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Hypoglycemia After Gastric Bypass Surgery Fatemeh Rahmani

Hypoglycemia After Gastric Bypass Surgery Fatemeh Rahmani. Agenda ● Definition ●Prevalence ●Etiology ●Pathophysiology ●Provacative test ●Risk factors ●Treatment.

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Hypoglycemia After Gastric Bypass Surgery Fatemeh Rahmani

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  1. Hypoglycemia After Gastric Bypass SurgeryFatemeh Rahmani

  2. Agenda●Definition●Prevalence●Etiology●Pathophysiology●Provacative test ●Risk factors●Treatment

  3. 54-year-old nurse with RYGB 9 y ago , no history of DM began to experience symptoms of hypoglycemia from 4 years ago occurred within 1 to 2 h after simple carb eating, initial evaluation : meal test BS= 34 mg/dL at 105 min after eating symptoms relieved by drinking juice

  4. PBHusually occurs 1y after surgerySymptoms occur 1-3h after eating Against the diagnosis1) 6-12 m in the postoperative period2)in the fasting state3) 4 hours after caloric intake4) with activity& during overnight (2-4am)‌

  5. 1)history of PP neuroglycopenia occurring 1-3 h after meals in a patient with history of bariatric surgery at least 1y before symptom 2)documented hypoglycemia (BS <54 mg/dL) at time of neuroglycopenic symptoms, and resolution of symptoms with treatment to raise glucose3) no hypoglycemia after a prolonged fast of at least 12 hours

  6. Agenda●Definition●Prevalence●Etiology●Pathophysiology●Provacative test●Risk factors ●Treatment

  7. inclusion criteria (April 2015- July 2016)-undergone RYGB surgery 1 y ago -were operated on by the same surgeon -had a negative hypoglycemic agent history -were18 years oldall patients received a standardized solid mixedmeal energy total :201kcal carb :34g (49.0%) fat :8g (32.0%) protein :3.8g (6.0%)

  8. tests were performed in the morning after overnight fast Blood samples were drawn every 30min until 150 min Patients with pHH underwent a second solid mixed mealtest1-2weeks later, low carb solid mixed meal consisting of energy total: 195kcal carb :9g[18.0%] fat :5g[22.0%] protein :26.9g[60.0%]cutt-off value : Bs <55mg/dL & INS >18pmol/L

  9. The purpose : evaluate the frequency of pHH with &w/o symptoms of hypoglycemia Most current literature considers pHH occurring with a frequency of<1-2%In our series ,25 expressed typical autonomous symptoms for pHH above 55mg/dL, due to the rapid drop in BSThese patients’ symptomses even w/o severe hypoglycemic episodes suggests that our finding of 1.0% is likely not fully representative of the actual pHH incidence

  10. ImportanceSevere hypoglycemia ●neuroglycopenic symptoms ●syncope ●motor vehicle accidents●increase morbidity and mortality in DM ●cardiac arrhythmia ●cardiovascular death in post bariatric surgery patients

  11. All patients underwent RYGB,SG,or DS at a single center 2002-2015 with postoperative glucose ≤70mg/dL 1)symptoms occurring >1y after surgery 2)normal FBS & insulin levels 3)correlation of symptoms & hypoglycemia

  12. 83 patients (1.4%)had symptomatichypoglycemia 23 :1episode 60: ≥2episodes 25 were admitted to the hospital for further management PPH: 32(38%) Infection :8(10%) Medication: 8(10%) Poor oral intake :8(10%) Unknown :27(32%)

  13. rate of symptomatic hypoglycemi & pp hyperinsulinemic hypoglycemia was 1.4%& 5%. Both conditions were most commonly seen after RYGB1/3 required hospitalization38% referred to endocrinologists for more evaluation 9 patients required nutritional intervention in the form of feeding tube placement or parenteral nutrition

  14. Rate of hypoglycemia is less after SG compared with RYGB In our cohort ,hypoglycemia occurred more frequently ●post-RYGB(88%) ● nondiabetic patients(54%) ●with a median of 781d between surgery & hypoglycemia

  15. What glucose threshold should be used Typical patterns of glycemia in a post-bypass patient ▪normal fasting glucose ▪exaggerated postprandial excursions compared with those without GI surgery ▪rapid rise in glucose shortly after food intake and a fast decline thereafterGlucose alone can not be used to define hypoglycemia (integration with symptoms)

  16. Agenda●Definition●Prevalence●Etiology●Pathophysiology●Provacative test●Risk factors ●Treatment

  17. The primary etiologies of PPHH ■Dumping syndrome ■factitious insulin/sulfonylurea administration ■nesidioblastosis ■Noninsulinoma pancreatogenous hypoglycemia – syndrome (NIPHS) ■Insulinoma

  18. Diagnosis of nesidioblastosis is 1 of exclusion -biochemical -provocative -radiologic testing -pancreatic resection - pathologic confirmation

  19. imaging is necessary to distinguish nesidioblastosis and insulinoma after the biochemical evaluation. Insulinoma can be identied in CT , Sono ,MRI. indium-111 pentetreotide (GLP-1) scan is the most sensitive for detecting occult insulinoma by highlighting somatostatin receptorpositive tumors Calcium stimulated selective mesenteric arteriography invasive , selectively sample insulin secretion from the pancreas ,useful in localizing the B-cell mass in cases of nesidioblastosis

  20. recurrent nesidioblastosis after distal pancreatectomy has been described in surgical therapy failure. Several series of open distal pancreatectomy in children for nesidioblastosis found that 100(52%)of 193 patients had recurrent symptoms after resection61 (32%) required an additional resection to ameliorate their symptomsAdults could differ from children in that the former has diffuse nesidioblastosis instead of focal and recurrent hypoglycemia in the initial postoperative period are commonly not transiently

