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Hi,

A surgeon from the Netherlands is writing a letter to the editor criticising

the MGB.

I have the oportunity to write a response.

Below is the Dutch Dr's letter and my response.

Any help and suggestions would be appriciated.

P.S. I think it would be of value for each of you to read both.

I think my argument is better I spent quite some time on it.

I have to get it back to the editor by Monday.

Thanks.

RR

To the Editors:

Galen, the great physician and philosopher born in A.D. 129 pronounced the

view that blood was continually being made and used up. This was the " truth "

for 1,400 years until Harvey successfully challenged Galen's

position. Laparoscopic surgery is revolutionizing many areas of both

General and Bariatric Surgery. Revolutions are by their very nature

inherently disruptive, often requiring a review of previously held

assumptions.

Dr. Greve's letter addresses the revolutionary aspects of laparoscopic

surgery to laud some aspects but he raises concerns about " . the

re-introduction of procedures by minimal (sp.) invasive surgeons that were

abandoned years ago because they were shown to be inferior in open surgery.

One of the examples is the laparoscopically performed Mini-Gastric Bypass. "

In his letter he likens the Mini-Gastric Bypass (MGB) to the old Mason loop

gastric bypass. He rightly points out the failings of the old loop bypass

[5-7]. Unfortunately he fails to note two important facts. One, the

Mini-Gastric Bypass is NOT the old loop gastric bypass, it is different, and

second, that the previously well documented problems and complications of

the old Mason loop gastric bypass that he refers to have not occurred in the

series of 817 MGB patients. In fact since we know that the old Mason loop

gastric bypass routinely led to the well documented complications described

by Dr. Greve and since these complications are not present in the series of

MGB patients it should be obvious, even to Dr. Greve, that they are not be

the same operation.

Dr. Greve also refers to the extensive literature on Billroth II anastomoses

and gastric cancer. He provides a prejudiced reference to that literature

to bolster his case. He refers to a variety of papers on the topic, many of

which are out of date and some that actually conclude the opposite of his

thesis! As a remarkable example of Dr Greve's careless use of the medical

literature he refers to the well-done New England Journal article by Schafer

et. al. (N Engl. J Med 1983 Nov 17; 309(20): 1210-3 The risk of gastric

carcinoma after surgical treatment for benign ulcer disease. A

population-based study in Olmsted County, Minnesota. Schafer LW, Larson DE,

Melton LJ 3d, Higgins JA, Ilstrup DM ). This study was performed " to

determine the long-term risk of gastric cancer in benign peptic-ulcer

disease. " In this study the Mayo Clinic group studied residents of Olmsted

County, Minnesota, who had surgery for peptic-ulcer disease in the 25-year

period 1935-1959. These patients were subsequently followed for over 5,635

person-years. The risk of development of a gastric cancer in this group was

compared with that expected on the basis of gastric-cancer incidence rates

for the local population. They found gastric carcinomas in only two of the

patients in the surgical group, as compared with an expected rate of 2.6

primary gastric carcinomas (relative risk, 0.8 [95 per cent confidence

interval, 0.1 to 2.7]). That is they found that the rate in the surgically

treated patients was actually lower than that seen in unoperated controls.

They concluded " there is no indication for endoscopic surveillance in

asymptomatic patients with previous gastric surgery for benign peptic-ulcer

disease. " Odd, yet Dr Greve uses this article in his reference list? One

has to wonder if he did not read the article?

Furthermore such epidemiological studies need to be viewed with some

caution. In a study from Sweden by Lundegardh et. al. (Br J Surg 1994

Aug;81(8):1164-7 Risk of cancer following partial gastrectomy for benign

ulcer disease. Lundegardh G, Adami HO, Helmick C, Zack M) The relative risk

of developing cancer after partial gastrectomy for benign ulcer disease was

examined in a population-based cohort comprising 6,459 patients operated on

between 1950 and 1958. Follow-up to 1983 revealed 1,112 patients with some

type of cancer versus 1,128 expected cases (relative risk 1.0), i.e. no

different than expected. The study found an increased risk for lung cancer

(relative risk 1.5 (95 per cent c.i. 1.2-1.7)) while the risk for cancers of

the nervous system was less frequent than expected (relative risk 0.5 (95

per cent c.i. 0.3-0.8)). Does this mean that a BII causes lung cancer and

protects against brain cancer?

