IL-12/23) are indicated for moderate-to-severe patients; JAK inhibitors and sphingosine-1-phosphate receptor (S1PR) modulators represent small-molecule precision options. Management of special populations requires a precise balance between efficacy and risk, with vedolizumab preferred during pregnancy, cautious use of corticosteroids and JAK inhibitors in elderly patients, and prerequisite antiviral or anti-tuberculosis therapy for patients with concurrent hepatitis B or latent tuberculosis infection. ② For difficult-to-treat and refractory IBD, a paradigm shift from phenotype-driven to multi-omics molecular subtyping is proposed, along with dynamic non-invasive monitoring technologies such as AI-assisted capsule endoscopy and plasma cell-free DNA (cfDNA) methylation profiling, and integrated management model of multidisciplinary team (MDT). IBD is essentially a systemic immune disorder; diagnosis and treatment require grasping clinical clues and evaluating the 3 imaging dimensions (bowel wall, mesenteric vessels and lymph nodes). The principles of “early diagnosis”, “individualized precision therapy”, and “whole-disease-cycle management” should be implemented in diagnosis and treatment of IBD, gradually shifting from symptom relief toward mucosal and histological healing, thereby improving patients’ quality of life.