Reactive Hypoglycemia and WLS

southernlady

Administrator
Staff member
Since I was diagnosed with RH back in 1991 and had diabetes as well, I made sure I got a DS to avoid aggrevating it. So when I was doing my research, I came across many links on the subject. I collected them into one post and am posting them here for others to see during their research.

NIPHS Noninsulinoma Pancreatogenous Hypoglycemic Syndrome

According to the article I say on the Mayo Clinic web site which has been moved:

Mayo Clinic doctors have recognized and reported on a seemingly rare but serious complication following gastric bypass called non-insulinoma pancreatogenous hypoglycemia syndrome (NIPHS) or post-bariatric surgery hypoglycemia. After a person eats, this condition can result in very low blood sugar levels that lead to severe neurologic symptoms, including visual disturbances, confusion and (rarely) seizures.

It’s not just Mayo doctors tho, I found other links as well:
Post-pradial Hypoglycemia

Noninsulinoma pancreatogenous hypoglycaemia syndrome (NIPHS) caused by an activating glucokinase mutation

Evaluation and Management of Adult Hypoglycemic Disorders: An Endocrine Society Clinical Practice Guideline


Electrical short-circuit in b-cells from a patient with non-insulinoma pancreatogenous hypoglycemic syndrome (NIPHS): a case report

Clinical features and morphological characterization of 10 patients with noninsulinoma pancreatogenous hypoglycaemia syndrome

Endocrine and Nutritional Management of the Post-Bariatric Surgery Patient: An Endocrine Society Clinical Practice Guideline
Late dumping can be due to reactive hypoglycemia and can often be managed with nutritional manipulation or be treated prophylactically by having the patient eat a small snack.

Postprandial hypoglycemia
Post-RYGB patients who present with postprandial symptoms of hypoglycemia, particularly neuroglycopenic symptoms, should undergo further evaluation for the possibility of insulin-mediated hypoglycemia. In a study conducted in one institution, only nine adult patients without a history of gastric bypass had surgically confirmed nesidioblastosis during the same period in which six patients were evaluated and treated for the condition after gastric bypass surgery (GBS) (245). The study described six patients with severe, intractable postprandial symptoms associated with endogenous hyperinsulinemic hypoglycemia. This complication, believed to be secondary to the RYGB anatomy in some patients, has necessitated partial pancreatectomy for relief of the symptoms and hypoglycemia. In these patients, histological examination demonstrated pancreatic islet cell hyperplasia. This complication may present from 2 to 9 yr after RYGB. In a recent study of 14 patients with hyperinsulinemic hypoglycemia, the glucose and insulin responses to mixed meals were measured (246). A subsequent study of six RYGB patients with postoperative hypoglycemia compared with lean and obese controls without hypoglycemia failed to find an increase in β-cell mass (247) and concluded that post-GBS hypoglycemia is not due to an increase in β-cell mass or formation. Rather, they concluded that postprandial hypoglycemia after GBS is due to a combination of gastric dumping and inappropriately increased insulin secretion, either as a failure to adaptively decrease insulin secretion after GBS or as an acquired phenomenon (247).
Surg Endosc. 2011 Jun;25(6):1926-32. Epub 2010 Dec 24.
Abnormal glucose tolerance testing following gastric bypass demonstrates reactive hypoglycemia.
Roslin M, Damani T, Oren J, Andrews R, Yatco E, Shah P.

Source
Department of Surgery, Lenox Hill Hospital, 186 East 76th Street, New York, NY, 10021, USA.

Abstract
BACKGROUND:
Symptoms of reactive hypoglycemia have been reported by patients after Roux-en-Y gastric bypass (RYGB) surgery who experience maladaptive eating behavior and weight regain. A 4-h glucose tolerance test (GTT) was used to assess the incidence and extent of hypoglycemia.

METHODS:

Thirty-six patients who were at least 6 months postoperative from RYGB were administered a 4-h GTT with measurement of insulin levels. Mean age was 49.4 ± 11.4 years, mean preoperative body mass index (BMI) was 48.8 ± 6.6 kg/m(2), percent excess BMI lost (%EBL) was 62.6 ± 21.6%, mean weight change from nadir weight was 8.2 ± 8.6 kg, and mean follow-up time was 40.5 ± 26.7 months. Twelve patients had diabetes preoperatively.

RESULTS:

Thirty-two of 36 patients (89%) had abnormal GTT. Six patients (17%) were identified as diabetic based on GTT. All six of these patients were diabetic preoperatively. Twenty-six patients (72%) had evidence of reactive hypoglycemia at 2 h post glucose load. Within this cohort of 26 patients, 14 had maximum to minimum glucose ratio (MMGR) > 3:1, 5 with a ratio > 4:1. Eleven patients had weight regain greater than 10% of initial weight loss (range 4.9-25.6 kg). Ten of these 11 patients (91%) with weight recidivism showed reactive hypoglycemia.

CONCLUSIONS:

Abnormal GTT is a common finding post RYGB. Persistence of diabetes was noted in 50% of patients with diabetes preoperatively. Amongst the nondiabetic patients, reactive hypoglycemia was found to be more common and pronounced than expected. Absence of abnormally high insulin levels does not support nesidioblastosis as an etiology of this hypoglycemia. More than 50% of patients with reactive hypoglycemia had significantly exaggerated MMGR. We believe this may be due to the nonphysiologic transit of food to the small intestine due to lack of a pyloric valve after RYGB. This reactive hypoglycemia may contribute to maladaptive eating behaviors leading to weight regain long term. Our data suggest that GTT is an important part of post-RYGB follow-up and should be incorporated into the routine postoperative screening protocol. Further studies on the impact of pylorus preservation are necessary.

PMID:
21184112
[PubMed - in process]
 
Last edited:

weaura

Well-Known Member
Thanks for the links; however not all of them work for me - may just be my computer - or me LOL :confused:
At the beginning of my extreme hypoglycemic episodes (in 2006) they thought I had nesidioblastosis (sp?), but eventually discovered I had an insulinoma.
Learned very quickly that I had to be my own advocate because the doctors all talked about it as a result of RNY, and even when we would tell them I didn't have a RNY, but had a BPDS, they were dismissive, as if I didn't know what I was talking about.
 

southernlady

Administrator
Staff member
Thanks for the links; however not all of them work for me - may just be my computer - or me LOL :confused:
At the beginning of my extreme hypoglycemic episodes (in 2006) they thought I had nesidioblastosis (sp?), but eventually discovered I had an insulinoma.
Learned very quickly that I had to be my own advocate because the doctors all talked about it as a result of RNY, and even when we would tell them I didn't have a RNY, but had a BPDS, they were dismissive, as if I didn't know what I was talking about.
I did a copy and paste from elsewhere so I may have some broken links. I need to recheck and if necessary, find the new ones.
 
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