Alterations in Gastrointestinal Physiologyafter Roux-En-Y Gastric Bypass
Todd A Ponsky, MD, Fredrick Brody, MD, FACS, Edward Pucci, MD
Morbid obesity is increasing exponentially in the US.
Although the Roux-en-Y procedure is an effective
Approximately 33.3% of Americans were obese in 1991,
therapy for weight loss, it alters normal digestion and
versus 25.4% in Currently, 54.5% of Americans
nutrient absorption. These alterations can be mild with
are overweight, with a body mass index Ͼ Diet and
no apparent sequelae or cause life-threatening complica-
exercise are implemented initially, they usually fail after
tions. After RYGB, severe malnutrition occurs in ap-
2 years. In response to this epidemic, surgical therapies
proximately 4.7% of the patients postoperativelyThe
for morbid obesity have evolved. There are several dif-
most common nutritional deficiencies in these patients
ferent weight loss operations available, including Roux-
are iron and vitamin There are numerous case
en-Y gastric bypass (RYGB), biliopancreatic diversion,
reports that document malnutrition that lead to myop-
duodenal switch, vertical banded gastroplasty, and the
LapBand. The most common procedure performed in
To understand the pathophysiologic mechanisms of
the US is RYGB, which is both a restrictive and malab-
RYGB, a review of normal nutrient absorption is re-
sorptive operation. Although there are several variations
quired. My colleagues and I describe normal nutrient
available for RYGB, the general principles are similar.
absorption followed by the malabsorptive physiology as-
The first part of the operation creates a gastric pouch of
approximately 20 cm3 to restrict oral intake. The secondcomponent of the operation involves construction of a
biliopancreatic limb that diverts bile and pancreatic
Nutrients are divided into five groups: protein, car-
fluid from the proximal to the distal small intestine. This
bohydrate, fat, vitamins, and minerals. Normal ho-
distal diversion creates a segment of small bowel that
meostasis and weight maintenance depends on the
allows food to pass without interacting with bile or pan-
digestion and absorption of each of these nutrients.
creatic fluid. This diversion delays the interaction of
Conversely, altered pathways of absorption result in
pancreatic enzymes and biliary secretions with the food
weight loss and potentially substantial deficiencies
bolus. Finally, this bypass effectively alters normal nutri-
Although this procedure can alter normal physiology,
it has the propensity to increase survival for morbidly
Amino acids are the basic components of protein. A
obese patients. A recent study by Patterson and col-
chain of 2 or more amino acids is called a peptide. The
suggests that life expectancy improves by almost
amino acids in a peptide are linked by the carboxyl group
11% after laparoscopic RYGB, compared with diet and
of one amino acid to the amino group of another. A
exercise alone. Flum and Dfound that morbidly
protein is composed of one or more long peptide chains.
obese patients had a 33% decreased hazard of death after
Smaller proteins, chains of less than 30 amino acids, are
referred to as oligopeptides and include somatostatinand vasopressin.
Where the peptide-laden food bolus enters the
Received November 4, 2004; Revised March 2, 2005; Accepted March 2,
mouth, cephalic stimulation through acetylcholine en-
hances acid production from gastric parietal cells. The
From the Department of General Surgery, The George Washington Univer-sity Medical Center, Washington, DC.
acid, along with acetylcholine, stimulates pepsinogen
Correspondence address: Fredrick Brody, MD, Department of General Sur-
release from chief cells. The gastric acid then facilitates
gery, The George Washington University Medical Center, 2150 PennsylvaniaAve NW, Suite 6B, Washington, DC 20037.
conversion of pepsinogen into pepsin. Cleavage of pep-
2005 by the American College of Surgeons
Physiologic Basis of Roux-en-Y Gastric Bypass
sinogen into pepsin requires a gastric pH Յ 5. Pepsin
drate absorption starts in the duodenum and is com-
then initiates the cleavage of protein into peptides. The
pleted usually by the first 100 cm of small intestine.
