Severe hypoglycemia after gastric bypass surgery for morbid obesity

Recently, hypoglycemia with endogenous hyperinsulinemia has been described after undergoing bariatric surgery because of morbid obesity. It has been theorized that after a gastric bypass surgery, some trophic factors affecting pancreatic beta cells could emerge. The authors present a case of morbidly obese patient with severe hypoglycemia 3 months after bariatric surgery. An abdominal helicoidally computed tomography scan showed a 1.7 cm tumor in the tail of the pancreas. Histopathology revealed an insulinoma with well-defined contours surrounded by pancreatic tissue with atrophic signs and with hyperplasia and hypertrophic phenomena compatible with nesidioblastosis in adjacent islets of the pancreatic duct. Authors hypothesize that maintenance of the stimulus produces hyperplasia/hypertrophy of the pancreatic islets and reemphasizes the dynamic qualities of pancreatic beta cells and the possibility of producing hyperplasia from the extreme resistance to insulin present in morbidly obese patients.     

Serum lipids after gastric bypass surgery for morbid obesity

Thirty-eight of 151 consecutive patients (25 percent) undergoing bypass surgery for morbid obesity had increased serum levels of total cholesterol (TC), triglycerides (TG) or both preoperatively. Ten patients had isolated TC elevation, six had isolated TG elevation and 22 had both TC and TG elevation. High density lipoprotein-cholesterol (HDL-C) levels were subnormal in 28 of the 38 patients (74 percent). Fasting lipid profiles were determined in the 38 hyperlipidemic patients at 6-month intervals postoperatively. Mean follow-up period was 29 months. By 6 months postop, patients had a greater than or equal to 20 percent mean reduction in TC and greater than or equal to 50 percent mean reduction in TG which were significant in comparison with preop levels and correlated with weight loss (P less than or equal to 0.05). Mean HDL-C levels had increased significantly vs. preop levels by 12 months postop (P less than 0.05). Lipid profiles became normal in 32 of the 38 patients (84 percent). Improvements in lipid profile were sustained in all patients with satisfactory weight loss but regressed after 12 months in patients who did not lose greater than or equal to 50 percent of their excess weight. These results suggest that abnormal serum lipid profiles can be permanently improved with sustained weight loss after gastric restriction surgery for morbid obesity.     

Absence of luminal intrinsic factor after gastric bypass surgery for morbid obesity

Abnormally low serum cobalamin levels (<180 pg/ml) have been observed in 154 of 429 patients (36%) at an average of 22 months (range 3–64 months) after gastric bypass surgery for morbid obesity. Twenty-four patients underwent a Schilling test and retrograde endoscopy of the bypassed gastric segment to determine the presence of intrinsic factor (IF) in gastric aspirates and in mucosal biopsies at 22±4 months after surgery. Five patients had a normal cobalamin level (405±44 pg/ml), and gastric juice intrinsic factor was present in three of them (11±7 ng/ml). Nineteen patients had a low cobalamin level (113±8 pg/ml), and gastric juice IF was found in only two subjects of this group (10 ng/ml each). Basal gastric juice IF concentration of healthy control subjects was 24±5 ng/ml. Schilling test results were normal in all five patients of the first group and in only nine patients of the group with cobalamin deficiency after surgery. To assess whether IF was present within the parietal cells of subjects with absent luminal IF, we studied gastric biopsy material of 14 patients using a well-characterized indirect immunoperoxidase method. IF was identified in fundic mucosal biopsy specimens of all 14 patients with absent gastric juice IF. We conclude that cobalamin deficiency occurs in a significant number of patients after gastric bypass and is associated with absence of gastric juice IF. We propose that this abnormality might be caused by inadequate secretion of IF from the bypassed stomach.This work was presented in part at the annual meeting of the American Gastroenterological Association, San Francisco, California, May 1986, and has appeared in abstract form (Gastroenterology 90:1533, 1986).     

