Introduction Small bowel cancer (SBC) is rare and accounts for 5% of all gastrointestional (GI) malignancies despite the small bowel forming 75% of the GI tract. ^[1] Typical non-specific symptoms lead to late diagnosis and poor prognosis. We aim to establish a better understanding of the natural history and genetic features of SBC.

Methods A regional UK cancer registry identified local SBC patients diagnosed from January 1991 to January 2011. We retrospectively reviewed medical records collecting data on patient demographics, environmental and medical risk factors, family history, natural disease progression and immunohistochemical analysis (IHC).

Results The registry identified 205 SBC patients, 58% male and 42% female, who were diagnosed at a mean age of 63 years. Patients presented with abdominal pain (23.3%, n = 60), altered bowel habit (16.7%), weight loss (15.0%), bowel obstruction (15.0%) jaundice (13.3%), anaemia (10.0%) and other (6.6%). Investigations included CT (85.7%, n = 35), MR (8.6%) and barium (11.4%) imaging; gastroscopy (37.1%) that detected 8 of 9 duodenal SBCs and were reported normal in 2 jejunal and 2 ileal SBCs, DBE (2.9%) and ERCP (2.9%) that detected 1 duodenal SBC each; emergency (8.6%) and staging laparotomy (8.6%). SBC anatomical and histological distributions are described in Table 1. Patients were diagnosed at disease stage I (11.4%, n = 35), II (22.9%), III (20.0%) and IV (45.7%). Treatment included curative surgery (66%, n = 38; 12 resections, 7 bypasses and 6 Whipple procedures and adjuvant chemotherapy (AC) in 20%) with a 60% success rate and recurrence in 16.7% within a year; palliative surgery (18.4%; 6 bypasses and AC in 66.7%) and medical palliation (15.6%). Mortality rates at 1, 2, 5 and 10 years were 74.3%, 79.8%, 91.7% and 98.2% respectively (n = 109). Environmental factors included smoking (47%, n = 53) and drinking alcohol (51.1%, n = 45). Co-morbidities included peptic ulcer disease (8.4%, n = 72), coeliac disease (4.2%), Crohn’s disease (1.4%) and ulcerative colitis (1.4%). Furthermore, 23.6% of patients (n = 89) had ≥1 other malignancies that were metachronous (83.3%), synchronous (12.5%) or both (4.2%). Family history included a 1^st or 2^nd degree relative with malignancy (28.2%, n = 39) or familial adenomatous polyposis (7.7%). IHC showed Lynch syndrome and adenomatous polyposis coli gene mutations in 42.1% (n = 19) and 40% (n = 10) respectively.

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Abstract PTH-128 Table 1

Anatomical and histological distribution of SBC

Conclusion Our understanding of SBC is limited by its insidious course, difficult assessment and rarity coupled with multiple histological subtypes. A more comprehensive understanding of SBC and it’s genetic predisposition may allow high-risk patient stratification to earlier identify and treat SBC thus improving its poor prognosis.

Reference

1. Ross et al. British Journal of Cancer 1991;63:143–145

Disclosure of Interest None Declared.