stomach absorbs very few peptides or amino acids. When the peptides and amino acids enter the duode-
num, the duodenal and jejunal epithelial cells release
Lipids are the largest energy source in the body and 93%
cholecystokinin Presence of food in the an-
of dietary lipids are absorbed in the proximal two-thirds
trum, antral distention, and vagal stimulation increase
of jejunum.Dietary lipids include free fatty acids, tri-
the production of gastrin. Gastrin stimulates CCK al-
glycerides, phospholipids, and cholesterol. When lipids
soCCK stimulates release of trypsinogen from pan-
enter the duodenum, the I and S cells, located within the
creatic acinar cells. Trypsinogen is released into the du-
duodenal mucosa, secrete CCK and secretin, respec-
odenum and cleaved into its active form, trypsin, by
tively. CCK and secretin stimulate gallbladder contrac-
enterokinase, an enzyme released from the duodenal
tion and pancreatic secretion. The pancreas secretes the
mucosal cells. Trypsin activates chymotrypsin and pro-
lipolytic enzymes lipase, cholesterol esterase, and phos-
carboxypeptidases A and B. Chymotrypsin and the pro-
pholipase A2. These enzymes digest distinct lipid com-
carboxypeptidases are produced from the pancreatic aci-
ponents. Lipase hydrolyzes triglyceride molecules into a
nar cells as well. All of these pancreatic enzymes
monoglyceride and two fatty acids. Phospholipase A2
hydrolyze proteins into amino acids or oligopeptides.
hydrolyzes phospholipids into a fatty acid, a phosphoric
Trypsin and chymotrypsin are endopeptidases that
acid, and a nitrogenous base. Cholesterol esterase cleaves
cleave internal peptide bonds while procarboxypepti-
cholesterol esters into free cholesterol. After fat digestion
dases cleave the carboxy terminals of the peptide chains.
by these distinct enzymes, bile-saltϪformed micelles
In the duodenum, brush-border peptidases digest oli-
emulsify the lipid byproducts. The strongly polar bile
gopeptides that are absorbed through the sodium-
acids align their hydrophilic tails externally and their
dependent amino acid cotransporters located along the
nonionized, hydrophobic heads internally to form a mi-
luminal border of the enterocyte. Although 50% of pro-
celle. This emulsification process provides a nonpolar
tein absorption occurs in the duodenum, the entire
environment to harbor and transport lipid byproducts
small bowel is capable of protein absorption. By midje-
into the aqueous blood. Ultimately, enterocytes absorbthe micelles. Once absorbed into the enterocyte, the
junum, the overwhelming majority of protein absorp-
triglycerides and cholesterol are resynthesized. These
compounds combine with other nonpolar lipids, phos-pholipids, and proteins to form lipoproteins called chy-
lomicrons. Chylomicrons are transported from the en-
Monosaccharides, including glucose, fructose, and ga-
terocyte into the lymphatic system and eventually into
lactose, are the most basic forms of carbohydrates. Di-
the thoracic duct that enters the bloodstream through
etary carbohydrates exist as disaccharides, such as su-
the left subclavian vein. Fat absorption, including fat
crose, maltose, or lactose or as polysaccharides such as
soluble vitamins, occurs throughout the entire small
starch. Initially, salivary and pancreatic amylase hydro-
bowel although excess bile salts are absorbed in the ter-
lyze polysaccharides into oligosaccharides, such as disac-
charides and trisaccharides. These oligosaccharides areadditionally broken down into monosaccharides by oli-
gosaccharidases in the brush border of the intestinal mu-
Surgical therapy for morbid obesity occurs through ei-
For example, the intestinal enzyme sucrase di-
ther restricting food intake or decreasing absorption
gests sucrose into the monosaccharides glucose and
from the intestinal tract. Several techniques reduce the
fructose. Maltase divides maltose into two glucose mol-
size of the stomach to induce early satiety and limit oral
ecules and lactase digests lactose into the monosacchar-
intake. These techniques include gastric banding or sta-
ides glucose and galactose. Glucose and galactose are
pling. Malabsorptive operations decrease the amount of
transported into the cell by active transport using a
bowel available for absorption and divert bile and pan-
Naϩ-Kϩ ATPase pump. Fructose is transported pas-
creatic enzymes from the proximal to the distal bowel.
sively through carrier-facilitated diffusion. Carbohy-
These two alterations limit food digestion and produce
Physiologic Basis of Roux-en-Y Gastric Bypass
malabsorption. There are several surgical options avail-
proteins function as enzymes and provide structural sup-
able to construct this restrictive or malabsorptive state.
