scott@vtx-cpd.com
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Hi Silvana,
I did a bit more digging into this as it really interested me. It looks as though GingiPro is available through Bova in the UK as well as Australia, although there are some important considerations around its use.
The combination contains EIDD-1931, doxycycline and meloxicam, which raises a few questions for me. Ideally, before considering something like this, I think I would want to be confident that concurrent periodontal disease had been properly assessed and treated, including dental radiographs and extraction of diseased teeth where appropriate. I would also want confirmation of FCV by PCR rather than using an antiviral empirically, and obviously the individual cat needs to be an appropriate candidate for an NSAID.
There are also some wider stewardship questions around whether doxycycline is necessary in every case and around antiviral use in cats without confirmed calicivirus. EIDD-1931 itself is interesting, but potential adverse effects and owner exposure/handling need consideration, particularly as there are teratogenicity concerns. Applying a medication directly to the gingiva of a cat with a very painful mouth may not always be particularly straightforward either!
The other limitation at the moment seems to be the evidence base. There are apparently good anecdotal results, but the optimal duration of treatment has not yet been properly studied or published. Molnupiravir/EIDD-related antiviral treatment on its own has also been investigated in FCV-positive cats with encouraging results, so I suspect this is an area we are going to hear considerably more about.
So, potentially very interesting, and I can certainly see a role for this type of antiviral treatment in carefully selected FCV-positive cats, but I think I would currently be a little cautious about the one-size-fits-all combination product approach until we have more published data.
Thanks for bringing it up — I genuinely hadn’t come across it before!
Scott
Replying to Silvana S. 26/08/2026 - 09:20
Thanks Silvana! I am in exactly the same place. I haven’t had the opportunity to use lorazepam for this yet either, but the results are interesting enough that I would definitely consider it in an appropriate case, alongside all the usual multimodal management of course.
It will be interesting to see whether the findings hold up in larger studies and, in the meantime, to hear what experiences people have as they start using it clinically.
Scott 🙂
Hi Silvana,
Super interesting, thanks for sharing. I haven’t used GingiPro myself and haven’t come across it clinically here in Canada. I’ll reach out to Sam Taylor and see if she has any experience with it or knows more about its availability.
I’ll let you know what I hear back.
Scott ::
Replying to Raquel M. 24/08/2026 - 12:41
Thanks Raquel.
I hope all is well with you! You are absolutely right, lorazepam is only one small part of managing these cats, and identifying an underlying cause where possible, analgesia, diet, weight management and particularly addressing environmental stress are probably much more important than simply reaching for another drug.
Great to hear your outpatient UO case did so well too. Sometimes we have to work with what is realistically possible for the owner, particularly when the alternative is euthanasia.
I think I am in a similar place with lorazepam. The results are interesting enough that I would certainly consider it, particularly in selected cats, but I would like to see the findings reproduced in a larger study before it becomes routine for every first-time UO.
The CE event sounds very timely! I would be really interested to hear what the criticalist thinks about lorazepam and whether they have started incorporating it into their own UO protocols.
Scott 🙂
Replying to Silvana S. 16/08/2026 - 16:59
Hi Silvana, thanks – that’s a really good question. I tend to use once-daily prednisolone as well where the clinical situation allows, and I think this study gives us a little more reason to favour that approach, particularly when PU/PD is becoming troublesome.
The morning dosing question is interesting because you will quite often see the recommendation that glucocorticoids should be given in the morning in dogs, with the rationale that this more closely matches endogenous cortisol production and might therefore be less disruptive to the hypothalamic-pituitary-adrenal axis. Some veterinary prednisolone product information specifically recommends morning administration in dogs for this reason. The difficulty is that the evidence for a strong circadian cortisol rhythm in dogs is actually much less convincing than it is in people. The ACVIM consensus literature notes that dogs do not demonstrate a clearly established circadian pattern of cortisol secretion, so I don’t think we have strong evidence that giving prednisolone at, for example, 8 am rather than 6 pm produces a meaningful clinical benefit.
For hypoadrenocorticism specifically, I generally recommend giving the replacement prednisolone once daily in the morning. Partly that is physiologically intuitive and partly it creates a simple, consistent routine for the owner, but I wouldn’t be concerned if an individual dog was receiving it consistently at another time of day and was clinically doing very well. Current AAHA guidance focuses much more on giving an appropriately low physiological daily dose and adjusting it according to clinical signs and steroid adverse effects than it does on a particular time of day. Many stable Addisonian dogs actually require less than 0.1 mg/kg/day of prednisone/prednisolone, with up to 0.25 mg/kg/day generally being sufficient for stable long-term management.
