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From: "Howard McCollister" <>
Subject: Re: dysphagia or GERD?
Date: 2 May 2003 10:15:14 -0500
Message-ID: <3eb28ad7$0$86586$>

"Terri" <> wrote in message
> Since someone close to me (age 44) has just been diagnosed with
> esophageal adenocarcinoma, I'll chime in here with a couple of questions
> re this disease. GERD/acid reflux is associated only with the
> adenocarcinoma variant of esophageal cancer? Is there any definitive
> evidence showing that treating GERD with PPI's actually reduces the
> incidence of esophageal adenocarcinoma? Do either of you know of any
> genetic predisposition connected to this disease? My brother has been
> told that his long term survival chances are about 1/3 and that these
> are pretty typical odds for it. Various scans (brain, lungs, abdomen,
> bone) have shown no metastases and his surgeon has told him that the
> original esophageal tumor is "relatively small" without defining what
> that means in terms of actual size. My internet research on medline
> suggests that tumor size is a critical prognostic variable in this
> cancer. Is all of the above reasonably accurate/correct?
> He was definitively diagnosed on April 15 (second endo and biopsies -
> first endo 10 days earlier was "suspicious" but biopsies were negative
> for malignancy) and will begin combined radiation and chemo on May 5 for
> 1 week, radiation alone for the next 3 weeks followed by another week of
> combined radiation and chemo. I can supply the names of the chemo drugs
> (3) that will be used if you are interested. He will have surgery 4
> weeks after the last week of combined chemo and radiation. Again, my
> research in internet, medline, and discussions with physician friends
> tell me that this is the current "best" treatment for this cancer. Would
> either or both of you view this as a reasonable assessment of the
> treatment he is being offered?
> There is one complication in his treatment. He learned several years ago
> during an IVP that he has only one kidney. The oncologist in charge of
> his case has suggested that she might reduce the chemo dosage and number
> of drugs somewhat (use 2 instead of 3 drugs) to avoid damaging his
> single kidney. While this strikes me as rational, a functioning kidney
> and recurrent or advancing esophageal cancer doesn't strike me as any
> better than "curing" the esophageal cancer only to end up on lifetime
> dialysis. He has a very large family of siblings (10) all of whom have
> very seriously offered him a kidney if they are a match, should he
> require one. I'm wondering whether the oncologist might be willing to be
> more aggressive if she were informed that there was a kidney available
> if it should be required (everyone is willing to have the testing done
> for matching). Any thoughts on this? Of course someone who has just had
> chemo, radiation and major surgery for esophageal cancer is not exactly
> the best candidate for further major transplant surgery, so maybe I'm
> just grasping at any straw I can find....
> I have learned in my crash course on this disease that there has been an
> explosion in the number of cases of this disease over the past 3 decades
> with the number increasing by 350%, mostly in middle-aged white males
> like my brother. Anyone have any ideas as to the reason for this
> increase?
> Any links to studies and other information would be greatly appreciated.

Esophageal cancer can be squamous cell carcinoma, or adenocarcinoma.
Adenocarcinoma of the esophagus starts in Barrett's esophagus, where the
lining has undergone metaplastic change from chronic acid reflux. The most
common type of esophageal cancer through history has been squamous cell
cancer since the esophagus is entirely lined with squamous mucosa, but the
incidence of squamous cell cancer of the esophagus is actually decreasing
while adenocarcinoma of the esophagus is rapidly increasing in incidence.
The theory for this, not proven by randomized, prospective study, is that
the use of effective anti-acid medication beginning 30 years ago (H2
receptor antagonists such as Tagamet) and now PPIs will effectively remove
acid from the stomach, upsetting the acid-base relationship and now allowing
alkaline bile salts to come out of solution in the stomach. Since these meds
have not addressed the reflux mechanism, that patient is now refluxing bile
salts, which are more damaging to the esophagus than acid. However, it's the
acid that causes the symptoms, so the patient feels better even though he is
accelerating the development of Barrett's esophagus. If you graph out the
increasing use of H2 blockers and now PPIs over the last 30 years, and
compare it to the graph of the incidence of adenocarcinoma of the esophagus
over that same period, you will find that the graphs are identical. Not
exactly a smoking gun, however the comparison is compelling, and it reminds
me exactly of the way that the link between tobacco and lung cancer became
evident. This info was related to me in a conversation with Tom DeMeester
and a slide with that graph on it comes up in almost every talk he gives. It
is therefore becoming increasingly suspected that the use of anti-acid
medication DOES NOT decrease the incidence of esophageal cancer, but in fact
may actually increase it.

The treatment you outline is completely appropriate. The only thing I would
add is that the esophagectomy can be done laparoscopically, something that
will speed recovery and decrease complications. Having done the procedure
that way several times, I would highly recommend that approach. Yes, the
size of the tumor is a very important prognostic factor, and since the size
is discernalbe preoperatively, that clinical staging guides the preop
chemo-radiation along with CT and PET scan. However, the actual prognosis
and additional post-op treatment will be far better understood after the
operation when the tumor and surrounding tissue and lymph nodes can be
definitely examined.

The kidney thing certainly throws a little twist into the situation and I'm
not sure how I would approach that since it's pretty far onto the fringes of
my knowledge base.

I do wish your brother and his family the best of luck.


From: "Howard McCollister" <>
Subject: Re: dysphagia or GERD?
Date: 3 May 2003 14:24:16 -0500
Message-ID: <3eb4169f$0$71551$>

"Terri" <> wrote in message
> CBI wrote:
> >
> > "Howard McCollister" <> wrote in message
> > news:3eb2c36d$0$34126$
> > >
> > >
> > >  It is now known that, somehow, H Pylori does protect against GERD
> > >  and it's complications to some degree, although the mechanisms are
> > >  not clear.
> >
> > The explanation I have always heard was that the inflammation of the
> > stomach caused less acid to be produced. Is there some thinking that
> > there is more (or less) to it than that?
> >
> > --
> > CBI, MD
> My newsreader just did something peculiar and eliminated 99% of posts,
> so I'm piggybacking this response.
> Thank you again Dr. McCollister, and I'm also interested into your
> response to CBI's question.
> I have another question re treatment of GERD. You noted in your response
> yesterday that treating the symptom (heartburn) by reducing/eliminating
> the reflux of acid into the esophagus might actually do more harm than
> good because the esophagus might then be exposed to more damaging bile
> salts, since the actual cause of the reflux of contents from stomach to
> esophagus has not been addressed when the drugs are used. The patient
> has less discomfort but s/he may actually be doing himself/herself more
> damage and increasing his/her risk of developing esophageal
> adenocarcinoma. What treatment do you recommend for GERD? Are the
> lifestyle changes of restricting food intake to at least three hours
> before lying down, elevating the head of the bed on blocks, reducing the
> size of meals especially the evening meal and evening snacks, and weight
> loss where necessary of any benefit?
> Terri

OK, you asked...

Acid reflux disease (GERD) is a mechanical problem. It relates to
dysfunction of the LES, whether it be baseline laxity (low resting LES
pressure) or transient inappropriate LES relaxation. Current studies
definitely tend to favor the latter as the primary cause for GERD in 60-80%
of cases. Therefore, the role of anti-secretory medications as a "cure" for
GERD doesn't make much sense in my mind. If there is no reflux-mediated
damage to the esophagus on EGD (stricture, erosion, Barrett's) then I have
no problem with using PPIs as a means of controlling the patient's symptoms,
but I think it's important to bear in mind the flip side -- we may very well
be increasing that patient's risk of esophageal cancer. We are not curing
the patient's disease, only controlling the symptoms of that disease. It's
not unlike treating a patient's painful inguinal hernia with pain

Note that (at present) I stop short of saying that everyone with acid reflux
disease should have an anti-reflux procedure. We aren't there - can't draw
that conclusion with certainty. Yet.

Since we postulate that reflux can be a significant contributer to the
development of esophageal cancer, then stopping the reflux should be our
primary goal. Just suppressing the symptoms with PPIs apparently isn't
enough, since they don't do anything to stop the reflux. They only change
the character of the refluxate. In fact, that may actually INCREASE the
incidence of esophageal cancer.

Toward that end, how do we stop the reflux? The lifestyle modifications are
an excellent place to start. Since a full stomach is a major contributing
factor to transient inappropriate LES relaxation, one should eat in a manner
such that the stomach is not overdistended (smaller meals). Since gravity
will aid reflux, one should go to bed on an empty stomach, and along those
same lines, elevating the head of the bed will also be beneficial. Since
increased intra-abdominal pressure will increase the pressure gradient
across the LES, then weight loss is also a great idea since that will
decrease the volume of the abdominal cavity. Since some foods (tomato spices
etc) will mediate transient inappropriate LES relaxation, they should be
avoided. Same for nicotine, caffiene, alcohol. All of the above are also
true if the reason for GERD is a lax LES (low baseline LES resting

Alternatively, there are anti-reflux procedures. Gold standard is the
gastric fundoplication, a time-honored (50 years) procedure that has been
refined to the point where it is 92-98% effective in stopping reflux in the
short term. Yes, there can be side effects of the operation, especially if
not done well (dysphagia, gas bloating), but these are minimized if modern
methods and concepts are followed. Recurrence rates are about 6-10%
depending on who is doing the procedure. The concept is wrapping (plicating)
the stomach to itself around the esophagus at the level of the LES. This
will splint the LES and prevent it from relaxing. It makes the LES into a
more effective one-way valve.