port to the body, protein deficiency has serious conse-quences, including poor wound healing, decreased im-
mune function, muscle weakness, weight loss, mental
apathy, anemia, pressure sores, depigmented hair or
In addition to a decreased dietary intake of proteins
skin, and diarrhea. The most severe form of protein de-
secondary to the gastric pouch, the RYGB induces pro-
ficiency is referred to as kwashiorkor. Currently, little
tein malabsorption. Under physiologic conditions, the
data exists about protein levels after RYGB. Protein de-
majority of protein is absorbed in the duodenum. After
ficiency was documented in 4.7% of patients after
RYGB, protein never enters the duodenum. Protein ab-
sorption is limited to the distal jejunum and ileum.
centage is low, the real percentage of protein deficiency is
Other components of the RYGB contribute to pro-
difficult to document because of the lack of data.
tein malabsorption. Pepsinogen, as discussed alreadycleaves protein into peptides. After RYGB, Sundbom
and colleaguesfound a substantial decrease in pepsino-
Similar to protein, RYGB alters carbohydrate digestion
gen levels from the gastric remnant. Decreased levels of
and absorption. Under physiologic conditions, most
pepsinogen are secondary to the vagotomy that occurs
carbohydrate absorption occurs within the first 100 cm
with gastric partitioning. Vagotomy negates cephalic
of small intestine after interacting with pancreatic
stimulation and decreases acid secretion and ultimately
amylase. Because ingested carbohydrates bypass the du-
decreases pepsinogen levels. Without pepsinogen, many
odenum, pancreatic amylase stimulation and release is
protein molecules are left intact and are not absorbed.
reduced. After passing from the gastric pouch, carbohy-
Even if the gastric remnant releases a basal level of pep-
drates travel through the Roux limb as intact polysaccha-
sinogen into the duodenum, pepsinogen does not inter-
rides. After passing the jejunojejunostomy, the polysac-
act with the ingested protein until it traverses the jeju-
charides interact with a small amount of basal amylase
nojejunostomy. This delays protein cleavage and small
that is secreted from the pancreas through the biliopan-
creatic limb. The limited pancreatic amylase hydrolyzes
Along with the restrictive component and decreased
the polysaccharides into oligosaccharides and allows
pepsinogen levels, decreased production of pancreatic
minimal carbohydrate absorption in the remaining
enzymes contributes to protein malabsorption. In 1971,
small intestine. The combination of decreased absorp-
Ito and Mdemonstrated a 40% reduction in pan-
tive surface area, decreased pancreatic amylase secretion,
creatic enzyme secretion after a gastric bypass. They con-
and delayed interaction of amylase with the polysaccha-
cluded that this finding resulted from decreased gastrin
rides limits carbohydrate absorption.
levels.Discussed here already, food in the antrum, an-
Carbohydrates are a major source of energy for body
tral distention, and vagal stimulation induce gastrin se-
metabolism and the sole energy source for the brain and
cretion. Gastrin then stimulates the release of CCK.
red blood cells. The liver and skeletal muscle store car-
Without food in the excluded antrum, antral distention
bohydrates as glycogen. In the absence of adequate car-
and vagal stimulation of G cells do not occur. Interest-
bohydrate substrate, fat and protein are broken down
ingly, Ito and Mason17 showed increased pancreatic se-
through gluconeogenesis into carbohydrates to provide a
cretion after restoration of gastric continuity; diminish-
nutritional substrate for the brain and red blood cells. A
ing the role of vagotomy on pancreatic secretion. Under
deficiency in carbohydrates can lead to a deficiency in
physiologic conditions, as peptides pass through the du-
odenum, the duodenum releases CCK and causes the
The anatomic alterations created during the RYGB
pancreas to secrete proteolytic enzymes. Theoretically,
probably contribute to dumping syndrome. The early
because the peptides never traverse the duodenum, this
phase of dumping occurs immediately after eating and is
physiologic process is omitted as well. Several studies do
characterized by abdominal cramping, nausea, vomit-
not show any changes in CCK levels after RY
ing, diarrhea, dizziness, palpitations, and diaphoresis.