A more balanced review of the medical literature on gastric stump cancer

shows that numerous long-term studies of BII patients have found no evidence

of an increased incidence of gastric cancer. In a recent study by Bassily

et. al. (J Gastroenterol Hepatol 2000 Jul;15(7):762-5 Risk of gastric cancer

is not increased after partial gastrectomy. Bassily R, Smallwood RA, Crotty

the records of a total of 569 patients who had a partial gastrectomy for

peptic ulcer disease between 1957 and 1976 were analysed. Five hundred and

seven of the group (83.5%) had a Billroth II procedure. They concluded that

" the risk of gastric cancer was not increased after Billroth II partial

gastrectomy. " In another study by Luukkonen et. al. (Hepatogastroenterology

1990 Aug; 37(4): 392-4 Decreased risk of gastric stump carcinoma after

partial gastrectomy supplemented with bile diversion. Luukkonen P, Kalima T,

Kivilaakso E) the risk of gastric stump cancer after gastric surgery for

peptic ulcer in the Finnish population was studied. A total of 285 patients

operated on for benign peptic ulcer between 1948 and 1954 were followed.

Only nine patients (3%) were lost to follow-up. Six patients of the total

285 developed gastric cancer 6, 7, 8, 21, 25 and 27 years after the

operation. (It is hard to see how the operation could have caused cancer in

6-8 years) The risk of contracting gastric cancer in a control population

(individuals who had no operation) of equal size and age during a similar

follow-up period was 8 cases. They concluded that the observed number of

gastric cancers (6 patients) did not differ significantly from the expected

number (8). This study, as well as many others, shows that the risk of

gastric cancer does not significantly increase after partial gastrectomy for

benign peptic ulcer.

As Dr Greve correctly points out there are some studies that appear to show

an increased risk of gastric stump cancer as compared to the general

population. Sadly, either on purpose or because of ignorance of the

literature, he does not recognize the flawed nature of these studies. In the

studies that show slight increases in the rate of gastric cancer following

BII, all of these studies include patients that have had the surgery for

peptic ulcer disease. The problem with this type of study design is the

fact that it has been well shown that gastric ulcer is associated with

gastric cancer. For example in a study by Molloy and Sonnenberg (Gut 1997

Feb; 40(2): 247-52 Relation between gastric cancer and previous peptic ulcer

disease. Molloy RM, Sonnenberg A) the association between peptic ulcer and

gastric cancer was studied among patients followed up at hospitals of the US

Department of Veterans Affairs. 3,078 subjects with cancer of the stomach

were compared with a control population of 89,082 subjects without gastric

cancer. In this study a previous history of gastric ulcer was associated

with a significantly increased rate of gastric cancer (relative risk 1.53,

95% confidence interval: 1.24 to 1.87). It is important to note that this

increased risk is similar to that seen in the studies showing an increased

risk of gastric cancer in BII surgical patients. Many other studies confirm

that unoperated peptic ulcer patients have an increased risk of gastric

cancer. In the study by Hansson et. al. from Sweden published in the New

England Journal of Medicine (N Engl J Med 1996 Jul 25;335(4):242-9, The risk

of stomach cancer in patients with gastric or duodenal ulcer disease.

Hansson LE, Nyren O, Hsing AW, Bergstrom R, fsson S, Chow WH, Fraumeni

JF Jr, Adami HO) they estimated the risk of stomach cancer in a large cohort

of hospitalized patients with gastric or duodenal ulcers. Altogether, 57,936

patients were followed through 1989, for an average of 9.1 years. The

incidence ratio for gastric cancer among 29,287 patients with gastric ulcers

was increased at 1.8 (95 percent confidence interval, 1.6 to 2.0) and

remained significantly increased throughout follow-up, which was as long as

24 years for some patients. Again, this value is very similar to that

reported for the increase seen in some studies of post-gastrectomy patients.

They concluded that gastric ulcer disease and gastric cancer have etiologic

factors in common. A likely cause of both is atrophic gastritis induced by

H. pylori. Thus the studies that find small increased rates of gastric

cancer in post gastrectomy patients may simply be identifying gastric ulcer

patients that are prone to develop gastric cancer regardless of their

surgical procedure.

