Right, they don’t have the UG/GG products. They have their own “FDA” approved products (I don’t know their governing body. Equestra is a granular product, but they also have 3 others whose form I don’t know: Gastrozol, Ulcershield, Omoguard.
I have no idea the concentration/dosing of those products.
Not that I’m going to be relying on my math before I start dosing my horse, but at 4mg/kg for a 1300lb horse I’m getting 118 pills a day? (4mg X 590 kgs = 2360/20mg per pill = 118 pills). I’m eager for my math to be wrong because it seems like if that is an acceptable daily treatment rate, the 3 pills daily he travels on for shows probably isn’t doing anything more than the fig newton it is stuffed into…
The problem is they only studied that high dose so we have no idea if half that would do the same thing, as Simkie was working through. And yes, your math is right, which makes using esomeprazole at that level just as $$$ as using GG/UG, even assuming it would work the same way.
But also, they used a purposefully buffered paste, which isn’t the same as the “delicate” capsules and contained granules that are meant to be swallowed whole, not crunched.
The problem is, there are people who have pre and post scope results have had miserable success with 3 capsules a day.
AND, there are people who have proven success.
AND, there are people who have scoped poor results with UG/GG
AND, there are people who have scoped success with UG/GG
One of the things from Dr Sykes (edited because I had Nielsen on the brain) latest study on tapering was that horses don’t seem to have reliable results to X dose. Some had treatment results from preventive dosing, and vice versa. That’s also was Simkie was getting at by mentioning the relatively low healing rates of normal buffered omeprazole Is that because Australia’s buffered product isn’t buffered well enough? I don’t know (remember) the details about the UG/GG trials that got them approved to remember either the details of the study parameters to begin to start pointing at the idea that even that wasn’t (or was) pretty darn good. Given what’s known history of lots of horses not resolving the “right” ulcers with omeprazole I’d say it’s always been an issue of individual metabolism
and thanks, I have water up my nose now!
Research very rarely replaces what’s come before. It’s additive. This doesn’t negate the other studies.
This study used a whoppingly large esomeprazole dose. They don’t really explain why. It could be that someone is looking to bring an esomeprazole paste to market and wants data that shows it blows omeprazole away. They may also want a dose that makes winging it with OTC human options unattractive. This paper does both of those things. Or, the driver behind the dose here could be something else entirely. We don’t know.
As with all research, it needs to be taken in context and weighed against what else is out there.
@JB and @Simkie - all great points. Even at 2mg per kg, 50+ pills a day seems so high compared to 3. But your reasoning about 3 pills working in some, and not knowing the exact purpose of the study or why they chose the dose they did make a lot of sense.
Thanks Simkie for such a thoughtful analysis of this paper (genuine, not sarcastic, thanks, as I haven’t read it).
Just wanted to add (and not directed just at you) that anyone can email the corresponding author and ask clarifying questions! Often researchers are happy to discuss their work in more detail, though this is counterbalanced by their busy schedules. I’ve certainly happily answered questions from strangers about my research (provided they were asked politely, obviously). So if anyone genuinely wants to know why they chose the protocol they did, I would shoot the lead author an email and ask! The worst they can do is not respond 
Yes, absolutely! I’ve often emailed the lead author to ask questions. I get a response about 50% of the time and they’re usually just thrilled to talk about their research.
What’s interesting here is the corresponding author appears to be a consultant, based in the UK. The other authors are all AUS based vets. I’m not sure I’ve ever seen that before?
Oh, yeah. Here it is. Luoda Pharma is looking to bring a esomeprazole paste to the market.
“David Rendle provides consultancy services to BOVA Aus, BOVA UK and Luoda Pharma, who have developed and produced the oral esomeprazole preparation that was investigated, and to other companies who produce oral omeprazole products for the treatment of equine gastric disease. Tania Sundra has received expenses from BOVA Aus for attending educational events. Other authors declare no conflict of interest.”
They’re an Australian company, so presumably bringing this to the Australian market. Curious they compared to a buffered paste omeprazole rather than the more common (in Aus) enteric granule paste formulas. Maybe the enhanced bio availability in the enteric products didn’t give them such a notable difference.
Are you talking about the Sykes tapering study?
Uh, no. That’s not at all what I was saying. The authors discussed the omeprazole results and their interpretation of them in the full text. A poorly buffered product isn’t on the list.
Sykes, yes, sorry, I was deep into some dewormer resistance conversations and had Nielsen on the brain
The point of mentioning that along with Syke’s study is that it’s POSSIBLE, maybe even PROBABLE, that the variable metabolism of omeprazole is what leads to low healing rates. It might not have been where you were going, but the connection is there. That’s all. No need to dissect this further if I misinterpreted your thought process.