Unlike fat or carbohydrate, protein is not stored. All
Increased gastric emptying after RYGB leads to rapid
protein in the body has some biologic function. Because
filling of the small bowel with hyperosmolar chyme.
Physiologic Basis of Roux-en-Y Gastric Bypass
This causes an osmotic shift of extracellular fluid into
decrease in serum calcium. Many patients experience
the bowel to restore isotonicity. Also, this shift causes
progressive bone loss over time. Vitamin D deficiency is
intestinal distention, abdominal cramping, nausea,
more likely to occur after a biliopancreatic diversion
vomiting, and diarrhea. Bowel distention causes the re-
than RYGB because a greater degree of fat malabsorp-
lease of vasoactive intestinal peptide and serotonin.
tion. Deficiencies of vitamin D and calcium after both
These two hormones are associated with diaphoresis,
types of malabsorptive procedures can increase bone
dizziness, and palpitations. Fluid shifts from the intra-
turnover and decrease bone mass.It is imperative
vascular space can accentuate the vasomotor symptoms.
to monitor hemoglobin, calcium, and thiamine levels
Early phase symptoms are accentuated by a surge in
In addition to vitamin D, any of the fat-soluble
The late phase occurs 1 to 4 hours after eating and is
vitamins can become deficient after RYGB. This in-
characterized by sweating, dizziness, and fatigue. A de-
cludes vitamins A, E, and K. There are reports of ocular
layed surge in insulin secretion with rebound hypogly-
deficiency after biliopancreatic diversions as a result of
cemia causes this phase. The primary treatment for
vitamin A deficiencyThere is no such data after
dumping syndrome includes a decrease in simple carbo-
RYGB. Vitamin K deficiency can lead to a decrease
hydrate intake. This can be a problem in patients with a
in vitamin K-dependent clotting factors. Coagulation
carbohydrate deficiency. Symptom improvement can
studies should be monitored closely for patients taking
occur by modifying the diet to small, frequent meals that
are high in fiber, protein, and complex carbohydrates
Cobalamin (vitamin B12) is absorbed in the terminal
ileum. In order for absorption to occur, cobalamin must
curs to some degree in approximately 70% to 75.9% of
be linked to the glycoprotein, intrinsic factor. Intrinsic
patients after bariatric surgeryAlthough this per-
factor is produced by parietal cells in the stomach and
centage seems high, the overwhelming majority of pa-
released after hormonal stimulation from acetylcholine,
tients only experience transient dumping as they modify
histamine, and gastrin. Pepsin and hydrochloric acid are
needed to separate B12 from the protein bolus in thestomach. Without hydrochloric acid in the proximal
pouch, RYGB patients cannot cleave B12 from the pro-
Under physiologic conditions, fat passes into the duode-
tein moiety. The excluded stomach and bypassed duo-
num and stimulates CCK. In turn, CCK stimulates the
denum prohibit binding of free B12 to intrinsic factor.
gallbladder and pancreas to release bile and lipolytic en-
Several investigators showed that bound B12 is not ab-
zymes. After RYGB, the secretion of bile and lipolytic
sorbed as well as administered crystalline B12 orally after
enzymes is reduced because lipids never pass through the
a RYGB or partial gastrectomySmith and col-
duodenum. Lipids, including triglycerides, phospholip-
leaguesfound that B12 was not digested and essentially
ids, and cholesterol, travel through the Roux conduit as
malabsorbed. They recommended supplementing with
intact structures until they reach the jejunojejunostomy.
either monthly parenteral B12 or daily oral crystalline
Delayed breakdown of dietary fats and the delayed for-
preparations. Meanwhile, a normal Shilling test can oc-
mation of micelles limit the amount of fat available for
cur after RYGB. This finding suggests that the bypassed
absorption. Undigested fat passes into the colon produc-
stomach continues to secrete some degree of intrinsic
ing fat malabsorption and steatorrhea.
factorand that B12 deficiency results from malab-sorption; not a decrease in intrinsic factor.
Restrictive procedures, such as gastric banding and
RYGB reconstruction can cause deficiencies in certain
gastroplasty, can cause vitamin and mineral deficiencies
vitamins and minerals. Iron, calcium, and thiamine (vi-
as well.There are several reports of vitamin A, C, D,
tamin B1) are absorbed primarily in the duodenum.
