07/19 Eddie Cabergoline question

Good morning, everyone

For the past year, Eddie and I have been on the Biosimilars forum (he's currently on Lantus/Glargine 12u BiD). Eddie had hypophysectomy for acromegaly in Dec 2020. He had a terrible hospital experience (incision dehiscence twice) and was in clinic for 28 days. They were able to get about 60% of the tumour and so in 2021 he had SRT (3 sessions). It's now 1.5 years later and while his insulin requirements went down after the SRT (Feb 2021), they're beginning to climb back up again. His spreadsheet tells the tale as does the fact he's residing in high numbers with the occasional dive followed only by long sustained time in the high zone, which makes me so concerned.

I think his acromegaly is active again. In March he had a CT scan to check on his status and although it showed a much reduced area the jury is out whether or not the CT showed scar tissue or if the tumour is there and just smaller from the SRT. Eddie is also 76% IAA and by the looks of things that's kicking in big time along with possible IGF-1.

I am going to take him to Victoria once they are back from summer break. In the meantime, I'm wondering about Cabergoline.

@FrostD I'm wondering what you think. I'm really quite challenged at the moment. Usually with Eddie and Blue (Eddie's brother who also has acromegaly and is OTJ [surgery/SRT] but just diagnosed with early CKD), it's one needing close attention at a time. Right now it's both and, well, wow...

 

I've been hemming and hawing about how to answer this, so I'll just do what I do "best" - objective, honest and straightforward. Please understand there is absolutely no judgment/condescension/tone or anything in this, it can be hard to convey over the internet.

It seems to me that one of the things you have to come to terms with is they're now older, senior cats. The days of perfect health are gone. You can treat or possibly cure one thing, but then another is going to crop up. Believe me I understand, I wish for perfect health as well, but the stress and anxiety of chasing it will absolutely wear you down - physically and emotionally.

You've already spent quite a bit on the two of them, at least from a US-cost perspective. Far more than I personally could afford or justify to spend. To put it quite bluntly, I think your goal of completely eradicating the tumor, getting rid of the diabetes,etc is a bit of a pipe dream. I think the expectations/hopes are setting you up for a hard failure and even more stress and anxiety.

Even if money were no object, I personally would not put him through more CTs/MRIs, SRT, etc. That is a lot on a little body, and the older he gets and the longer than growth hormone is affecting the rest of his body (heart), the more risky it becomes.

Now all that said, every single one of us is different in how far we're willing to go, how much we're willing to spend, what sacrifices we're willing to make. I absolutely understand that to a lot of people here, their cats are the equivalent of a human child. That means no limits, no boundaries. If this were one of my kids, you bet I'd be weighing risks, chasing down everything I could, regardless of cost. But quality of life matters as well, for BOTH of you.

Cabergoline in a post SRT + IAA cat is, simply put, incredible risky. Now comes the part I believe nearly everyone here will disagree with....if it were me personally as Eddie's caregiver, I would try the cab instead of another round of imaging and SRT. My goal at that point would be more...palliative?.... care - hoping the cab would keep the other acro effects in his body at bay. BUT, and this is a huge BUT -

My concern for you is primarily your work and sleep schedules. I am not sure you can test as often is required to keep him safe, especially when school starts. If you end up in a situation where the cab starts working, another round of cells dies off, and IAA takes a break....that's an incredibly dangerous situation. July 2021 on my SS - you can see just how much I was having to test and feed to keep him safe - just from cab alone.

If you will do another round of SRT, then I wouldn't bother. It can take up to 6 weeks to see cab effects, by then he'd have his scans. And cab has to be tapered down before SRT...so you'd ramp him up then just as soon take him back down.

To summarize - I think cabergoline in Eddie's situation potentially very dangerous. While I personally would do it (again no more SRT) as I am home all the time, can handle broken/little sleep, can manage hypos, etc - that is a risk I personally am willing to take. I do not believe it is the right decision for you.

 

This is one thing I really appreciate about you: straight-shooter. There is so much to say in response but I'm letting your comments settle in. The one thing I will affirm is that I'm not ready to give up yet and I really don't think Eddie is either. I'm going to do some deep reflection, though, on your good words, for which I am grateful.

 

It's taken me quite a while to write this post today. Before you read on, know that whatever you decide to do we'll support you. What I write is my opinion, my circumstances/experiences, not yours.

Acromegaly is the symptoms you see as a result of hypersomatotropism, which is the benign pituitary tumour. The tumour (not the acromegaly) has been there all this time. What SRT does is neuter the tumour cells so that as they die off, they do not reproduce. Until they die off, the tumour cells are still active and producing excess growth hormone, which in turn causes the acromegaly. I remember one cat (Grayson) who after SRT from around 16 units, up to 50 units before the SRT started to kick in quite a bit later. Yes, he also had IAA, which just adds another complication. At the one year anniversary of SRT, he was down to 20 units. Still above his preSRT dose, but way less than what it would have been had he not had treatment.

Eddie's max dose was 15 units? That's what I see on the spreadsheet. What was the max dose from the earlier days? I'm not sure his post SRT insulin dose journey is atypical. He's also a very complicated cat treatment wise so far, so not much to compare him to. I also went back to your post where you quoted that Dr. Hammond thought the CT scan showed scar tissue, not regrowth. That was less than 3 months ago.

You do know that only a minority of cats that have SRT go OTJ. You have one cat that's done that already, so you've already beaten the odds. Don't expect the same of Eddie. If he does, that's a bonus. What the majority of SRT cats get is a longer life, with much reduced insulin dose, and more importantly, less excess growth hormone and it's nasty side effects. I call that a huge win. Most of these cats are older cats, and many die of other causes. The cat Grayson passed with a blood cancer, totally unrelated to the acromegaly. What the SRT does is make the life they have left much better.

The thing about having an acrocat, is that at some point you come to the realization that there is only so much you can do to help. The rest is literally up to the cat's body and luck. In many ways you remind me of me. My vet told a new tech that I had spent the equivalent of a brand new small car on Neko. Worth it as far as I was concerned for "the world's bestest cat". I still miss her a lot, think of her often. The music in her tribute video was fitting. I did everything I could for her, that made sense to do. At some point, things no longer made sense and I had to let her be a cat and enjoy what time she had as much as she could, and stop subjecting her to treatments that may or may not have worked, just to keep her around for me. I also considered cabergoline, though it was brand new at the time with no experience out there. But I decided that with all she had going on, it was just one too many thing.

