Related Experiment Video
Updated: May 11, 2026
05:42
Robotic Enucleation of an Intra-Pancreatic Insulinoma in the Pancreatic Head
Published on: January 3, 2020
Somatostatin analogues for pancreatic surgery
Kurinchi Selvan Gurusamy1, Rahul Koti, Giuseppe Fusai
1Department of Surgery, Royal Free Campus, UCL Medical School, London, UK. kurinchi2k@hotmail.com.
The Cochrane Database of Systematic Reviews
|May 2, 2013
Summary
Prophylactic somatostatin analogues may reduce complications after pancreatic surgery but do not affect mortality. Further high-quality trials are needed to confirm these findings for routine use.
Area of Science:
- Gastrointestinal Surgery
- Surgical Oncology
- Pharmacology
Background:
- Pancreatic resections carry significant risks, with morbidity rates of 30-60% and mortality of 5%.
- The use of synthetic somatostatin analogues to mitigate these risks is debated among surgeons.
Purpose of the Study:
- To evaluate the efficacy of routine prophylactic somatostatin analogue use in patients undergoing pancreatic surgery.
Main Methods:
- A systematic review and meta-analysis of 21 randomized controlled trials involving 2348 patients.
- Data were extracted and analyzed using fixed-effect and random-effects models.
Main Results:
- Somatostatin analogues significantly reduced overall postoperative complications (RR 0.70; 95% CI 0.61 to 0.80) and pancreatic fistulas (RR 0.66; 95% CI 0.55 to 0.79).
- No significant differences were observed in perioperative mortality (RR 0.80; 95% CI 0.56 to 1.16) or re-operation rates.
- The impact on clinically significant pancreatic fistulas was not significant when clearly distinguished.
Conclusions:
- Somatostatin analogues show potential in reducing perioperative complications but not mortality.
- Further high-quality, adequately powered trials are essential to solidify these findings.
- Current evidence suggests potential benefit, warranting consideration for routine use in pancreatic resection.
Related Concept Videos
01:24Glucagon-like Receptor Agonists
Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...
01:06Oral Hypoglycemic Agents: Glinides
Repaglinide (Prandin) and Nateglinide (Starlix), known as glinides, are oral insulin secretagogues that stimulate insulin release from pancreatic β cells by closing the ATP-sensitive potassium channels (KATP channel). Repaglinide controls insulin release from pancreatic β cells by managing potassium efflux. It shares two binding sites with sulfonylureas and also has a unique site, indicating overlapping mechanisms of action. With a rapid onset and a 4-7 hour duration, it effectively manages...
01:23Dipeptidyl Peptidase 4 Inhibitors
Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a significant...