There is also the Stretta procedure
( This treats the LES
directly, stimulating collagen deposition in the substance of the LES and
thereby tightening it up, as well as ablating afferent nerve fibers to the
LES that contribute to transient inappropriate LES relaxation. It's very
effective, entirely outpatient, return-to-work-the-next-day. It's not
appropriate for everybody, but can be an excellent tool.

There are some other technologies for anti-reflux. Endo-cinch
(  has been around awhile, but is
dying AFAIK, since it doesn't work, according to randomized prospective
testing based on post-procedure pH testing.

Medtronic will be marketing GateKeeper, another method of LES repair This procedure has
been in development by Endonetics since before the concept of transient
inappropriate LES relaxation was perceived as an important factor in GERD,
and GateKeeper doesn't address that problem. Still in clinical trials, it
remains to be seen how effective it is in randomized prospective testing.

GERD in a nutshell, according to HMc.  FWIW. Sorry for the length of the

From: "Howard McCollister" <>
Subject: Re: dysphagia or GERD?
Date: 4 May 2003 00:52:13 -0500
Message-ID: <3eb4857b$0$37857$>

" CBI" <00doc at mindspring dot com> wrote in message

> OK - so what do you do with those people who you don't do an anti-reflux
> proceudure on besides lifestyle modification? Specifically, I'm wondering if
> you use prokinetic agents, such as  Reglan,  more or earlier than others.
> --

I do use Reglan, but I have not been impressed that it's very useful. IMHO
it tends to act more efficaciously in the stomach than in the espohagus.
Propulsid (cisapride) was a much better drug as a prokinetic agent for
treatment of reflux, but there was that pesky ventricular fibrillation issue
and it's off the market.

People come to me and I lay out their options. If they don't have EGD
evidence of reflux damage, I advise lifestyle mods and put them on meds to
try to control their symptoms, but I put them on an EGD recall list so we
can do followup EGDs every 2-5 years for surveillance for Barrett's etc. If
those measures don't do the trick and they do get reflux damage or remain
symptomatic, I tell them we need to stop their reflux and the options are
religious adherence to the lifestyle mods, maybe Reglan, laparoscopic
gastric fundoplication, or Stretta procedure.


From: "Howard McCollister" <>
Subject: Re: dysphagia or GERD?
Date: 3 May 2003 13:30:32 -0500
Message-ID: <3eb40945$0$71556$>

" CBI" <00doc at mindspring dot com> wrote in message
> "Howard McCollister" <> wrote in message
> news:3eb2c36d$0$34126$
> >
> >
> >  It is now known that, somehow, H Pylori does protect against GERD and
> >  it's complications to some degree, although the mechanisms are not
> >  clear.
> The explanation I have always heard was that the inflammation of the
> stomach caused less acid to be produced. Is there some thinking that
> there is more (or less) to it than that?
> --

The current concept is just that AFAIK; the presence of H Pylori decreases
the potency of the refluxate. However the data is very unclear, at least in
my mind. The data is conflicting relative to whether or not this applies
just to patients with H Pylori-mediated clinically evident inflammation or
includes patients who are (or have been) H Pylori-positive but have no
clinical symptoms. Is it the inflammation, or just the presence of H Pylori,
or only H Pylori-mediated inflammation? Honestly, I don't know.

Throw into the mix the fact that some doctors that will empirically treat
someone for H Pylori only on the basis of UGI symptoms. Then there is the
question of treating them only on the basis of H Pylori-postive serum
antibody testing, and then again the question of treating those symptomatic
patients based only on urease-positive breath testing. These studies don't
tell me much about the protective role of H Pylori in GERD, but they do make
me more convinced that H Pylori should only be treated on the basis of
EGD-observed gastro-duodenal inflammation/ulceration that are
biopsy-positive for the organism on H&E stain or direct urease testing (CLO
or HP-Fast etc).


From: "Howard McCollister" <>
Subject: Re: dysphagia or GERD?
Date: 4 May 2003 10:07:52 -0500
Message-ID: <3eb52bc0$0$50385$>

"Tursica123" <> wrote in message
> McCollister wrote:
> Hiatus hernias are not dangerous. Prolonged *acid reflux* (not hiatus
> hernia) can predispose to *esophageal* cancer. Hiatus hernia and acid
> reflux are *not* the same thing. The definitive test for hiatus hernia
> is upper GI endoscopy -- barium swallow is almost useless in such
> diagnosis. You can't treat hiatus hernia with medicine any more than you
> can treat an inguinal hernia with medicine.
> I would take issue with these statements!
> First of all, hiatal hernias can often be associated with reflux since
> the GE junction is abnormal.  You cant treat a hiatal hernia per se, but
> you can treat the reflux symptoms.
> Secondly, barium UGI is probably better at delineating the anatomy of
> the hiatal hernia in relation to the hiatus, especially with complex
> hiatal hernias.  If I had a patient with a suspected hiatal hernia
> and/or dysphagia, I think UGI is a better 1st line test as it is less
> invasive and often more informative.
> Finally, a hiatal hernia can be dangerous.  Type 2 and 3 hernias can
> incarcerate and strangulate the stomach.  Although, this is rare.  But
> it is often the justification for surgically repairing an otherwise
> asymptomatic hiatal hernia.

First, I agree that hiatus hernia can be associated with reflux. However,
the GE junction is not necessarily abnormal, but does happen to be
abnormally located part of the time which subtracts from it's resting
pressure. Technically, you are correct, of course.

Second, what would prompt you to believe the patient had a hiatus hernia?
You mean he came in complaining of reflux symptoms, right? In which case
you're ordering a UGI, why? To evaluate effects of the patient's reflux?
Pointless. What do you tell the patient if the UGI is negative? I don't
understand why doctors think UGI is a useful test in the frontline diagnosis
and treatment of GERD.

So you diagnose a hiatus hernia (the 1 in 3 cases where UGI picks it up).
The hiatus hernia isn't important, it's the condition of the distal
esophagus, especially the presence of Barrett's esophagus. How is the UGI
going to help you determine whether or not this hiatus hernia is clinically
significant, doctor? Personally, I would consider ordering a UGI if I found
a paraesophageal hernia at EGD, otherwise, it is of no value in this
circumstance. It has a high false negative rate, and has little or no
diagnostic relevance to the disease you are trying to diagnose and treat --

Third, old doctors like me refer to Type 2 and Type 3 hiatus hernias as
paraesophageal hernias. Technically, you are correct again. However, try to
view that post in the context of the reply to Richard's reply. You might be
inclined to think of me more as a hotheaded surgeon trying to make a point
as opposed to an ignorant fool.


From: "Howard McCollister" <>
Subject: Re: dysphagia or GERD?
Date: 4 May 2003 19:34:17 -0500
Message-ID: <3eb5b0f5$0$81623$>

"Tursica123" <> wrote in message

> I agree that endoscopy plays a major role in assessing upper GI
> complaints. It's strenghth is mainly in assessing mucosal changes as
> well as the ability to biopsy and treat (dilate).  I think UGI is better
> at defining the anatomy of the stomach in relation to the hiatus and
> diaphragm and assessing gastric emptying. As you said, UGI is
> particularily good for evaluating complex paraesophageal hernias (Type 2
> and 3).
> I just dont want people to think that all hiatal hernias are benign and
> have no relationship to GERD symptoms.  I also dont want people to think
> that barium is an outdated test.

I don't disagree that I overstated the case a little about the benignancy of
hiatus hernia relative to it's contribution to GERD.

