scott@vtx-cpd.com

Replying to Iulia M. 07/08/2025 - 17:27

Hi Lulia,

Chlorphenamine can certainly be effective, but its shorter duration of action and higher sedation potential can be limiting. Cetirizine generally allows once-daily dosing, causes less sedation, and has some evidence in dogs, mainly small pharmacokinetic and clinical studies—suggesting it may help control allergic symptoms, particularly in atopic dermatitis. Direct head-to-head comparisons in veterinary patients are lacking, so choice is still based largely on individual response and tolerability. In my experience, cetirizine is worth trialling if chlorphenamine gives only partial control or causes unwanted sedation.

Hope you have a great week.

Scott 🙂

Replying to Julia Biernat 11/08/2025 - 09:45

Hi Julia,

Thank you so much for joining the course and thank you for your question!

I think this is an area where the use of PPIs in liver disease is often a bit over-generalised.

In most stable chronic hepatopathies, I don’t use PPIs routinely. My main indications would be when I have reasonable clinical suspicion or confirmation of an upper GI bleed — for example, haematemesis, melaena, or gastric/duodenal erosions or ulceration seen on endoscopy — and I think the bleed is likely due to a combination of portal hypertension–related mucosal congestion, secondary erosive gastritis, or concurrent drug effects (e.g., corticosteroids, NSAIDs). I might also consider a PPI if there’s marked hyperacidity suspected in a case with concurrent GI disease or after a known ulcerogenic insult.

If I have a patient with evidence of bleeding but significantly prolonged clotting times, then yes, I’d generally want to correct the coagulopathy before performing any invasive diagnostics and ideally before starting acid suppression. This is particularly relevant if you think the bleed is related to mucosal friability secondary to hypocoagulability rather than an acid-mediated ulcer. In those cases, fresh frozen plasma (FFP) is my first step, as it provides both clotting factors and, in some cases, volume support for hypoalbuminaemic patients.

In terms of how often I see GI bleeding purely due to clotting factor abnormalities, I’d say it’s uncommon as the sole cause in liver disease. When it does occur, it’s usually in the context of advanced decompensation, either severe synthetic failure with markedly prolonged PT/aPTT or DIC. In those situations, GI bleeding is often part of a broader haemorrhagic tendency affecting multiple sites (e.g., petechiation, ecchymoses, haematuria). I do occasionally see bleeding in patients with severe thrombocytopaenia — whether from DIC, immune-mediated mechanisms, or bone marrow suppression — but in my experience, portal hypertensive gastropathy or erosive gastritis from systemic illness are more frequent contributors in liver patients.

For additional context, the ACVIM consensus on acid suppressant use notes that although hepatic disease has been associated with gastroduodenal ulceration (GUE) in dogs, evidence that it is a direct cause is scarce, and the prevalence of upper GI bleeding in dogs and cats with hepatic disease has not been established. The pathogenesis is uncertain. In humans, altered mucosal blood flow from portal hypertension (hypertensive gastropathy) is the most common cause for GI bleeding, while in dogs, decreased hepatic degradation of gastrin with subsequent hyperacidity has been proposed — though experimental data do not support hypergastrinemia as a major factor. Experimental bile duct ligation can produce ulceration in dogs. In people, gastric acid suppression generally does not reduce bleeding from portal hypertensive gastropathy because these patients already tend to have hypochlorhydria, although PPIs may indirectly help by raising gastric pH enough to stabilise clots. There is one retrospective canine study in which implementation of lifelong PPI therapy around the time of intrahepatic shunt closure was associated with a lower rate of death from GI haemorrhage, but the underlying mechanism was unclear and may not have been related to the hepatic dysfunction itself.

Overall, the consensus opinion is that there is weak evidence to support prophylactic acid suppression in dogs and cats with hepatic disease in the absence of clinical or endoscopic evidence of GI bleeding. My own approach mirrors this, I reserve PPIs for patients with documented or strongly suspected ulceration or erosive gastritis, rather than using them as blanket prophylaxis in all liver cases.

I hope you have a wonderful week!

Scott 🙂

Replying to Angela Tiivel 10/08/2025 - 09:53

Hi Angela,

Thanks for your message. I understand how frustrating it can be to lose access to products like Denamarin, Zentonil, and Samylin, as they are widely used in many countries for hepatic support. In situations where these aren’t available, the goal is to select from what you do have access to, ensuring you can still provide adequate doses of the key active ingredients with the strongest evidence for liver protection, namely S-adenosylmethionine (SAMe) and silybin (the bioactive extract of milk thistle), ideally in combination with antioxidants such as vitamin E.

Of the products you mentioned, VETEXPERT Hepatiale Forte Advanced would probably be my first choice for most cases, as it contains SAMe together with phosphatidylcholine, which aids hepatocyte membrane stability and can improve bioavailability of silybin if given together in some cases. However, if the formulation you have does not already include silybin, I would look at adding this separately, either through a combination product or a stand-alone silybin supplement with proven bioavailability (often in the form of silybin–phosphatidylcholine complexes).

DRN Epato and Bioiberica Prolivet are also reasonable options — both can provide useful support depending on their exact composition in your market. Epato products often contain silybin, phosphatidylcholine, and sometimes artichoke extract or other antioxidants; Prolivet typically contains silybin and other liver-supportive nutrients. The main thing is to check the label for the actual amount of silybin and/or SAMe per tablet or capsule, as the doses in many nutraceuticals are quite low compared to those used in published studies.

When selecting and dosing:

SAMe: Aim for a therapeutic dose of roughly 18–20 mg/kg once daily on an empty stomach. This helps maximise absorption and avoids degradation by food.

Silybin: Aim for 4–5 mg/kg once daily (or divided twice daily), ideally in a phosphatidylcholine-bound form for improved absorption.

Vitamin E: May be beneficial in chronic hepatopathies or where oxidative stress is suspected, but dosing should be tailored to avoid excess.

If a single product doesn’t contain both SAMe and silybin in adequate amounts, you can combine two complementary products to reach the desired doses. For example, you might use Hepatiale Forte Advanced to supply adequate SAMe and then pair it with Epato to provide the silybin component.

Regarding your comment on liver enzyme improvements after discontinuing Apoquel, there have been occasional reports of mild ALT or ALP elevations in dogs on oclacitinib, though it’s not considered a common side effect. In cases where there’s a temporal association between starting Apoquel and enzyme elevation, particularly if other causes are not identified, a trial off the medication can help clarify the relationship. If Apoquel is needed for pruritus control but liver enzyme elevations persist or worsen, switching to an alternative antipruritic may be considered.

I really hope you are enjoying the course.

Best regards,

Scott

Replying to Victoria R. 08/08/2025 - 14:31

No problem!

I am looking forward to trying it too!

Scott 🙂

Replying to Sarah Keir 02/08/2025 - 18:25

Hahahaha!

There has to be a home for our old university gowns!

Scott 🙂

Replying to Riley D. 03/08/2025 - 21:02

Hey Riley,

Thanks for sharing the case. I’ll be curious to see how things go with his check up and whether you detect any effusion you can tap for RT-qPCR.

For what it’s worth, I’ve just been following an older kitty, “Emma Jane,” with a long, twisty file: chronic pleural effusion, persistent hyper-globulinaemia, a static right-ventricular mass, previous pericardiectomy, and a relapse of presumptive FIP now on a second 84-day GS course. Her echo shows mild HCM-type changes plus that ventricular mass, and her troponin’s been intermittently high—so I’m watching her as another possible example of the cardiac-FIP spectrum. The one thing that does not make sense with her is her age!

Keep us posted.

Cheers,

Scott