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Small bowel adenocarcinoma (SBA) is a malignant epithelial neoplasm arising from the mucosa of the small intestine (duodenum, jejunum, or ileum).

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It is rare, accounting for ~30–40% of all primary small bowel malignancies and <5% of all gastrointestinal cancers.

Epidemiology

Incidence: ~1–2 cases per 100,000 per year.
Peak age: 50–70 years.
Gender: Male predominance (≈ 1.5:1).
Sites (descending frequency):
- Duodenum (esp. 2nd part) – ~55%
- Jejunum – ~30%
- Ileum – ~15%

Etiopathogenesis

Chronic mucosal inflammation and carcinogen exposure increase risk.

Pathogenesis parallels that of colorectal adenocarcinoma (APC, KRAS, p53 mutations).

Condition	Mechanism / Association
Crohn’s disease	Chronic inflammation → dysplasia → carcinoma (esp. ileum)
Celiac disease	Chronic villous atrophy → carcinoma
Familial Adenomatous Polyposis (FAP)	Multiple duodenal adenomas (esp. periampullary)
Peutz–Jeghers syndrome	Hamartomatous polyps → malignant transformation
HNPCC (Lynch syndrome)	MSI pathway mutation
Adenomas	Malignant transformation (adenoma–carcinoma sequence)
High animal fat diet, alcohol, smoking	Environmental carcinogens

Pathology

| Gross types | • Annular (circumferential constricting) lesion – “apple-core” or “napkin-ring” appearance. • Polypoidal / exophytic mass – intraluminal growth. • Ulcerative / infiltrative – mucosal ulceration, wall thickening. | | --- | --- | | Microscopy | Gland-forming adenocarcinoma (well → poorly differentiated). | | Mode of spread | • Local infiltration of mesentery and adjacent organs. • Lymphatic → mesenteric nodes. • Hematogenous → liver, lung, peritoneum. |

Clinical Presentation

Nonspecific and delayed (average delay in diagnosis 6–12 months).

Intermittent crampy abdominal pain.