Interventional radiologic treatment of complications following gastric bypass surgery for morbid obesity

Complications of gastric bypass surgery include leakage from the gastrojejunal anastomosis with abscess formation and anastomotic stenosis. Using interventional radiologic techniques, we have treated 18 patients with such complications following surgery for morbid obesity, with clinical success in 11. Procedures included 9 abdominal abscess drainages and 7 balloon dilatations of stenotic or occluded gastrojejunal anastomoses. Eight of 9 abscesses resolved completely; 3 of 7 balloon dilatations resulted in long-term clinical improvement. We describe the techniques used as well as problems encountered in these patients.     

Renal tubular acidosis secondary to jejunoileal bypass for morbid obesity

Renal handling of acid and base was studied in patients with persistent metabolic acidosis 3-9 years after jejunoileal bypass for morbid obesity. Excretion of acid was studied before and after intravenous infusion of NH4Cl and excretion of bicarbonate after infusion of NaHCO3. Bypass patients showed impaired capacity for acidification of urine. The lowest urinary pH was 5.53 +/- 0.10 in 10 bypass patients and 4.76 +/- 0.06 in 6 controls. The corresponding values for standard bicarbonate in plasma were 15.0 +/- 0.3 mM and 15.8 +/- 0.3 mM. Glomerular filtration rate was identical in the two groups. Fractional loss of bicarbonate in urine was higher in controls than in bypass patients. The renal impairment is classified as distal renal tubular acidosis.     

Atrophic beriberi. A complication of jejunoileal bypass surgery for morbid obesity.

Four months after jejunoileal bypass surgery for morbid obesity, a 37 year black woman who ate a grossly inadequate diet was hospitalized complaining of diffuse abdominal pain, complete loss of appetite, burning feet, generalized weakness and inability to walk without assistance; she had had a weight loss of 100 pounds. Physical findings were limited to the neurologic examination and revealed bilateral glove hypesthesia to midforearms, bilateral stocking hypesthesia to the ankles and partial loss of all sensory modalities. She also had distal muscle weakness with inability to make a firm fist or to stand without assistance. Routine laboratory studies were not diagnostic. She was admitted to the surgical service with a diagnosis of electrolyte imbalance secondary to gastrointestinal losses; she was fed a high-protein diet as tolerated and given intravenous electrolyte therapy, but her neurologic condition deteriorated severely over a two week period. She had a complete loss of deep tendon reflexes in all extremities; the extent of sensory loss increased slightly and motor function disappeared completely below the knees with minimal function in the thighs. Hip motion remained normal. Finger and wrist extension were absent and flexion was very poor, although shoulder and central nervous system functions were all intact. Several serum vitamin studies made at that time showed only a severe depletion of thiamine. Atrophic beriberi secondary to jejunoileal bypass surgery and poor diet was appreciated for the first time. Replacement therapy with thiamine followed by an elemental diet containing all essential nutrients administered through a jejunostomy tube resulted in gradual improvement. Atrophic beriberi should be suspected whenever peripheral neuropathy develops after jejunoileal bypass for morbid obesity.     

Metabolic bone disease after gastric bypass surgery for obesity

BACKGROUND: The popularity of gastric bypass surgery for treatment of morbid obesity has been increasing in recent years. Osteomalacia and osteoporosis are commonly observed in patients who have had partial gastric resections for treatment of peptic ulcer disease. Recently, we encountered four patients with previous gastric bypass surgery who had metabolic bone disease similar to that reported in the older literature in patients who had partial gastrectomies. METHODS: Review of clinical data of four patients who developed osteomalacia and osteoporosis 9 to 12 years after gastric bypass surgery for morbid obesity. RESULTS: All subjects were women, 43 to 58 years old. Three had Roux-en-Y gastric bypass, and the other had a biliopancreatic diversion 9 to 12 years prior to presentation. Weight loss averaged 41.8 kg. Patients reported fatigue, myalgias, and arthralgias. They had symptoms for many months or years before the correct diagnosis was established. All were osteopenic or osteoporotic with hypocalcemia, very low or undetectable 25-hydroxyvitamin D levels, secondary hyperparathyroidism, increased 1,25-dihydroxyvitamin D levels, and increased serum alkaline phosphatase. CONCLUSIONS: Relatively little has been published in the general medical literature about this postoperative complication of bariatric surgery. Yet, nearly all patients after bariatric surgery will receive their long-term follow-up from a primary care physician. Physicians and patients need to be aware of this complication and take measures to identify and prevent it.     