E, K, B1, B2, and B6 deficiencies. Many of these find-
After RYGB, these vitamins never enter the duodenum
ings were present in patients taking regular multivitamin
and their absorption is decreased considerably. Because
vitamin D is a fat-soluble vitamin, it is poorly absorbed
tients admitted for either malnutrition or excessively
after the RYGB. Ultimately, this leads to an additional
rapid weight loss after a horizontal gastroplasty. They
Physiologic Basis of Roux-en-Y Gastric Bypass
found substantially decreased levels of serum thiamine
sume adequate amounts of protein and calories can feel
and folate compared with preoperative levels. Thiamine
weak and develop nutritional deficiencies. Caloric in-
and folate levels were low in 50% and 65% of these
take should be between 1,000 and 1,500 cal/kg and
patients, respectively. These values can have far-reaching
patients with an initial body mass index of Ͻ 50 kg/m2
indications as more patients undergo the LapBand
should consume 60 to 70 g of protein per day. Patients
with a body mass index 50 to 70 kg/m2 can need up to100 g of protein per day.
Prevention and control of deficienciesRYGB decreases the quantity of food patients consume.
Daily oral supplementation with a chewable multivita-
Ursodiol, which increases the solubility of bile salts, re-
min, as a result, is recommended. Although there is little
duces the risk of developing gallstones to approximately
published data about treatment regimens for micronu-
2% if taken at 300 mg four times a day. Without urso-
trient deficiencies after RYGB, low serum levels of iron,
diol, gallstones can occur in 30% of patients with con-
B12, and folate require either a multivitamin or specific
siderable weight loss from either medical or surgical
supplementation of the deficient micronutrient. A min-
methods.Ursodiol is given as long as the patient
imum daily dose of 350 ug of oral B12 is sufficient to
continues to lose considerable weight (Ͼ 3% of body
maintain normal serum levels after a RYGBand 500 ug
weight per month) or for the first 6 months after an
of oral B12 is sufficient to correct the majority of defi-
operation. Cost and the rather large size of the pill limit
ciencies. Intramuscular injections can be used as well.
This regimen entails an injection of 1,000 ug followed
Physical activity is recommended postoperatively. A
every 2 to 4 weeks with 100 to 500 ug to maintain
strenuous activity program on a very low calorie diet
normal serum levels. Nasal sprays and gels can also pro-
causes an excessive loss of lean body mass and an unde-
vide effective prophylaxis. Meanwhile, low folate levels
sirable effect. A knowledgeable physical therapist or ex-
are corrected with multivitamin supplementation,
ercise physiologist should guide any activity greater than
which typically contains 400 ug of folate.
walking in the early postoperative period.
A complete blood count and serum levels of iron,
Meanwhile, adequate fluid intake prevents constipa-
total iron-binding capacity, and vitamin B12 should be
tion, hypotension, urinary tract infections, kidney
obtained in patients preoperatively and again postoper-
stones, and hyperuricemia. Patients should sip small
atively at 6-month intervals during the first 2 years.
quantities of liquid on a regular basis to avoid these
These levels should be checked annually thereafterAl-
problems. They should avoid excessive sweating to limit
though most surgeons do not measure serum calcium
volume depletion in the early postoperative period. In
addition, most patients should discontinue diuretics
relatively harmless. In addition to a multivitamin, 1,200
postoperatively as some degree of volume depletion
Multivitamins and oral iron supplements do not con-
The demand for bariatric surgery increases as the epi-
sistently correct low serum iron levYet, only 50%
demic of morbid obesity continues to worsen. In 1990,
of low Hgb levels are associated with iron deficiency.
surgeons performed approximately 4,900 bariatric proce-
Many patients with severe iron deficiency anemia (Hgb
dures compared with 100,000 procedures in 2000. Clearly
Ͻ 10 g) respond rarely to oral iron supplementation
bariatric surgery achieves a sustained weight loss with long-
alone. Patients do respond to a variety of therapeutic
term folloand resolves associated comorbidities
measures including IM iron injections, IV iron dextran,
including diabetes and hypertension.The principles
SC injections of erythropoietin and blood transfusions.