As to UGI, I believe that the anatomical relationship of the GEJ to the
hiatus is of little importance in the primary investigation of GERD. In the
case of GERD alone, the presence or absence, as well as size of a hiatus
hernia can be more sensitively determined by EGD. More importantly, it's
clinical relevance can be determined with EGD by accurate mucosal
evaluation, whereas UGI contributes little or nothing to that. I'm saying
that with GERD, it's the mucosa, not the anatomy, and (for the most part)
not the function either. Not in the initial workup. Naturally, esophageal
function must be evaluated at some point -- at the very least,
preoperatively. But in plain ol' GERD, all relevant information is gathered
by EGD, ambulatory pH testing, and manometry. UGI brings nothing to the

Having said that, I agree that I would get a UGI before an EGD in a patient
whose primary complaint was dysphagia only, or in any other situation where
I felt that the patient's symptoms might relate to abnormalities of
esophageal or gastric function. It won't replace manometry for accurate
evaluation of esophageal dysmotility, but in many of those situations, UGI
can provide a nice overview of upper GI relationships. There is a fairly
large subset of GERD patients whose primary complaint is chest pain, or
dysphagia. In fact, only about 40% of GERD patients complain of classic

I order many barium studies for one reason or another, and I don't think
contrast GI studies are outdated either. It's just that in many areas, as
has been common in medicine, they have been superceded by tests that have
been shown to be more sensitive, more specific, and more diagnostically


From: "Howard McCollister" <>
Subject: Re: dysphagia or GERD?
Date: 4 May 2003 10:19:25 -0500
Message-ID: <3eb52ed2$0$34171$>

"Terri" <> wrote in message
> Howard McCollister wrote:
> >
> > " CBI" <00doc at mindspring dot com> wrote in message
> > news:b91pmp$hde$
> >
> > >
> > > OK - so what do you do with those people who you don't do an
> > > anti-reflux proceudure on besides lifestyle modification?
> > > Specifically, I'm wondering if you use prokinetic agents, such as
> > > Reglan, more or earlier than others.
> > >
> > > --
> > > CBI, MD
> > >
> > >
> >
> > I do use Reglan, but I have not been impressed that it's very useful.
> > IMHO it tends to act more efficaciously in the stomach than in the
> > espohagus. Propulsid (cisapride) was a much better drug as a
> > prokinetic agent for treatment of reflux, but there was that pesky
> > ventricular fibrillation issue and it's off the market.
> > 
> > People come to me and I lay out their options. If they don't have EGD
> > evidence of reflux damage, I advise lifestyle mods and put them on
> > meds to try to control their symptoms, but I put them on an EGD recall
> > list so we can do followup EGDs every 2-5 years for surveillance for
> > Barrett's etc. If those measures don't do the trick and they do get
> > reflux damage or remain symptomatic, I tell them we need to stop their
> > reflux and the options are religious adherence to the lifestyle mods,
> > maybe Reglan, laparoscopic gastric fundoplication, or Stretta
> > procedure.
> >
> > HMc
> Nice to see my questions asked and answered before I've even figured out
> how to formulate the question. Thanks, both of you.
> If religious adherence to lifestyle modifications *without meds*
> controls the "heartburn" for the most part (heartburn once a month or so
> treated with a couple of gaviscon tablets) does surveillance still need
> to be continued? Would this scenario fall into the once every 5 years
> follow-up rather than every 2? If I read your detailed response from
> yesterday correctly, you would recommend surgical correction of the
> mechanical problem for anyone with reflux damage. Is this still true if
> the lifestyle modifications work to cure the symptoms? I guess what I'm
> really asking is how significant is the degree and frequency of
> heartburn?
> In my brother's case he had had severe heartburn for many years (20+)
> that he had treated with otc antacids and for which he had never sought
> medical attention, but he says it had actually pretty much disappeared
> for the past 5 years or so. I'm making a wild assumption that the reflux
> of the acid into his esophagus over the years had finally destroyed the
> nerve fibers in the esophageal lining that should have carried the
> heartburn "message" and that's why his heartburn stopped. Is that
> possible? Difficulty swallowing and pain on eating was what sent him in
> search of medical attention a little more than 6 weeks ago, a search
> that resulted in the diagnosis of esophageal cancer. In retrospect
> (hindsight being 20-20) he says that he had had some slight difficulty
> with eating for more than 8 months but had shrugged it off as of no
> significance.
> Terri

If there is damage or change to the distal esophagus, I  would recommend
surgical correction of the reflux as one option, and try to make the patient
aware of the consequences of the condition of their lower esophagus. The
patients may opt for surveillance, in fact most do if their symptoms are
under control. As to the timing of followup EGDs, I would be inclined to use
a shorter interval in patients with severe signs or symptoms, longer in
patients with a more normal appearing esophagus and whose symptoms are under
good control.

Yes, it is very common for people with advanced Barrett's to come in with a
history of  severe heartburn, and then it kind of "went away a few years
ago, doc". I see this all the time, and it makes it harder to convince those
patients that they have a problem and submit to yearly EGD and biopsy. Your
postulated mechanism of "burned out" nerve fibers appears to be very close
to the mark. I have heard your brother's scenario many, many times.


From: "Howard McCollister" <>
Subject: Re: dysphagia or GERD?
Date: 5 May 2003 18:52:32 -0500
Message-ID: <3eb6f89b$0$34189$>

"J" <> wrote in message
> Howard McCollister wrote:
> > "Yes, it is very common for people with advanced Barrett's to come in
> > with a history of severe heartburn, and then it kind of "went away a
> > few years ago, doc". I see this all the time, and it makes it harder
> > to convince those patients that they have a problem and submit to
> > yearly EGD and biopsy. Your postulated mechanism of "burned out" nerve
> > fibers appears to be very close to the mark. I have heard your
> > brother's scenario many, many times.
> Well, that's scarey !  Because I haven't had heartburn for over 20
> years, yet I have GERD and swallowing problems.
> Years ago, if I ate too much and bent over, I could feel it come up.
> So does the tissue harden (scar?) so that on EGD (and no biopsy) the GI
> doctor could perhaps be fooled into thinking there's nothing wrong?
> Or what triggers from the above state to cancer? bad luck?
> J

There are many factors that can contribute to swallowing problems, including
esophageal dysmotility. It may not relate to anatomic abnormalities of the
LES, including hiatus hernia. Esophageal dysmotility can be a function of
longstanding GERD, contibuting to poor function of the esophagus with
resultant swallowing problems. Definitive test would be 48 hour ambulatory
pH testing and esophageal manometry. EGD is definitive for Barretts
esophagus, at least in the hands of someone who knows what to look for.

Your esophageal problems have been a long odyssey. I don't recall whether or
not you have had pH testing, but if not, I would find that baffling since
that is how the diagnosis of GERD is made. Esophageal manometry would
likewise be a crucial test in the workup of your swallowing problems. As I
stated (somewhere, I'm sure), the diagnosis of hiatus hernia does not
necessarily imply GERD, and vice versa.

Ambulatory pH testing is how GERD is diagnosed. EGD does not diagnose GERD,
it diagnoses the *compications* of GERD. UGI is less valuable for that.
Stricture, that's about it.

As to which long standing GERD with Barrett's esophagus develop cancer of
the esophagus, bad luck does play a role. Think of it like lung cancer. Not
all long term smokers develop lung cancer.


From: "Howard McCollister" <>
Subject: Re: Upper Esophagus Acid Reflux
Date: 1 Aug 2003 20:41:25 -0500
Message-ID: <3f2b1618$0$5416$>

"Steve Harris" <> wrote in message
> "Howard McCollister" wrote in message
> news:3f1e1d0e$0$99072$
> > Most doctors erroneously treat acid reflux with medicine (proton pump
> > inhibitors such as Prilosec) and call it good, but this only treats
> > the symptoms, not the disease itself, by reducing or stopping the
> > symptom-causing acid in the refluxate.
> It's not an error. It not only treats the symptoms, but also
> the side effects down the line. You can die from the
> surgery. There is no evidence that anybody dies from
> decision to have drug treatment RATHER than surgery.
> In such a case, talk about curing the disease or the
> symptoms is silly. What you want is not to die.

The relationship between alkaline reflux and esophageal cancer is well
studied and documented ( Antireflux surgery is the
only method of preventing this, whereas as anti-secretory medication
exacerbates the problem by augmenting the precipitation of carcinogenic bile
salts in the stomach.

Treating the symptoms of acid reflux is fine if those symptoms are indeed
adequately treated and there is no evidence of end-stage GERD (Barrett's
esophagus). If there is, than such half-measures are inadequate.


From: "Howard McCollister" <>
Subject: Re: Upper Esophagus Acid Reflux
Date: 2 Aug 2003 15:52:12 -0500
Message-ID: <3f2c23e3$0$4937$>

"Steve Harris" <> wrote in message
> "Howard McCollister" <> wrote in message
> news:3f2b1618$0$5416$
> > Treating the symptoms of acid reflux is fine if those symptoms are
> > indeed adequately treated and there is no evidence of end-stage GERD
> > (Barrett's esophagus). If there is, than such half-measures are
> > inadequate.
> >
> > HMc
> The abstract I posted shows you are wrong. Now it's your
> turn to post randomized studies supporting your conclusion.
> Good luck.

I confess I didn't work very hard at completing your assignment, Steve. I
didn't really find any randomized studies. However, I am dismayed that you
give so much credence to the concept of drawing meaningful conclusions about
treatment of GERD relative to esophageal cancer based on a study with a mean
followup of 6 years. Until an ADEQUATE randomized prospective study comes
along, I am going to rely on the science of the subject.