Dr Greve also left out any references to the actual magnitude of the

increased risk seen in the post gastrectomy patients. As described above

the majority of studies find no increased risk of gastric cancer in BII

patients, but in the studies that do find an increase in risk, how much

increase is found and how does this compare to other factors involved in the

development of gastric cancer? Let us look at these issues to put Dr

Greve's incendiary remarks in proper perspective.

Hundreds of articles have looked at factors that might affect the

development of gastric cancer. A large number of studies have indicated

that salted, smoked, pickled, and preserved foods (rich in salt, nitrite,

and preformed N-nitroso compounds) are associated with an increased risk of

gastric cancer. In contrast, strong evidence has been provided that high

consumption of fresh fruit and raw vegetables and a high intake of

antioxidants are associated with a reduced risk of gastric cancer. Domestic

refrigeration and reduced salt consumption are considered to play a role in

explaining the decreasing rate of gastric cancer over time. Familial factors

have been suspected to play a role in GC susceptibility, and recently germ

line mutations in the E-cadherin gene were identified in a few families.

Overall, it is evident that several factors (including diet, individual

susceptibility and H. pylori infection) interact in a complex multifactorial

process, leading over a long period of time to GC (J Gastroenterol. 2000; 35

Suppl 12:84-9 Epidemiology of gastric cancer: an evaluation of available

evidence. Palli D). Now with all of these factors where is post-gastrectomy

positioned as a risk factor?

As Dr Greve fails to point out, evidence supports that gastric cancer has an

environmental etiology, of which diet appears to be the most important

component (Cancer 1993 Mar 1; 71(5): 1731-5 Dietary factors and gastric

cancer risk. A case-control study in Spain. Ramon JM, Serra L, Cerdo C,

Oromi J.) Epidemiologic studies show that there is an approximately a

threefold increased risk of gastric cancer for frequent consumption of fresh

and processed meats (odds ratio (OR) = 3.1 and 3.2 respectively). Gastric

cancer risk rises with increasing intake of smoked and pickled foods (OR

3.67) Increased risk of gastric cancer has also been demonstrated for

frequent consumption of dairy products (OR = 2.7) and fish (OR = 2.2). All

of these changes are as much as twice as high as that seen with the studies

showing an effect of gastrectomy on gastric cancer risk. Studies also show a

decreasing risk of stomach cancer with increasing frequency of vegetable

consumption. Intake of citrus fruits (OR 0.47) and raw-green vegetables (OR

0.56) appear to be protective. Consumption of salty snacks more than twice

per month has been associated with an 80 percent increased risk (Am J

Epidemiol 1999 May 15; 149(10): 925-32 Dietary factors and the risk of

gastric cancer in Mexico City. Ward MH, -Carrillo L.) These findings

are consistent with many studies around the world that indicate important

roles for salt, processed meats, and vegetable consumption in gastric cancer

risk. There are hundreds more articles like these but we can summarize

these findings as follows: BII post gastrectomy patients are at little or

no increased risk of gastric cancer. If either they or their physicians are

concerned it about gastric cancer it appears that very simple dietary

modifications can have a much greater impact on the patient's lifetime risk

of gastric cancer than that of the gastrectomy, i.e. avoiding processed

meats, smoked and pickled foods while increasing one's intake of fresh

fruits and vegetables, with or with out supplementation with additional

antioxidant vitamins.

Helicobacter Pylori

Evidence of a positive association between Helicobacter pylori infection and

gastric cancer risk has been provided by most prospective studies that

overall suggest a two- to threefold increase in risk. Randomized

intervention studies on H. pylori eradication and its effects on gastric

cancer predisposing conditions (atrophic gastritis and intestinal

metaplasia) are in progress and represent a priority for epidemiological

research in view of the potential preventive applications. Again studies

clearly show that H Pylori not gastrectomy appears to be the risk factor

associated with gastric cancer and physicians who feel this is of concern

can provide treatment to eradiate H. Pylori to patients.

Scores of studies have looked at the tens of thousands of patients that

undergo BII operations on an annual basis (est. 16,000 per year is the US.)

In these studies routine screening or follow up of such patients to look for

incipient gastric cancer has not generally been recommended as valuable.

Finally if Dr. Greve were really and honestly concerned about the risk of

BII causing gastric cancer one wonders why his letter would be directed to

the journal of Obesity Surgery. As noted above thousands and thousands of

patients undergo BII type gastrojejunostomy on a yearly basis and it would

seem his zeal in protecting the public against the risk of the BII type

anastomoses might more profitably be directed elsewhere, at the thousands of

general surgeons that routinely perform the BII anastomoses on a daily

basis. It seems odd for him to focus on this relatively small subset of BII

patients.

