eMedicine Specialties > Oncology > Carcinomas of the Gastrointestinal Tract

Malignant Neoplasms of the Small Intestine: Treatment & Medication

Author: N Joseph Espat, MD, MS, FACS, Professor and Chief of Surgical Oncology, Vice-Chairman of Department of Surgery, Roger Williams Medical Center
Coauthor(s): Ponnandai S Somasundar, MD, FACS, Assistant Professor of Surgery, Boston University; Surgical Oncologist, Roger Williams Medical Center; Director of Oncology, Kent County Hospital; Piero Marco Fisichella, MD, Assistant Professor of Surgery, Stritch School of Medicine, Loyola University; Director, Esophageal Motility Center, Loyola University Medical Center
Contributor Information and Disclosures

Updated: Apr 30, 2008

Treatment

Medical Care

  • Because of its low prevalence, few clinical trials have been performed to assess the efficacy of chemotherapy for treating small-bowel cancer.
    • The largest published study was in 1984 by Jigyasu et al and involved 14 subjects with metastatic small-bowel adenocarcinoma who were treated with 21 chemotherapy regimens, most containing 5-fluorouracil (5-FU). Two minor responses and one partial response occurred, with a median survival of 9 months.19
    • In their 1984 review of 65 patients with small-bowel adenocarcinoma, Ouriel and Adams reported a mean survival of 10.7 months in 6 patients with metastatic disease treated with 5-FU–based regimens, compared with a mean survival of 4 months in 6 patients with metastatic disease who received no chemotherapy. An additional 6 patients with recurrent disease were also treated with chemotherapy and had a mean survival of 11.5 months, compared with 21 patients with recurrent disease who received no chemotherapy and survived a mean of 7.9 months.20
    • More recently, a 1998 British study by Crawley et al reported 8 patients with advanced small-bowel adenocarcinoma treated with infusional 5-FU–based regimens and found a response rate of 37.5% and a median survival of 13 months.21
  • Newer agents found to be effective for colorectal carcinoma also may be active for small-bowel adenocarcinoma.
    • As reported by Polyzos and colleagues in 2003, 3 subjects with 5-FU–refractory small-bowel adenocarcinoma were treated with salvage irinotecan therapy. Two patients achieved a minor response and had improvement of their symptoms.22
    • Also in 2003, Bettini and colleagues found that the FOLFOX 4 regimen (ie, combination infusional 5-FU, oxaliplatin, and leucovorin) was safely administered as adjuvant chemotherapy in 3 patients with resected small-bowel adenocarcinoma associated with celiac disease.23
  • Because these are uncontrolled studies with few patients, drawing conclusions regarding the benefit of chemotherapy for small-bowel adenocarcinoma, either in the metastatic or adjuvant setting, is difficult. In patients with a good performance status, any attempts using the regimens mentioned seem reasonable.
  • Similarly, few studies have assessed the efficacy of cytotoxic chemotherapy for small-bowel sarcomas. An analysis by Fernandez-Trigo and Sugerbaker from 1993 reported on 7 randomized prospective studies of subjects with nonextremity sarcomas and found no survival benefit with the addition of adjuvant chemotherapy after surgery.24
  • Studies of chemotherapy in patients with metastatic GI soft tissue sarcomas have also yielded disappointing results.
    • For example, the Southwest Oncology Group, as reported by Zalupski et al in 1991, found that only 3 (7%) of 43 subjects with GI sarcomas responded to a combination of doxorubicin and dacarbazine, whereas 21% of subjects with leiomyosarcomas of other sites responded to the same combination.25
    • A trial reported by Blair et al in 1994 found that a combination of ifosfamide and etoposide produced no responses among 10 patients with GI sarcomas.26
  • Evidence indicates that in general, small-bowel sarcomas and GISTs are more resistant to chemotherapy than sarcomas in other sites. A 2000 Dutch study by Plaat et al found greater expression of multidrug-resistance proteins in GISTs compared with non-GI leiomyosarcomas.27
  • Unlike conventional chemotherapy, the recently developed novel agent imatinib mesylate (also known as STI571 and Gleevec) has shown promising activity in GISTs. Imatinib is a small molecule that selectively inhibits the tyrosine kinase activity of bcr-abl, c-kit, and PDGFR.
    • In 2002, Demetri et al reported a multinational study of 147 subjects with advanced GISTs who were randomized to receive 400 mg or 600 mg of imatinib daily. Results demonstrated a 54% partial response rate and 28% stable disease, with a median duration of response greater than 24 weeks and no differences in response between the two doses.28
    • Another study of imatinib by the European Organization for Research and Treatment of Cancer, as reported by van Oosterom et al in 2002, indicated a 54% partial response rate and 37% stable disease rate, with a duration of response greater than 10 months, among 35 subjects with GISTs.29
  • These studies have led to the US Food and Drug Administration approval of imatinib for advanced GISTs. However, its effect on survival and its role in the adjuvant setting remain to be defined by the results of ongoing randomized clinical trials.
  • The FDA has recently approved Sunitinib (Sutent) as targeted therapy for patients in whom imatinib fails in the form of disease progression or inability to tolerate the drug.