SRT requires sedation, at least for two days, maybe up to four depending on how the particular place treats, and other factors. Twice now Eddie has had adverse reactions to sedation. In your post after his last bad reaction during anaesthesia for a CT scan, you said Victoria uses a different sedation med, but who's to say he'll do any better on it? I strongly suggest that if you do really want to go ahead with another SRT that you get an echocardiogram done on Eddie by a boarded cardiologist, before you book SRT again. A xray or radiograph is not enough to show you whether his heart can take it. A cardiologist can also advise on anaesthesia and which meds are appropriate if any. CSU requires an echo before SRT, as well as up to date blood work, to make sure the kidneys are also OK with anaesthesia. I personally think the risk to Eddie for SRT again is pretty high. It's not something I would do, but I'm not you and you may have a different risk tolerance than I do. Neko had the all clear from her cardio vet before her second SRT, but almost didn't make it, in a teaching hospital that had all the expertise at hand (cardiologists, anaesthesia experts). Her radiation was reduced to just the one day. I felt awful afterwards and the event helped me realize that there was only so much I could do and some things no longer made sense to do as the risk outweighed the possible reward.

I think I'm echoing a lot of what Melissa has already said, plus I've walked in those second SRT shoes and regretted it. Ask yourself "what would Eddie want to do?". Cats live in the moment, day to day. Cats are so much more than his numbers. If his BG is high, increase the insulin dose. If the BG is his only acro side effect, that's not a big reason to treat.

 

Ok, can you elaborate a bit on why dangerous? Is it because of what seems my ability to manage, monitor, test, feed, etc? I get it re: the personally. I don't hear you any other way. If you think cab is not the right decision for me and you'd step away from SRT, what options would I have? It's kind of like being between the devil and the deep blue sea, as my mother used to say.

But, Melissa, I really appreciate your good words here and your care. I never hear what you say as being judgemental or condescending, for that matter. You have experience and I'm learning. I get it. Whatever path I take, it's on me. Nevertheless, it really does help to feel like we're in this together.

 

Acromegaly is the symptoms you see as a result of hypersomatotropism, which is the benign pituitary tumour. The tumour (not the acromegaly) has been there all this time. What SRT does is neuter the tumour cells so that as they die off, they do not reproduce. Until they die off, the tumour cells are still active and producing excess growth hormone, which in turn causes the acromegaly. I remember one cat (Grayson) who after SRT from around 16 units, up to 50 units before the SRT started to kick in quite a bit later. Yes, he also had IAA, which just adds another complication. At the one year anniversary of SRT, he was down to 20 units. Still above his preSRT dose, but way less than what it would have been had he not had treatment.

Well, I guess what remains of the tumour is there. That's what I'm unsure of. This is kind of like a Schrödinger's cat situation. What is going on inside of Eddie's head (in so many ways). Eddie is at his 17 month mark since SRT. I get different opinions with regard the efficacy of SRT: the radiation oncologist suggests it's 9-12 months, as do the folks at WSU, so I'm up in the air about the timeliine.


Eddie's max dose was 15 units? That's what I see on the spreadsheet. What was the max dose from the earlier days? I'm not sure his post SRT insulin dose journey is atypical. He's also a very complicated cat treatment wise so far, so not much to compare him to. I also went back to your post where you quoted that Dr. Hammond thought the CT scan showed scar tissue, not regrowth. That was less than 3 months ago.

Yes, I believe 15u was the max dose. I didn't have a SS before I joined FDMB although I did curves and sent them to the IM vet. Eddie's journey is so complicated; it's complicated by the fact he was in WSU for 28 traumatic days, came back with a feeding tube and was on a pharmacological overload including Trazadone. He wasn't using the kitty box, he was so food-driven he was scary to behold, was reactive and completely asocial. This went on for months. The journal I kept is awful and is so disturbing to read but I didn't give up on him. By the end of 2021 he was starting to regulate (that means so many things: using kitty box, not so food-driven, still a bit reactive and a-social but far, far better).

You do know that only a minority of cats that have SRT go OTJ. You have one cat that's done that already, so you've already beaten the odds. Don't expect the same of Eddie. If he does, that's a bonus. What the majority of SRT cats get is a longer life, with much reduced insulin dose, and more importantly, less excess growth hormone and it's nasty side effects. I call that a huge win. Most of these cats are older cats, and many die of other causes. The cat Grayson passed with a blood cancer, totally unrelated to the acromegaly. What the SRT does is make the life they have left much better.

I don't know what the future holds for Eddie. I do know, I'll try my best for him. And, as you see, I'm taking him for a blood panel, etc. so as to determine where he's at. "Etc" means I am going to get an IGF-1 test done.

The thing about having an acrocat, is that at some point you come to the realization that there is only so much you can do to help. The rest is literally up to the cat's body and luck. In many ways you remind me of me. My vet told a new tech that I had spent the equivalent of a brand new small car on Neko. Worth it as far as I was concerned for "the world's bestest cat". I still miss her a lot, think of her often. The music in her tribute video was fitting. I did everything I could for her, that made sense to do. At some point, things no longer made sense and I had to let her be a cat and enjoy what time she had as much as she could, and stop subjecting her to treatments that may or may not have worked, just to keep her around for me. I also considered cabergoline, though it was brand new at the time with no experience out there. But I decided that with all she had going on, it was just one too many thing.

I guess I've yet to arrive at that realization if only because, as I've learned here, ECID. I take it as a compliment that I'm doing the best I can do for Eddie (and Blue) and so far things make sense. It's a strange journey because we have to take it with our acrocats and often be at odds with veterinarians, which is horribly ironic. It makes sense to me to investigate cab, if only because it might help with his insulin in relation to IGF-1/IAA. Eddie's medications are not all that many and he has more good days than ever. In fact, he seems unperturbed by either high or low BG. Go figure.

