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In the October episode of Chattering with ISFM, host Nathalie Dowgray presents two detailed discussions on important feline health topics - gastrointestinal and renal health.
First, Yaiza Gomez-Mejias interviews Sina Marsilio on feline chronic enteropathies, with a particular focus on gastrointestinal lymphoma and the diagnostic challenges of distinguishing small cell lymphoma from IBD. Marsilio discusses recent advances in the field, drawing from her recent work on the ACVIM consensus guidelines for ‘diagnosing and distinguishing low-grade neoplastic from inflammatory lymphocytic chronic enteropathies.’
Later, Kelly St. Denis speaks with Jonathan Stockman about his JFMS Clinical Spotlight article, ‘Dietary Phosphorus and its Impact on Renal Disease in Cats’. They examine phosphorus metabolism, the risks associated with high-phosphorus diets, and effective strategies for managing phosphorus levels to support feline kidney health.
For further reading material please visit:
For ISFM members, full recordings of each episode of the podcast is available for you to listen to at portal.icatcare.org. To become an ISFM member, or find out more about our Cat Friendly schemes, visit icatcare.org
Host:
Host:
Nathalie Dowgray, BVSc, MANZCVS, PgDip, MRCVS, PhD, Head of ISFM, International Society of Feline Medicine, International Cat Care, Tisbury, Wiltshire, UK
Speakers:
Yaiza Gomez-Mejias, LdaVet MANZCVS (Medicine of Cats) CertAP (SAM-F) Acr AVEPA, ISFM Community Coordinator and Small Animal Clinician
Sina Marsilio, Dr.med.vet., PhD, DACVIM (SAIM), DECVIM-CA, Assistant Professor of Medicine & Epidemiology at UC Davis.
Kelly St. Denis, MSc, DVM, DABVP (Feline), Co-editor of the Journal of Feline Medicine and Surgery and JFMS Open Reports, St Denis Veterinary Professional Corporation, Powassan, Ontario, Canada
Jonathan Stockman, DVM, DACVIM (Nutrition), Associate Professor in the Department of Clinical Veterinary Sciences & JFMS Author.
Creators & Guests
Host
Nathalie Dowgray
What is Chattering With ISFM?
Welcome to Chattering With ISFM, the official monthly podcast of the International Society of Feline Medicine, hosted by Nathalie Dowgray (Head of ISFM). Each month, we chatter about cats and cat-friendly practices with industry experts and contributors to The Journal of Feline Medicine and Surgery. Each episode contains highlights from our longer discussions and interviews, which are accessible to ISFM members at portal.icatcare.org. If you would like access to our full episodes, would like to become an ISFM member, or find out more about our Cat-Friendly schemes, visit icatcare.org.
Hello and welcome to the October
episode of Chattering with ISFM.
I'm Nathalie Dowgray, Head of ISFM
and host of this month's podcast.
This month, Kelly St Denis is going
to be speaking with Jonathan Stockman
about his JFMS Clinical Spotlight
article, Where Are We With Dietary
Phosphorus and Renal Disease?
But first up this month, Yaiza Gomez
Mejias is speaking with Sina Marsilio
on the latest in feline chronic
enteropathies, including GI lymphoma.
Which are the different types
of cells involved in feline
gastrointestinal lymphoma?
This lymphoma is made of
small, mature lymphocytes.
That's important to realise in
contrast to the classic multi centric
lymphoma that we see in dogs where
they show up with big lymph nodes.
That's not the case for low grade
intestinal T cell lymphoma or LGITL, the
cells are mature small T lymphocytes.
This lymphoma makes up about
75 to 80 percent of all
feline intestinal lymphomas.
These lymphocytes are about the size
of a neutrophil, these cells mostly
affect the mucosa, either the lamina
propria or the epithelium, in which
case we talk about an epitheliotropic
lymphoma, or they can be also mixed.
In the duodenum, we might have moderate
to severe lymphoplasmacytic enteritis.
And so that makes it really hard for
the pathologist to know what's going on.
Small cell lymphomas are almost always
diffuse, which means that they don't
build masses or things like that.
We see enlarged cell lymphomas
diffuse in the gut cell wall.
So why is it difficult for
pathologists to differentiate?
If we think about IBD in cats, most
experts would agree that lymphoplasmacytic
enteritis is by far the most common
form of inflammatory bowel disease
in dogs and cats, and that cellular
infiltrate consists of, again, small
mature lymphocytes intermixed with plasma
cells and other inflammatory cells like
neutrophils, eosinophils, or macrophages.
In LGITL, the dominant cell infiltrate
are small mature lymphocytes.
Which again can be intermixed
with other inflammatory cells.
Think about these small lymphocytes,
a small mature cells also mean that
there is a very low mitotic index, which
means, of course, that clinically this
disease is progressing very slow and
so it almost has an indolent behaviour.
All of us have encountered cases
where we do see muscularis or
mucosal layer thickening, or both.