Surgical Care

  • Surgical resection provides the only hope of cure for patients with small-bowel adenocarcinomas. This is possible in approximately two thirds of patients. The remaining have unresectable disease as a result of extensive local disease or metastases to regional lymph nodes, the liver, or the peritoneum.
  • Use wide local excision on lesions in the distal duodenum, jejunum, or ileum.
    • Patients with lesions in the proximal duodenum, including those in the periampullary region, should undergo pancreaticoduodenectomy, which now has an operative mortality rate of less than 5%.
    • Several studies have shown that patients who undergo resection have an improved 5-year survival rate of 40-60%.
    • Surgery is indicated for palliation in patients with symptomatic advanced disease, such as intestinal obstruction.
    • Ileal tumors are more likely to develop intestinal obstruction than jejunal tumors. Emergency surgery for these patients relieves the obstruction but precludes a complete and negative margin resection.
  • Despite the efficacy of imatinib for GISTs, surgical resection remains the primary therapy for small-bowel sarcomas, although 35-50% are unresectable because of metastatic disease. Similar to proximal duodenal adenocarcinomas, small-bowel sarcomas located in this region should be resected with a pancreaticoduodenectomy.
    • Those in the distal duodenum, jejunum, or ileum should be resected with wide margins; tumors close to the ileocecal valve may require a right hemicolectomy.  DeMatteo et al reported a  series from Memorial Sloan-Kettering of 200 patients with GISTs showing median survival of patients with complete excision was 66 months, as opposed to those with incomplete resection at 22 months, justifying the removal of adjacent organs to obtain complete resection of the primary disease.7
    • Lymph node metastasis is rare, and therefore an extensive lymph node dissection is not recommended.
    • Resection appears to prolong survival, but recurrence with widely metastatic disease is typical.

Consultations

  • Gastroenterologist: This specialist may assist in diagnosis through upper GI endoscopy and colonoscopy.
  • Radiation oncologist
    • Although no survival benefit is achieved with adjuvant radiotherapy after surgery for small-bowel adenocarcinoma or sarcoma, radiotherapy may be useful as a palliative procedure for pain relief or obstructive symptoms in patients with advanced disease. Also, radiotherapy may be of benefit for controlling chronic tumor-related blood loss.
    • While postoperative radiotherapy has been shown to improve local control for sarcomas of the extremities, its role for GIST and GI sarcomas is not clear. Adjuvant brachytherapy and intraoperative radiation are also being investigated for treatment of GI sarcomas.

Medication

No standard regimen demonstrates benefit in an adjuvant or metastatic setting for small-bowel adenocarcinoma. Because of the similarity to colorectal adenocarcinoma, a regimen containing 5-FU with leucovorin (ie, Roswell Park, Mayo Clinic) may be used. Newer agents active in colorectal carcinoma, such as irinotecan and oxaliplatin, may also be considered, in combination with 5-FU. Small-bowel sarcomas, most of which are c-kit –positive GISTs, are resistant to cytotoxic chemotherapy. However, patients with advanced disease may be treated with imatinib.

Chemotherapeutic agents

Chemical substances or drugs that treat neoplastic diseases by interfering with DNA synthesis.


Fluorouracil (Adrucil)

Fluorinated pyrimidine analog. Metabolite, FdUMP, inhibits thymidylate synthase that is essential in folate metabolism. 5-FU metabolites FUTP and FdUTP inhibit RNA and DNA synthesis by incorporating into RNA and DNA, respectively.

