Where would I find the latest vet research on giving Ranitidine long term? When our horse left the vet school after being scoped and treated for ulcers, they didi not seem to know how to prevent a reoccurrence and just said Ulcergard. Clearly, that is not practical for every day use and Ranitidine daily was prescribed by another vet. Now I have read it leads to kidney issues in humans. Is any vet school doing research on what it does to horses if fed daily long term? TIA!!
I would never use any acid reducer long-term until the horse proved he can’t be managed otherwise. I would look to why the horse did (or you suspect) develop ulcer, and work on management first. More turnout, better herd situation, feeding some alfalfa (especially before work), possibly one of the better gut support supplements, before resorting to an acid suppressor. They simply need proper acid production to appropriately break down food and digest/absorb nutrients.
I"m shocked that a vet school would not suggest management changes :no: Regular vets, that doesn’t shock me so much 
The time my horse got scoped at the vet hospital they recommended alfalfa and a 1/4 tube daily for prevention. The vet whom did the follow up clean scope was from a private clinic was a big fan of relyne GI for prevention, small amounts of alfalfa and a slow feeder.
The effectiveness of ranitidine depends on what is causing the acid in the horse. It only blocks histamine, and it can develop tolerance in some users, where more is needed to be effective. My understanding is that there is more than one chemical compound causing acid secretion in horses (there are three in humans), so if it is caused by something other than histamine, ranitidine will not work.
Proton pump inhibitors (PPIs), such as GastroGuard or omeprazole, function more upstream, like a lock and key mechanism, attaching to parietal cells that produce hydrochloric acid and shutting off acid manufacture. Therefore PPIs work to fight excess acid production regardless of its cause.
So, they are two different classes of drugs that have different mechanisms of action. Here’s an older study that compared the two in TB racehorses: https://www.ncbi.nlm.nih.gov/pubmed/16313043
I’m given to understand that there are no long-term adverse effects of ranitidine, other than the tolerance issue.
The report that looked at kidney disease in humans taking PPIs is still being debated. There was not one specific study that found PPIs to cause kidney problems. Rather, meta data (data collection looking at many studies) showed that there MAY be an association between PPIs and kidney disease (and heart disease as well), but a cause and effect connection could not be made. The results of the report were serious enough that it was recommended that people taking PPIs be warned about the possible side effects. Please note that this has nothing to do with ranitidine, which is not a PPI.
In using PPIs, you need to assess whether the risk of kidney and heart disease (which hasn’t been extensively studied in equines) is greater than the risk of untreated excess acid production and/or ulcers. Also, removing other factors in equine ulcers, like stress, may decrease the need for continuous pharmaceutical treatment of any kind.
So, you’re probably safe with ranitidine, but it may stop working over time or you may need to give a larger dose. And it may not work if the cause of your horse’s acid is not histamine. If you switch to a PPI, the long-term adverse effects are not conclusive, but there is potential for risk in humans that may or may not be extrapolated to equines.
Hope that all makes sense. Not a vet but worked in the gastroenterology department of a pharma company and managed PPI hospital contracts. Have also done EGUS seminars with equine experts. Your vet is the ultimate voice of authority, but it’s good to go armed with knowledge IMO. Best of luck to you.
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In regards to PPI. Could there be a risk to using long term gastrogard? I am currently using 1/4 tube daily on my own horse.
Raniditind is a histamine blocker, but in such a way that stomach acid is reduced. Same result, just a different mechanism from PPIs. It just doesn’t reduce acid for as long as PPIs do with the “same” dose (ie treatment vs prevention).
But also, PPIs vs H2 blockers have different values for fore gut vs hind gut ulcer issues. Ranitidine can help with both, PPIs help with fore and can make hind issues worse.
I’d still not use either as prevention until it’s a last resort.
Anything that lowers acid will have some negative impact on nutrient absorption, there’s just no away around it. Long-term effect in horses specifically hasn’t been studied, afaik, not just because of $$, but it’s so uncommon for that to happen. But since B12 still requires sufficient acid to be released from its protein binders in the stomach (so it can be bound to intrinsic factor to be usable) it’s likely to become a deficiency in horses as well, even at a prevention dose, even if it takes a lot longer. Magnesium too.
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Yes, PPIs can change hindgut flora. And you’re right about the nutrient absorption.
I disagree in part, though, about the “same result, different mechanism.” SOMETIMES this is the case, but you’re likely to have more failure to control acid with ranitidine if excess histamine isn’t causing the problem.
Can you explain (more) about how histamine production either causes ulcers (if that’s what you’re implying, I can’t tell), or if excess (or “excess”) histamine production can cause symptoms similar to those of ulcers?
I was really just referring to the fact that H2 blockers do lower acid production, just like PPIs do, even if it’s via different mechanism.
I totally agree with you that the symptoms a horse has may not be related to either excess acid production (probably extremely rare), or the erosion of the stomach lining via the prostaglandin reduction that comes from certain COX inhibition.
I think it’s unknown at this point, and it’s not even fully understood in humans. Like I said above, you have to weigh the risks and the benefits and try to use the medication for as short a time as possible, doing everything else to try to reduce causes of EGUS: eliminate stress, extend feeding time/reduce pre-event fasting, reduce diets high in fermentable carbohydrates that precipitate the generation of volatile fatty acids, etc.
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Histamine is only one precursor to acid production. Other peptides, like gastrin and acetylcholine, also stimulate acid production in humans, and I’m guessing they do in horses too (or similar peptides). They bind with the parietal cells of the stomach and turn on the “acid factory.”
Ranitidine is a histamine blocker, so it will shut down acid production precipitated by histamine. However, if other peptides are also stimulating the parietal cells, the stomach will still make hydrochloric acid, even with ranitidine on board.
PPIs block ALL acid production by binding preferentially to the stomach parietal cells, preventing the production of acid. Even in the presence of histamine or other peptides, no acid will be manufactured.
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