Immunohistochemical study of p53, c-erbB-2, and PCNA in barrett's esophagus
with dysplasia and adenocarcinoma arising from experimental acid or alkaline
reflux model.

Kawaura Y, Tatsuzawa Y, Wakabayashi T, Ikeda N, Matsuda M, Nishihara S.

Department of Surgery, Ishikawaken Saiseikai Kanazawa Hospital, Japan.

PURPOSE: An immunohistochemical study of p53, c-erbB-2, and proliferating
cell nuclear antigen (PCNA) in Barrett's esophagus with dysplasia and
adenocarcinoma, arising from experimental acid or alkaline reflux, was
performed in dogs. METHODS: Cardiectomy was performed in group A (n = 26) as
an acid reflux model, and total gastrectomy was performed in group B (n =
24) as an alkaline reflux model. After surgery, the esophageal mucosa was
observed and biopsied endoscopically every 3 months over a period of 6
years. Immunohistochemical staining of p53. c-erbB-2, and PCNA was
performed, using biopsied specimens. RESULTS: In group A, Barrett's
esophagus developed in 14 of the 26 dogs. Low-grade dysplasia occurred in 5
of the 26 dogs, and in 1 of these 5 dogs, it developed into high-grade
dysplasia. In this animal, adenocarcinoma arose 63 months after the
operation. In group B, Barrett's esophagus developed in 10 of the 24 dogs.
Low-grade dysplasia was observed in 4 of the 24 dogs. In 1 of these 4 dogs,
the dysplasia became high-grade and adenocarcinoma occurred 66 months after
the operation. In group A, PCNA was positive in adenocarcinoma; the PCNA
labeling index (LI) was 58. c-erbB-2 and p53 were negative in all animals in
group A. In group B, PCNA was positive in Barrett's esophagus with
high-grade dysplasia and adenocarcinoma; the PCNA LI was 77. p53 was
positive in adenocarcinoma. c-erbB-2 was negative in adenocarcinoma.
CONCLUSIONS; The results of this study provided evidence of the
dysplasia-carcinoma sequence arising from alkaline reflux, as well as from
acid reflux. To the best of our knowledge, this is the first report of the
use of an alkaline reflux model and a 6-year study using dogs to observe the
course of Barrett's esophagus.

[Adenocarcinoma of the esophagogastric junction: association with Barrett
esophagus and gastroesophageal reflux--surgical results in 122 patients]

[Article in German]

Schumpelick V, Dreuw B, Ophoff K, Fass J.

Chirurgische Klinik, Medizinischen Fakultat, Rheinisch-Westfalische
Technische Hochschule (RWTH), Aachen.

OBJECTIVE: To investigate the surgical results of adenocarcinoma of the
esophagus and esophagogastric junction and its relationship with
gastroesophageal reflux disease (GERD) and Barrett's esophagus. Background:
The incidence of adenocarcinoma of the cardia is continuously rising.
Specialized intestinal metaplasia in Barrett's esophagus seems to be the
source of these tumors. Barrett's esophagus is end stage GERD. In
experimental studies alkaline reflux give rise of Barrett's esophagus and
adenocarcinoma. PATIENTS: 122 patients with adenocarcinoma of the cardia and
 121 patients with squamous cell tumor of the esophagus. METHODS: All
esophageal resections between 11/85 and 2/95 were retrospectively analyzed.
The relationship of gastroesophageal reflux disease, Barrett's esophagus and
malignancy was compared between both groups using parameters of case history
and histological sections. Survival was analyzed for tumorstage, T-and
N-stage and R-classification. RESULTS: 5.9% of the adenocarcinomas were
stage I, 44.1% stage II, 41. 5% stage III and 8.5% stage IV. Heartburn,
regurgitation, consumption of H2 blockers or Barrett's mucosa were
significantly more frequent for adenocarcinomas. A 5 year survival of 100%
was seen for stage I tumors. Invasion of t he muscular layer reduced
survival to 50%, lymph node invasion to 20%. R0-resection had a survival of
40%. CONCLUSIONS: A relationship of GERD and adenocarcinoma of the cardia
seems to be likely in our cases. Most patients had advanced malignancy.
Survival is good only for early cases. Prevention of tumor genesis with
effective antireflux surgery in case of alkaline reflux seem to be the best
therapeutic decision.

Increased expression of epidermal growth factor receptors in Barrett's
esophagus associated with alkaline reflux: a putative model for

Jankowski J, Hopwood D, Pringle R, Wormsley KG.

Department of Medicine, Dundee University.

A 49-yr-old male was reviewed who had a 10-yr history of reflux esophagitis.
He presented initially with frequent heartburn of moderate severity and, on
subsequent endoscopy, was noted to have erosive esophagitis and, at that
time, a high maximal gastric acid output. During the next 5 yr, his symptoms
and acid output diminished. Eight years after presentation, he was noted to
have developed a small area of Barrett's metaplasia, without dysplastic
change. Ten years after the initial presentation he was completely
asymptomatic, despite having extensive Barrett's metaplasia, now with high
grade dysplasia. As a result, he was referred for esophagogastrectomy. At
the time of surgery, he had alkaline reflux, with antacid gastric contents
and, subsequently, hypochlorhydria was proven by a pentagastrin test. A
second individual (male, 46 yr) who presented initially with reflux symptoms
and gastric-type metaplasia, underwent gastric secretory studies that
revealed a peak acid output of 16 mmol/L in 1986. During the period 1989 to
1991, his symptoms progressed despite H2 antagonist therapy. In this regard
he was reinvestigated, and his peak acid output in 1991 was 0 mmol/L, and
subsequent esophageal biopsies demonstrated intestinal metaplasia in four of
six biopsies (two biopsies had high-grade dysplasia; the two others had
gastric-type metaplasia). He has refused esophageal resection, and is being
reviewed regularly at the endoscopy clinic. Flow cytometric analysis of the
esophagus in both individuals revealed expression of epidermal growth factor
receptor which was increased in the areas of high grade dysplasia, compared
with Barrett's mucosa without dysplasia or normal cardiac mucosa. We
conclude that alkaline reflux may accelerate the development of Barrett's
esophagus (and intestinal type metaplasia) in patients with gastroesophageal
reflux disease. The increased expressed of epidermal growth factor receptors
in Barrett's mucosa with dysplasia compared with Barrett's mucosa without
dysplasia may reflect the higher malignant potential of the former mucosa.

Surgical therapy in Barrett's esophagus.

DeMeester TR, Attwood SE, Smyrk TC, Therkildsen DH, Hinder RA.

Creighton University School of Medicine, Department of Surgery, Omaha,

Seventy-six patients with Barrett's esophagus were cared for during a
10-year period. Fifty-six patients (74%) presented with complications of the
disease. There were 20 strictures, 7 giant ulcers, 11 cases of dysplasia,
and 29 patients with carcinoma. In patients with benign disease, 93% had
mechanically defective sphincters and 83% had peristaltic failure of the
lower esophageal body. Esophageal pH monitoring showed excessive esophageal
exposure to pH less than 4 in 93% and excessive exposure to pH more than 7
in 34% of the patients tested. Ninety-three per cent of patients with
excessive alkaline exposure had complications, compared to only 44% with
normal alkaline exposure (p less than 0.01). Gastric pH monitoring, serum
gastrin levels, and gastric acid analysis supported a duodenal source for
the alkaline exposure. Antireflux surgery was performed using Nissen
fundoplication in 30, Belsey partial fundoplication in 3, and Collis-Belsey
gastroplasty in 2. Six required resection with colon interposition. Good
symptomatic control was achieved in 77% after antireflux surgery. Four
patients had symptoms and signs of duodenogastric reflux; three required a
bile diversion procedure. Fifteen patients had an en bloc curative resection
with colon interposition. One patient with high-grade dysplasia on biopsy
was found to have intramucosal carcinoma after simple esophagectomy. Five
tumors were intramucosal, seven were intramural, and four were transmural.
Lymph node involvement occurred only in the latter two. Actuarial survival 5
years after curative resection was 53%. Median survival time for patients
after palliative resection or no resection was 12 months. Study of en bloc
specimens indicated that extent of resection should be adapted to extent of
disease: esophagectomy for intramucosal disease, en bloc esophagectomy with
splenic preservation for intramural and transmural disease. Serum CEA was
useful in detecting recurrent disease after surgery when the primary tumor
stained positively for CEA.

Role of intragastric and intraoesophageal alkalinisation in the genesis of
complications in Barrett's columnar lined lower oesophagus.

Attwood SE, Ball CS, Barlow AP, Jenkinson L, Norris TL, Watson A.

Department of Surgery, Royal Lancaster Infirmary.