  21. NIPHS rare syndrome characterized by endogenous HH in adults that is not caused by an insulinomaPancrease show similar pathological feature of nesidioblastosisService et al. In 1999 in 5 adults found symptoms of PP neuroglycopenia secondary to hyperinsulinemic hypoglycemia due to excessivebeta –cell growt these patients had negativeimaging studies, negative 72 h fasts, and positive selective arterial calcium stimulation tests indicative of pancreatic beta-cell hyperfunction

  22. Another possible but rare cause of hypoglycemiain post-RYGB patients is insulinomaThe persistence of hypoglycemic episodes after dietary adjustments led to consideration of an autonomous source of hyperinsulinemia, and MRI and CT iden-tified an insulinoma. Insulinoma can present with hypoglycemia in both fasting and postprandialstates (rarely)

  23. Which patients with hypoglycemia after bariatric surgery require a prolonged fasting test and imaging

  24. For patients with typical PPH and no fasting hypoglycemia, don’t need prolonged fasting tests.In patients with fasting hypoglycemia who do not appear well, additional diagnostic testing (AI, critical illnes, malnutrition associated with excessive weight loss or food aversion) should be consideredImaging studies should not be performed unless the history and biochemical testing demonstrate that fasting hypoglycemia is present and is caused by excessive insulin secretion, or other atypical clinical features raise suspicion for other pathology

  25. Agenda●Definition●Prevalence●Etiology●Pathophysiology●Provacative test●Risk factors ● Treatment

  26. PPHH ( late dumping syndrom )is seen mainly after RYGB. The pathophysiology of this is not well understood it is believed to be due to alterations in ▪glucose regulatory mechanism ▪incretin hormones ▪INS sensitivity ▪increased β-cell hyperplasia/ activity/ sensitivity PPHH usually occurs 1 y after bariatric surgery, with normal glucose and insulin levels in the fasting state

  27. early dumping:typically occurred within 1h of eating due to concentrated nutrients and carb rapidly entering the small bowel and occurred in 1/3 gastrectomy patients.(9-21%)late dumping: typically occurred 2–3 h after eating, associated with hypoglycemia and generally developed later in the post-operative course, but with an etiology that was less clear(1-6%)

  28. Several factors implicated ,including increase in incretins Incretins are gut-derived hormones that are released into the blood post-prandially, and stimulate insulin release from the beta cells of the islets of Langerhans 2 incretins that are most often implicated are: a) Glucagon-like peptide-1(GLP-1) b) Gastric inhibitory peptide (GIP;also known as glucose-dependent insulinotropic polypeptide)

  29. levels of GLP-1 increase after bariatric surgery, due to the rapid transit of unabsorbed nutrients to the jejunum &ileum, the distal portion of which is the site of Lcells, the source of GLP-1Rabiee et al. in 2011 studied 4 post-RYGB patients and reported 3-4 fold increase in GLP-1 levels 1y after surgery & 2 fold increase in GIP levelGoldfine et al. in 2007 found incretin levels to be 5-10 fold higher in post-RYGB patients compared to controls

  30. GLP-1 has been ▪increase beta cell mass in prolieration ▪decreasing- beta cell apoptosis ▪induce hypertrophy of pancreatic cellsother possible mechanisms:-lack of reduction of b-cell mass which was increased during the preoperative obese state-increased insulin sensitivity following weight loss-inappropriate beta cell secretion following early entry of ingested nutrients into the small intestine -abnormal counter-regulatory hormonal (glucagon) responses

  31. GLP-1 has 2 functions: ▪antihyperglycemic hormone increasing B-cell sensitivity to glucose to induce glu-dependent insulin secretion with inhibition of glucagon secretion▪initiator of the “ileal brake” to slow small bowel motility in response to the rapid delivery of food into bowel resulting in the activation of the “ileal brake” at the consequence of profound insulin secretion and subsequent hypoglycemia

  32. Plasma GIP levels andGLP-1levels in four patients with neuroglycopenia occurring 2–3 years after Roux-en-Y gastric bypass (colored symbols, cases 1–4) and in five asymptomatic patients 1 year after Roux-en-Y gastric bypass (controls—open circles) following a standardized test meal

  33. Loss of pylorus in RYGB causes faster GI transit and absorption of simple sugars that evoke a stronger GLP1 response resulting in higher insulin level called Postprandial hyperinsulinemic hypoglycemia

  34. In patients with post-RYGB hypoglycemia, elevation of GIP &GLP-1 persist for years after surgery with hypersecretion of INS in setting of normal BS INS sensitivity as well as b-cell GLP-1 receptor availability, sensitivity to GLP-1, and sensitivity to glucose are normal in patients with post-RYGB hypoglycemiaso an inappropriately exuberant INS response with subsequent hypoglycemia is due to excessive secretion of GLP-1 after oral nutrients

  35. Agenda●Definition●Prevalence●Etiology●Pathophysiology●Provacative test ●Risk factors ●Treatment

  36. provocative tests GTT is not well tolerated in previous history of UGI - hyperosmolar liquid provokes dumping syndrom-10% of healthy people have glucose <50 mg/dL in 180 min of the challenge, without neuroglycopenia. an oral GTT should play no role in the evaluation of meal-induced hypoglycemia particularly in individuals after GI surgery and dumping syndrome

  37. provocative testingmixed meal (protein,carbohydrates ,fat) -no currently accepted standard for meal testing;- solid& liquid mixed meal are used with carb 40-75g some believe liquid meal has no place in the evaluation of patients with accelerated& unregulated transit of calories into the proximal small intestine but others believe it provides reproducible stimulus

  38. Agenda●Definition●Prevalence●Etiology●Pathophysiology●Provacative test ●Risk factors ● Treatment

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