Gastric Enterovirus Infection: A Possible Causative Etiology of Gastroparesis

weyland

Well-Known Member
Gastric Enterovirus Infection: A Possible Causative Etiology of Gastroparesis.

Barkin JA1, Czul F2, Barkin JS2, Klimas NG3, Rey IR3, Moshiree B2.
Author information


Abstract

BACKGROUND:

Gastroparesis (GP) is a disabling chronic gastroenterologic disorder with high morbidity that severely impacts patients' quality of life. GP can present acutely after a viral-like gastrointestinal illness resulting in speculation that in some patients, neurologic damage caused by the infection might underlie the pathogenesis of idiopathic gastroparesis (IGP).
AIMS:

The aim of this study is to document case reports of Enterovirus (EV) infection as a possible cause of IGP.
METHODS:

Eleven patients referred with a diagnosis of GP underwent workup to exclude known causes of GP. Those with a history of flu-like symptoms or gastroenteritis prior to onset of GP symptoms had gastric biopsies taken during upper endoscopy to assess for the presence ofgastric mucosal EV infection. Data on presenting symptoms, extra-intestinal symptoms and conditions, prior nutritional support requirements, upper endoscopy findings, and response to therapy were cataloged.
RESULTS:

Eleven patients were diagnosed as IGP. Nine had active EV infection on gastric biopsies and were included (7/9 female, mean age 43 years). Eight out of nine received EV treatment with antivirals and/or immune therapies, with a wide degree of variability in treatment regimens. Four out of eight who received EV treatment had symptomatic improvement. One patient had stable symptoms. Three patients are currently undergoing therapy.
CONCLUSIONS:

Gastric EV infection was frequently detected (82 %) in patients undergoing investigation for IGP. Antiviral and/or immune therapies against EV seem to be favorable, as most of our patients had resolution of their GP symptoms after treatment. This is the first study to identify EV as a possible infectious etiology of IGP.
Full text from sci-hub.

While not specifically on ME patients, over half of them did have ME and autonomic dysfunction in addition to gastroparesis. Nice to see some other ME clinicians looking at enteroviruses finally.
 

weyland

Well-Known Member
Some details on how they were treated:
Four of eight patients (50 %) who received EV treatment had symptomatic improvement (Table 2). Their treatment regimens were as follows: One treated with intravenous immunoglobulin (IVIG) alone; one treated with IVIG, ribavirin, Isoprinosine, Equilibrant, CoQ-10, and EnteraGam; one treated with IVIG, Isoprinosine, Equilibrant, and CoQ-10; and one treated with EnteraGam and naltrexone. Treatment agents used, along with dosage, interval, and duration varied widely by patient. In the two patients who received treatment and were previously on total parenteral nutrition (TPN), one was able to be weaned off of TPN completely along with deactivation of her gastric pacemaker, and the other was able to be weaned from daily to thrice weekly TPN, with stable weight. One patient who received treatment with CoQ-10 and naltrexone had stable symptoms. There are currently three patients (38 %) undergoing therapy and pending follow-up. One is being treated with IVIG and EnteraGam; one is being treated with IVIG, CoQ-10, naltrexone, Enteromend, and ImmunXT; and one is being treated with famciclovir, CoQ- 10, and naltrexone.
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
Full text from sci-hub.

While not specifically on ME patients, over half of them did have ME and autonomic dysfunction in addition to gastroparesis. Nice to see some other ME clinicians looking at enteroviruses finally.
Another post-viral onset group! And look at all that enterovirus infection. I wonder if they used a similar test as Dr. Chia????

And this is from Klimas! I completely missed this study - thanks for posting it!

Check this out regarding gastroparesis. I had no idea the vagus nerve controlled stomach contractions as well....wow...I gotta send this to someone.

Gastroparesis (gastro- from Ancient Greek γαστήρ gaster, "stomach" and πάρεσις -paresis, "partial paralysis"), also called delayed gastric emptying, is a medical condition consisting of a paresis (partial paralysis) of the stomach, resulting in food remaining in the stomach for an abnormally long time. Normally, the stomach contracts to move food down into the small intestine for additional digestion. The vagus nerve controls these contractions.