So my short answer would be: morning is my preference, particularly for Addisonian dogs, but I don’t think we currently have good evidence that morning administration is clinically superior to evening administration in an otherwise stable dog. Consistency, using the lowest effective replacement dose, monitoring the individual dog’s clinical response, and remembering to increase glucocorticoid supplementation appropriately during periods of stress are probably much more important.
Great question.
Scott 🙂
Replying to Laura S. 04/08/2026 - 15:11
Hi Laura,
That is a really good question, and yes, I absolutely think cholecystocentesis is something that can be performed at GP level provided you are comfortable identifying the gall bladder ultrasonographically and can maintain good visualisation of the needle throughout the procedure. In many ways, I think it can be an incredibly useful and relatively accessible diagnostic procedure, particularly in exactly the situation you describe where referral, liver biopsy, or more advanced investigations are financially unrealistic for the owner.
I would probably say, however, that I would want someone to be reasonably confident with ultrasound guided FNAs before making cholecystocentesis their next procedure. The gall bladder is obviously a less forgiving target than the liver, so being able to confidently visualise your needle and needle tip is really important. If your confidence with liver FNAs is growing, though, I certainly do not think cholecystocentesis should be regarded as something that can only be performed in a referral hospital.
Cholecystocentesis can be completed using a percutaneous transhepatic ultrasound-guided approach, by laparoscopic assistance, or during exploratory abdominal surgery. If completed under ultrasonographic surveillance, a transhepatic approach allows adjacent liver tissue to provide a tamponade effect, limiting bile leakage. Whatever approach is used for cholecystocentesis, it is prudent to empty the gallbladder of most bile to limit postcentesis leakage. Samples of collected bile are used for cytologic evaluation and culture of aerobic and anaerobic bacteria and fungi. It is important to empty the gallbladder to collect bile with particulate debris or sediment in gravitationally dependent regions, as this material typically contains bacterial biofilm that will disclose organisms detected by cytologic evaluation and culture.
In terms of technique, I generally prefer a transhepatic approach where possible. In other words, I pass the needle through a small amount of liver parenchyma before entering the gall bladder rather than puncturing the exposed gall bladder wall directly. The idea is that the surrounding hepatic tissue provides some tamponade to the needle tract and potentially reduces the risk of bile leakage afterwards. I would use a relatively small gauge needle, typically around 22 to 25 gauge depending on the patient and the viscosity of the bile, attached to a syringe. A butterfly needle can certainly be used if that is what you are most comfortable controlling, although personally I think the most important consideration is not whether it is a butterfly or a standard needle but whether you can see and control the needle tip throughout the procedure.
There are obviously situations where I would be much more cautious. If the gall bladder wall looks compromised or discontinuous, there is pericholecystic fluid, there is concern about impending rupture, or I suspect a gall bladder mucocele with significant wall compromise, I would not regard that as a straightforward diagnostic cholecystocentesis. Equally, if there is significant coagulopathy or the gall bladder is extremely small and difficult to access safely, the risk benefit calculation changes.
I do think bile sampling can be extremely valuable when you suspect bacterial cholangitis or cholecystitis. One of its major advantages is that bile culture can provide information that bloodwork, ultrasound and even liver cytology cannot. If I am considering several weeks of antimicrobial therapy for suspected bacterial biliary disease, I would much rather have aerobic and anaerobic culture and susceptibility results to guide me, particularly because antimicrobial resistance amongst biliary isolates is certainly something we encounter.
Regarding performing cholecystocentesis at the same time as a liver biopsy, yes, I think that can be very sensible when the clinical picture supports it. If I am investigating suspected cholangitis or cholangiohepatitis and I am already obtaining hepatic tissue, then obtaining bile for cytology and culture at the same time can give you complementary information. The liver biopsy tells you what is happening within the hepatic tissue and biliary structures, while the bile sample can help determine whether bacteria are present and, importantly, what they are susceptible to. I suspect that is the context in which Penny was recommending it.
Complications of cholecystocentesis may include intraperitoneal bile leakage (decreased by using a transhepatic approach), haemorrhage, haemobilia, bacteraemia, and a biliary-cardiac reflex (vasovagal reaction). The latter adverse reaction is mediated by the vagal nerve, is more common in cats, and may result in ventilatory arrest, severe bradycardia, and death.