SRT requires sedation, at least for two days, maybe up to four depending on how the particular place treats, and other factors. Twice now Eddie has had adverse reactions to sedation. In your post after his last bad reaction during anaesthesia for a CT scan, you said Victoria uses a different sedation med, but who's to say he'll do any better on it? I strongly suggest that if you do really want to go ahead with another SRT that you get an echocardiogram done on Eddie by a boarded cardiologist, before you book SRT again. A xray or radiograph is not enough to show you whether his heart can take it. A cardiologist can also advise on anaesthesia and which meds are appropriate if any. CSU requires an echo before SRT, as well as up to date blood work, to make sure the kidneys are also OK with anaesthesia. I personally think the risk to Eddie for SRT again is pretty high. It's not something I would do, but I'm not you and you may have a different risk tolerance than I do. Neko had the all clear from her cardio vet before her second SRT, but almost didn't make it, in a teaching hospital that had all the expertise at hand (cardiologists, anaesthesia experts). Her radiation was reduced to just the one day. I felt awful afterwards and the event helped me realize that there was only so much I could do and some things no longer made sense to do as the risk outweighed the possible reward.

Eddie's sedation issues were at WSU and the last CT scan. He had no issues at all with the sedation used by the radiation oncologist for his SRT. But your point regarding an echocardiogram done by a boarded cardiologist is well-taken. I am not entirely committed to a second SRT (Blue had 18 sessions of fractionated radiotherapy @ WSU and only one SRT session at VCA Calgary) for Eddie. In fact, I'd just like to learn more about cab in the meantime.

I think I'm echoing a lot of what Melissa has already said, plus I've walked in those second SRT shoes and regretted it. Ask yourself "what would Eddie want to do?". Cats live in the moment, day to day. Cats are so much more than his numbers. If his BG is high, increase the insulin dose. If the BG is his only acro side effect, that's not a big reason to treat.[/QUOTE]

What would Eddie want to do? Good question. His in-the-moment answer is "have a snack" or "go out onto the catio in the sun".

I'm really appreciating the support here and by that I mean the willingness to share perspectives while knowing that ECID as is every one of us. It also helps knowing I'm in this with other like-minded (as in the sense of really caring and willing to walk the walk kitty-folks) people. Thank you, Wendy.

 

Dangerous in the sense of a hypo, yes. I'm a little biased given Mr Kitty's downward BG spiral, but these are large doses and depots we're working with. So yes, what I observe as your ability to test given school schedule, sleep needs, etc I do worry. I could be wrong! I just recall a few busy days/nights that really took it out of you.

No SRT and no cab really just leaves you with letting him be. Giving the last round of SRT time to settle, letting the IAA run out, and managing the diabetes with insulin as needed.

As I mentioned, the sole reason I personally would do the cab is the hope of slowing the other acro effects like soft tissue growth, heart issues, etc. I believe cab is pretty expensive in Canada though.

The really difficult thing about this, no matter if it's your first pet or your 100th, is you get to a point where you have to start guessing how much life you think they have left. Terribly depressing. And when considering treatment options, you have to start questioning how much life it would extend, with what quality, etc.

Before all of Mr Kitty's other diagnoses, we strongly considered the 5-8k for SRT because he was only 10 or so, that's potentially a lot of life left. Just decided to try the cab first. But then all these other things cropped up and have shifted what we're willing to do. Turned out when he was just sort of "twilighted" for a chest tap he had to be resuscitated...so who knows what may have happened with SRT (though as Wendy mentioned, an echo may have caught some potential issues).

I guess this is a long way of saying I absolutely feel for you, it's stuck between 3 rocks and 3 hard places trying to figure out what is best for everyone involved.

I suppose if I were you, my sequence of events would be:
1. Start with the bloodwork, an echo, then possibly imaging. Figure out your yes/no to another round of SRT then.
2. If yes SRT, I see cab as totally out of the picture for a long time
3. If no SRT, then I'd revisit the cab situation and see what you can/can't feasibly do. Maybe a Libre is a possible option, or a pet sitter to come at least once a day. Or brining him with you to school, I have no idea ha

And yes, I just always want to be doubly sure that when I'm giving my opinions they're clearly identified as such! Or that you/others reading these threads aren't like man, she's a judgmental jerk lol

 

That's the million dollar question. The tumour is smaller. Had it gone down even further and is way up in size, or is it still slowly going down to it's current size and still going down smaller? It could be either. CSU told me up to two years for SRT effects, and I've seen somewhere 2-3 years.

Cab has no impact on IAA, it's a completely different condition. How much cabergoline helps IGF-1 is also suspect. A couple have studies have shown "not much". A couple people here have gotten subsequent IGF-1 tests after starting cabergoline and results were actually up. It does however seem to help excess growth hormone output which is a good thing. Unfortunately there is currently no test for feline growth hormone levels, so it can't be measured. Side note, SRT also does not impact IGF-1 levels. CSU told me not to bother retesting and from what I've seen here, even if SRT is actively working you can still have higher IGF-1 levels. Testing IGF-1 again will tell you nothing about what the tumour is doing. So it might satisfy curiosity, but won't lead to actionable steps.

I am focused on the heart testing because my own experience with Neko showed how fast things can change with our acros. I've also seen a lot of acrocats here take a sudden turn to the worse with their hearts. I've heard that heart issues can be "silent killers". And actually experienced that in a non diabetic. My other cat who had an echo, which showed no action required at that time, though enough questions his vet thought we should get a follow up in 6 months to be sure. 3 days before his follow on echo, he had a thromboembolism.

I agree with Melissa on the blood work, then echo. Not sure about imaging - it's only been 4 months since the last one and not sure what imaging will tell you that's worth the risk. I'd wait until you have echo results, then revisit what to do next.

A question for you, have you seen any change/addition of acro side effects in the last six months?

 

This is what I mean about Schrödinger's cat. Even the CT scan was inconclusive since it was not possible to know if what they were looking at was a tumour decreasing (and decreasing?) in size or, vascularization or scar tissue or just a smaller tumour, sitting there.

