10/26 Oberon +8.5 375, AMPS 462/1.9, +2 406, +4 373, +6 367, +9 398, PMPS 388/1.9, +2 311, +4 302

Hope the R helps :).

By any chance, was the full panel TAMU GI panel done? I don’t see it. If so, are there any plans of repeating it to see what the Spec fPLI is doing?
I know you said the US read was Triaditis. Unfortunately, antibiotics may or may not “fix” Triaditis. If the inflammation was initially caused by an infection and it’s treated, the inflammation may decrease and normalize, but not always. In addition, any infection found can be secondary vs primary to the Triaditis. If inflammation is still present, it can cause resistance. I am going to attach a photo that shows the issues that occur just with chronic pancreatitis alone vs Triaditis which would obviously worsen the situation.

upload_2020-10-26_8-36-25.jpeg
 

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No, the only thing we really did in terms of triaditis was the ultrasound. The original plan was to do 28 days of Baytril, but he started gagging just at the smell of the tablets so we switched to 7 d of Veraflox. I ought to follow up with the internist next week (that whole dept is apparently shut down for covid this week).
 
Hopefully, they get back up and running & everyone is ok there:). Nothing worse than gagging just from the smell of a medication :(.
Are they going to repeat the US?

I was just thinking again about differentials with respect to diagnosis and common underlying issues/causes known to result in insulin resistance:bookworm:.

The other question I had was, was there any mention of of doing an ACTH Stimulation test given the Dex suppression result was borderline? This may be helpful (sometimes it is and sometimes it’s not :)). Some include it as part of the work up.
I’ve attached the article in case it’s of any help :).

One thing that is very interesting, and I am not sure if they have been able to identify if it occurs with cats, is that there can be cyclicity with all causes of Cushings. It was once thought to be rare, but now they know it is more common than once thought.

People can cycle in and out of active periods of the disease over months or years (sometimes even day to day or within weeks). I wonder if this may be the situation in some cases where there is suspected IAA in a cat? If there are borderline results for Cushings or enough indications that there is in fact another underlying issue, such as ACTH dep cushings, is that really the primary problem? Do some cats eventually “cycle out” of the active part of the disease process and achieve remission from DM within months or even years, or with some cats, maybe they don’t completely cycle out of the active disease but instead experience the waxing and waning (also common) of the active cycle & therefore, the DM becomes more easily controlled/regulated? It would offer a logical explanation for the reduction in insulin required or even for eventual remission with some cases if no other active inflammatory disease states are at play.

Things that make you go hmmmm;)!! It seems they have made great strides in being able to better identify more mild cases of endo issues whereas years ago, these cases flew under the radar and all of it was considered very rare. Not so much now.

I just think the differential diagnosis are important to think about and keep in mind because, similar to dental issues that are often mentioned on the board, other disease states like Triaditis, pancreatitis, Cushings (even if mild), all offer the potential for the use of additional treatment options that may help reduce the time it takes to get the DM controlled and regulated again (or achieve remission :)).
 

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Holding steady in the high 300s at PMPS... this is going to be the 9th cycle at 8.5 and I can give him 1.25 U of R. Alternatively, maybe it's time to bump him up to 9.0 (and skip R tonight)? I think there's a case to be made for either one.
 
I didn't want to wait too long and shoot late (should have thought about this and posted earlier!), so I went with the more conservative approach and held off on the increase but gave 1.25 U of R. It'll probably be easier for me to monitor this evening than tomorrow if the R triggers another dive (long teaching day; I'll be around but busy off and on), though I don't think it's likely. But it does really look like he needs a Lantus increase. Other than the dip he's still stuck in the pinks for the most part. I can do that tomorrow morning.
 
I will be curious.... but I would think R not only because of the glucose value but also because of the ketones right now. If you increase the Lantus it doesn’t seem like that will make a dent in the BG or ketones like the R might
 
Lisa & Oberon said:
I didn't want to wait too long and shoot late (should have thought about this and posted earlier!), so I went with the more conservative approach and held off on the increase but gave 1.25 U of R. It'll probably be easier for me to monitor this evening than tomorrow if the R triggers another dive (long teaching day; I'll be around but busy off and on), though I don't think it's likely. But it does really look like he needs a Lantus increase. Other than the dip he's still stuck in the pinks for the most part. I can do that tomorrow morning.
Click to expand...

Funny you sent as I was sending :). Good point that you can watch tonight. Always important ;)!
 
But there have been times where you’ve got the ketones lower and even the BG a bit lower and that would seem like a good time to increase the Lantus. So, R and then increase the Lantus. Just a thought :)
 
:) Actually, when he's coming out of a dip is a pretty good time. He's still low then so I can't give R, but climbing rapidly.

Slight possibility of a dip tomorrow, though I think the next day is more likely. (Current pattern is every 3-4 days.) I don't think I want to wait that long to increase, so I may just go ahead and do it tomorrow.
 