This disease, even though maybe
ultrasonographically we might see it in
the muscularis, has no correlation with
anything, except for the mucosal changes.
This really is a mucosal disease.
Despite attempts from other studies,
nobody has found a cutoff that
would definitively say, okay, if
the gut wall is this thick, or if
the abdominal lymph nodes are this
thick, it would be definitely LGITL.
It's really hard for the clinical
pathologist to make any diagnosis of
small cell lymphoma just based on the
finding of small mature lymphocytes
and some reactive lymphocytes.
If we see that there's like sheets and
sheets of these monomorphic looking small
lymphocytes that obliterate the entire
mucosa and don't make space for anything
else, I think it's a pretty clear case.
But then if we do have these nests
and plaques and accumulations
of small lymphocytes, that's
when things get tricky.
So other types of lymphoma that
we should not forget about is
high grade large cell lymphomas.
These can be either of
T or of B cell origin.
High grade large cell could be both.
They are often located in the ilium or the
iliopoietic junction or stomach and they
often make masses, rather than diffused
lesions, but they can be diffused.
And they can be in the
mucosal or transmural.
When we do have severe, they often
produce severe abdominal lymphadenopathy,
thickening of the bowel wall.
They can also be in other organs and
cause hepatomegaly or splenomegaly.
And those findings, of course,
we would find on abdominal
ultrasound, which would be great.
But I want to stress here, the absence
of ultrasonographic findings does
not exclude large cell lymphomas.
The absence of any findings in ultrasound
doesn't mean that there's nothing there.
But the other thing that is fantastic
about ultrasound in that aspect is
that we can do fine needle aspirates.
We might see sheets of large, very
immature lymphoblasts, that have cellular
abnormalities, pleomorphism, multiple
nucleoli or even nuclei, present.
And then if we are really lucky,
we might see actually mitosis.
And so, this indicates that the
mitotic index is really high.
Fine needle aspirates are really
phenomenal way of diagnosing the disease.
And also if we think about that cellular
composition, it also becomes clear where
that usually is a much more aggressive
clinical course because a higher mitotic
index correlates with more rapid growth
and a more aggressive clinical course.
That makes it clear why we shouldn't
treat that just with metronomic
chemotherapy, but with more cytotoxic
chemotherapy, such as CHOP protocols.
Some people call it a subform.
Some call it a separate form.
I want to talk about large
granular lymphocyte lymphomas.
Similar to large cell lymphomas, these
are composed of large lymphocytes.
They make up about one third of
large cell lymphomas and consist
of cytotoxic T cells or NK cells.
Histologically,
they're characterised by eosinophilic
granules in the cytoplasm.
They can cause either mass like lesions,
but they can all or segmental thickening
and they're often readily diagnosed
by fine needle aspirates as well.
While large cell lymphomas have
a relatively poor prognosis,
unfortunately, large granular lymphocyte
lymphomas have a grave prognosis
and a very aggressive clinical
course.
Do you think the difference between
small cell lymphoma and inflammatory
bowel disease is relevant?
I think if it was me, I would want
my doctor to give me all the options
and then I can decide, right?
While I agree that a cat with
chronic intestinal disease likely
has IBD or LGITL, there are
intermediate and large cell lymphomas.
There's mast cell disease.
There's infectious disease,
including histoplasmosis, at
least here in the United States.
There's gastrointestinal
eosinophilic sclerosing fibroplasia.
All of those are important differentials
for cats with chronic GI disease, right?
We mentioned that neither clinical
science, nor serological testing,
nor ultrasound, nor cytology, none
of those have been found to have, to
reliably differentiate between the two.
The only reliable way to differentiate
is to collect intestinal biopsies.
The beauty of our profession, I believe,
is that there is no algorithm that
works for every single patient, right?
Because it depends so much on whether
I have a cat that has lost a lot
of weight rapidly, according to
the owner, and maybe doesn't have
so much time to do a diet trial.
I might push harder for biopsies because
we just don't have much time to lose,
versus in a cat that might be very stable,
I would suggest maybe a treatment trial.
If I have a stable 10 year
old cat, otherwise healthy,
maybe mildly underweight,
the risk for taking
biopsies is really small.
But if I have a cat with severe HCM,
obviously the calculation changes.
I believe your question is the difference
between small cell lymphoma and IBD
relevant for therapeutic options, right?
So it is true that many cats with
LGITL respond to prednisolone
treatment alone, at least for a while.
And then on the other hand, cats
which are refractory IBD can
be treated with Chlorambucil.
So in the real world, the treatment
is very similar currently.
You might argue could you not
go on an escalating treatment
regimen starting with Pred?
Then assess and escalate
to Chlorambucil if need be?
And I think again,
perfectly valid options.
It's possible that we will see
better and more targeted therapies
in the future, but currently the
treatment is very similar and you
could argue there isn't a clinically
relevant difference at this point.
Thank you so much.
That's fascinating.