Patients with Barrett's columnar lined lower oesophagus have severe acid
gastrooesophageal reflux and may develop complications, including
ulceration, stricture, and carcinoma. The aim of this study was to establish
if a relationship exists between the pH profile in the oesophagus and
stomach and the development of complications in patients with Barrett's
columnar lined lower oesophagus. Twenty four hour ambulatory oesophageal pH
monitoring was performed in 26 patients with Barrett's columnar lined lower
oesophagus and combined with 24 hour ambulatory gastric pH monitoring in 16.
Ten of the 26 with Barrett's columnar lined lower oesophagus had
complications including stricture (eight), deep ulceration (one), and
carcinoma (one). Oesophageal acid exposure (% time < pH 4) was similar in
patients with or without complications (19.2% v 19.3% p > 0.05). Oesophageal
alkaline exposure (% time > pH 7) was greater in patients with complications
(24.2% v 8.4% p > 0.05). Of the 16 patients who underwent gastric pH
monitoring there was a clear relationship between gastric and oesophageal
alkalinisation in 13. These results support the hypothesis that
complications in Barrett's columnar lined lower oesophagus develop in
association with increased exposure of the oesophagus to an alkaline
environment which appears to be secondary to duodenogastric reflux. The
routine use of 24 hour ambulatory gastric pH monitoring in conjunction with
oesophageal pH monitoring can help identify those patients at risk.

From: "Howard McCollister" <>
Subject: Re: Barrett's and cancers
Date: 5 Aug 2003 13:26:36 -0500
Message-ID: <3f2ff627$0$4943$>

"pbeyer" <> wrote in message

> Howard McCollister wrote:
> > "Steve Harris" <> wrote in message
> Appreciate that data is incomplete as to the outcomes of medical vs
> surgical treatment of GERD but hopefully lifestyle measures may have
> some value as they do in other cancers-- eg etoh avoidance, good diet,
> not smoking, etc.
> Pete

There is reason to be optimistic that  that may be correct. In terms of
esophageal cancer, the point is to stop reflux, not just stop the acid. If
one accepts that up to 80% of reflux episodes are due to transient
inappropriate lower esophageal sphincter relaxation, the lifestyle changes
you mention above, as well as some others, are important since all of those
things (alcohol, nicotine, some spicey foods, full stomach) will contribute
to those LES relaxations.


From: "Howard McCollister" <>
Subject: Re: GERD, allergies, or something else?
Date: 15 Aug 2003 12:27:10 -0500
Message-ID: <3f3d172f$0$66792$>

"mark peteritas" <> wrote in message
> Can H. Pylori cause esophagitis?  Has anyone had symptoms where it
> just feels like the esophagus is swollen/irritated?  I rarely ever get
> heartburn anymore, but the one thing I have noticed is, if I take
> prevacid 30mg twice a day, the symptoms become accutely worse.  This
> almost seems like an infection to me.  Interestingly, if I stop the
> prevacid for a day or so, I do get mild heartburn, but it actually
> feels sort of soothing, and I don't have the swollen feeling or
> difficulty swallowing while the heartburn is there.  I just can't
> stand this uncomfortable swallowing feeling.
> Anyone have any experience with something like this?
> I have an endoscopy scheduled for sept 2nd, and am doing a 24hour pH
> test on Sept 11, so hopefully those 2 tests will reveal something...

No, H. Pylori has nothing to do with GERD. In fact, for reasons that aren't
entirely clear, an H. pylori infection tends to ameliorate GERD.

The EGD and 24 hour ambulatory pH test will be definitive. The pH test will
tell whether or not you do have esophageal reflux, and the EGD will
demonstrate whether or not you have the COMPLICATIONS of GERD, such as
erosive esophagitis, stricture, or Barrett's esophagus.

24 hour catheter-based ambulatory pH testing is a little problematic and its
accuracy is impaired compared to more modern methods. It's important, while
the catheter is in place, to live a normal life. That is, eat the things you
normally eat, do your normal activities etc. These things are hard to do
when you have a tube down your nose connected to a device on your belt. A
better test is 48 hour wireless ambulatory pH testing. This test uses a
small, capsule-sized pH sensor that wireless transmits pH data to a
pager-sized device you wear on your belt, or keep within 4 or 5 feet of you.
There is no cather, it is completely comfortable, you can shower, eat or do
any other normal activity. It is far more accurate than catheter-based pH

Look at for information on this method of pH testing
and ask your gastroenterologist if it's available to you.


From: "Howard McCollister" <>
Subject: Re: GERD, allergies, or something else?
Date: 18 Aug 2003 22:51:05 -0500
Message-ID: <3f419e17$0$5665$>

"mark peteritas" <> wrote in message

>   I read about the Stretta procedure, which sounds
> interesting.  Has anyone had that procedure, or does anyone have any
> advice on it?

I have done the Stretta procedure many times. Patient selection is critical
to success of this procedure, but in the appropriate patient, it is an
excellent option. It is entirely outpatient, has very few complications,
very few side effects, and no activity or diet restrictions. The major
disadvantage is that it can take months for the effects to manifest
themselves. It has about an 80% - 90% success rate (off all meds within 1
year). Can't be done in patients with a large hiatus hernia. Relative to
anti-reflux procedures, I do about 60% lap fundoplications and 40% Stretta.

If you have a history of erosive esophagitis observed on EGD, then the pH
testing has little value since it is already established that you have
severe GERD and that is the point of pH testing. You will need esophageal
manometry, however, to make sure you have adequate esophageal function and
no underlying motility disorders.


From: "Howard McCollister" <>
Subject: Re: GERD, allergies, or something else?
Date: 22 Aug 2003 17:58:13 -0500
Message-ID: <3f469f55$0$307$>

"mark peteritas" <> wrote in message
> Thanks for the feedback.  I am definitely intrigued by the Stretta
> procedure.  I am very young (25 years old) to be having GERD this bad.
>  I want to weigh my options and make the appropriate choices, in terms
> of meds, or surgery, and if surgery, which one.  I have heard that the
> long term relapse rate is quite high with the lap fundoplications, and
> the complications such as dysphagia, difficulty belching, vomiting,
> etc., scare me a bit.  I like the idea of the Stretta procedure, but I
> guess it is too new to know if it will work long term (like for the
> rest of my life).  Do you have any thoughts on this?  Can a Stretta
> procedure be done more than once if needed?
> Last endoscopy, i was diagnosed with erosive esophagus (just 1 ulcer,
> I believe).  No hiatus hernia at that time (1.5 years ago).  I was on
> 30mg of prevacid since then, until it stopped working earlier this
> summer.  I am trying aciphex 20mg right now, but I can't tell if it is
> helping any better yet.  It just seems surprising to me that I could
> still have symptoms, while on prevacid 30mg, which is pretty strong,
> right?
> I will find out more results in a little over a week when I have
> another endoscopy done.
> Are there any chances that being on a moderate/high dose of PPIs can
> allow problems such as yeast esophagitis, or something of that nature
> to happen in an immuno-competant person?  I feel like I am digging
> with a question like that, but this came on very suddenly, and has
> been very persistant for a couple months.

At 25, with a history of erosive esophagitis , the chances that PPI's will
control your GERD for the rest of your life are negligible, even with
lifestyle modifications. Long term use of PPI's will result in increasing
polyp formation in your stomach due to the trophic changes of unopposed
gastrin, but there is no evidence to support the assertion that it will
increase your risk of gastric cancer.

Stretta is new. It's specific long-term effect isn't known. However, the
long term effects of radiofrequency energy on human tissue are known. Once
collagen is deposited in the LES, and the afferent nerves are ablated, the
science of the issue would lead one to believe that the effects are
permanent. There are no long term studies to prove this, however. Yes,
Stretta can be done more than once.

Lap fundoplication is a good operation. The recurrence rate is 6-10% at 5
years in competent hands, the specific recurrence rate is surgeon-dependant.
Dysphagia tends to be a temporary phenomenon, about 2-6 weeks and depends
very much on the pre-operative motility of the esophagus. The decreased
ability to belch can be problematic, but tends to decrease with time as the
patient learns to not swallow air (now that he doesn't need to do that to
clear acid from the esophagus). IME, most patients find that to be an
acceptable trade-off compared to a lifetime of poorly-controlled, or
uncontrolled, GERD.


From: "Howard McCollister" <>
Subject: Re: ENT or gastro doc for endoscopy? (aug 25)
Date: 25 Aug 2003 10:00:09 -0500
Message-ID: <3f4a23cb$0$53399$>

"Kilroy Bass" <> wrote in message
> What specialist is best recommended for endoscopy?  I went to ENT for
> throat pain, he said it might related to GERD.  He recommended surgery
> if symptoms persist in order to look in esophagus.  Unless he means
> endoscopy, I've read that gastroenterologists do endoscopies too.
> Is a ENT surgery the same as an endoscopy?  He said it might cost
> around $3000 with anesthesia and other stuff.  Or does ENT do the
> scalpel routine?
> Recommendations?