Stimulated erythropoiesis with secondary iron loading leads to a decrease in hepcidin despite an increase in bone morphogenetic protein 6 expression

The BMP/SMAD signalling pathway plays an important role in iron homeostasis, regulating hepcidin expression in response to body iron levels. However, the role of this pathway in the reduction in hepcidin associated with increased erythropoiesis (and secondary iron loading) is unclear. To investigate this, we established a mouse model of chronic stimulated erythropoiesis with secondary iron loading using the haemolytic agent phenylhydrazine. We then examined the expression of components of the BMP6/SMAD signalling pathway in these animals. We also examined this pathway in the Hbb(th3/+) mouse, a model of the iron loading anaemia β-thalassaemia intermedia. Increasing doses of phenylhydrazine led to a progressive increase in both liver iron levels and Bmp6 mRNA expression, but, in contrast, hepatic Hamp expression declined. The increase in Bmp6 expression was not associated with a corresponding change in the phosphorylation of hepatic SMAD1/5/8, indicating that stimulated erythropoiesis decreases the ability of BMP6 to alter SMAD phosphorylation. Increased erythropoiesis also reduces the capacity of phosphorylated SMAD (pSMAD) to induce hepcidin, as Hamp levels declined despite no changes in pSMAD1/5/8. Similar results were seen in Hbb(th3/+) mice. Thus the erythroid signal probably affects some components of BMP/SMAD signalling, but also may exert some independent effects.     

Small-intestinal and colonic changes after biliopancreatic bypass for morbid obesity

Morphologic and functional adaptations of the functioning intestine were evaluated in 41 patients before and after biliopancreatic bypass for morbid obesity. This surgical procedure diverts pancreatobiliary secretions via the duodenum and the jejunum into the colon, the remaining small intestine being anastomosed to the stomach after antrectomy. In the proximal ileum there was an 80% increase of the height of villi; the specific activities of maltase, sucrase, and aminopeptidase in brush border membranes remained unaffected, and that of lactase tended to decrease. In the distal ileum villi heights increased only by 58%, and disaccharidase activities (except for maltase) were slightly enhanced. In the colon the mucosa displayed, in some patients, focal appearance of true villi, and brush border enzyme activities increased concomitantly. We conclude that biliopancreatic bypass induces an adaptation of all intestinal segments of the functioning intestine; this adaptation tends to compensate for the shortening of the gut continuity.     

Intussusception following jejunoileal bypass for morbid obesity: Report of a case

Summary A man who had undergone jejunoileal bypass for morbid obesity had cramping abdominal pains for which no cause could be found, despite repeated clinical examinations and numerous investigations. Only during anesthesia could the large mass formed by the intussusception be palpated. following reduction of the intussusception and refixing to the anterior abdominal wall, all symptoms abated.     

Gastric emptying of liquid before and after gastroplasty for morbid obesity

Gastric emptying of a liquid meal was investigated with a radionuclide method before and 1 week and 3 and 12 months after gastroplasty operation for morbid obesity. Gastroplasty results in a small proximal pouch with a narrow stoma to the remaining stomach. The total gastric emptying was delayed 3 months after gastroplasty (p less than 0.01). Twelve months after gastroplasty, emptying of the proximal pouch was faster than at 3 months (p less than 0.01). This may indicate dilatation of the stoma between the two gastric pouches during this period. Surprisingly, the total gastric emptying 12 months after gastroplasty was not only faster than at 3 months but also faster than before surgery. The explanation, therefore, cannot only be attributed to a dilated stoma, and hormonal mechanisms may be involved. A lack of correlation between preoperative weight and emptying was observed, but because the material consists of only obese subjects, no conclusion can be drawn about the postulated role of gastric emptying in developing obesity. Emptying of the total stomach and of the proximal pouch failed to correlate with postoperative weight losses. The weight loss after gastroplasty evidently bears little, if any, relation to the postoperative changes in gastric emptying of liquids.     