Now over to Kelly St.
Denis and Jonathan Stockman
to discuss dietary phosphorus
and renal disease in cats.
Welcome, Dr Stockman.
Thank you
Why is phosphorus important?
Phosphorus is at the heart of
nutritional management of kidney
disease in cats because a lot of
the derangements in hormones are to
do with phosphorus metabolism with
chronic kidney disease in cats.
When we have chronic kidney disease,
some of the things that may occur
are we can have an increase in
the parathyroid hormone, which is
obviously intimately involved in
regulating calcium and phosphorus.
We may have a decrease ability
in the kidneys ability to remove
excess phosphorus from the body.
We have less activation of vitamin
D, which is also important for
calcium and phosphorus metabolism.
So all of these things play together.
When we have kidney disease and
contribute to the progression
of disease and worsening of the
clinical status of the patient.
We know we have to monitor phosphorus
because hyperphosphatemia is a
negative indicator to address.
High phosphorus and calcium also have
the risk of the calcium phosphorus
product and mineralization of
tissues, which also contributes
to the progression of the disease.
So these are all things that come into
play together and can really impact the
patient's wellbeing and how quickly they
progress through the disease, which is
obviously what we're trying to prevent.
We're trying to avoid the disease
from progressing as much as possible.
In addition to that, what I
highlighted in the paper as well is
again the topic of excess dietary
phosphorus even in healthy adult cats.
Our study was the first one to
show that these changes can happen
very quickly if they receive a
lot of bioavailable phosphorus.
And also that these changes are truly
indicative of kidney damage that leads
to chronic kidney disease and not
something that is potentially reversible.
In the article, you do talk about
monitoring dietary phosphorus,
but other options such as
calcium to phosphorus ratio.
And I wondered if you could tell us how
are we supposed to navigate this if it
is so difficult for us to monitor just
based on total dietary phosphorus alone?
It's tricky because manufacturers
don't have to declare the total
amount of phosphorus in the diet.
Some provide information on the
label, but it's totally voluntary.
Even when they do it's the total
dietary phosphorus, so we don't
know how much is bioavailable.
And you mentioned organic inorganic.
And that's the type of language that
we've been using for a very long time.
And in the literature there is some
evidence that suggests that the
solubility of phosphorus in water
is crucial for the bioavailability.
And it tends to be the inorganic
phosphors, salts that are water soluble,
that are more bioavailable for cats.
Those compounds are added to cat
food that can be very bioavailable
and at high amounts, increasing the
risk for kidney damage and disease.
There are other things that impact
phosphorus bioavailability, including
the calcium to phosphorus ratio.
When we have a higher ratio, it seems to
reduce the bioavailability of phosphorus.
So a calcium phosphorus ratio of
above one is safer in terms of
high phosphorus risk of inducing
kidney disease than a low calcium to
phosphorus ratio of let's say 0.5, 0.6.
Also, the other thing that can
be a little bit protective is the
amount of magnesium in the diet.
So magnesium, together with
calcium, may complex with phosphorus
preventing its absorption.
So this is another thing
that can be helpful.
But the calcium phosphorus ratio, you
can find the relative bioavailability
of, and so obviously, when the calcium
and phosphorus ratio is a little
bit higher, it's a little bit more
protective or the bioavailability is a
little bit reduced for the phosphorus.
And this is something that potentially
you can find on the label if the
manufacturer decides that they want to
list it, but again, this is voluntary.
And usually, that will be a minimum
value analysed in the diet, but it
doesn't tell you what the maximum is.
So it's a bit of a limited information.
Where do early kidney and kidney
disease diets fall into this, in
terms of making decisions about that?
If you're a newly diagnosed cat in very
early stages of kidney disease to start
with those early disease diet, especially
when they're in stages one through two.
But then one of the monitoring steps
that I would consider is maybe at that
point, when they're on the diet for a
little while, still measuring PTH and
FDF23 and then if elevated, transition
to a more phosphorus restricted diet.
If those hormones are very elevated, that
can be an indication that we could benefit
from even more phosphorus reduction.
There is evidence that FGF23
elevation on its own is a negative
and can lead to cardiovascular
disease and other complications.
So it is something we should consider.
Thank you.
Thank you all for listening.
If you are an ISFM member don’t forget
you can access the full version of
the podcast and all the other ISFM
member benefits including congress
recordings, monthly webinars, the
clinical club, the discussion forum
and much more at portal.icatcare.org.
If you are looking for more free
CPD from ISFM in November we have
a number of open access webinars.
First up, on the 19th we have a
webinar on Microbiota analysis,
evidence and perspectives on
clinical practice for vets.
And thats with Miquel
Montserrat and that’s brought
to you by Purina.
On the 25th of November, we have our
final Cat Friendly Clinic webinar
for the year, that’s on Cat Friendly
Hospitalisations, with Yaiza Gomez Meijas.
We'll be back again next month,
with more from the world of
feline medicine and JFMS.