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Winter 2005
Nesidioblastosis
and Standard of Care
Edward E. Mason MD, Ph.D.
he Summer
2005 IBSR Newsletter article, “Obesity Surgery, Insulin, GLP-1 and Cancer – A
Literature Review”, explained the benefits from bypass operations with regard
to reducing plasma insulin stimulation of cancer growth and preventing or
curing type-2 diabetes mellitus (T2DM) by stimulating the secretion of GLP-1
from the distal ileum. Now we are confronted
with two reports of life saving pancreatectomy in patients with
nesidioblastosis following Roux-en-Y gastric bypass (RYGB). Service et al found one patient had
insulinomas and five had a diffuse overgrowth of beta cells.1 Patti
et al reported three similar patients.2 One had a reversal of the RYGB without relief
before the pancreatectomy. What may be a
rare complication can become too frequent in absolute numbers when treating an
epidemic with the projected 200,000 RYGB operations for 2006. Patients
need effective and life saving treatment, but continued follow-up for life has
become even more important.
In 1999 I suggested further study of transposition of the distal ileum
to a juxta-duodenal position so the ileum would be exposed to glucose more
frequently to possibly prevent or cure T2DM, without the complications of
bypass operations.3 The operation should not be used in humans
until we learn how to avoid hypoglycemia from excessive insulin secretion.
Patients must know what is
being done and the possible consequences.4 Nesidioblastosis should be explained as a
possible but rare result. If it occurs
it will probably require another major operation. The result of that second operation could be
permanent insulin dependent diabetes if the entire pancreas is removed or
failure to control the attacks of hypoglycemia if some pancreas is left in
place. However, there may be the choice
of a restriction operation without bypass.
For the majority of patients in 2006, the choice will be either RYGB
(bypass) or no operation at all. Restriction
operations should be offered and may, at some time, be recommended as the
operation of choice.5 Surgeons need to prepare for the time
when there may be sufficient reason for no longer using bypass operations. Encourage your colleagues to join a registry
that is attempting to obtain lifelong information about outcome. Together we can solve whatever problems arise
and improve the outcome for these patients.
One variable that summarizes the most serious complications of both
obesity, and the surgical treatment of obesity, is length of life. MacDonald et al observed a marked survival advantage for patients with diabetes following
RYGB.6 No difference in survival was found following bypass or restriction
operations performed from 1986 to 1999 in a survival
analysis by the IBSR.7 We
found a mortality rate of 3.45% (654/18,972) for patients followed an average
of 8.3 years.
Here are some additional suggestions for patient education. The normal stomach can hold over three pints
of food and liquid. As digestion begins,
the pyloric muscle at the lower end of the stomach controls emptying. This muscle is regulated by osmoreceptors in
the duodenum that keep the mixture of food, bile and digestive juices at the
same concentration as body fluids. However,
if glucose reaches the distal ileum, the ileal brake hormone (GLP-1), is
secreted into the blood stream. GLP-1
has two ways of slowing the movement of nutrients through the normal digestive
tract. 1) It acts upon the pyloric
muscle to decrease gastric emptying and 2) it slows intestinal
peristalsis. GLP-1 also stimulates beta
cells in the pancreas to grow and to produce more insulin. To prevent prolonged action of GLP-1 the circulating
enzyme, dipeptidyl peptidase-4, inactivates GLP-1.
Gastric bypass causes weight reduction through interference with all of
this elaborate, automated control of storage in the stomach, metering of food
entering the intestine, and regulation of the rate of movement of the digesting
food stream through some 23 feet of small bowel. RYGB prevents or cures T2DM but it also
interferes with the normal regulation of insulin secretion. Stimulation of GLP-1 release by exposing the
distal small bowel to glucose prevents T2DM, but continual stimulation of the
pancreas may result in overgrowth of insulin producing cells and, in some
patients, the secretion of insulin becomes excessive and out of control. This causes blood sugar levels to be too low
for survival. The only treatment then becomes a major
operation to remove enough of the pancreas to rid the patient of excessive
insulin. The use of a one time major
operation to regulate the concentration of sugar in the blood is inferior to
the continually active and elaborate control mechanisms that normally regulate
blood sugar levels.
What should the response of surgeons performing bypass operations for
obesity be to these reports? A surgeon
cannot solve a patient’s weight problem without some participation by the
patient and change in that patient’s environment
and life style. The informed patient must decide what is best for their remaining
life. Unfortunately, we do not know the
lifelong frequency of some complications from these operations. It is a difficult task explaining complex
potential consequences and surgeons
must continue to gather information from longer follow-up. If necessary, surgeons need to be prepared to
make changes if it becomes apparent that bypass operations produce more
complications, than cures. RYGB causes
weight loss but also loss of many important body regulatory systems that keep a
normal person healthy. Lifelong medical
care following gastric bypass is expensive and difficult to obtain, but it is
necessary. In the meantime, help each
patient find the best treatment for what we expect to be a long and more
pleasant life following surgical treatment for obesity.
1. Service
GJ, Thompson GB, Service J, Andrews JC, Collazo-Clavell ML, Lloyd R. Hyperinsulinemic
hypoglycemia with nesidioblastosis after gastric-bypass surgery. NEJM
353, 249-254, 2005.
