Vol 44 # 4 December 2012 - Kma.org.kw

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275 Bariatric Surgery and Hypoglycemia December 2012 gastric banding (n = 2,917) for obesity, the relative risk of severe hypoglycemia was five-fold higher in the gastric bypass patients compared with controls [12] . However, it is noteworthy (and reassuring) that the absolute rate of post-bariatric hypoglycemia was low (< 1%). Furthermore, the Roux-en-Y gastric bypass procedure was more frequently associated with hypoglycemia than other forms of bariatric surgery, including vertical banding gastroplasty and gastric banding [12] . The median time from surgery to hypoglycemic symptoms in the Swedish survey was 2.7 years, consistent with the post-operative latency of 1 - 5 years reported in other series [5,13-15] . Of note, the frequency of accidental deaths was higher in postbariatric surgery patients than in reference cohorts, which may indicate undiagnosed hypoglycemia and possible underestimation of the number of patients with hypoglycemia [12] . Classically, hypoglycemia in post-gastric bypass patients occurs postprandially or during the postabsorptive period (as opposed to during fasting). Post-gastric bypass hypoglycemia usually is associated with the concurrence of low serum glucose levels (typically < 60 mg/dl) and inappropriately elevated or measurable levels of insulin and C- peptide. The mechanisms behind post-gastric bypass hyperinsulinemic hypoglycemia are not well-understood. In 2005, Service et al reported a series of six patients with symptomatic postprandial hyperinsulinemic hypoglycemia that developed on average 30 months after gastric bypass surgery [16] . Insulinoma was ruled out using imaging studies and selective arterial calcium stimulation test [16] . These patients then underwent either extensive or spleenpreserving distal pancreatectomy, and islet specimens were obtained for histological study. The pancreatic islet sections obtained from the patients reported by Service et al showed evidence of nesidioblastosis (hypertrophic beta cells, with enlarged or normalappearing islets; small scattered clusters of endocrine cells; and ductuloinsular complexes) [16] . The authors thus concluded that insulin hypersecretion from nesidioblasts was responsible for post-gastric bypass hypoglycemia in their patients [16] . However, reexamination of the pancreatic histology by Meier et al raised doubts about the presence of true nesidioblasts [17] . Instead, evidence of increased beta cell nuclear diameter was observed in post-gastric bypass patients compared with controls [17] . Thus, the hypoglycemia in such patients could have arisen from a combination of exaggerated “dumping” syndrome and increased insulin secretion per beta cell. Another mechanism proposed for the insulin hypersecretion and possible islet cell proliferation was enhanced glucagon-like peptide 1 (GLP-1) secretion from L cells in distal ileum, resulting from the rapid transit of nutrients following gastric bypass surgery [16] . Indeed, studies identifiedexaggeratedGLP-1response and attendant insulinotropic and glucagonostatic effects as mechanisms for post-gastric bypass hypoglycemia [18,19] . Since the mechanisms underlying post-bariatric hypoglycemia are not fully understood, a standard approach to management has not yet been developed. Mild hypoglycemia may be evaluated and treated in an outpatient setting. However severe hypoglycemia likely requires hospitalization and evaluation to rule out etiologies such as insulinoma. Without randomized controlled studies, the therapeutic approach to severe post-bariatric surgery hypoglycemia has been empirical. Management usually begins with dietary modification, including frequent small meals with low carbohydrate content. Pharmacological approaches that have had variable success include diazoxide, acarbose, octreotide, and calcium channel blockers [6, 13, 20] . For patients with refractory hypoglycemia, surgical intervention may be warranted, either to reverse the gastric restriction procedure or reduce the mass of insulin-secreting pancreatic tissue [5- 7, 14- 16] . In summary, severe hyperinsulinemic hypoglycemia is a rare but serious sequel of gastric bypass surgery. It usually presents a few years after the surgery and is accompanied by neuroglycopenic symptoms including confusion, seizure, syncope or coma. Future studies should be directed at unraveling the mechanisms, identifying risk factors, and developing optimal surveillance and management strategies for post-gastric bypass hypoglycemia. While awaiting the results of definitive studies on the subject, clinicians should be cognizant of the risk of hypoglycemia, educate gastric bypass patients on the warning symptoms of impending hypoglycemia and appropriate corrective measures. REFERENCES 1. Ogden C, Carroll M, Kit B, Flegal K. Prevalence of obesity in the United States, 2009 - 2010. NCHS Data Brief 2012; 82:1-7. 2. Haslam DW, James WP. Obesity. Lancet 2005; 366:1197- 1209. 3. Rucker D, Padwal R, Li SK, Curioni C, Lau DC. Long term pharmacotherapy for obesity and overweight: updated meta-analysis. BMJ 2007; 335:1194-1199. 4. Klein S, Fontana L, Young VL, et al. Absence of an effect of liposuction on insulin action and risk factors for coronary heart disease. N Engl J Med 2004; 350:2549- 2557. 5. Ritz P, Hanaire H. Post-bypass hypoglycaemia: a review of current findings. Diabetes Metab 2011; 37:274-281. 6. Ashrafian H, Athanasiou T, Li JV, et al. Diabetes resolution and hyperinsulinaemia after metabolic Roux-en-Y gastric bypass. Obes Rev 2011; 12:257-272.