Have you read the full text here? The authors discuss the overall low omeprazole response rate.
Yes, I have, that’s what I was referring to. I didn’t feel the need to repeat that since you already laid it out.
That’s why I also questioned the study(ies) done to get GG approved for treatment, and that is what I haven’t read, or it’s been so long I don’t remember the details.
I’m really trying hard to understand where you’re coming from, but you haven’t explained why you think the authors conclusion on why the omeprazole response was lower aren’t valid. And while you point to “variable metabolism” as outlined in the Sykes tapering study as a cause…that’s awfully hard to follow, because Sykes doesn’t discuss “variable metabolism” at all in his tapering study.
Which is here. https://onlinelibrary.wiley.com/doi/10.1111/jvim.16795
From context, I’m guessing that you’re referring to how Sykes reported pretty broad response to omeprazole (and esomeprazole) horse to horse. But that applies to all preps, not just this paste in the Rendle paper, so it’s still really unclear why you think something like that is a driver for lower response to omeprazole in this study. Sykes used Gastrogard in his study and still found “The results of this study were surprising as the overall efficacy of omeprazole in raising ventral gastric pH was less than previously reported.”
I’m not sure what you’re reading, but nowhere did I suggest the findings aren’t valid
I SAID, that their findings work well with what Sykes said about variable reactions to some doses of omperazole, And then I simply added that I don’t know/remember the research on GG that got it approved so have no idea how that relates to these findings
But also, it’s reality that omeprazole isn’t healing some horses in situations where it should - proper dose, right kind of ulcers, etc, so it SHOULD mean that there are indeed some horses who aren’t getting the full metabolic benefits of even the right dose.
Sykes DOES discuss variable metabolism in his video on tapering, and it’s the entire basis for why tapering doesn’t work
Go to 7:10 if you want to start right where he’s talking about what was found when they started dropping doses (ie a taper)
“some horses absorb very little omeprazole, some horses absorb a lot of omeprazole, and that really dictates how they respond to different doses”
That chart (on the variability) isn’t in the paper link
What I was reminded of though is that at the 4mg/kg dose, the impact was much more reliable than lower doses, so that answers that about the treatment dose work done for approval.
I wasn’t referring to any comparison of esomeprazole
I hope that’s clear now
Okay, so you’re referencing a webinar where Sykes is discussing his tapering research, not a paper that has been published. Great, thanks for clarifying, that’s helpful. Do you know where that data is published, if it is? …nevermind, I’ll try to find it later.
Yes, Sykes has certainly demonstrated variable individual response to omeprazole and esomeprazole, a few times.
But it’s still not clear why you think any additional explanation beyond Rendle’s is necessary. Why do you think there’s anything more to it beyond what he’s proposed?
Or why you think “variable metabolism” is impacting this study (not just possibly, but probably!) but not other omeprazole studies with better results. Do you think this particular population was somehow more likely to have poorer response to omeprazole than every other study showing better results? Why?
This was a relatively large study with 73 horses in the omeprazole treatment group and 74 in the esomeprazole group. Unless the authors were selecting specifically for omeprazole resistant horses, and purposefully placing them in the omeprazole treatment group, “variable metabolism” doesn’t seem like a very likely thing to blame the poor omeprazole response.
Individual response to omeprazole will vary in every study. Unless specifically selected for or against, by, say, screening for previous response to omeprazole. Sure, in a particularly small sample, those variable responders might skew results one way or the other. But this isn’t a small sample.
Btw, the language in the gastrogard insert is:
Dose Confirmation: GastroGard (omeprazole) Paste, administered to provide omeprazole at 1.8 mg/lb (4 mg/kg) daily for 28 days, effectively healed or reduced the severity of gastric ulcers in 92% of omeprazole-treated horses
Clinical Field Trials: GastroGard Paste administered at 1.8 mg/lb (4 mg/kg) daily for 28 days healed or reduced the severity of gastric ulcers in 99% of omeprazole-treated horses
(Emphasis mine.)
This isn’t even counting successful treatment as grading at one or lower. This is just “reduced severity.” They don’t state what percentage of horses achieved grade 0.
How do you get Nexium pills in the stomach without the horse chewing them?
They are very small. Horses don’t thoroughly chew every bite.
If this is a concern, however, you could dose with a balling gun, or you could dose with a buffer of some sort before dosing the Nexium.