This is also such a mystery and I'm trying to understand. It's the pituitary gland that secretes GH and from what I've read, "GH is ... a potent insulin antagonist and almost all acromegalic cats have concurrent diabetes mellitus." Furthermore, "Feline HST is caused by a functional GH secreting pituitary tumour. Unlike many hormones which act on a specific target gland, GH affects almost all tissues in the body either directly or indirectly by increasing the secretion of a hormone from the liver known as insulin-like growth factor 1 (IGF-1). " And, so what we are measuring in IGF-1 is secondary, really, to the level of GH (which, as you point out, can't be or hasn't been measured). So, first question: if the pituitary has been removed (transphenoidal hypophysectomy), what is causing an increase in IGF-1 from the liver since there is no pituitary to release or secrete GH??? To make matters even more mysterious, "it is the antagonistic action of GH on insulin that causes many of clinical signs of HST in cats." There's something odd in this circularity since logically there would be no GH to call upon the liver to secrete IGF-1! Almost all cats with a diagnosis of HST have concurrent DM because the ability of insulin to promote glucose uptake into tissues is reduced in the presence of excessive of GH. Therefore, "the end result of chronic GH-induced insulin antagonism is hyperglycaemia and secondary glucosuria, i.e. DM."

Is anyone else finding this somewhat of a shell game? Like how on earth can Eddie be hyperglycaemic if there is no organ producing GH!! Does the tumour mimic the pituitary and secrete GH?? Is that it????? Further, is cab most effective in reducing insulin requirements in non-HST cats with DM? Round and round... @FrostD @Wendy&Neko Is there something in this equation I'm missing?

That sounds so intense! I will definitely look into the echo and perhaps even blood pressure.

This is where Schrödinger's cat makes an appearance. I will certainly do all of the precursor to anything like that.

Not really. Eddie weighs a ton but he still gets around. Jumps down from his cat tower, doesn't have wheezy breathing or snoring, facial features still pretty much the same, nothing that looks like neuropathy or arthritis...

 

There's always growth hormone circulating, whether there's a tumor or no. It is the tumor though that secretes excess.

It is my understanding they do not remove the entire pituitary, just aim to get only the tumor. So the pituitary itself will still produce some level of GH. It's not like thyroid removal where you then have to supplement for the rest of life with replacement meds.

My biology and biochemistry are about 5 years rusty now, but I also suspect there is a little more to IGF-1 production than strictly affected by GH. A quick Google says the thyroid also comes into play, as does the body's natural insulin/pancreas, liver health, etc. It's like during pregnancy, both GH and IGF 1 nearly double...yet I have no tumor. So yes, a shell game of sorts where everything is intertwined. The wonders and frustrations of biology!

(I also would not do the imaging, just sounded like you had decided you already wanted it...and I assumed it would be a prerequisite for possible next round of SRT)

 

Note: I edited your post 9 above to show my words quoted followed by your answers. That makes it a lot easier to read than the one monster quote, to see who said what. Post 5 and 6 above was an intermingle of who said what too, making it harder to reply to. In future, just grab the part of the text you want to reply to, then add your comments, then grab the next bit of text you want to reply to, repeat.

You are beyond my knowledge of endocrinology. That's why even in internal medicine there are specialists in this. All I know is that even at RVC where they have done way more hypophysectomies than anywhere else, not all the cats go OTJ. You'd think they would. But maybe not all the pituitary tumour is removed? Dunno.

Another one of those catch-22's. Almost all cats with HST have been diagnosed because they are diabetic. There have been cats with HST who are not diabetic, but only a few discovered. Is that because no one thinks to look for a pituitary tumour in cats with symptoms that might be acromegaly but don't recognize it as such? In the couple cases I've seen written up, it was due to enlarged organs (hearts).

@FrostD - Typically imaging is the first day of several days when SRT is done.

 

Hi Wendy, my reply to @FrostD might help clear up the mystery. Could you please explain what you mean by "grab[ing] the part of the text" to which I want to reply? Do I copy and paste below? Look what happens when conversations get quite involved!!

 

By capturing part of the text, I mean highlighting the specific part you want to reply to, then hitting the Reply popup, adding your reply, then going back and highlighting the next part you want to reply to. See how my replies in post 11 ended up?

Your reply to Melissa in 12 is one big jumble. Without work, I can't figure out what is your reply and what is the original text that Melissa said. Also, if you quote something, please state the source. I like read the entire document, not just selected pieces.

 

Ok, I'll try that next time but here is the jist of the jumble:

Melissa: "There's always growth hormone circulating, whether there's a tumor or no. It is the tumor though that secretes excess."

Jodey: It is my understanding they do not remove the entire pituitary, just aim to get only the tumor. So the pituitary itself will still produce some level of GH. It's not like thyroid removal where you then have to supplement for the rest of life with replacement meds.
Transphenoidal hypophysectomy involves removal of the entire pituitary and the tumour. So, we're back to mystery. Because the pituitary is the "master gland", hormone replacement is necessary: i.e. Leveothyroxiine, which Eddie (and Blue) will take forever: "Transsphenoidal hypophysectomy is a technically challenging surgery to perform, whereby a tumour affecting the pituitary gland is removed from the base of the brain through the soft palate in the mouth." I also read "Successful treatment of acromegaly is known to normalize serum insulin-like growth factor 1 (IGF-1) levels within days after surgery. However, our clinical observations indicate that many cases of acromegaly show delayed normalization of serum IGF-1 levels after complete tumor resection." Ok, now that sounds promising. One study says "Successful treatment of acromegaly is known to normalize serum insulin-like growth factor 1 (IGF-1) levels within days after surgery. However, our clinical observations indicate that many cases of acromegaly show delayed normalization of serum IGF-1 levels after complete tumor resection."
This might be the answer: "Results: In all patients (46 cats), serum IGF-1 levels returned to the normal reference values for age and sex during the observational period (12-132 months). The mean duration from the time of surgery until IGF-1 normalization was 10 months (range, 3 days-57 months). Twenty-seven patients (59%) reached normal IGF-1 ranges within 3 months of surgery, whereas 19 patients (41%) experienced delayed (>3 months) IGF-1 normalization. Eleven patients (24%) recovered normal IGF-1 levels 12 to 57 months after surgery. The possibility of delayed IGF-1 cure was increased 8.8-fold with an immediate postoperative IGF-1 level increase of 100 μg/L.
Conclusion: Satisfactory remission of acromegaly by IGF-1 criteria was delayed in a large proportion of acromegalic patients, especially those with high postoperative IGF-1 levels. Hence, additional treatment can be delayed in clinically stable acromegalic patients who show no evidence of residual tumors on postoperative magnetic resonance imaging and a normal growth hormone suppressive response to a glucose load."
57 months!! How about that?