that induce weight loss can result in deficiencies of protein,
Total abdominal hysterectomy might be required in
fat, carbohydrate, vitamins, and minerals. Understanding
some patients with menorrhagia. Prophylactic oral sup-
the physiologic basis of weight loss is crucial to produce
plements containing 650 mg of elemental iron in pre-
weight loss without causing malnutrition. Because the
number of RYGB continues to increase, more research is
Adequate protein and calorie consumption is neces-
needed to define the physiologic mechanisms associated
sary to maintain muscle mass. Patients unable to con-
Physiologic Basis of Roux-en-Y Gastric Bypass
17. Ito C, Mason EE. Gastric bypass and pancreatic secretion. Sur-
Study conception and design: Ponsky, Brody
18. Kellum JM, Kuemmerle JF, O’Dorisio TM, et al. Gastrointesti-
nal hormone responses to meals before and after gastric bypass
Analysis and interpretation of data: Ponsky, Brody
and vertical banded gastroplasty. Ann Surg 1990;211:763–770;
Drafting of manuscript: Ponsky, Brody, Pucci
19. Rubino F, Gagner M, Gentileschi P, et al. The early effect of the
Roux-en-Y gastric bypass on hormones involved in body weight
regulation and glucose metabolism. Ann Surg 2004;240:236–242. 20. Meyer JH. Nutritional outcomes of gastric operations. Gastro-
enterol Clin North Am 1994;23:227–260. 21. Carvajal SH, Mulvihill SJ. Postgastrectomy syndromes: dump- 1. Whitman J. Medical complications of obesity. Clin Fam Pract
ing and diarrhea. Gastroenterol Clin North Am 1994;23:261–
2. Kuczmarski RJ, Flegal KM, Campbell SM, Johnson CL. In- 22. Hsu LK, Benotti PN, Dwyer J, et al. Nonsurgical factors that
creasing prevalence of overweight among US adults. The Na-
influence the outcome of bariatric surgery: a review. Psychosom
tional Health and Nutrition Examination Surveys, 1960 to
23. Monteforte MJ, Turkelson CM. Bariatric surgery for morbid 3. Flegal KM, Carroll MD, Kuczmarski RJ, Johnson CL. Over-
obesity. Obes Surg 2000;10:391–401.
weight and obesity in the United States: prevalence and trends,
24. Mallory GN, Macgregor AM, Rand CS. The influence of
1960–1994. Int J Obes Relat Metab Disord 1998;22:39–47.
dumping on weight loss after gastric restrictive surgery for mor-
4. Patterson EJ, Urbach DR, Swanstrom LL. A comparison of diet
bid obesity. Obes Surg 1996;6:474–478.
and exercise therapy versus laparoscopic Roux-en-Y gastric by-
25. Newbury L, Dolan K, Hatzifotis M, et al. Calcium and vitamin
pass surgery for morbid obesity: a decision analysis model. J Am
D depletion and elevated parathyroid hormone following bilio-
pancreatic diversion. Obes Surg 2003;13:893–895. 5. Flum D, Dellinger E. Impact of gastric bypass operation on 26. Slater GH, Ren CJ, Siegel N, et al. Serum fat-soluble vitamin
survival: a population-based analysis. J Am Coll Surg 2004;199:
deficiency and abnormal calcium metabolism after malabsorp-
6. Faintuch J, Matsuda M, Cruz ME, et al. Severe protein-calorie
tive bariatric surgery. J Gastrointest Surg 2004;8:48–55; discus-
malnutrition after bariatric procedures. Obes Surg 2004;14:
27. Coates PS, Fernstrom JD, Fernstrom MH, et al. Gastric bypass 7. Skroubis G, Sakellaropoulos G, Pouggouras K, et al. Compari-
surgery for morbid obesity leads to an increase in bone turnover
son of nutritional deficiencies after Roux-en-Y gastric bypass
and a decrease in bone mass. J Clin Endocrinol Metab 2004;89:
and after biliopancreatic diversion with Roux-en-Y gastric by-
28. Brolin RE. Gastric bypass. Surg Clin North Am 2001;81:1077– 8. Kushner R. Managing the obese patient after bariatric surgery: a
case report of severe malnutrition and review of the literature. 29. Polizzi A, Schenone M, Sacca SC, et al. Role of impression
JPEN J Parenter Enteral Nutr 2000;24:126–132.