Gastroparesis may occur when the vagus nerve is damaged and the muscles of the stomach and intestines do not properly function. Food then moves slowly or stops moving through the digestive tract.
 

weyland

Well-Known Member
I haven't read the study but they must be ME/CFS patients with gastroporesis - no?
Yes exactly. It was a small study with only 11 patients, all diagnosed with idiopathic gastroparesis. 56% of those eleven patients also had ME and 56% also had confirmed autonomic dysfunction by tilt table.
 

Onslow

Active Member
A few points:

[1] They say 19%-32% of healthy controls have active EV infection, so that would tend to suggest that EV reactivates similar to HHV and what we're seeing in CFS is perhaps just reactivation.

[2] They don't seem to have established causality between the enterovirus infection and the gastroparesis.

[3] They (and others) speculate that gastroparesis is caused by viruses damaging the vagus nerve. However there isn't any evidence that that is the case. Given that gastroparesis tends to resolve by itself after a few days or a week by itself (I had it myself a number of times when I had CFS), that would tend to suggest that there isn't any "damage" as such. Also, given that we know that the brain causes reduced parasympathetic function even in healthy individuals after exercise (see the recent Japanese fatigue review posted by Cort), that would suggest that it is likely the brain causing the vagus nerve hypofunction, and that it is related causally to the fatigue (i.e. generated in the brain).
 

Remy

Administrator
Full text from sci-hub.

While not specifically on ME patients, over half of them did have ME and autonomic dysfunction in addition to gastroparesis. Nice to see some other ME clinicians looking at enteroviruses finally.
Interesting!

Wish they'd specified the doses they used though...especially for IVIG.
 

weyland

Well-Known Member
They say 19%-32% of healthy controls have active EV infection, so that would tend to suggest that EV reactivates similar to HHV and what we're seeing in CFS is perhaps just reactivation.
No, enterovirus doesn't reactivate because it lacks the ability to form latency in the first place.

[2] They don't seem to have established causality between the enterovirus infection and the gastroparesis.
They did, that was the point of the treatment. Half of the treated patients had symptomatic improvement.

Given that gastroparesis tends to resolve by itself after a few days or a week by itself
I'm guessing these patients wouldn't be on total parenteral nutrition or have gastric pacemarkers if they were just having a little bout of gastoparesis for a few days. These were likely chronic cases.
 

Onslow

Active Member
No, enterovirus doesn't reactivate because it lacks the ability to form latency in the first place.
Why do up to 32% of healthy, unsymptomatic controls have enterovirus infection then?

They did, that was the point of the treatment. Half of the treated patients had symptomatic improvement.
It was uncontrolled, so there are a variety of possible reasons for improvement.
 

weyland

Well-Known Member
Why do up to 32% of healthy, unsymptomatic controls have enterovirus infection then?
Because they are extremely common viruses that can cause transient asymptomatic infection in the gut mucosa of healthy people. It's already been shown in ME patients that the enterovirus infections present persist for months or years and moves beyond the gut into the muscles and brain and probably nerves as well.
 

Onslow

Active Member
Because they are extremely common viruses that can cause transient asymptomatic infection in the gut mucosa of healthy people. It's already been shown in ME patients that the enterovirus infections present persist for months or years and moves beyond the gut into the muscles and brain and probably nerves as well.
I don't think that has been shown at all. If so, please post a review (and not something by Chia reviewing his own work).
 

weyland

Well-Known Member
I don't think that has been shown at all. If so, please post a review (and not something by Chia reviewing his own work).
We don't only rely on secondary sources here, if that's what you want you should head back to wikipedia.

Myalgic encephalomyelitis--a persistent enteroviral infection?

Chronic enterovirus infection in patients with postviral fatigue syndrome.

Enteroviruses and postviral fatigue syndrome.

Enterovirus in the chronic fatigue syndrome.

Viral Isolation from Brain in Myalgic Encephalomyelitis
 
Last edited by a moderator:

Cort

Founder of Health Rising and Phoenix Rising
Staff member
I wish we had more certainty on the enterovirus infection in ME/CFS such as an outside lab validating Dr. Chia's findings. That would be huge, I would think, for his hypothesis. I can't understand why that has never happened.
 

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