The point about gall bladder rupture is interesting because I would distinguish between an accidental needle related bile leak and a gall bladder that is already severely diseased and genuinely at risk of spontaneous rupture. I would not assume that every gall bladder that leaks following cholecystocentesis was inevitably going to rupture anyway, and equally I would not regard accidental rupture as universally fatal. The prognosis is going to depend enormously on the underlying gall bladder pathology, the degree and duration of bile contamination, whether infection is present, and how quickly the problem is recognised and treated.
If I genuinely suspected that the gall bladder had ruptured during the procedure, that would become a surgical emergency rather than something I would try to manage medically. I would involve a surgeon immediately. Management would generally involve exploratory laparotomy, assessment of the gall bladder and biliary tract, copious abdominal lavage, and addressing the source of leakage. Depending on what the gall bladder actually looks like, that may mean cholecystectomy rather than simply suturing the puncture site. I would also provide appropriate analgesia and supportive care, and if septic bile peritonitis were suspected, institute appropriate antimicrobial therapy while obtaining samples for culture wherever possible.
I therefore would not want the potential complication to put you off performing cholecystocentesis altogether. It is about patient selection and technique. In an appropriately selected patient with an intact gall bladder wall, a good transhepatic window and continuous ultrasound guidance, I think it is a very reasonable procedure for a GP with developing ultrasound skills to work towards. Perhaps the ideal first few cases would be performed alongside somebody with more ultrasound experience if that opportunity exists, simply because having someone beside you to confirm the approach and needle position can make that initial transition much less intimidating.
And importantly, in the situation you describe where an owner cannot afford referral or liver biopsy, a carefully selected cholecystocentesis may provide genuinely useful diagnostic information rather than simply being viewed as a lesser alternative to referral.
I hope that helps!
Scott
Replying to Lesley M. 09/08/2026 - 17:01
Really interesting thought, Lesley, and not completely off the wall at all! We already use the same principle with intraoperative autotransfusion.
And in principle, yes, some of the blood left within the abdomen will be reabsorbed over time, so there is potentially a degree of natural “autotransfusion” occurring. The difficulty is that this process is relatively slow and unpredictable, and therefore wouldn’t give us the immediate restoration of circulating red cell mass that we would want following significant haemorrhage. There are also potential downsides to deliberately leaving a large volume of blood behind, including peritoneal inflammation and discomfort, and potentially infection depending on the surgical situation.
Where your idea becomes really interesting is autotransfusion itself. Rather than discarding that blood, could we collect and reinfuse it during surgery, particularly when donor blood is limited? That can certainly be useful in appropriate cases, although suspected malignancy has traditionally made people cautious because of the theoretical concern about returning tumour cells to the circulation. Interestingly, none of the dogs in this particular study received autotransfusion, so unfortunately the paper doesn’t help us answer that question.
So yes, physiologically some of that abdominal blood will ultimately be reabsorbed, but I’m not sure there would be an advantage to deliberately leaving it there after surgery versus actively collecting and reinfusing it when autotransfusion is considered appropriate.
Definitely not an off-the-wall thought though!
Scott 🙂
Replying to Lesley M. 09/08/2026 - 17:04
Hi Lesley, this is the company we use here in North America: https://animalbiome.vet/pages/vet_fmt_capsules
I’m not sure whether they currently ship to the UK, but definitely worth having a look! I’d be interested to know if you find a UK supplier too.
Scott 🙂
Replying to Rosanna Vaughan 30/07/2026 - 15:57
Hi Rosanna,
Thanks very much. I’m glad you found it helpful. I’ve become a real fan of Senvelgo in the right patient.
For CGMs, I still use the FreeStyle Libre 2 a lot. It’s the system I’m most familiar with, it’s the one most of the published veterinary literature has used, and I find it reliable enough for following trends rather than focusing on individual glucose readings. I don’t routinely chase every number, as I think looking at the overall glucose pattern alongside the clinical picture is much more useful.
That said, I have also had several patients start using the FreeStyle Libre 3, and I’ve been really impressed with it. The sensor is noticeably smaller, which seems to make it better tolerated by many cats, and the continuous real-time data are excellent. If owners are comfortable with the technology, I think it’s a really nice evolution of the Libre system.