From now on, will include citation info. I do know better but was on the clock!

 

That would make sense then, I would expect the levels to normalize eventually if the entire pituitary is removed and then supplemented.

Im on my phone, the way to split the quotes is to use the hard coding (with the brackets and back slashes and stuff...I can explain more later but I'm hoping Wendy has an easier way if you're on the computer).

 

Good morning,
I'm still trying to wrap my head around some issues raised in this conversation. Above @Wendy&Neko says, "What SRT does is neuter the tumour cells so that as they die off, they do not reproduce. Until they die off, the tumour cells are still active and producing excess growth hormone, which in turn causes the acromegaly."

And then @FrostD Melissa says, "There's always growth hormone circulating, whether there's a tumor or no. It is the tumor though that secretes excess."

I must be thick-headed or something because it is my understanding that it is the pituitary alone that releases GH and it is the liver that responds by releasing IGF-1.

Do you see where I'm getting stuck? Is the tumour mimicking the pituitary gland? Can a tumour release GH or does the liver just get "confused" and continue to release IGF-1 leading the researchers (in the article I quoted above but didn't cite) to say, "The possibility of delayed IGF-1 cure was increased 8.8-fold with an immediate postoperative IGF-1 level increase of 100 μg/L" and that's why IGF-1 levels can remain high for up to 57 months? Perhaps the liver needs a reset.

Meanwhile the IM vet just wrote me to say, "I have not used cabergoline before. Without knowing that his DM is the result of increased GH, I do not feel comfortable to try it."

 

The tumor is just an overgrowth of the pituitary, therefore causing excess growth hormone. Wendy and I are saying the same thing, just a little differently. A pituitary without a tumor is still making GH, a pituitary with a tumor is making more GH.

Having us tie it all together is well beyond our pay grade

At least in humans, what I am seeing is that if and when the growth hormone and IGF 1 levels return to normal appears to depend a lot on the size of the tumor, the location, the skill of the surgeon, if they can remove the whole tumor. From what I am reading, apparently some tissue can be left behind and regrow, or in rare cases there are rumors elsewhere causing problems.

 

Shame about the IM vet...the cab side effects, especially for male cats, are so minimal.

 

I like how you said there may be "rumors" elsewhere causing problems. But anyway, as the world turns, all I know is that the pituitary has been removed along with the tumour or as much of the tumour as could be excised. Therefore, and I agree, it's above our pay grade but no pituitary ought to equal no GH. LOL.
In Eddie's case, he got SRT to deal with the remained of the tumour that could not be safely removed surgically along with the pituitary.
Gah.
We need more emojis.

 

Well, I'm not giving up on that. I will, however, go the echo route as both you and Wendy have discussed and make a decision from there.

 

Could you ask him what you think is causing the DM and a higher than normal dose requirement? If not increased GH, then it's got to be IAA cause I can't think of anything else that would cause it. And if it is just the antibodies, he is right that cabergoline won't do a thing for it.

 

In a subsequent email the IM vet wrote,
IM Vet to me:
"This is my understanding:
If no GH tumor then unlikely elevated IGF-1. Thus: if IGF-1 elevated and CT looks clear suspicion of GH tumor remnant. I do not deal with this question often.
Your question is one you should ask the radiation oncologists.
DM can have many causes, excess GH being one of them. Therefore, DM can occur in the absence of GH tumor and hyperglycemia can occur without any organ producing GH."

I wrote to the vets at WSU with the same question I posed here and that I put to the IM vet since I seemed to be going in circles. There was one additional twist I read today and included it in the email to them:

Me to WSU: "Today I was reading about Growth-Hormone-Release-Hormone and I’m wondering if there’s a connection with that hormone (released from the hypothalamus) given that its main role is to stimulate the pituitary gland to produce and release growth hormone into the bloodstream. What if there is no pituitary gland? What's happening with all these hormones? I keep running into this question and no one seems prepared to answer it.

I included this in my email to WSU: “The action of growth hormone-releasing hormone on the pituitary gland is counteracted by somatostatin, a hormone also produced by the hypothalamus, which prevents growth hormone release” (https://www.yourhormones.info/hormones/growth-hormone-releasing-hormone/) There seems a trifecta or more of complications here.

For me and Eddie, this all boils down to one question: since he’s having tests done would you advise me, given the above, what tests are more/most appropriate?"

WSU is really good about responding to questions. I've also asked them about Blue and therapy for CKD. We'll see what happens. Stay tuned.

 

To go further off the deep end here...and a bit off topic

Does IAA only develop in response to exogenous insulin?

Theoretically, let's say pituitary is entirely removed successfully, pancreas is perfectly fine, and GH/IGF normalize. If the cat has IAA, at that point couldn't you discontinue insulin and BG should normalize after a bit? I hope the way I phrased that makes sense.

 

Cabergoline is a somatostatin analogue, hence why it is used in these situations. I am not sure if that's what you are referring to in the quotes above.

I think it all circles back to - is Eddie's tumor completely dead? I don't think there is a way to answer that for certain. A normalized IGF would probably draw that conclusion, but if it's not then it's just more questions. Is it dead but you're waiting for his body to normalize? Is it dying off and you just have to wait? Or is it ramping back up? We already know there isn't a direct correlation between IGF and tumor size/activity.

 

I did read that Cab was a somatostatin analogue which is another reason I'm surprised the IM vet didn't know about it.

Those are the questions of the day, to be sure. I wish I could learn more. The endocrine system is truly marvellous.

 

If not a normalized IGF-1, is that just because it takes time to normalize, or because there is some excess growth hormone still being produced? Meaning, a higher IGF-1 on retest won't give you a definitive answer.

There is appallingly little research or information about IAA in cats out there. We don't test cats not on insulin to see if they have IAA. Sandy's Black Kitty took 5 years after being off of insulin for his IAA to go back to normal levels. We also have no way of knowing if Eddie's pancreas is perfectly fine, though I saw hints that Neko's was at least partly working. Don't discontinue insulin cold turkey. Just follow the dosing methods and reduce the insulin as the BG numbers tell you they need less insulin. Even cats with "just" IAA, when the IAA breaks, don't necessarily go off of insulin, but could go to lower doses.