In fact it is obvious why he has chosen to misrepresent the medical

literature and or selectively present it in his letter. His real purpose is

revealed in the concluding remarks of his note where he says, " Minimal

invasive surgery . should improve and utilize the experience gained in open

surgery and not re-invent surgical techniques. " His real concern is that

the laparoscopic surgery has modified an open technique. Yet is that not

what all of us actually hope for, that newer and better techniques will be

devised over time and that these newer techniques will be put to the service

of our patients.

Surgeons have a long history of fighting against change. Surgeons fought

antisepsis, changes in breast cancer surgery, closed suction drainage and

uncounted other improvements in medical care. Rather than welcoming change

surgeons have shown themselves instead to be hidebound conservatives

unwilling to see the light of a new day. They have failed to embrace change

so often that it has come to be a defining characteristic of surgery.

The Mini-Gastric Bypass is a remarkable new development in Bariatric

surgery. It is supported by the most extensive database and data collection

effort ever put forth to document the outcomes of a Bariatric surgical

procedure. To date more than 817 patients have undergone the procedure.

The complication rate is 5.3% over all, the mortality rate is 0.12%, the

operative time averages 38 + 9.2 minutes, the mean hospital stay is 1.1 + 1

day and the hospital charges are 1/3 to ¼ that charged by others. There are

no hernias, pulmonary emboli or episodes of DVT in the series to date. And,

the surgery is easily revised or reversed. The weight loss is comparable or

better than any other reported series.

While more work needs to be done, it is clear that rather than calling for

laparoscopic surgeons not to be innovators, all of the members of the

medical community must continually question our past beliefs. If new data

exposes past theories to the harsh light of reality then so be it. We

should all be long past the days of Galen.

Should laparoscopic surgeons reinvent bariatric surgical procedures?

The exciting development of minimal invasive surgery has in recent years

significantly altered the approach of many surgeons to the morbidly obese

patient. After the introduction of the adjustable silicone gastric banding,

which was adapted for laparoscopic placement by Belachew and colleagues,

many laparoscopic surgeons entered the field of bariatric surgery. In Europe

most bariatric procedures nowadays are performed laparoscopically. Even more

exciting is the performance of more complicated procedures by minimal

invasive techniques. Not only the gastric bypass but also the

biliopancreatic diversion as developed by Scopinaro and its variations, such

as the duodenal switch, are now performed either by hand assisted

laparoscopic or even complete laparoscopic procedures[1-3]. The advantages

are obvious, minimal surgical trauma with quick post-operative recovery,

short hospital stay and minimal risk of wound problems. Laparoscopy may even

provide superior access with a good view of the anatomy in the morbidly

obese patient.

Main issue of minimal invasive surgery is access to the operation field. The

procedures performed are similar to the procedures performed by open

surgery. Minimal invasive surgery should not alter the indication to perform

any kind of surgical procedure simply because you only need a few small

incisions. It is therefore puzzling to note that procedures that have been

performed, and fine-tuned, for decades by open surgery are altered by

laparoscopic surgery. But even more concerning is the re-introduction of

procedures by minimal invasive surgeons that were abandoned years ago

because they were shown to be inferior in open surgery. One of the examples

is the laparoscopically performed mini-gastric bypass, a small proximal

gastric pouch with a Billroth II type anastomosis, for the morbidly obese

patients as reported during the last meeting of the American Society for

Bariatric Surgeons (ASBS)[4]. This type of procedure has been used

extensively by open surgery (loop gastrojejunostomy according to Mason) but

was shown to be insufficient and causing to many complications[5-7]. The

preliminary results of laparoscopic loop gastric bypass appear to be

acceptable with respect to weight loss, however complications mainly occur

in a later stage. Moreover, it is well known from the very large experience

in the past with distal gastrectomies for peptic ulcer disease, that these

patients have a significantly increased risk to develop a carcinoma in the

gastric remnant after 15-20 years [8-18]. Unfortunately morbidly obese

patients are usually young when operated and thus will be exposed to long

term biliary reflux, suggested to be a causative factor in malignant

degeneration of gastro-intestinal mucosa[19-21]. A typical example where

lessons learned in the past should not be disregarded.