Adult

Single-agent adjuvant regimens
Roswell Park: 500 mg/m2 IV qwk for 6 wk, repeat cycle q8wk for total of 4-6 cycles
Mayo Clinic: 425 mg/m2 IV on days 1-5, repeat cycle q4wk for total of 4-6 cycles
Combination regimens
IFL (combined with irinotecan): 500 mg/m2 IV bolus qwk for 4 wk; repeat cycle q6wk
FOLFOX 4 (combined with oxaliplatin): 400 mg/m2 IV bolus, followed by 600 mg/m2 IV infusion over 22 h on days 1 and 2; repeat cycle q2wk

Pediatric

Not established

Methotrexate and trimetrexate administered prior to 5-FU increases formation of FUTP and enhances cell killing and toxicity; increased risk of bleeding with anticoagulants, NSAIDs, platelet inhibitors, and thrombolytic agents; enhanced bone marrow toxicity with other immunosuppressive agents

Documented hypersensitivity; bone marrow suppression; serious infection; poor nutritional status; active ischemic heart disease; MI within 6 mo

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Nausea, oral and GI ulcers, depression of immune system, hemopoiesis failure (bone marrow suppression), hand-foot syndrome, neurologic toxicity, and cardiac ischemia may occur; adjust dosage in renal impairment


Leucovorin (Wellcovorin)

Racemic mixture of 5-formyltetrahydrofolate. Metabolized to reduced folate 5,10-methylenetetrahydrofolate, which forms ternary complex with FdUMP and thymidylate synthase, enhancing inhibition of the latter.

Adult

Roswell Park: 500 mg/m2 IV over 2 h qwk for 6 wk, administered before 5-FU; repeat cycle q8wk for total of 4-6 cycles
Mayo Clinic: 20 mg/m2 IV on days 1-5, administered before 5-FU; repeat cycle q4wk for total of 4-6 cycles
IFL: 20 mg/m2 IV bolus, after irinotecan and before 5-FU, qwk for 4 wk; repeat cycle q6wk
FOLFOX 4: 200 mg/m2 IV over 2 h on days 1 and 2, prior to bolus 5-FU; repeat cycle q2wk

Pediatric

Not established

May decrease serum levels and efficacy of phenobarbital, phenytoin, and primidone; rescues against toxic effects of methotrexate

Documented hypersensitivity; pernicious anemia; vitamin-deficient megaloblastic anemias

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Allergic reactions, nausea, and vomiting may occur with administration; do not administer intrathecally or intraventricularly; use in pernicious anemia or vitamin B-12 deficiency megaloblastic anemias may cause hematologic remission, but allow neurologic manifestations to progress


Irinotecan (Camptosar)

Camptothecin derivative that inhibits topoisomerase I, resulting in double-stranded DNA damage. Approved as first-line therapy in combination with 5-FU and leucovorin or as second-line, single-agent therapy after 5-FU for advanced colorectal cancer.

Adult

Single-agent: 125 mg/m2 IV over 90 min qwk for 4 wk, repeat cycle every 6 wk; alternatively, 350 mg/m2 IV over 90 min q3wk
IFL combination: 125 mg/m2 IV over 90 min before leucovorin and 5-FU, qwk for 4 wk; repeat cycle q6wk

Pediatric

Not established

Because can cause diarrhea and dehydration, use of laxatives and diuretics may need to be reduced or omitted during treatment; patients who received prior abdominal or pelvic radiation therapy are at increased risk for severe myelosuppression; concurrent use with radiation not recommended

Documented hypersensitivity; ongoing severe diarrhea or neutropenic fever from prior treatment with irinotecan; significant liver function abnormalities including any degree of jaundice

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Can induce early and late diarrhea; early diarrhea may be accompanied by cholinergic symptoms (eg, rhinitis, increased salivation, miosis, lacrimation, diaphoresis, flushing); atropine (0.25-1 mg IV/SC) may be given to prevent or treat these symptoms; late diarrhea occurs more than 24 h after irinotecan and can be severe and life-threatening; late diarrhea should be treated promptly with loperamide, and fluids and antibiotics should be given if dehydration and fever occur; if diarrhea grade 2 or higher occurs, subsequent doses should be reduced
Severe neutropenia is another toxicity, which has resulted in deaths from sepsis; patients with neutropenic fever or ANC <1000 should have subsequent doses reduced
In clinical trials, patient with baseline performance status of 2 had higher rates of hospitalization, early death, and other complications; therefore, treatment in these patients should be closely monitored


Oxaliplatin (Eloxatin)

Organoplatinum complex that acts as an alkylating agent. Metabolites cross-link with DNA, inhibiting DNA synthesis and function. Combination with 5-FU and leucovorin (FOLFOX 4 regimen) is approved for treatment of advanced colorectal cancer.