 

It does make sense but I'm starting to wonder if, in the course of things, IAA is increased after pituitary removal as a (secondary?) response to exogenous insulin as being next in line antagonistic response to DH. When the pituitary is removed and DH isn't being released (or ought not to be) perhaps there's a next-in-line response that happens with exogenous insulin. I'm not sure if that made sense because it's so slippery but there might be something to the idea that in acro cats exogenous insulin after hypophysectomy prompts a defence that takes the form of increasing IAA? Jeeze, I don't know. I wish I had a big white board as I also like to think visually and would love to chart this out.

 

So totally agree with this!~ Which makes it all the more curious that Eddie's insulin dose keeps increasing. I'm wondering if there's the "paradox effect" going on here...given all we've been discussing.

 

Oh right I would never go cold turkey, was just purely from a curiosity/theoretical standpoint

 

This. ^^^^^

This is hugely important. Highlight it with a marker, bold it, italicize it, post it in your refrigerator, make it your mantra. Whatever. But don’t overlook it.

I’m going to be blunt so please take it in the positive, caring vein in which it is intended.

I think you’re too focused on the dose. And, at risk of losing what’s good by chasing the perfect. (I hear your brain shutting down now, but please don’t; I’ve been there and I care).

I’m also not clear that you have realistic expectations.

Since Eddie is doing “better than ever” per your own assessment, what exactly are you projecting needs to happen to believe you’re on the right path? I understand that you want his BG to be in better ranges, but does the dose have to go to zero as occurred with Blue? Because that just might not happen. And you need to accept that as both realistic and completely normal. I’ll share a little story. I helped treat a dog who had lymphoma. Her nodes were the size of golf balls when diagnosed. She wasn’t a candidate for the gold standard CHOP protocol, so we went with a different treatment which was typically less successful and had a lower average survival time. The dog went into remission and stayed there. The 6 month survival hope turned into two years and she never came out of remission. Lost her to kidney disease instead. BUT, and this is one of two points of the story. The dog going and staying in remission on that treatment was my only experience and so it became my expectation. The IM vet and oncologist were in disbelief at the results, but it was all I knew. They emphasized that “this just doesn’t happen” but it was hard not to subconsciously think it was normal. I still have to remind myself of it today as a few friends have been through treatments with their dogs, all with the expected unfortunate outcomes. So please, don’t let your experience with Blue color your expectations for Eddie.

My second point of telling the story is that there is inherent risk of focusing too much on one thing. Yes the dog went into remission and stayed there. But because she was staying in remission longer than expected, we had to decide whether to keep her on the chemo drug (potentially hard on the kidneys) or stop the drug and risk relapse. We were in uncharted territory. There were no clinical studies or even individual cases in the literature that we could find to guide us. No one had kept a dog on that drug for that long, so far as we knew. But I will always wonder… did we blow her kidneys by focusing too much on the cancer? Will you blow Eddie’s kidneys by focusing too much on the insulin dose/tumor status/IGF-1 numbers and the ensuing tests/treatments/sedation as you chase that ghost??? How will you feel if you lose him on the table simply trying to get another CT scan? Because you’ve had s couple of close calls. I’d call those warning shots and heed their message.

There’s nothing wrong with striving to do better for our kitties, to research and tweak and experiment with creative solutions to help them. God knows I’m one of those people who has spent hours sitting on floors at University Vet Teaching hospitals challenging specialists to do out-of-the-box thinking and to find answers. Have you heard the quote used in medicine that “when you hear hoofbeats, think horses, not zebras?” Well, I have brought so many zebras to my vets that we laugh about it. So I get where you’re at. But rather than focusing on extensive clinical tests, I suggest you try to do a few more things at home.

First, you’re always asking “why” on the high numbers. So here’s your mission: find the lows. Don’t assume what’s going to happen — prove it. Get in extra tests and don’t feel bad about it. And feed only at your regularly scheduled times, not at every test. When you see nicer numbers, test more not less. Find where if bottoms out. And do it again.
And again. And again. Wendy brought up the possibility of low numbers and bouncing — we can’t prove it or disprove it, but you can.

And as for cabergoline, I’m concerned that you’d be playing with fire. Until you can show the ability to test more throughout the cycle and overnight, and until you rule out simpler answers like bouncing (think horses, not zebras), I think you’d only be muddying the waters and risking catastrophic outcome.

My two cents.

 

Hi JL
thanks for sharing your thoughts. My brain is not shutting down so don't worry. On the contrary, I'm trying to work with what I know and with what I can learn about the correlations I've been discussing here (GH, IGF-1, etc.). The insulin numbers are concerning if only because they may be a sign of IGF-1 levels. So, the point I'm making without belabouring it is that I'm exploring what is good, better or best for Eddie, this one little cat (well, he's not so little). If I talk a lot about BG, that really is of less significance than is the relation of BG to GH and IGF-1 as insulin antagonists. I mean, I wish Eddie was diabetic. Period. But he's not, and caring for him is as complicated as it could get. I'm not trying to manufacture what happened with Blue but sharing anecdotally, which everyone here does, what happened with Blue as part of the Blue-Eddie Nation here at my house. If I'm letting what happened with Blue colour my expectations, I can be forgiven, because they are brothers, for one thing. When i hear folks taking about their experiences with their cats--and everyone does it--I listen because sometimes there's something relatable. Acromegaly is just bad and there are so many moving parts. I'm focusing on clinical trials, etc. not only because I want to help Eddie but also because I'm trying to educate myself. And what I learn matters at home. I said Eddie's (current) medications are not all that bad and for that I'm grateful. The good days he's having, I cherish.

And, honestly, if I'm asking "why" on high numbers, it really is because I'm here alone and on foot with Eddie. I do it, in part, to reach out, make conversation, make contact, even if someone says, it's a bounce. Yeah, ok, there's folks out there that get it.

The last time I saw the IM vet he said to stop testing so much. Of course, I don't really listen to that, especially since in the last few while since Eddie saw him, insulin has increased from 11u-14u. I'm testing. I'm on it.

Anyway, the Zebras and I, Eddie and Blue, thank you!

 

Eddie is diabetic, but what is often called type 3, diabetes caused by other conditions.