Minimal invasive surgery is a great improvement in the field of bariatric

surgery. However it should improve and utilize the experience gained in open

surgery and not re-invent surgical techniques.

JWM Greve, Md, PhD

Department of Surgery

University Hospital Maastricht

PO Box 5800

6202 AZ Maastricht

The Netherlands

E-mail: JW.Greve@...

References

1. Naitoh, T., et al., Hand-assisted laparoscopic digestive surgery

provides safety and tactile sensation for malignancy or obesity. Surg

Endosc, 1999. 13(2): p. 157-60.

2. Lonroth, H., Laparoscopic gastric bypass. Obes Surg, 1998.

8(6): p. 563-5.

3. Nguyen, N.T., et al., A comparison study of laparoscopic

versus open gastric bypass for morbid obesity [in Process Citation]. J Am

Coll Surg, 2000. 191(2): p. 149-55

4. Rutledge, R., The Mini-Gastric Bypass: Experience with the

First 300 Cases. Obesity Surgery, 2000. 10(2): p. 133.

5. Mason, E.E. and C. Ito, Gastric bypass in obesity. Surg Clin

North Am, 1967. 47(6): p. 1345-51.

6. Mason, E.E. and C. Ito, Gastric bypass. Ann Surg, 1969. 170(3):

p. 329-39.

7. Mason, E.E., et al., Optimizing results of gastric bypass. Ann

Surg, 1975. 182(4): p. 405-14.

8. Bushkin, F.L., Gastric remnant carcinoma. Major Probl Clin

Surg, 1976. 20: p. 106-13.

9. Cheung, L.Y., Reflux of bile acids, gastritis, and gastric

remnant carcinoma [editorial]. Am J Surg, 1987. 153(4): p. 403-4.

10. Ewerth, S., et al., The incidence of carcinoma in the gastric

remnant after resection for benign ulcer disease. Acta Chir Scand Suppl,

1978. 482: p. 2-5.

11. Graem, N., A.B. Fischer, and H. Beck, Dysplasia and carcinoma in

the Billroth II resected stomach 27-35 years post-operatively. Acta Pathol

Microbiol Immunol Scand [A], 1984. 92(3): p. 185-8.

12. Greene, F.L., Early detection of gastric remnant carcinoma. The

role of gastroscopic screening. Arch Surg, 1987. 122(3): p. 300-3.

13. Greene, F.L., Management of gastric remnant carcinoma based on the

results of a 15- year endoscopic screening program. Ann Surg, 1996. 223(6):

p. 701-6; discussion 706-8.

14. Klarfeld, J. and G. Resnick, Gastric remnant carcinoma.

Cancer, 1979. 44(3): p. 1129-33.

15. Loscos, J.M., et al., Cancer of the gastric stump. Gastrointest

Endosc, 1986. 32(2): p. 75-7.

16. Orlando, R.d. and J.P. Welch, Carcinoma of the stomach after

gastric operation. Am J Surg, 1981. 141(4): p. 487-91.

17. Pickford, I.R., et al., Endoscopic examination of the gastric

remnant 31-39 years after subtotal gastrectomy for peptic ulcer. Gut, 1984.

25(4): p. 393-7.

18. Schafer, L.W., et al., The risk of gastric carcinoma after

surgical treatment for benign ulcer disease. A population-based study in

Olmsted County, Minnesota. N Engl J Med, 1983. 309(20): p. 1210-3.

19. Kobayasi, S., et al., Gastric and small intestinal lesions

after partial stomach resection with Billroth II or Roux-en-Y reconstruction

in the rat. Cancer Lett, 1994. 85(1): p. 73-82.

20. Kojima, H., K. Kondo, and H. Takagi, [The influence of reflux of

bile and pancreatic juice on gastric carcinogenesis in rats]. Nippon Geka

Gakkai Zasshi, 1990. 91(7): p. 818-26.

21. Langhans, P., et al., Gastric stump carcinoma--new aspects

deduced from experimental results. Scand J Gastroenterol Suppl, 1981. 67: p.

161-4.

Rutledge, M.D., F.A.C.S.

The Center for Laparoscopic Obesity Surgery

4301 Ben lin Blvd.

Durham, N.C. 27704

Telephone #:

Fax #:

Email: DrR@...

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