Oh yeah :).....forgot about the magic scanner!!!! Maybe I wouldn’t be on the great feces mission to get the perfect samples for microbiome testing :confused:.
T literally ruined my “catch” the other day by throwing litter at it mid air while my face was IN RANGE :eek:. Guess he let me know how he felt about my little study....LOL
 
Oh hell no :p! He could win the award for most neophobic cat in the world :banghead:. I have a camera in the litter room and set an alert but of course I was across the house so was late enough that he was able to beat me! He was like “I’ve got serious poop to cover so I don’t know what you are doing in MY box but it is not of my concern!” INCOMING.....litter literally midair like he did it on purpose to teach me a lesson :eek:!
 
Tomlin said:
One thing that is very interesting, and I am not sure if they have been able to identify if it occurs with cats, is that there can be cyclicity with all causes of Cushings. It was once thought to be rare, but now they know it is more common than once thought.
Click to expand...
In my time here, we've had exactly 1 Cushings (PDH) cat go into remission from Cushings and also diabetic remission. Story here. Like acromegaly, the pituitary tumour can pulse. I've seen quite a few more acrocats go into remission and out again. Of course, there are probably more that don't get tested because there are no obvious clinical signs or their dose remains low.

We have yet to see a cat with both Cushings and IAA. Most people start with the UCCR test to differentiate. Bonus, it just means collecting urine samples at home, unless you've got a cat like T at home. :p

Oberon does need that Lantus increase.
 
R already kicking in at +2... wonder if he's actually going to dip or if he's just messing with me. Unless something really weird happens tonight he'll get the Lantus increase tomorrow morning.
 
:bighug:
Wendy&Neko said:
Of course, there are probably more that don't get tested because there are no obvious clinical signs or their dose remains low.

We have yet to see a cat with both Cushings and IAA.
Click to expand...

This is exactly why I am questioning and thinking about current recommendations based on what the endos know now vs in the past:). Many of these cases are being completely missed :banghead:. How many of the cats on this board have been tested for HST? The current standard by leading endos at the U settings is to test every cat when initially diagnosed with DM. Unfortunately, in the past, Cushings and HST, were identified and diagnosed with different clinical symptoms & diagnostic values in mind. They were also not on the radar except when it was obvious because it was thought to be “extremley rare”, “doesn’t usually happen”. One will never see what they don’t look for o_O! Unless and until the current standards are recognized, followed & there is an open mind to the reality of these disease states being more common than once thought, cases will continue to fly under the radar & be missed until the condition is more serious and causes additional (and often more serious) health issues.

I am not certain about IAI with Cushings only because the much of the current info out there is that antibodies exist in many cats (and dogs and people:) ) and they often have no clinical implications. For this reason, they have essentially made IAI a diagnosis of exclusion and recommend that even with a positive test for antibodies, other underlying causes/disease states/issues, that they know for certain cause or contribute to insulin resistance, be ruled out first. If you miss other diagnosis, you also miss the opportunity for potentially more effective and efficient treatment options available. You may also not get the DM regulated at all, or it may be time limited, if the primary problem is not identified and addressed.

Wendy&Neko said:
Most people start with the UCCR test to differentiate.
Click to expand...

This is another more recent change. Like with Oberons IM, many IMs will actually not start with the UCCR and will instead go right to the Dex suppression test. UCCR is now recommended to be used as the test of choice when the index of suspicion is low (and it requires a minimum of 2 home “first catch” samples from a miniumum of 2 consecutive days). If there is any suspicion of a problem, they go right to the dynamic test aka Dex Suppression Test. Keep in mind if any of the UCCRs come back as elevated, the next step is the Dex Suppression Test. Even transient stress and illness (which in Oberons case there was Triaditis with possible bacterial infection) can result in a false positive test. In that case, several days are wasted collecting urine and waiting for results when one could instead be further along in the diagnostic process. This is why they don’t recommend UCCR when there is enough suspicion & clinical evidence of a problem—-move right to the Dex Suppression Test.

In Oberons situation, the unregulated DM or Triaditis, could have resulted in the increased Dex test/borderline result. Even if they had done the UCCR, transient stress &/or illness is able to result in a false positive & then you are back to the Dex test. In the end it would seem it would be important to address the Triaditis issue, get the DM regulated (to a point) and then potentially re run tests—maybe try the UCCR if it is pretty easy to catch several days of the first urine :) in hopes that it is negative which would then would be pretty conclusive.

Again, my questions for ruling out the differential diagnoses from IAI are not to disprove that the IAI is a primary or contributing problem, but instead to make absolutely sure that there is no other underlying problem that could be causing the insulin resistance:bookworm:. It would be important to identify or rule them out not only for regulating the DM right now but also, hopefully, to be able to avoid additional or more serious health issues in the future :bighug:.
 
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