I’m dredging this up to ask a question. My 3 year old went into training (colt starting) and immediately displayed ulcer symptoms (refusing grain, kicky, bucky, listless, cranky). I put him on 28 days of ulcergard, administered by the staff and I’m not sure that it was consistently given or given at the same time every day. I tried to then taper him on the pop rocks (two packets a day) but he refused the grain with the pop rocks. Switched then to abler paste and I don’t think that is effective. He’s bitey and kicky, but he is eating his grain. I’d like to give this a try (this is simple economics–it’s not in my budget to pay $1,500/month for training board and $1,000/month for gastrogard). My questions:
TIA!
You’ve had this horse on a PPI for quite awhile without a resolution of symptoms? Scope him. Understand what you’re dealing with. There’s plenty that can happen in the stomach that isn’t addressed solely by a PPI, and plenty that can make a horse crabby in this way that’s not in the stomach at all.
To answer your questions:
I personally would not dose twice a day. Others have. You can look at the literature and decide if that’s something you’re comfortable with.
Yes, it matters if dosing is more than 24 hours apart. How large is the window?
Nexium does indeed raise the pH of the stomach for longer than 6 hours. At six hours post 40 mg dose, the pH of the stomach was >5 iirc as reported in the Pereira paper.
Yes, there are risks with long term dosing, namely risk to the hind gut and potential alteration of magnesium and calcium absorption.
But this doesn’t sound like a horse that needs further treatment with a PPI. This sounds like a horse that needs workup to understand what’s bothering him, because treatment with a PPI had been ineffective.
Treatment with ulcergard (full tube x1/day for 28 days). He went back on food, stopped bucking, stopping trying to bite and kick. When I went to taper him (onto abler pop rocks, 2 sachet per day), he stopped eating the grain again and didn’t get the meds. Both times that he stopped eating (when he first got there and then when I tried to taper on the pop rocks, they didn’t tell me until he hadn’t eaten for several days). So then I went to once per day full tube of Abler paste and he has been on that since Sunday, but it does not seem to be effective. That may be because they started giving it to him at all times of day and evening (once in front of me at 7pm because they forgot), after eating, and may have skipped it for a day, or because he had a rebound and we just haven’t given it long enough. I have enough tubes of abler paste to complete another 28 days. There is a better chance that he will get his daily dose if we put it in am food bags. I will not scope him while he is in training because of the withholding of food for 12 hours and the fact that I think he is already stressed at this facility (this is only the second time he’s been away from home since I got him here as a weanling); I would scope him when I bring him home and can control everything. He is in the middle of his second month of colt starting so I do not want to bring him home now–he needs another month at least (I will bring him home as soon as I can start riding him), possibly two. The training part of the journey is excellent.
Ulcers are a reasonable deduction because he went off his grain completely for four or five days and they did not tell me (he was eating voraciously at home) when I first brought him out there. His grain baggies were made up with a preventative dose of abprazole, but he didn’t get it because he refused to eat it. I went out to watch them work him and he was trying to buck the western saddle off (with the hind strap). He NEVER bucked under saddle in the year that I was ground driving and lunging him prior to sending him for training. He also tried to bite and kick me when I was posture prep grooming him in his stall on his sides. That’s why I started treating him with ulcergard. As soon as we got about 6 or 7 days of ulcergard in him, he stopped the bucking and they were able to get on him. He stopped trying to bite and kick me when I was grooming him. He then worked very well while he had ulcergard on board. I was looking to taper but have not found a reliable solution. If I have to put him back on ulcergard for the six to 10 weeks longer that he will be there, I will, but it will really stretch my budget. I have two other horses and one that has other veterinary needs right now. I was hoping to give this a try and see if it doesn’t curb the rebound of symptoms and provide a more reliable means of delivery when I can’t really depend on the barn to be consistent. I did have a horse many years ago that I scoped and had to rescope and rescope (subject to an insurance claim), and because the administration by the barn staff was so inconsistent, he needed to be on the gastrogard and sulcrafate for three cycles before the ulcers were healed and I could taper him.
I spoke to his breeder last week and she told me that his year older full sister gets ulcers every time she goes to a show. They are managing it with preventative ulcergard and outlast.
Omeprazole alone can raise pH enough to make squamous ulcers feel better, but won’t get them healed(well), so when you stop the drug, the pH lowers again, and the squamous ulcers hurt (more) again. That’s why scoping is best
Honestly, I’d take him out of training and put that money towards scoping and suitable treatment. If the ulcers are due to the stress of the whole training scenario, which is what squamous ulcers are highly linked to - stress - then you’re not likely going to fix him while in training, especially if they developed so quickly. He may simply not be mentally ready for “colt starting”
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