Interesting Article of the Difference a Pyloric Valve Can Make

Sep 13, 2011

 I'm going to highlight the interesting parts in red, and my comments will be in blue. Enjoy this article and please take this lesson to heart! Here's the link: http://jcem.endojournals.org/content/95/4/1851.long#sec-2

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We present a patient with severe post-RYGB neuroglycopenia (Not enough blood sugar to fuel the brain) who had gastrostomy tube (GT) placement in the remnant stomach during hospitalization for small bowel obstruction. She experienced markedly reduced frequency of hypoglycemia and improved nutritional status. Standardized administration of identical liquid meals orally (via surgically altered gut) vs. GT (via nonbypassed gut) was conducted to determine metabolic correlates of improved symptoms.

SUBJECT AND METHODS

The subject is a 35-yr-old female with a history of morbid obesity who underwent RYGB 3 yr earlier, at which time her weight was 96 kg and BMI was 38.9 kg/m². Twelve months after surgery, she had lost 45 kg, and despite improving dumping symptoms, she was experiencing symptomatic hypoglycemia, with tachycardia, diaphoresis (Sweating a lot because of shock), and a loss of consciousness episode when plasma glucose was 32 mg/dl. Symptoms were worse after carbohydrate intake, ameliorated (made better) by fasting, and minimally responsive to acarbose, diazoxide, and octreotide 1000 μg/d (These are medication to treat the low blood sugar problem). Postprandial (after a meal) plasma glucose, insulin, and C-peptide concentrations were documented as 15 mg/dl, 33 μU/ml, and 7.5 ng/ml, respectively. Radiological imaging was negative for pancreatic mass (I think this means there was no tumor or mass on her pancreas that would explain her low blood sugar problems), and antiinsulin antibodies and sulfonylurea screen were negative (Basically they couldn't find anything that would explain the low blood sugar issue). After the patient developed a small bowel obstruction, a GT (a feeding tube) was placed in the original stomach for decompression and nutrition. The patient requested to maintain the GT for nutrition after discharge because she noted decreased frequency of hypoglycemia. Improvement in hypoglycemic symptoms and energy status continued, and she was ultimately able to return to work. She continues to take overnight GT feedings, decreasing her reliance on oral carbohydrates during waking hours, and consequently, hypoglycemic episodes. No hypoglycemia occurs during overnight feeds, and weight is stable at 4 kg above pre-GT weight.

To formally assess the metabolic basis for improvement in hypoglycemia resulting from GT feeds, standardized testing was conducted in the Stanford University General Clinical Research Center. Written informed consent, approved by the Stanford Human Subjects Committee, was obtained. After an overnight fast, the subject was admitted for blood sampling via iv catheter. One 240-ml can of Ensure liquid formula (250 kcal, 6 g fat, 40 g carbohydrate, 9 g protein) was administered over 15 min by mouth. Blood samples were obtained at baseline and 30, 60, 90, 120, and 150 min afterward. The following morning, after overnight fasting, the procedure was repeated, but the liquid meal was delivered via GT. For comparison, insulin and glucose values were obtained from 10 healthy nonsurgical females matched for BMI and age, and to six healthy females with normal fasting glucose but who had attained glucose elevations (>200 mg/dl) similar to our subject 30–60 min after oral glucose challenge (75 g). Of note, the latter subjects, hereafter referred to as “glucose controls,” were all overweight/obese [BMI, 28.0 ± 4.4 kg/m²) and extremely insulin-resistant [top 5%). Glucose concentrations were measured via oximetric method and insulin via RIA. Total GLP-1 and GIP were determined using C-terminally-directed antisera (code 89390 and R65), which detect the sum of the intact peptides plus the primary metabolite. Glucagon concentrations were determined using antiserum 4305, which is specific for glucagon of pancreatic origin.

RESULTS

At the time of metabolic evaluation, the subject weighed 47.2 kg (BMI, 19.0 kg/m²). Compared with the GT liquid meal, oral ingestion produced a peak glucose at 30 min twice as high (243 vs. 129 mg/dl), followed by symptomatic hypoglycemia at 90–120 min (60 vs. 80 mg/dl) and continued lower glucose levels throughout the 180 min test (77–78 vs. 92–106 mg/dl). Insulin concentrations at 30 min were 8-fold higher (406 vs. 48 μU/ml) but dropped rapidly, reaching 19 μU/ml at the onset of hypoglycemia. In comparison, at the time glucose peaked in the six glucose-matched controls, insulin concentrations were 166 ± 80 μU/ml. Thus, our subject’s peak insulin was 144% higher than similarly hyperglycemic controls, despite the fact that the controls were obese and insulin resistant, and thus expected to have higher insulin responses to oral glucose. In the 10 BMI-matched controls, insulin and glucose responses were essentially identical to values in our subject when the liquid meal was administered via GT.

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Part two of this article is on another post. For some reason I couldn't copy and paste anymore on this post. 


 

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