ENT doctors have nothing to do with GERD except for the occasions where the
reflux is so bad that it gets up into the posterior pharynx. In those cases,
they may stumble across the diagnosis that has apparently eluded your
primary care doctor for these many years.

You do indeed need an upper GI endoscopy (EGD), but the ENT doctor's role in
your diagnosis and treatment is over. Make an appointment to see a
gastroenterologist, or laparoendoscopic surgeon.

Be aware that EGD does not diagnose GERD, it only diagnoses the
*complications* of GERD such as erosive esophagitis, pre-cancerous Barrett's
esophagus, stricture. A negative EGD does not mean you don't have GERD, it
only means that your GERD hasn't damaged your esophagus. Yet.


From: "Howard McCollister" <>
Subject: Re: ENT or gastro doc for endoscopy? (aug 25)
Date: 26 Aug 2003 11:32:22 -0500
Message-ID: <3f4b4922$0$99704$>

"PF Riley" <> wrote in message
> On 25 Aug 2003 10:00:09 -0500, "Howard McCollister"
> <> wrote:
> >
> >Be aware that EGD does not diagnose GERD, it only diagnoses the
> >*complications* of GERD such as erosive esophagitis, pre-cancerous
> >Barrett's esophagus, stricture. A negative EGD does not mean you don't
> >have GERD, it only means that your GERD hasn't damaged your esophagus.
> >Yet.
> It sounds like a pet peeve of yours is when people think EGD is done
> to "rule out" GERD.

Yes, it is. I see this all the time. Patients come in with years of
disabling GERD symptoms. I suggest reflux and they say no, they had an EGD
and were told it was normal and that they therefore they couldn't have GERD.
Or worse, their doctor has tried to diagnose their GERD with an Upper GI
xray contrast study. UGI xray for simple GERD is a waste of electrons.


From: "Howard McCollister" <>
Subject: Re: ENT or gastro doc for endoscopy? (aug 25)
Date: 26 Aug 2003 13:46:50 -0500
Message-ID: <3f4b7336$0$2491$>

"Orac" <> wrote in message
> Correct. Most cases of GERD are diagnosed clinically, although it is
> possible to do esophageal manometry and pH monitoring to produce hard
> evidence of GERD in the absence of esophagitis or Barrett's esophagus.
> It IS important to make sure these complications have not yet occurred.
> --

Yes. But I do believe that pH testing is uneccessary if the patient without
esophageal damage on EGD responds to the empiric use of anti-secretory
medication and/or lifestyle changes.

If they DO have erosive esophagitis, stricture, Barrett's, then pH testing
is likewise uneccesary since those findings clearly make the diagnosis of
severe GERD, and pH testing adds nothing.


From: "Howard McCollister" <>
Subject: Re: ENT or gastro doc for endoscopy? (aug 25)
Date: 27 Aug 2003 14:54:27 -0500
Message-ID: <3f4d0389$0$97272$>

"Kent H." <> wrote in message
> Remember Howard that the first endoscopists were the nosepickers. Other
> than recognizing that I would agree with your comment.

Certainly, but I was responding based on the modern practice of medicine.
The first endoscopist may very well have been Galen, but that's not any more
relevant to this poster's situation in the here-and-now than any other
aspect of ancient endoscopic history. And if you want to acknowledge
history, don't forget to give homage to surgeons next time you get your hair
cut. ;)

ENT specialists haven't been doing upper GI endoscopy at any point in the 30
years since I started medical school. There was a time when you could get
your ears cleaned, your tonsils removed, and your vision refracted all in
the same office visit by the same (EENT) specialist, too. But that also is
about as relevant as my med school pharmacology class.

History is interesting, and instructive, but one has to be careful not to
let the past influence the present too much, which happens too often in this
line of work. Medicine already has plenty of curmudgeons.


From: "Howard McCollister" <>
Subject: Re: Abdominal bloating and water retention?
Date: 14 Jan 2004 15:26:14 -0600
Message-ID: <4005b355$0$70185$>

"jhaviland" <> wrote in message
> I've been to my doctor and she didn't have any firm ideas why I am
> bloating so significantly.  I would like to have any ideas for the
> next time I see her.
> I am a 51 year old postmenopausal woman, in generally good health.
> Over the past week and a half, I've gained about 10 lbs of what seems
> to be fluid in my gut area.  I had some bloating in the 2 weeks
> previous but much less.  My doctor prescribed laxatives, both
> stimulant and bulk, drinking 8-10 glasses of water, and PrevAcid and
> another GERD reducing agent metroclopramide.  The idea was to 'blast'
> out my gut.  This happened but didn't reduce the bloating although I'm
> more able to eat now without reflux.
> Previous to this I had trouble with GERD and taken Pepcid and Prilosec
> in the last month.  I had also changed my diet to eliminate caffine
> and other irritating foods.  I don't have a fever, have no history of
> liver disease, and am not taking other meds.  My diastolic blood
> pressure was up for me (110/80) but not greatly.
> Any ideas?   I've very uncomfortable and not able to function
> normally.

When people with GERD complain of bloating, the usual cause by far is air
swallowing. This is common in such patients as a means of clearing the
esophagus of refluxed stomach acid. The stomach becomes distended with air.
Some of that air is belched out, but a lot of it passes on into the
intestinal tract, which also becomes distended with air, causing the
bloating you describe.

Fortunately, such bloating is not dangerous; just uncomfortable.
Unfortunately, there is no good way to treat it. You will see a lot of
advertisements for surfactants (Gas-X) - but these just turn small bubbles
into large bubbles. The total volume of air is unchanged and you will still
be bloated. Enzymatic agents such as BeanO will only affect the methane gas
that is produced by digestion of some foods, won't affect swallowed air.

The only solution is to tell you to stop swallowing air. I'm sorry that I
can't give you any advice on how to do that...


From: "Howard McCollister" <>
Subject: Re: New Medical Device? .. (Stomach PH)
Date: 11 Aug 2004 11:55:14 -0500
Message-ID: <411a4eef$0$82995$>

"Ed Friedman" <> wrote in message

> As a side note, doctors who routinely use this test for stomach acid
> report that the vast majority of their patients who suffer from GERD,
> acid reflux, acid "indigestion", etc. exhibit hypochlorhydria instead of
> hyperchlorhydria.

The definitive diagnosis of GERD / "acid reflux" is made on the basis of
ambulatory pH testing, where a pH sensor is placed in the lower esophagus 6
cm above the lower esophageal sphincter. Acid refluxing into the esophagus
is documented over a 24-48 hour period.  The two entities may be confused if
based solely on clinical presentation but a very basic GERD workup will
easily distinguish symptomatic hypochlorhydria from GERD.


From: "Howard McCollister" <>
Subject: Re: spasm of the throat
Date: 11 Feb 2005 09:15:10 -0600
Message-ID: <420ccb58$0$12329$>

"Damian" <> wrote in message
>I had posted this on the asthma site and got 2 replys maybe someone
> here could be of help.
> I went to the ENT Dr. yesterday because I was having throat spasms. At
> the time it feels like I can't breath in or out, I start dry heaving and
> then vomit.  I will cough for a long time, maybe 2-3 days after.  I
> was very surprised when the Dr said this was all a part of my asthma. I
> thought something was wrong with my throat because sometimes my voice
> kind of goes off in two directions at the same time.  If I am in a crowd
> and have to raise my voice to talk the same thing happens.  He said it
> is probable someone's perfume or dust in the air. He is a really nice
> guy told me my pulm. Dr can treat this. It's not that I don't believe
> him I am just really surprised that all this is my asthma.
> My main question would be how do you treat throat symtoms?  Do inhalers
> help this?  And is my asthma out of control if this is happening 2-3
> times a week?  I have an appt. with the pulm Dr in a few weeks but
> would appreciate some feedback so I can hold my own during our
> conversation.

There's a distinct possibility that your throat problem AND your asthma are
due to GERD.

Only about 40% of people with acid reflux disease actually have typical
"heartburn". The other 60% have a variety of symptoms, including asthma,
hoarsness, and "throat problems".

I think your ENT doctor is not keeping up with his reading.


From: "Howard McCollister" <>
Subject: Re: spasm of the throat
Date: 14 Feb 2005 13:50:35 -0600
Message-ID: <4210ea36$0$21034$>

"Damian" <> wrote in message
> To Howard my asthma is from an industrial accident about 10 years ago.
> I am not saying I don't have reflux but I had some GI bleeding and they
> did an endoscopy wouldn't I have had some indication to the tissues
> that I had reflux?

