Helicobacter pylori and sudden infant death syndrome
(10/26/00)
Dear Friends,
A number of articles hit the news the past few of days regarding Helicobacter
pylori and sudden infant death syndrome. The news refers to a study
published in the Archives of Diseases in Childhood titled, "An Association
Between Sudden Infant Death Syndrome (SIDS) and Helicobacter Pylori
Infection," led by J.R. Kerr of the Infectious Diseases Research Group at
the University of Manchester (U.K.). The public has been on an
information roller coaster, the result of an explosion of media reports. We need to help
people separate myth from fact and risk factor from cause. We will post information as it
becomes available to us.
Please keep the following in mind:
- A similar study made similar claims in 1997.
- The study's authors do not claim to have determined the cause of
SIDS.
- The study's authors do not present an explanation as to how a mild
infection caused by H Pylori can cause SIDS or sudden death. They
conclude that H Pylori infections increase SIDS risk, but offer no
explanation from this study as to how or whether they really do.
- When it comes to media coverage of SIDS, we often feel a sense of frustration in
being confronted with misleading headlines, announcements of so-called breakthroughs and
statements taken out of context.
- Please read the article, "Mass Media's" Role in SIDS Education, at <http://sids-network.org/media.htm>.
- You can search MEDLINE for pylori
and SIDS information.
We are currently gathering more information about this specific research and will keep
you updated.
Thanks!
Chuck Mihalko
Executive Manager
SIDS Network
Comments from the SIDS Alliance.
Proposed link between Helicobacter pylori and sudden infant death syndrome.
Pattison CP, Marshall BJ
Med Hypotheses 1997 Nov 49:5 365-9
Abstract
Helicobacter pylori may be linked to sudden infant death syndrome (SIDS)
through synthesis of inflammatory cytokines, particularly interleukin-1, which
can produce fever, activation of the immune system, and increased deep sleep. A
relatively minor respiratory or enteric infection, together with overwrapping
and prone sleep position could then induce terminal hypoxemia. Alternatively, H.
pylori produces large amounts of urease which, if aspirated in gastric juice,
could reach the alveolae, react with plasma urea, and produce ammonia toxicity
leading to respiratory arrest. Epidemiological similarities between H. pylori
and SIDS are presented along with possible transmission mechanisms for H. pylori
which support this hypothesis.
Author Address
Department of Medicine, Trinity Lutheran Hospital, Kansas City, Missouri,
USA.
Comments from Dr. Carl Hunt
22 Jun 1998
What do the DR's on this list think of this theory. It is the first thing I have
seen that I can relate to my baby. He had the reflux really bad, I brought it to my DR's
attention at his 2 month check-up, he said not to worry. It seemed worse when I fed him
formula. I breast fed him 95% of the time, but the night before he died I fed him 2 4oz
bottles of formula. Oh I would like an answer but I pray it is nothing I did-like feed him
formula.
The relationship between SIDS and gastroesophageal reflux remains very confusing and
controversial. Lots of babies have reflux and sometimes it can be a significant
problem----but it is not clear that this is associated with any increased risk for SIDS.
In regard to the recent animal data re Helicobacter pylori, I have not yet seen the
original data. However, based on what I have heard so far, it is much too premature to try
and relate these experimental findings to infants, whether in relation just to reflux or
in regard to potential impact on SIDS risk. Overall, clinical studies have indicated that
Helicobacter pylori, which is associated with stomach problems rather than reflux, is not
as significant a problem in infants in the SIDS age range as it is in older children and
adults.
Hope these comments are helpful.
Dr. Carl Hunt
January 13, 2003
On your website under the section dealing with Helicobacter pylori and
SIDS there is an item dated 22nd June 1998 with comments from Dr Carl Hunt.
Could this death have been caused by Anaphylaxis Shock? Consider our case!
Our daughter gave birth to a baby girl on 10th Sept. last. Healthy baby
and breast fed. Baby had a persistent navel infection which required 3 courses
of antibiotics to clear up. The 3rd course was intravenous and had to be given
in hospital so Mum and baby interned for a week. During this hospital stay the
baby was fed once, or perhaps twice, on factory prepared liquid formula without
any problems. After returning home our daughter decided to supplement breast
feeding with formula as she wanted to return to work this month. Baby at this
stage 9 weeks old. She used the same brand of formula at home as in hospital but
in the powdered form [this has different formulation]. First feed no problem.
After second feed she decided to change baby. As she was doing so baby turned
bright red and lost consciousness. Baby rushed to nearby hospital and revived
with steroids etc. We know of 3 other similar recent cases in counties Tipperary
and Cork. All switching from initial breastfeeding. All the babies were saved by
the prompt action of parents, hospitals and General Practitioners. Our
granddaughter might well have died had our daughter put her straight to bed. How
many SIDS deaths are due to Anaphylaxis Shock? Like the baby in the case on your
website our daughters baby suffered from reflux, now controlled by medication.
Fascinating medical history, and thank God for the good outcome!
SIDS infants do not die of anaphylaxis, at least there is no evidence given
IgE levels are not increased and the tissues do not show increased numbers of
eosinophils, and those present have not released their granules into the
surrounding tissues,
Reflux remains controversial with specific reference to SIDS. Unfortunately
most autopsies of SIDS cases do not include microscopic sections of the
gastroesophageal junction or the distal esophagus where the findings of chronic
reflux esophagitis (or for that matter, allergic esophagitis) can be identified.
In my experience when these sections are included, there is virtually no
evidence of chronic reflux. OF COURSE, it is important to remember also that
these SIDS infants are young and may not have had the reflux long enough to have
developed the tissue changes. No doubt the clinicians are able to address this
question better than a pathologist.
Good luck,
Henry Krous, MD
San Diego