One of the reasons I had asked about other acro symptoms, and you answered none really, is that can be an indicator of excess growth hormone and IGF-1 activity. When Neko’s dose started going up and I considered her second SRT, she was getting some soft tissue growth in her mouth, breath was getting a little wispy (sign of growth in the pharynx) and arthritis was getting worse, a sign of bony growth. Plus the bony growth on her jaw. So I had physical signs of worsening condition and increased GH and IGF-1. That plus increasing dose meant tumour regrowth.

One other thing to confuse the IGF-1 picture, we have had members retest IGF-1 and find it higher, in spite of insulin dose going down post SRT or cabergoline. So don’t correlate increasing need for insulin with increasing IGF-1.

 

Eddie's face (mouth, jaw, etc), really look pretty much the same and he has no wheezy breathing at all. Here is a history of his IGF-1:

EDDIE: IGF-1
10/6/20 IGF-1 355
1/12/21 IGF-1 269 (Pre- hypophysectomy)
6/14/21 IGF-1 235 (Post-hypophysectomy + SRT (2/21)
2/11/22 IGF-1 156 = 4501 ng/dL
9/25/22 IGF-1 TODAY

The question still remains about the relationship between GH and IGF-1. Where does GH come from if the pituitary has been removed?

Interesting: Diabetes Type 3. I've not heard of that...Let's see what the blood panel shows.

 

What a long, long thread but I guess it's good to keep it in one place.

@Wendy&Neko @FrostD

I was grateful to be able to have an in-depth conversation with the IM vet. We talked for nearly an hour this time. He came prepared. I had emailed him with some questions and he provided me with a printed copy of his responses. He also seemed to be amenable to considering cabergoline after doing his own research and providing me with printed copies of 4 studies, 3 in favour of cabergoline and one more neutral (image of article titles attached).

I told him I wanted to get an echo done before anything else and he is going to refer Eddie to a clinic on the lower mainland. He agrees that Eddie numbers (including the low ones) are still too high. He does not, however, want to prescribe another insulin schedule (as in one extra, for example).

He does think the numbers are associated with GH and he also thinks (although he admitted to not knowing for sure) that while the tumour might be on its last legs, it can produce GH (again, he says, this is not certain as there is no way of measuring GH in cats, only the secondary level, the IGF-1 in response to GH. He said, "I do not know the total pathway of GH production and if it is produced in other areas other than pituitary". I asked him if it's possible a pituitary tumour can "mimic" the pituitary and release GH even when that gland has been removed and he thought that it plausible. I got a response from Annie Chen-Allen from WSU (and Tina Owen) who said said "I agree with Tina, the IGF-1 elevation is most likely due to residual tumor secreting GH. The only way to know if residual tumor is getting any bigger is with comparison imaging, ideally MRI over CT.
Since the IGF-1 came down from 6/2021 to 2/2022, it will be interesting to see what the IGF-1 value is from today. If it continues to decrease, it may suggest residual tumor is dying off – either thru the effects of radiation or lack of blood supply. If the IGF-1 is higher and insulin requirement is higher, it would make sense to repeat a MRI at some point, depending on when the last one was done." They also said, the IM vet (Sarah Guess) at WSU was going to get back to me as well as the intensive care vet, Linda Martin. They are so great.

Anyway, back to the IM vet conversation: He wants to see what the IGF-1 results are before Cabergoline, which, of course, makes sense. He has, however, changed his tune regarding Cabergoline. He wants to rule out some secondary condition ("another insulin counter acting disease [eg. any chronic inflammation] regarding insulin resistance that might not include the tumour. He said it's possible Eddie's pancreas is feeling overwhelmed.

He wants to refer to Boundary Bay Veterinary Specialists where there are both cardiologists and oncologists.

So, the results are forthcoming. He couldn't do a urine test as Eddie was nervous in the clinic and just released a flood before they could get a sample. I'm looking forward to the results and will upload them here. The IGF-1 will take about 10 days, though.

In the meantime, he passed this on:
Dose of 10μg/kg cabergoline q48h PO for 6 months
8 x 0.5 mg tablet costs around $150 (USD)
https://www.canadapharmacyonline.com/DrugInfo.aspx?name=Dostinex0405
I do not know if this can be compounded

All of this is moot, of course. But knowledge steadies the boat.

 

The first member here to use cabergoline (Nat and Marvin) is from Montreal and got it cabergoline. Coincidentally, he was off insulin in a couple of really "interesting" weeks. What Melissa said about almost round the clock monitoring can be really true for some.

I think your IM vet has a good plan, double check first for any other conditions that could be causing insulin resistance, there are a few of them. Regarding the comments from WSU, see my comments in post 33 about IGF-1, and it being an unreliable indicator of what is happening in Eddie's head. His last reaction to a CT scan would have me very concerned about doing that or an MRI anytime soon.

Boundary Bay is a good hospital. I think they are the only two cardio vets in BC maybe? The one Neko went to moved back to Italy. The original oncologist there, Sarah, is also great to deal with, and one of the owners. I went as a support person for a friend whose dog was treated there, and I took the dog there a few times by myself while she dealt with a family emergency. At that time Dr. Charney was on the board of Yonkers that did Cyberknife (also a treatment for acromegaly), so we had a few discussions about that, as I was just planning Neko's SRT at the time.

Thanks for putting the titles of papers up . Do you have the actual articles there? I'd like to read the full articles. The last paper there, I attached an electronic version in this thread: https://felinediabetes.com/FDMB/thr...betes-mellitus-and-hypersomatotropism.259213/ I think it's been a useful paper for a few people who needed to convince their vet. Note, although a number of people start on cabergoline every other day, they usually move to every day dosing.

Link to the abstract of the first paper on Cushings being treated with cabergoline (first paper I've seen on that being tried for Cushings). It's just a study of one, but the cat went OTJ after two doses!!

Link to the abstract on quality of life after treatment of acrocats, and comparing different types of treatment. This would be a good one for people trying to decide between types of treatment.

Link the abstract on 3 cases of cats going into remission on cabergoline. This was an early article from the same group who published the last larger study article. Note that Marvin went OTJ in August 2017, before this article was published. Some where I have a copy of this one tucked away, so just looking for the second and third one. I can get it elsewhere if you don't have them.