No. Not necessarily. EGD won't diagnose GERD, it will only diagnose the
complications of GERD. Disabling and symptomatic GERD can be present in the
face of a completely normal EGD. Obviously, if EGD demonstrates the
complications of GERD (erosive esophagitis, stricture, Barrett's esophagus)
then GERD can be presumed. Otherwise, the only way to diagnose GERD
definitively is with ambulatory esophageal pH testing or impedance


From: "Howard McCollister" <>
Subject: Re: 24 Hour Ph Questions - 2nd try
Date: 18 Mar 2005 07:14:02 -0600
Message-ID: <423ad3a7$0$11317$>

"Pete" <> wrote in message
> Hi everyone,
> I am sending this again in hopes that someone can comment on the
> questions I had about the 24 hour ph test I had recently.
> I have written the group in the past.  I currently take 20 mg of
> prilosec in the morning and it seems to be working after the previous
> PPI (prevacid) that I took for seven years stopped working.  I tried
> Protonix after that and it didn't work either.  I tried both at high
> doses.  I went through hell and lost my old gastro after he cut my
> fundic polyps twice (which I believe had something to do with my
> prevacid ceasing to work - you may recall this story).
> I am on my last gastro where I live (Hagerstown, MD) and he is from the
> older school and doesn't believe in cutting hyperplastic fundic polyps
> (I believe the younger doctors like to remove them).  I don't know what
> I can do if the PPI's keep making the polyps grow or if the prilosec
> stops working.  Surgery is out of the question.
> I went to Baltimore (Univ of Maryland) to get a second opinion and the
> gastro recommended a 24 hour ph and manometry, and for my current gastro
> to take some specimens in my duodenum in my next EGD to check for
> lymphangectasia (which is a one in a million and usually results in
> diarrhea which I don't have - I think this will be a waste of time and
> an unnecessary invasion).
> I have a copy of the 24 hour ph report and manometry, which was done by
> another university gastro who works in the "swallowing center".  They
> don't do the test where I live.
> I have some questions about the test results that make no sense to me.
> I tried to ask my gastro today and he didn't even know they mailed him a
> copy of the test report, and had to go fumbling through my chart looking
> for it, and he could not answer my questions and said he would have to
> look at the graphs I was referring to later.  I don't think he knew how
> to read them, or had ever seen a report like this before, because he
> does not order the test.
> I am an engineer and study medicine, and am pretty good at reading
> charts and graphs, and I could easily see how to interpret the ph
> waveform which has the 24 hours (in military time) on the x-axis and the
> ph values on the y-axis (one set for the proximal sensor which was 5 cm
> above the LES and the other set for the distal sensor which is about 10
> cm in the stomach below the LES - total of 15 cm between sensors).
> Sorry for the long lead in.  My main question is as follows.  I consider
> the stomach to be a reservoir and have an ambient ph value which would
> be mimicked in the esophagus as you refluxed up acid and acid fumes (or
> bile) into the esophagus.  Therefore, I do not see how the ph of the
> esophagus can ever be lower than that of the stomach unless a puddle of
> acid is sitting in the esophagus and the LES remains closed and the
> stomach went from acid to basic all of a sudden (perhaps from refluxing
> bile through the pyloric sphincter into the stomach).
> Anyway, from 3:30 AM til 9:00 AM (recumbent position), the ph in my
> stomach was significantly higher than the ph in my esophagus [stomach
> was 7-8 and above (graph stops at 8), and the esophagus was approx in
> the 6 range].  I got up around 9:15 AM, and the stomach ph still stayed
> higher than the esophagus (but not as pronounced) until I had the probe
> removed around noon. The histogram analysis also clearly indicates a
> higher percentage of the time that the stomach was above ph 7 versus the
> esophagus.
> Twenty mg's of Prilosec will not raise the ph of the stomach near that
> much and I believe the stomach acidity should go up during the night
> (i.e. lower ph) as the PPI wears off after taking it in the morning.  My
> stomach acid decreased during the night (after 3:30 AM) and even went to
> the basic side of the neutral 7.0.  This makes no sense to me unless I
> am refluxing bile into the stomach, and if so why didn't the bile also
> reflux into the esophagus, unless the LES stayed tight.  Incidentally
> the stomach ph was significantly more acid than the esophagus between
> 12:30 AM (when I went to bed) and 3:00 AM.
> I will quote the "impression" the gastro wrote in the report.  "Gastric
> acid breakthrough late in the day and at night as expected on PPI qAM
> without evidence of associated pathologic gastroesophageal reflux".  I
> don't agree with this because of my statements above, and I saw no acid
> breakthrough after 11:30 PM (I assume acid breakthrough means the ph of
> the esophagus dropping below 4 - correct me if I'm wrong).  He wrote
> nothing about this quandary I am asking about.
> I apologize for this being so long but I was trying to save you from
> saying you need more information, etc. If I could show you the charts it
> would all be there.  I know that basic can burn just as bad as acid, but
> I can not live without the PPI acid blockers.  If I stop them I will
> start burning within a day, and the H2 blockers don't touch it.
> Please comment on this the best you can.  It's a shame I can't talk to
> my doctor about this.  I tried.  Thanks for reading this and I look
> forward to your comments.
> Pete

Ambulatory pH testing is pretty straightforward, and it appears that you are
overthinking the test and results.

If you are getting acid in your esophagus more than about 4% of the time, or
if your DeMeester score is more than about 15, especially on PPI's, then you
have acid reflux. Acid reflux is defined as esophageal pH less than 4.
Normal esophageal pH is about 6, anything higher than that usually indicates
alkaline reflux. Nightime reflux may be related to PPIs wearing off, but are
far more likely to be related to the recumbant position.

Normally, it would be considered pointless to do a pH test while a patient
is on PPIs, and I rarely, rarely would do that. The idea is to determine if
there is reflux, and under what conditions, and how much of the time. If
there is, that reflux can be addressed by the usual manner and the point is
to control the symptoms. PPI do not stop reflux, they only change the nature
of the refluxate. The problem is not the acid, it's the acid in the
esophagus permitted by a dysfunctional LES. When we discuss PPIs or any
other anti-secretory medication, we're talking about symptomatic treatment

So, it's apparent that you have GERD - there appears to be no question about
that. The only other question that needs to be addressed is whether or not
your medications are controlling your symptoms to your satisfaction. If you
have no endoscopic evidence of Barrett's esophagus, stricture, or erosive
esophagitis, and the medication is keeping you comfortable, then you need do
nothing further except for periodic surveillance (by EGD), every two years
or so. If medication isn't controlling your symptoms to your satisfaction,
then you will need to consider some sort of anti-reflux procedure. Enteryx
and Stretta are effective about 70% of the time. Nissen fundoplication is
successful about 93% of the time (initially), but has as much as a 20-25%
failure rate over the succeeding 10 years.

I am currently out of the country in the remote central highlands of Haiti.
My internet access has been spotty due to problems with our satellite link.
I'll be glad to help you, but it will be a week or so before I have
unfettered access to the internet.


From: "Howard McCollister" <>
Subject: Re: 24 Hour Ph Questions - 2nd try
Date: 18 Mar 2005 14:50:13 -0600
Message-ID: <423b3ea8$0$11883$>

"Pete" <> wrote in message
> Howard...thank you for your response.  Could you please address my main
> concern as to why my esophagus had a higher ph than my stomach after
> 3:30 AM (I explained it in detail in my message).  This does not make
> sense unless my possible explanation is valid.  Thank you...Pete

There could be many reasons, but IMHO they don't make any difference
relative to your problem with GERD. It could be as simple as acid in the
esophagus and acid + bile in the stomach. From my review of what you've
posted here, I fail to understand why your doctor would care about gastric
pH. My simplistic surgeon's-view of your situation leaves me interested only
in acid in your esophagus - how often and under what circumstances.


From: "Howard McCollister" <>
Subject: Re: Burping excessively
Date: 10 Apr 2005 15:23:02 -0500
Message-ID: <42598ad5$0$50257$>

"Mitch" <> wrote in message
> Yes ... she is probably suffering from a Hiatal Hernia that is causing
> acid reflux.  It is incredibly painful and awful to deal with.  It can
> take many years to cure this condition which requires smaller meals,
> less acid, more exercise and more water ... things like citrus juice
> and coffee need to be sacrificed completely.
> What she should not do is get hooked on drugs like Prevacid and
> Prilosec and other heartburn medication.  All that does is kill the
> acid in the stomach to stop the gas, but that doesn't stop the problem,
> it only masks it.

Excessive belching and bloating in patients with GERD is caused by air
swallowing, which the patient does, more or less unconciously, in order to
clear the lower esophagus of the refluxate.

The cause of GERD is a malfunction of the lower esophageal sphincter, either
a low resting pressure, or transient inappropriate LES relaxation.
Esophageal reflux occurs when the pressure in the stomach exceeds the
contraction pressure of the LES at any given moment. The term "hiatus
hernia" refers to an anatomic abnormality where the upper part of the
stomach has actually slipped up into the doesn't describe any
kind of disease condition. Hiatus hernia can contribute to GERD, but doesn't
have to. Not all patients with hiatus hernia have GERD, and not all patients
with GERD have a hiatus hernia.