The LibreLink app works very well for owners, and if they’re happy to share the data through LibreView it makes remote review straightforward. That has probably changed my diabetic monitoring more than anything else over the past few years.
In terms of placement, I generally position the sensor over the lateral thoracic wall, just caudal to the scapula. I clip quite a generous area, degrease the skin thoroughly with alcohol and let it dry completely before application. I then reinforce the adhesive with a little tissue glue around the outer adhesive pad rather than underneath the sensor itself. Finally, I cover the whole thing with a light body suit or recovery shirt for the first week if the cat will tolerate it. Since doing that, I lose very few sensors.
A lot of my clients have also really liked using the commercially available adhesive sensor covers that fit over the Libre sensor. They seem to help keep the sensor in place, particularly in more active cats or those that like to groom excessively, and they’re relatively inexpensive.
One other tip I’ve found useful is to prepare owners that the sensor doesn’t have to last the full 14 days to be worthwhile. Even three to five days of home glucose data is often far more informative than a traditional in-hospital glucose curve, particularly in cats that develop significant stress hyperglycaemia.
I’d be interested to hear how you get on with your first Senvelgo case.
Scott 🙂
Replying to Silvana S. 30/07/2026 - 09:49
No problem!
Ultimately, I am using this drug more and more ‘off label recommendation’ and finding it still works well. It is a very interesting drug!
Scott 🙂
Replying to Silvana S. 30/07/2026 - 10:09
Hello!
This feedback is really helpful. I will absolutely take this in to consideration when we are reviewing the course.
Thank you again for your brilliant contribution.
Scott
Hi Sophie,
That’s a really good question, and I think the answer depends very much on the individual patient and what we think caused the pancreatitis in the first place. I hope you are enjoying the course! Feedback always welcome.
Historically, we recommended prolonged fasting and then lifelong low fat diets for many dogs after pancreatitis. However, our understanding has changed considerably over the last 15 to 20 years. There is now mounting evidence in both human and veterinary medicine that dogs with acute pancreatitis benefit from early enteral nutrition. Enteral nutrition is superior to total parenteral nutrition because it helps maintain intestinal motility, preserves gastrointestinal barrier function, supports a healthy intestinal microbiome, and prevents villous atrophy. Studies in dogs have shown that feeding within 48 hours of hospitalisation is well tolerated, results in an earlier return to voluntary food intake, and reduces gastrointestinal complications. As a result, dogs that are not vomiting should be offered food as soon as possible, while those that remain anorexic should be considered for nutritional support via a feeding tube rather than being left unfed.
The question of what to feed long term is actually much less clear. There is currently very little evidence defining the ideal maintenance diet after recovery from acute pancreatitis. My own approach is that a dog with a single uncomplicated episode of acute pancreatitis that makes a complete clinical recovery does not necessarily need to remain on a low fat diet for life. I will generally keep them on a highly digestible low fat diet for the first one to two weeks after discharge and then reassess. If they continue to do well, have no concurrent disease, no persistent hyperlipidaemia, and this was their first episode, I am often happy to transition them back onto a good quality maintenance diet while advising owners to avoid high fat treats, table scraps, and obvious dietary indiscretions. This is very much in keeping with the current nutritional recommendations, which suggest tailoring long term feeding to the individual patient rather than automatically recommending lifelong fat restriction for every dog.
Where I am much more inclined to recommend long term fat restriction is in dogs with recurrent pancreatitis, chronic pancreatitis, documented hyperlipidaemia, breeds predisposed to lipid disorders such as Miniature Schnauzers, or dogs that clearly developed pancreatitis following a high fat dietary indiscretion. Those patients probably do benefit from remaining on a commercially formulated low fat diet, and I would also recommend avoiding fatty snacks and treats.
It is also worth remembering that pancreatitis is not always caused by dietary fat. Many cases are idiopathic, while others are associated with endocrinopathies, hypertriglyceridaemia, obesity, medications, or concurrent gastrointestinal disease. Because of that, I try not to automatically prescribe lifelong dietary fat restriction for every dog that has had pancreatitis without considering the underlying cause.
For dogs with chronic pancreatitis, my recommendations are different. These patients often do benefit from an ultra low fat diet as part of their long term management, particularly as many also have concurrent chronic inflammatory enteropathy, hepatitis, diabetes mellitus, or hyperlipidaemia. They may also require antiemetics, appetite stimulants, analgesia, and occasionally immunosuppressive therapy if there is suspicion of an immune mediated component and they have failed more conventional management.
