VIPoma medical therapy: Difference between revisions
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=Medical management of advanced local or metastatic disease= | =Medical management of advanced local or metastatic disease= | ||
*There has been limited use of chemotherapy in patients with VIPoma. However, streptozocin based chemotherapy is considered best. | *There has been limited use of chemotherapy in patients with VIPoma. However, streptozocin based chemotherapy is considered best. | ||
*Most successful and favourable combination regimen of chemotherapy is Streptozocin with doxorubicin together with somatostatin analogues. | *Most successful and favourable combination regimen of chemotherapy is Streptozocin with doxorubicin together with somatostatin analogues. 5-FU can be used as alternative to doxorubicin for concerns of adverse effects but is inferior. | ||
*Molecularly targeted therapy eg. Sunitinib (tyrosine kinase inhibitor) is approved for treatment of progressive, unresectable, locally advanced or metastatic well differenctiated VIPoma. It is used in combination with somatostatin analogue. | *Molecularly targeted therapy eg. Sunitinib (tyrosine kinase inhibitor) is approved for treatment of progressive, unresectable, locally advanced or metastatic well differenctiated VIPoma. It is used in combination with somatostatin analogue. | ||
*Other molecular targeted therapy undergoing research for treatment are Everolimus (mTOR inhibitor) and Bevacizumab ( anti-VEGF monoclonal antibody) | *Other molecular targeted therapy undergoing research for treatment are Everolimus (mTOR inhibitor) and Bevacizumab ( anti-VEGF monoclonal antibody) | ||
Revision as of 20:09, 8 January 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Madhu Sigdel M.B.B.S.[2]Parminder Dhingra, M.D. [3]
Overview
Initial treatment in patient with VIPoma is prompt replacement of fluid and correction of electrolyte imbalance and acid-base disturbance.[1]
Medical Therapy
Symptomatic treatment
- Initial treatment in patient with VIPoma is prompt replacement of fluid and electrolyte losses. The IV fluid of choice is isotonic normal saline with added potassium and bicarbonate as necessary.
- Somatostatin analogues like short acting octreotide (50-100mcg every 8 hours) are useful for controlling diarrhea by blocking the release of VIP. Octreotide is later replaced by longer acting depot preparation of somatostatin analogues like sandostatin (20 mg IM every 4 weeks) and Lanreotide (120mg subQ every 4 weeks)
- Steroids are used in diarrhea of VIPoma refractory to somatostatin (prednisone 60 mg per day).
- Sunitinib a tyrosin kinase inhibitor has some evidence of symptomatic and biochemical control in somatostatin analogue resistant VIPoma.[2] It is also a medical treatment for locally advanced unresectable or advanced metastatic VIPoma.
Medical management of advanced local or metastatic disease
- There has been limited use of chemotherapy in patients with VIPoma. However, streptozocin based chemotherapy is considered best.
- Most successful and favourable combination regimen of chemotherapy is Streptozocin with doxorubicin together with somatostatin analogues. 5-FU can be used as alternative to doxorubicin for concerns of adverse effects but is inferior.
- Molecularly targeted therapy eg. Sunitinib (tyrosine kinase inhibitor) is approved for treatment of progressive, unresectable, locally advanced or metastatic well differenctiated VIPoma. It is used in combination with somatostatin analogue.
- Other molecular targeted therapy undergoing research for treatment are Everolimus (mTOR inhibitor) and Bevacizumab ( anti-VEGF monoclonal antibody)
References
- ↑ Vinik A. Vasoactive Intestinal Peptide Tumor (VIPoma) [Updated 2013 Nov 28]. In: De Groot LJ, Beck-Peccoz P, Chrousos G, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-. Available from: http://www.ncbi.nlm.nih.gov/books/NBK278960/
- ↑ Dimitriadis GK, Weickert MO, Randeva HS, Kaltsas G, Grossman A (2016). "Medical management of secretory syndromes related to gastroenteropancreatic neuroendocrine tumours". Endocr Relat Cancer. 23 (9): R423–36. doi:10.1530/ERC-16-0200. PMID 27461388.