Adult

FOLFOX 4: 85 mg/m2 IV over 2 h (with leucovorin, before 5-FU) on day 1; repeat q2wk

Pediatric

Not established

Because of renally excretion, coadministration of nephrotoxic drugs may potentially affect clearance

Documented hypersensitivity (also other platinum compounds); should be given cautiously in patients with preexisting neuropathy

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

May cause acute, reversible, peripheral, sensory neuropathy precipitated by cold exposure; may also cause a persistent peripheral sensory neuropathy characterized by paresthesias; other common adverse events of FOLFOX 4 include neutropenia, thrombocytopenia, nausea, vomiting, diarrhea, and rare cases of pulmonary fibrosis

Tyrosine kinase inhibitors

Inhibit tyrosine kinase activity of c-kit, bcr-abl, and PDGFR oncogenes.


Imatinib mesylate (Gleevec)

Small molecule that selectively inhibits tyrosine kinase activity of c-kit, bcr-abl, and PDGFR. Available in 100-mg caps.

Adult

400 mg/d or 600 mg/d PO for adult patients with unresectable or metastatic GIST

Pediatric

Not established

Because of metabolism by hepatic cytochrome P-450 3A4 enzyme, plasma levels may be affected by other drugs that alter activity of this enzyme (eg, clarithromycin, cyclosporine, erythromycin, itraconazole, ketoconazole, phenytoin, simvastatin)

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Most common toxicities include fluid retention and edema, nausea, diarrhea, abdominal discomfort, muscle cramps, fatigue, and skin rash; most events are mild to moderate in severity; adverse events may be more common at 600 mg/d versus 400 mg/d

Multikinase inhibitors

Elicit actions via multiple tyrosine kinase inhibitors implicated in tumor growth, pathologic angiogenesis, and metastatic progression.


Sunitinib (Sutent)

Mulitkinase inhibitor that targets several tyrosine kinase inhibitors implicated in tumor growth, pathologic angiogenesis, and metastatic progression. Inhibits platelet-derived growth factor receptors (ie, PDGFR-alpha, PDGFR-beta), vascular endothelial growth factor receptors (ie, VEGFR1, VEGFR2, VEGFR3), stem cell factor receptor (KIT), Fms-like tyrosine kinase-3 (FLT3), colony-stimulating factor receptor type 1 (CSF-1R), and the glial cell-line derived neurotrophic factor receptor (RET).
Indicated for persons with gastrointestinal stromal tumors (GISTs) whose disease has progressed or who are unable to tolerate treatment with imatinib (Gleevec). Delays median time to tumor progression.

Adult

Standard dose: 50 mg PO qd on a schedule of 4 wk on treatment followed by 2 wk off treatment, then repeat cycle
Dose modification: Increase or reduce dose in 12.5-mg increments based on individual safety and tolerability
Coadministration with potent CYP4503A4 inhibitors: Minimum dose of 37.5 mg PO qd during treatment phase of cycle
Coadministration with CYP4503A4 inducers: Maximum dose of 87.5 mg PO qd during treatment phase of cycle

Pediatric

Not established

Potent CYP4503A4 inhibitors (eg, ketoconazole, itraconazole, clarithromycin, atazanavir, indinavir, nefazodone, nelfinavir, ritonavir, saquinavir, telithromycin, voriconazole) may increase plasma concentrations; CYP4503A4 inducers (eg, dexamethasone, phenytoin, carbamazepine, rifampin, rifabutin, phenobarbital) may decrease plasma concentrations; St John's wort induces metabolism and decreases plasma concentrations unpredictably (do not take concurrently)

Documented hypersensitivity; concurrent administration with St John's wort

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Common adverse effects include diarrhea, skin discoloration, mouth irritation, weakness, and altered taste; may cause fatigue, hypertension, bleeding, swelling, and hypothyroidism; in clinical trials, decreased left ventricular ejection fraction to below lower limits of normal in 15% of patients (monitor for CHF and discontinue if clinical manifestations of CHF develop); may cause hemorrhagic events that may include epistaxis or rectal, gingival, GI, genital, or wound bleeding