cytology during hypovitaminosis A. Br J Ophthalmol 1998;82:
9. Hsia AW, Hattab EM, Katz JS. Malnutrition-induced myopathy
following Roux-en-Y gastric bypass. Muscle Nerve 2001;24:
30. Anastasi M, Lauricella M, Ponte F. Surgical therapy for obesity
can induce a vitamin A deficiency syndrome. Doc Ophthalmol
10. Loh Y, Watson WD, Verma A, et al. Acute Wernicke’s enceph-
alopathy following bariatric surgery: clinical course and MRI
31. Livingston E. Obesity and its surgical management. Am J Surg
correlation. Obes Surg 2004;14:129–132. 11. Salas-Salvado J, Garcia-Lorda P, Cuatrecasas G, et al. Wernicke’s 32. Schade SG, Schilling RF. Effect of pepsin on the absorption of
syndrome after bariatric surgery. Clin Nutr 2000;19:371–373.
food vitamin B12 and iron. Am J Clin Nutr 1967;20:636–640. 12. Tabrez S, Roberts IM. Malabsorption and malnutrition. Prim 33. Schilling RF, Gohdes PN, Hardie GH. Vitamin B12 deficiency
after gastric bypass surgery for obesity. Ann Intern Med 1984;
13. Reilly K. Endocrine function of the gastrointestinal tract. In:
Savage E, Fishman S, eds. Essentials of basic science in surgery. 34. Mason EE, Munns JR, Kealey GP, et al. Effect of gastric bypass
Philadelphia: J B Lipincott Company; 1993:191–207.
on gastric secretion. Am J Surg 1976;131:162–168. 14. Szeto W, Buxby G. Nutrition, digestion, and absorption. In: 35. Smith CD, Herkes SB, Behrns KE, et al. Gastric acid secretion
Kreisel D, Krupnick A, Kaiser L, eds. The surgical review: An
and vitamin B12 absorption after vertical Roux-en-Y gastric
integrated basic and clinical science study guide. Phildelphia:
bypass for morbid obesity. Ann Surg 1993;218:91–96.
Lippincott, Williams, and Wilkins; 2001:272–291. 36. Halverson JD. Micronutrient deficiencies after gastric bypass for 15. Udekwu A. Gastrointestinal physiology. In: Simmons R, Steed D,
morbid obesity. Am Surg 1986;52:594–598.
eds. Basic science review for surgeons. Philadelphia: W B Saunders
37. Behrns KE, Smith CD, Sarr MG. Prospective evaluation of gas-
tric acid secretion and cobalamin absorption following gastric
16. Sundbom M, Mardh E, Mardh S, et al. Reduction in serum
bypass for clinically severe obesity. Dig Dis Sci 1994;39:315–
pepsinogen I after Roux-en-Y gastric bypass. J Gastrointest Surg
38. Miskowiak J, Honore K, Larsen L, Andersen B. Food intake
Physiologic Basis of Roux-en-Y Gastric Bypass
before and after gastroplasty for morbid obesity. Scand J
acid in patients participating in a very-low-calorie diet program. 39. Naslund I, Jarnmark I, Andersson H. Dietary intake before and 52. Sugerman HJ, Brewer WH, Shiffman ML, et al. A multicenter,
after gastric bypass and gastroplasty for morbid obesity in
placebo-controlled, randomized, double-blind, prospective trial
women. Int J Obes 1988;12:503–513.
of prophylactic ursodiol for the prevention of gallstone forma-
40. Andersen T, Larsen U. Dietary outcome in obese patients treated
tion following gastric-bypass-induced rapid weight loss. Am J
with a gastroplasty program. Am J Clin Nutr 1989;50:1328–
Surg 1995;169:91–96; discussion 96–97. 53. Raum W. Postoperative medical management of bariatric pa- 41. MacLean LD, Rhode BM, Shizgal HM. Nutrition following
tients. In: Martin LF, ed. Obesity surgery. New York: McGraw-
gastric operations for morbid obesity. Ann Surg 1983;198:347–
54. Marcus B, Pinto B, Clark M, et al. Physician-delivered physical 42. Rhode BM, Arseneau P, Cooper BA, et al. Vitamin B-12 defi-
activity and nutrition interventions. Med Exerc Nutr Health
ciency after gastric surgery for obesity. Am J Clin Nutr 1996;63:
55. Schauer PR. Open and laparoscopic surgical modalities for the 43. Mallory GN, Macgregor AM. Folate status following gastric
management of obesity. J Gastrointest Surg 2003;7:468–475.