So, in summary, I think the key is to individualise the plan. A first episode of acute pancreatitis does not automatically mean lifelong fat restriction. I tend to use a low fat diet during recovery, then reassess based on recurrence, concurrent disease, hyperlipidaemia, and the suspected underlying cause. For recurrent or chronic pancreatitis, I am much more likely to recommend long term dietary fat restriction.
Let me know if you have any other questions.
Scott 🙂
Replying to Rachel C. 15/07/2026 - 16:44
Thanks Rachel, I completely agree. I still think faecal testing has an important role, particularly early in the work-up to exclude parasites and other infectious causes before moving on to more invasive or expensive investigations such as ultrasound or endoscopy. I don’t think this paper suggests we should stop doing faecal testing, but rather that we need to be much more cautious about how we interpret bacterial PCR results. Simply detecting organisms like Clostridium perfringens or E. coli doesn’t necessarily mean they are causing the diarrhoea, and using those results alone to justify antibiotics is probably not appropriate. For me, it’s a useful reminder to interpret faecal PCR in the context of the whole clinical picture, rather than in isolation.
I hope you are well!
Scott 🙂
Hi Rachel,
Thanks for your questions, and I’m glad you enjoyed the lecture.
One of the main things I’m always keen to emphasise is that liver enzymes are not liver function tests. They are markers of hepatocellular injury or cholestasis, but they tell us very little about how well the liver is actually functioning. Equally importantly, liver enzymes can increase because of disease outside the liver. The liver is an incredibly sensitive organ and responds to a huge range of systemic insults, so I always encourage clinicians to interpret liver enzyme elevations within the context of the entire clinical picture rather than assuming they represent primary liver disease.
If I have a patient that is “not quite right”, has mild to moderate liver enzyme elevations, and an essentially unremarkable ultrasound, I don’t routinely jump to liver FNAs or gall bladder aspiration. Unless there is genuine suspicion of a primary hepatobiliary disorder, such as cholangitis or cholangiohepatitis, I don’t think those procedures are necessarily the next logical step.
The first thing I ask myself is whether these are persistent liver enzyme elevations. We certainly see transient increases that resolve completely on repeat testing and never recur. Because of that, if the patient is clinically stable, I don’t think it is unreasonable for the first step simply to repeat the biochemistry in two to four weeks to determine whether the abnormalities persist.
The second thing I commonly do is start a course of Denamarin. I will often add ursodeoxycholic acid, provided there is no evidence of complete biliary obstruction. I’m very comfortable using those medications together. They are generally very safe, and I think they provide sensible supportive therapy while you determine whether the abnormalities are transient or persistent. I would then reassess the liver enzymes after a few weeks.
If the liver enzymes normalise, then you’ve probably avoided unnecessary invasive diagnostics. If they remain persistently elevated, particularly if the ALT is greater than five times the upper reference interval, or the values continue to increase, then I think the conversation changes. At that point, if you’ve excluded obvious extrahepatic causes, the only way to obtain a definitive diagnosis may be liver sampling, whether that is cytology or biopsy depending on the individual case.
I also think it is worth remembering that ultrasound is an excellent tool, but it is not a test of liver function and it is not particularly sensitive for many inflammatory or metabolic hepatopathies. A completely normal appearing liver does not exclude significant microscopic disease, just as a very abnormal looking liver does not necessarily indicate severe dysfunction.
With respect to gall bladder aspiration, I certainly would not perform it routinely. For me, the main indication is suspected bacterial cholangitis or cholecystitis where obtaining bile for culture and cytology is likely to change management. This is particularly relevant in cats because bacterial cholangitis is considerably more common than in dogs.
Other situations where I would consider cholecystocentesis include patients with persistent cholestasis or hyperbilirubinaemia where I am concerned about an ascending biliary infection, dogs or cats with ultrasonographic evidence of abnormal bile such as echogenic debris, thickened gall bladder walls or changes suggestive of cholecystitis, patients with recurrent or poorly responsive hepatobiliary disease despite empirical antibiotics, and cases of pyrexia of unknown origin where the biliary tract remains a potential source of infection. It is also appropriate when you are concerned about antimicrobial resistance and culture results are likely to influence your antibiotic selection.