More on Malignant Neoplasms of the Small Intestine

Overview: Malignant Neoplasms of the Small Intestine
Differential Diagnoses & Workup: Malignant Neoplasms of the Small Intestine
Treatment & Medication: Malignant Neoplasms of the Small Intestine
Follow-up: Malignant Neoplasms of the Small Intestine
References
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Further Reading

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Keywords

small bowel cancer, small-bowel cancer, small bowel neoplasm, small-bowel neoplasm, small bowel malignancy, small-bowel malignancy, small bowel tumor, small-bowel tumor, small bowel mass, small-bowel mass, small intestine malignancy, small intestine tumor, small intestine cancer, gastrointestinal malignancy, gastrointestinal tumor, gastrointestinal cancer, GI cancer, GI malignancy, GI tumor, gastrointestinal mass, GI mass, gastrointestinal neoplasm, GI neoplasm, small bowel adenocarcinoma, small-bowel adenocarcinoma, adenocarcinoma, GI adenocarcinoma, small intestine adenocarcinoma, GI adenocarcinoma, familial adenomatous polyposis, FAP, gastrointestinal stromal tumor, GIST

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Contributor Information and Disclosures

Author

N Joseph Espat, MD, MS, FACS, Professor and Chief of Surgical Oncology, Vice-Chairman of Department of Surgery, Roger Williams Medical Center
N Joseph Espat, MD, MS, FACS is a member of the following medical societies: Alpha Omega Alpha, American Association for Cancer Research, American College of Surgeons, American Hepato-Pancreato-Biliary Association, American Medical Association, American Society for Parenteral and Enteral Nutrition, American Society of Clinical Oncology, Association for Academic Surgery, Central Surgical Association, Chicago Medical Society, International Hepato-Pancreato-Biliary Association, Pancreas Club, Sigma Xi, Society for Leukocyte Biology, Society for Surgery of the Alimentary Tract, Society of American Gastrointestinal and Endoscopic Surgeons, Society of Surgical Oncology, Society of University Surgeons, Southeastern Surgical Congress, Southern Medical Association, and Surgical Infection Society
Disclosure: Nothing to disclose.

Coauthor(s)

Ponnandai S Somasundar, MD, FACS, Assistant Professor of Surgery, Boston University; Surgical Oncologist, Roger Williams Medical Center; Director of Oncology, Kent County Hospital
Ponnandai S Somasundar, MD, FACS is a member of the following medical societies: American College of Surgeons, American Hepato-Pancreato-Biliary Association, Association for Academic Surgery, Association of Surgeons of India, and Society of Surgical Oncology
Disclosure: Nothing to disclose.

Piero Marco Fisichella, MD, Assistant Professor of Surgery, Stritch School of Medicine, Loyola University; Director, Esophageal Motility Center, Loyola University Medical Center
Piero Marco Fisichella, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, Association for Academic Surgery, Society for Surgery of the Alimentary Tract, and Society of American Gastrointestinal and Endoscopic Surgeons
Disclosure: Nothing to disclose.

Medical Editor

Lodovico Balducci, MD, Professor of Oncology and Medicine, University of South Florida College of Medicine; Division Chief, Senior Adult Oncology Program, H Lee Moffitt Cancer Center and Research Institute
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Benjamin Movsas, MD, Vice-Chairman, Department of Radiation Oncology, Fox Chase Cancer Center
Benjamin Movsas, MD is a member of the following medical societies: American College of Radiology, American Radium Society, American Society for Therapeutic Radiology and Oncology, and American Society of Clinical Oncology
Disclosure: Nothing to disclose.

CME Editor

Rajalaxmi McKenna, MD, FACP, Consulting Staff, Department of Medicine, Southwest Medical Consultants, SC, Good Samaritan Hospital, Advocate Health Systems
Rajalaxmi McKenna, MD, FACP is a member of the following medical societies: American Society of Clinical Oncology, American Society of Hematology, and International Society on Thrombosis and Haemostasis
Disclosure: Nothing to disclose.

Chief Editor

Jules E Harris, MD, Visiting Professor of Medicine, Division of Hematology/Medical Oncology, Department of Internal Medicine, University of Arizona College of Medicine at Tucson; Consulting Staff, Arizona Cancer Center
Jules E Harris, MD is a member of the following medical societies: American Association for Cancer Research, American Association for the Advancement of Science, American Association of Immunologists, American Society of Clinical Oncology, American Society of Hematology, and Central Society for Clinical Research
Disclosure: GlobeImmune Salary Consulting; Amplimed Consulting fee Consulting

 
 
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