From: "Howard McCollister" <>
Subject: Re: Burping excessively
Date: 10 Apr 2005 18:11:02 -0500
Message-ID: <4259b226$0$50272$>

In article <42580ad2$0$14796$>,
> "Ryan" <> wrote:
>> Whenever my partner feels sick to the stomach she starts burping
>> consistently for hours. Nothing seems to stop it. It interrupts her
>> sleep and it makes her feel sicker. Tonight it was from overeating. She
>> has been burping for over 2 hours before bed with no sign of it ending.
>> Any ideas on what causes it? I've personally never known anyone to do
>> that before.

One of the things that contributes the most to transient inappropriate LES
relaxation is a full stomach. In addition, the full stomach increases the
pressure gradient across the already-inappropriately-relaxed LES making
reflux all the more likely. When patients do reflux gastric contents back
into their esophagus, the typical reaction is to swallow air to clear the
esophagus. It's easy to postulate your partner overeating, swallowing air to
clear the esophagus, belching the swallowed air, but the increased air in
the stomach makes it fuller, which in turn promotes more reflux, which
causes more air swallowing, and on and on it goes ad nauseum (literally).

Nothing to do about it, really. The only way the cycle can be broken is by
decreasing intragastric pressure, which will happen eventually as the
stomach empties itself. The key to keeping it from happening is to avoid
overeating, and avoid substances that decrease the LES tone, such as
alcohol, tobacco, caffiene, certain spices. Weight loss is also an important
component in GERD patients who are obese. That intraabdominal fat also will
contribute to increased intraabdominal pressure, which increases the
gradient across the LES.


From: "Howard McCollister" <>
Subject: Re: Pain after GERD Surgery
Date: 30 May 2005 14:11:02 -0500
Message-ID: <429b64ea$0$50307$>

"Peter Hutchins" <> wrote in message
> Howard,
> thanks for the reply.
> Nexium and other nmedications were completely ineffective prior to the
> operation and it was determined that she had severly damaged the bottom
> half of her eshophagus to the point where the muscles were no longer
> responding correctly when she swallowed food (a barium swallow test was
> performed as well as a pH test). She did have a haitus hernia and that too
> was repaired at the same time of the Fundoplication.
> As for her recovery, it started off as expected with liquid diets and
> gradually adding solid food. Motility we believe is much better as there
> is no issue with getting any food into the stomach...but there has been no
> suggestion of any manometry to assess that definitively.
> We have discussed the pain with the surgeon, and his reply was "wait and
> see" although he did order an EGD found nothing abnormal. In terms of
> follow-up tests, there was no post-op ambulatory pH test because it's
> believed that the operational was sucessful.
> At the request of the family doctor we've had CTScans, XRays, and
> breathing tests to determine if there is anything related to respiratory
> issues, but aside from hasn't turned up anything.
> What would you suggest? We're trying to educate ourselves and determine
> what approach we can take with the surgeon/family doctor so that  we can
> all decide on a plan of attack.

One of the most common causes of chest pain in GERD patients is an
esophageal motility disorder. Barium swallow as a means of diagnosing that
is a blunt tool in the extreme. In your wife's case, I would be all the more
suspicious of that because of the normal EGD and lack of response to PPI's

Esophageal manometry is far more accurate in assessing motility, either
station pull-through technique or (preferably) impedance manometry. Diffuse
esophageal spasm, hypertensive LES, or nutcracker esophagus are entities
that need to be ruled out and that can only be done by manometry. Barium
swallow will be of little or no help. I think that performing a
fundoplication without pre-op manometry is a deviation from the standards of
care. Hypertensive LES can be exacerbated by a full fundoplication and lead
to exactly the kinds of symptoms your wife describes.

The reason I would suggest repeat pH testing is that her problem is
exacerbated by lying down. One other thing to consider is that asthma is
part of GERD in about 40% of cases and goes away after successful
anti-reflux surgery. Her original asthma may have been atopic (allergic) in
nature, but the fact that she still has that at least suggests the
possibility that she's still having some reflux.


From: "Howard McCollister" <>
Subject: Re: Why No GI Transplants?
Date: 3 Sep 2005 08:21:02 -0500
Message-ID: <4319a2ee$0$281$>

"John Schutkeker" <> wrote in message
> "Howard McCollister" <> wrote in
> news:431843d5$0$235$
>> Esophageal replacement is done pretty routinely these days, using a
>> either a gastric tube (non-reversed) or a length of transverse colon.
>> Gavriliu's Operation (not Heimlich) is of historical interest only.
> Why aren't they both of historical interest?  Is Gavriliu a Frenchman?
> If so, has esophageal transplant ever been tried here in America?
> I'm trying to think of a way to do it without sacrificing part of my
> colon.  No doubt that will give me problem using the toilet, and I'd
> also be worried about sepsis from surgical exposure to the feces in my
> colon.
> The advantage of nobody doing transplants is that (putting aside the
> fact that the organs aren't being harvested) there will be a theoretical
> oversupply of organs.  That means that my odds of getting a good tissue
> match would be high.  Am I correct in concluding that should reduce my
> reliance on immunosuppressive drugs?
> The bad thing would be that it's an experimental procedure, and my
> insurance wouldn't cover it.  So I'd be in debt for a hundred grand when
> it was over.
>> State of the art is
>> laparoscopic/thoracoscopic esophagectomy with cervical
>> esophagogastrostomy.
> The great thing about this is that they're using stents now, which is a
> non-surgical alternative that's also state of the art.  I'm still at
> stage II erosive esophagitis, with no sign yet of Barrett's disease.
> But this has clearly become progressive, so it will be coming in the
> foreseeable future?
> How aggressive is Barrett's cancer?  That's a squamous cell carcinoma,
> right?  Isn't that a non-aggressive tumor?

You seem to be laboring under a number of serious misimpressions. Your
research has been incomplete, you have grossly misunderstood it, or your
doctor has done a poor job of explaining things to you.

Gavriliu's operation and the Heimlich operation are the same operation
(reversed gastric tube). They were both described in the '50's. Gavriliu did
it first, Hemilich did it several years later and took credit. It doesn't
matter, that operation is rarely done anymore and has no applicability to
your situation anyway.

Esophageal stenting is by no means "state of the art". They have been around
for decades, but are only used for frank cancers of the esophagus that can't
be cured. They are used for palliation only in patients who are terminal.
The only recent advance in stenting has been expanding mesh stents, which
are indeed an improvement over the old plastic Celestin tubes, but have
absolutely no place in someone who has erosive esophagitis only, or even
Barrett's esophagus. Palliation for terminal cancer. Only. If your doctor
were to suggest that you have an esophageal stent placed, he is saying to
you that you are going to die of your esophageal cancer within a matter of

There is no such thing as "Barrett's Cancer". Barrett's esophagus is not
cancer. It is a *pre* cancerous condition that sets the stage for the
possibility of adenocarcinoma (not squamous cell cancer) of the esophagus.
The majority of people with Barrett's esophagus will *not* develop
adenocarcinoma of the esophagus, just as not every smoker will develop lung
cancer. Your situation, you say, is that you don't even have Barrett's
esophagus, so I suppose you could say you have a pre-pre-pre-cancerous
condition. (reflux->Barrett's->Barrett's with dysplasia->adenocarcinoma).

Cancer of the esophagus, adenocarcinoma or squamous cell carcinoma, tends to
be aggressive and 5 year survival is very low.

As I said several posts ago, there are no esophageal transplants in the
sense that you are referring to. *IF* you were to develop severe dysplasia
in Barrett's esophagus (*very* precancerous), or *IF* you were to develop
frank invasive cancer of the esophagus, your surgeon would recommend an
operation where the esophagus is removed and the stomach is mobilized up
into your chest and connected to the esophageal remnant in the neck or
proximal chest. Note that this is not a "reversed-gastric tube". Also note
that this is not a transplant, it's just a "rearrangement" of your own
tissue. There is no potential for rejection - it is your own body tissue, so
no immunosuppressive drugs are needed. There are no esophageal transplants.
They don't harvest some dead guy's esophagus to put into you. About the only
circumstance where they would use your colon instead of your stomach is if
you had had previous gastric surgery that precluded the used of your

None of these things are experimental. They are all established therapies
that insurance companies pay for.

I don't know what "Stage II" erosive esophagitis is. Erosive esophagitis is
an *acute* condition that has to be addressed acutely and cured. It's
diagnosed only by EGD, is treated with high dose PPI medication (Nexium
etc), and a followup scope is indicated to be sure that the erosive
esophagitis is cured. If erosive esophagitis can't be controlled with
acid-suppressing medication, or if erosive esophagits keeps coming back,
then surgery is indicated to stop the reflux.

People who have GERD, especially with recurrent esophagitis, need ongoing
surveillance with EGD every 1-3 years to determine whether on not Barrett's
esophagus is developing or progressing.

You need to sit down with your doctor and clarify your situation and


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