2. Patti ME, McMahon G, Mun EC, Bitton A, Holst JJ,
Goldsmith J, Hanto DW, Callery M, Arky R, Nose V, Bonner-Weir S, Goldfine AB. Severer
hypoglycemia post-gastric bypass requiring partial
pancreatectomy: evidence for inappropriate insulin secretion and pancreatic islet
hyperplasia. Diabetologia 48:
2236-2240, Epub Sep 30, 2005
3. Mason
EE. Ileal
transposition and enteroglucagon/GLP-1 in obesity (and diabetic?) surgery:
Review of the Literature. Obesity Surgery 9: 223-228, 1999.
4. Mason
EE, Hesson WW. Informed consent for obesity surgery. Obesity
Surgery 8: 419-428, 1998.
5. Mason
EE Development
and future of gastroplasties for morbid obesity. Archives
of Surgery. 138: 361-366, 2003.
6. MacDonald
KG, Long DS, Swanson MD, et al. The gastric bypass operation reduces the
progression and mortality of non-insulin dependent diabetes mellitus. J Gastrointestinal Surgery 1: 213-230, 1997.
7. Zhang
W, Mason EE, Renquist KE, Zimmerman B, IBSR Contributors. Factors Influencing
Survival Following Surgical
Treatment of Obesity. Obesity Surgery 15: 43-50, 2005.
F.U.D.
By
Kathleen Renquist
he
marketing term F.U.D. stands for Fear, Uncertainty, and Doubt. “By creating FUD, a company can discredit its
competitors without actually lying,” explained Ann Tvedt, U of I Department of Surgery
business manager. Here are some examples
of FUD regarding the IBSR:
1. The
IBSR has over 50,000 patients with no infections. Looking at any IBSR publications shows this
statement is FALSE. And we do not even
have 50,000 patients yet, so this statement represents two falsehoods.
2. We
can download our data to the IBSR. An alternative software vender could download data, but we can not use
it unless it is in IBSR format. However,
a company can provide data in an ASCII flat file formatted
so that we can merge the data into the IBSR aggregate data set. Personalized
Programming, the creators of Medical Manager, did just that for Dr. Alex
MacGregor in the early 90’s. It was
unfortunate no interest by other bariatric surgeons was generated to use that system.
It is the vendor’s responsibility to develop the module and not the
IBSR’s. There is a $100.00 per hour fee
for IBSR staff to work in conjunction with the vendor to test application
accuracy. But, this really does not take
long.
3. The
IBSR collects international data only. IBSR data is largely from U.S.A. data collection sites (93%). The National Bariatric Surgery Registry
(NBSR) was renamed in 1996.
4. Surgeons
using the IBSR software have no data on their computer locally. The IBSR is a single-user program that
resides on the members local PC. Surgeons
entering their data have it available to them locally all the time. Any field in the data base can be exported to
another product to analyze.
The user of a web system would still have to export data to some other
area if they wanted to do studies on the data individually or pay for that specialized reporting service to be done or programmed.
5. The
software loses data. There
is a difference between losing data and excluding data. The IBSR software and reports compare
complete patient information at follow-up with that of the same patient
population at initial visit or
operation. This pairing of initial and outcome data provides more accurate outcome
comparisons. If a patient is missing
follow-up, or is followed but the specific data in question is missing in
follow-up, or the patient had the data in follow-up but is missing it initially, then that patient is excluded in the
analysis. For the untrained eye, this
may look like the software is losing data.
In fact, it was not entered or submitted.
Be wary of software reports that provide information for one patient population
initially or at operation, then
another set of data from different patients at follow up. You can tell when this is the method used as
the total number of patients in each group is not the same. This is a common practice when reporting
results, but it should not be used for comparing outcome. It does provide quick, easy, and misleading
results.
6. The
IBSR is no longer in business. This
is false and we are still open for business.
As long as the aggregate data set of 45,000+ is useful, we should
have many things to do. New and old
members are welcome. The IBSR remains an
educational, non profit organization associated with the University.
If you find
interesting comments about the IBSR, I would like to hear them and determine if
they are fact or FUD. Please email me at
kathleen-renquist@uiowa.edu – thank you.
IBSR
Publications, 1986-2005
Kathleen Renquist, BS
any NBSR/IBSR publications can be obtained in the public domain. However, the vast majority are for IBSR
members. Feature articles of the IBSR
Newsletters from 1995 are located on the IBSR web site www.surgery.uiowa.edu/ibsr,
as well as several IBSR Power Point presentations. Apart from the IBSR web site, the following
publications have been prepared for the IBSR membership since 1986.
22 Exhibits
at the ASBS (18), ACS (4).
6 Poster presentations
37 Pooled
reports
>400 Individual surgeon reports
78 Newsletters
14 Peer
reviewed articles
10 Presentations,
mostly the ASBS
>500 Statistical requests
9 Manuals
13 Software
revisions or upgrades
18 Forms
(PFF’s, Data Entry, Scanner, HSQ), with various updates and revisions.
The IBSR has many publications but most are only for the IBSR membership. This work has taken time away from writing
papers in refereed or peer reviewed journals.
However, look for several publications to surface in the coming years due
to assistance of interested IBSR members and University of Iowa
researchers. Thanks to the dedication
from our IBSR surgeon members, the fruits of this labor are being realized.
Winter 2005 IBSR Newsletter Volume
20, Number 4
UI
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