Pattern of progression in liver injury following jejunoileal bypass for morbid obesity

Liver biopsies from 34 patients with morbid obesity, performed before and 5-9 months after jejunoileal bypass, were studied. The patients were divided into four groups according to preoperative findings: A: no or slight steatosis (15 patients), B: moderate-severe steatosis (6), C: steatohepatitis (steatosis + lobular lymphocytic inflammation) (8), D: steatofibrosis (steatosis + pericellular fibrosis) (5). In Group A, 12 patients showed postoperative progression to either moderate/severe steatosis, steatohepatitis, or steatofibrosis. In Group B, all patients progressed to steatohepatitis or steatofibrosis, and one developed septate fibrosis. All patients in Group C progressed to steatofibrosis, and 5 developed septate fibrosis or cirrhosis. In Group D, 3 developed bridging fibrosis. Mallory bodies appeared postoperatively in 11 patients (32%), all of whom preoperatively had either severe steatosis, steatohepatitis, or steatofibrosis. Only patients with postoperative pericellular fibrosis and Mallory bodies developed deranged architecture: 6 septate/bridging fibrosis, and 3 cirrhosis. Five patients, all with deranged architecture, developed reversible liver insufficiency. Progressive liver injury after jejunoileal bypass appears to reflect aggravation of a pre-existing liver lesion. The sequence of events: increasing steatosis, lobular lymphocytic inflammation, pericellular fibrosis, Mallory bodies, and deranged architecture is similar to that of the alcoholic liver lesion, indicating common pathogenetic mechanisms.     

Dietary intake before and after gastric bypass and gastroplasty for morbid obesity in women

Fifty-one morbidly obese women were randomized to surgical treatment with gastric bypass (GBY) or gastroplasty (GPL). Their dietary intake was assessed preoperatively and 12 months postoperatively by two methods: diet history and 4-day weighted intake. Their protein intake was also checked against urinary nitrogen losses. There was a good correspondence between the results of the two dietary methods and also between estimated protein intake and urinary loss. This makes the results reliable. After 1 year the GBY patients demonstrated a mean weight loss of 41.6 +/- 10.8 kg (P less than 0.001 versus GPL) and a mean energy intake preoperatively of about 2400 kcal/day and postoperatively of 1050 kcal/day (P less than 0.05 versus GPL). The GPL patients lost 28.9 +/- 9.6 kg as a mean and had a preoperative intake of about 2500 kcal/day and a postoperative intake of about 1300 kcal/day. There were only minor changes in the quality of the food from the preoperative to the postoperative situation. Postoperatively the daily intake of several nutrients was below minimum values of recommended or required intake.     

Anemia following Roux-en-Y gastric bypass for morbid obesity; a 5-year follow-up study

Objectives: Patients are at risk of anemia post Roux-en-Y gastric bypass (RYGB). We sought to determine the prevalence of anemia and related nutritional deficiencies 5 years after RYGB and to evaluate adherence to nutritional supplements with iron, vitamin B12, and folate.

Material and methods: Patients operated with RYGB 2004–2006 were eligible for evaluation. Blood samples were collected and use of nutritional supplements was recorded preoperatively, and at outpatients’ consultations 1, 2, and 5 years postoperatively. Of 203 patients operated, 184 (91%) completed the 5 year follow-up and were included in the study. Of these, 97% had valid measurements of hemoglobin both at baseline and after 5 years.

Results: During the 5 years after RYGB, the prevalence of anemia increased from 4% preoperatively to 24% in females, and from 0% to 7% in males. Ferritin levels decreased gradually in both genders. Iron deficiency increased from 6% preoperatively to 42% at 5 years in females, and from 0% to 9% in males. Vitamin B12 deficiency was not altered while folate deficiency decreased from 10% preoperatively to 1% at 5 years. Five years after surgery 25% reported the use of supplements with iron, while 83% used vitamin B12 and 65% used multivitamins with folate.

Conclusions: We observed a long-term increase in anemia and iron deficiency after RYGB in both genders, but most pronounced in women. Our postoperative protocol for prevention of vitamin B12 and folate deficiencies appear acceptable. Iron status and iron supplementation seems to need stronger emphasis during follow-up after RYGB.