December 2012 KUWAIT MEDICAL JOURNAL 276 7. Patti ME, Goldfine AB. Hypoglycaemia following gastric bypass surgery-diabetes remission in the extreme? Diabetologia 2010; 53:2276-2279. 8. Buchwald H, Avidor Y, Braunwald E, et al. Bariatric surgery: a systematic review and meta-analysis. JAMA 2004; 292:1724-1737. 9. Adams TD, Gress RE, Smith SC, et al. Long-term mortality after gastric bypass surgery. N Engl J Med 2007; 357:753-761. 10. Higa KD, Boone KB, Ho T. Complications of the laparoscopic Roux-en-Y gastric bypass: 1,040 patients - what have we learned? Obes Surg 2000; 10:509-513. 11. Dagogo-Jack S. Hypoglycemia in type 1 diabetes mellitus: pathophysiology and prevention. Treat Endocrinol 2004; 3:91-103. 12. Marsk R, Jonas E, Rasmussen F, Näslund E. Nationwide cohort study of post-gastric bypass hypoglycaemia including 5,040 patients undergoing surgery for obesity in 1986-2006 in Sweden. Diabetologia 2010; 53:2307- 2311. 13. Kellogg TA, Bantle JP, Leslie DB, et al. Post-gastric bypass hyperinsulinemic hypoglycemia syndrome: characterization and response to a modified diet. Surg Obes Relat Dis 2008; 4:492-499. 14. Patti ME, McMahon G, Mun EC, et al. Severe hypoglycaemia post-gastric bypass requiring partial pancreatectomy: evidence for inappropriate insulin secretion and pancreatic islet hyperplasia. Diabetologia 2005; 48:2236-2240. 15. Z’graggen K, Guweidhi A, Steffen R, et al. Severe recurrent hypoglycemia after gastric bypass surgery. Obes Surg 2008; 18:981-988. 16. Service GJ, Thompson GB, Service FJ, et al. Hyperinsulinemic hypoglycemia with nesidioblastosis after gastric-bypass surgery. N Engl J Med 2005; 353:249- 254. 17. Meier JJ, Butler AE, Galasso R, Butler PC. Hyperinsulinemic hypoglycemia after gastric bypass surgery is not accompanied by islet hyperplasia or increased beta-cell turnover. Diabetes Care 2006; 29:1554-1559. 18. Salehi M, Prigeon RL, D’Alessio DA. Gastric bypass surgery enhances glucagon-like peptide 1-stimulated postprandial insulin secretion in humans. Diabetes 2011; 60:2308-2314. 19. Rabiee A, Magruder JT, Salas-Carrillo R, et al. Hyperinsulinemic hypoglycemia after Roux-en-Y gastric bypass: unraveling the role of gut hormonal and pancreatic endocrine dysfunction. Surg Res 2011; 167:199-205. 20. Won JG, Tseng HS, Yang AH, et al. Clinical features and morphological characterization of 10 patients with noninsulinoma pancreatogenous hypoglycaemia syndrome (NIPHS). Clin Endocrinol (Oxf) 2006; 65:566-578.
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