bypass surgery. (The great folate mystery). Obes Surg 1991;1:
56. Schauer PR, Ikramuddin S. Laparoscopic surgery for morbid
obesity. Surg Clin North Am 2001;81:1145–1179. 44. Brolin RE, Gorman JH, Gorman RC, et al. Are vitamin B12 and 57. Schauer PR, Ikramuddin S, Gourash W, et al. Outcomes after
folate deficiency clinically important after roux-en-Y gastric by-
laparoscopic Roux-en-Y gastric bypass for morbid obesity. Ann
pass? J Gastrointest Surg 1998;2:436–442. 45. Brolin R. Metabolic deficiencies and supplements following 58. Pories WJ. Why does the gastric bypass control type 2 diabetes
bariatric operations. In: Martin L, ed. Obesity surgery. New
mellitus? Obes Surg 1992;2:303–313. 46. Brolin RE, Leung M. Survey of vitamin and mineral supplemen- 59. Pories WJ, MacDonald KG Jr, Morgan EJ, et al. Surgical treat-
tation after gastric bypass and biliopancreatic diversion for mor-
ment of obesity and its effect on diabetes: 10-y follow-up. Am J
bid obesity. Obes Surg 1999;9:150–154.
Clin Nutr 1992;55[2 Suppl]:582S–585S. 47. Martin L. Managing postoperative complications after bariatric 60. Pories WJ, MacDonald KG. The surgical treatment of morbid
surgery. In: Martin L, ed. Obesity surgery. New York: McGraw-
obesity. Curr Opin Gen Surg 1993;195–205. 61. Pories WJ, Swanson MS, MacDonald KG, et al. Who would 48. Brolin RE, Gorman RC, Milgrim LM, Kenler HA. Multivita-
have thought it? An operation proves to be the most effective
min prophylaxis in prevention of post-gastric bypass vitamin
therapy for adult-onset diabetes mellitus. Ann Surg 1995;222:
and mineral deficiencies. Int J Obes 1991;15:661–667. 49. Brolin RE, Gorman JH, Gorman RC, et al. Prophylactic iron 62. Pories WJ. So you think we are bariatric surgeons? Think again.
supplementation after Roux-en-Y gastric bypass: a prospective,
double-blind, randomized study. Arch Surg 1998;133:740–
63. Pories WJ. Improving diabetes care in North Carolina. N C Med 50. Cowan G, Hiler M, Martin L. Reoperative obesity surgery. In: 64. Pories WJ. Diabetes: the evolution of a new paradigm. Ann Surg
Martin L, ed. Obesity surgery. New York: Mcgraw-Hill; 2004:
65. Schauer PR, Burguera B, Ikramuddin S, et al. Effect of laparo- 51. Shiffman ML, Kaplan GD, Brinkman-Kaplan V, Vickers FF.
scopic Roux-en Y gastric bypass on type 2 diabetes mellitus. Ann
Prophylaxis against gallstone formation with ursodeoxycholic
Surg 2003;238:467–484; discussion 465–484.
Cannabis et Trouble Déficit de l’Attention (TDA) David Bearman, M.D., Californie (USA) http://davidbearmanmd.com/ Traduction autorisée par l’auteur http://mcforadhd.free.fr/ Les symptômes principaux des types les plus connus du TDAH (Trouble Déficit de l’Attention / Hyperactivité) sont (1) suractivité motrice, (2) inattention et (3) impulsivité (American Psychiatric Associat
HIP IMPINGEMENT Femoroacetabular impingement, or hip impingement, has emerged in recent years as a major cause of hip pain and eventually arthritis. Hip impingement means that there is a bony conflict in the hip. This conflict occurs when the hip is brought up into flexion. Activities that involve repetitive hip flexion and pivoting are frequently implicated in the development of hip impingemen