Conversely, I would generally avoid gall bladder aspiration in patients with a gall bladder mucocele, evidence of gall bladder rupture, significant coagulopathy, severe gall bladder wall necrosis, or where the result is unlikely to alter my management.
So, my approach is usually to ask three questions. Firstly, do I think this is primary liver disease? Secondly, is there evidence of liver dysfunction rather than simply liver injury? Thirdly, will obtaining liver or bile samples genuinely change my treatment plan? If the answer to that last question is no, and the patient is clinically stable, I think it is entirely reasonable to repeat the blood work, provide supportive hepatoprotective therapy with Denamarin and, where appropriate, ursodeoxycholic acid, and reassess before moving on to more invasive diagnostics.
Thanks again for the excellent questions.
Scott 🙂
Replying to Silvana S. 22/07/2026 - 09:55
Hi Silvana,
Thank you for your excellent question. I hope you are doing well.
This is exactly the sort of case where I think we need to step back and think about what is driving the diabetes rather than simply treating the blood glucose.
Hyperthyroidism is one of the recognised causes of insulin resistance, and the new AAHA guidelines list uncontrolled hyperthyroidism as an important concurrent disease that should be identified before selecting an SGLT2 inhibitor. They recommend screening cats over seven years of age for hyperthyroidism and generally favour insulin in cats with significant concurrent disease or where metabolic stability is uncertain.
If the cat is otherwise bright, eating well, well hydrated, has no ketosis, and is genuinely stable, I don’t think there is necessarily an urgent need to stop Senvelgo immediately. However, I would focus aggressively on getting the hyperthyroidism under control and monitor the diabetic response very closely. There is certainly be a possibility that improving the hyperthyroidism will reduce insulin resistance and substantially improve diabetic control.
My concern would be that ongoing weight loss and polyphagia make it difficult to know how much of the clinical picture is due to persistent diabetes versus uncontrolled hyperthyroidism. If those signs persist despite improving thyroid control, or if ketones become a concern, I would have a fairly low threshold for transitioning to insulin.
That said, I don’t think we necessarily need years of direct experience before carefully applying these drugs outside the original label population. It seems to me that they can be extremely valuable in selected cases that are not completely stable or entirely conventional, provided we understand the risks, monitor closely and have informed owners.
Interestingly, a recently published case series explored the use of velagliflozin in non ideal diabetic cats with concurrent diseases. While hyperthyroidism was not included, the authors successfully managed cats with conditions such as chronic kidney disease and hypersomatotropism, in some cases using combination therapy and intensive CGM and ketone monitoring. Their experience suggests that, in carefully selected patients with close monitoring and informed owner consent, there may be scope to use SGLT2 inhibitors outside the original label recommendations.
My own experience has probably reinforced that view. I have used these drugs successfully in several patients that would not have been considered ideal candidates in the original clinical trials. One cat, had IRIS stage 3 chronic kidney disease, significant biliary disease, was receiving corticosteroids and multiple medications for CKD, and still responded remarkably well to treatment. I have also used an SGLT2 inhibitor successfully in a cat with progressive FIP receiving corticosteroids, and in another cat with severe non regenerative immune mediated anaemia that was being treated with cyclosporine and prednisolone. All three of those cases responded very well, despite being far from straightforward.
Obviously these are anecdotal experiences rather than evidence, and I certainly would not advocate indiscriminate off label use. However, they have given me confidence that with careful case selection, very close monitoring, particularly of ketones during the early treatment period, and clear communication with owners, these drugs may have a broader role than we initially thought.
So, in your case, I certainly wouldn’t dismiss Senvelgo simply because the cat has hyperthyroidism. I would be inclined to treat the hyperthyroidism aggressively, monitor the diabetes and ketones closely, and then reassess how the cat is doing clinically over the following few weeks. If the clinical picture improves, I think it is entirely reasonable to continue. If not, then transitioning to insulin would be my next step.
I hope that helps.
Scott 🙂
Case Reports J Feline Med Surg 2026 Feb;28(2):1098612X251414198. doi: 10.1177/1098612X251414198. Epub 2026 Jan 3.
SGLT2 inhibitor therapy in diabetic cats: first clinical experiences with non-ideal candidates
Achilles Vanneste 1, Emma Van Heuckelom 1, Dagmar Vannieuwenhuyse 1, Charlotte De Voogt 1, Sylvie Daminet 1
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PMID: 41482870 PMCID: PMC12929899 DOI: 10.1177/1098612X251414198 -
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