 

Cabergoline is typically compounded into a liquid, with and oil-suspension base being common but someone posted that they received it in a water base. Someone also posted that they had it compounded into capsules I think. A liquid base is more flexible since the dose can easily be changed.
https://pccarx.com/Blog/flavoring-options-for-veterinary-compounding

 

Thanks for posting the links to the articles. The IM vet gave me hardcopies. He's much better in person than over email. As I mentioned, now he's interested in cabergoline and not so opposed as he was not being "familiar" with it.

Hi Larry, yes, I did know that about cabergoline but the IM vet is new to its use and, until he did some research, was against using it if only because it was not "familiar" to him.
In the event we do go that route, there is a compounding pharmacy here in Kelowna, BC. Eddie will be referred to a cardiologist (about 4 hours away) for now. In the meantime, just awaiting geriatric panel and IGF-1 results...

 

Hi

Hi Wendy,
thanks so much for links to these articles. The vet provided me with hardcopies and I didn't have time to track down the urls as you have done.

Heard from compounding pharmacy that they can do cabergoline if it comes to that. Waiting to hear from cardiologist (Boundary Bay) and, of course, to get the test results. The only delay will be that the IM vet works only two days a week (M-T) and if the results come this week I won't hear until next. But we go on.

Doing a curve today to determine increase, I guess to 15u. IM vet says pancreas is probably overwhelmed and that is contributing to resistance.

 

Sounds like the IM vet is being thorough and trying to check for/rule out other causes for the higher dose before making assumptions. I think that’s a very good idea.

Did you ever send blood to Texas A&M University for a full GI panel (fPLI/fTLI/folate/cobalamin)? That tests for pancreatitis, EPI, and folate and cobalamin levels. Things can sometimes simmer just below the surface without dramatic symptoms and, given that you’ve previously described Eddie’s stools as bordering on soft regularly, it might be worth doing. GI issues/inflammation can definitely affect BG. Even if you don’t think any of those things are likely, it never hurts to rule them out, especially if your thought process is heading toward cabergoline or SRT.

Also, did you ever run a full thyroid panel through Michigan State University? A percentage of post-SRT cats become hypOthyroid. We sent Tubby’s blood a couple of times to MSU to make sure we stayed on top of his status.

How old is your insulin pen? Are all of your recent pens from the same order/batch? Have you always used a biosimilar or did you at some point switch from brand name Lantus to a generic? (Just covering the “low hanging fruit”)

Good to hear that you’re going to a cardiologist. Tubby had multiple cardiac tests and echocardiograms. It was definitely worth doing, although in his case there wasn’t always full agreement amongst the experts whether he had any real problems or whether what they were seeing was “normal” for an acro cat. But they were able to rule out obvious or extensive disease, so we just continued to monitor.

What is the status of Eddie’s mouth dental wise? Tubby had dental issues and bony overgrowth. The dental specialist worked on him pretty extensively about a month after SRT. He definitely needed the work, but I kind of regret not waiting a bit longer. Even though I discussed it in great detail with the folks at CSU as well as the IM vet and dental specialist, I’ll always wonder whether the additional anesthesia so soon after SRT contributed to the kidney issues that took him.

Finally, on the topic of kidneys … did you do an SDMA test? Tubby’s kidneys took a notable hit after SRT and the dental so I would definitely do everything possible to monitor and protect those kidneys.

 

I never have run a fully thyroid panel through MSU. That is a really good suggestion. Eddie could well be hyPOthyroid given that he has gained so much weight.

The insulin pen we're currently using is the last in the pack of 5! It might well be reduced in efficacy. I have opened the new pack and taken out a new cartridge which I will use tonight but stay at the same dose, just in case the other has become less effective. Still always at brand name Lantus, though. I will definitely keep a close(r) eye on him with this change.

Dental wise, he needs treatment. That was on the roster, to be sure but it's been an issue because of his hypersensitivity to sedation (remember he stopped breathing). But we do know the three sedatives that he cannot take. He is able to go with the gas (what is the name? I could look it up and it works for him as long as there's an anesthesiologist present), which he had at WSU (3x) and for three fractions of SRT. It was at WSU that they discovered the two sedatives and the third was discovered with his last CT scan).

He did not have an SDMA on June 22nd, his last panel, but I think I may have requested it this time (results pending). In April, when he had the CT incident, this is the report from his emergency hospitalization:

"Chemistry results from IDEXX VetLab In-clinic Laboratory Requisition ID: 41133 Posted Final"

"Test" "Result" "Reference Range"

"ALB =" "29 g/L" "23 -" 39
"ALKP =" "50 U/L" "14 -" 111
"ALT =" "56 U/L" "12 -" 130
"BUN/UREA =" "6.6 mmol/L" "5.7 -" 12.9
"Ca =" "2.21 mmol/L" 1.95 -2.83
"Chloride =" "116 mmol/L" "112 -" 129
"CHL =" "4.15 mmol/L" 1.68 -5.81
"CREA =" "165 umol/L" "71 -" 212
"GGT =" "0 U/L" "0 - 4"
"GLU =
OSM calc = PHOS =" "11.01 mmol/L
320 mmol/kg
1.53 mmol/L" "H" "3.95
1.00" "- 8.84
- 2.42"

"Potassium =" "4.5 mmol/L" "3.5 - 5.8"
"Sodium =" "158 mmol/L" "150 - 165"
"TBIL =" "8 umol/L" "0 - 15"
"TP =" "71 g/L" "57 - 89"
"GLOB =" "42 g/L" "28 - 51"
"ALB/GLOB =" 0.7
"BUN/CREA =" 10
"Na/K =" 35

"Diagnostics:
- ketones: 0
- BG: on arrival 5AM 9.7mmol/L, 13.2 at 1130AM
- CBC: adequate platelets on manual, all other WBC normal. HCT wnl 32.3%
- Biochemistry: hyperglycemia (12.27mmol/L), mild elevation in creatinine (259 umol/L), mild elevation in sodium"
(166mmol/L)
- T4 13nmol/L normal
- SDMA normal (10ug/dL)
- fPL: normal
- UA: on analyser cocci suspected, on microscope clumps of cocci, scant neutrophils, +++ adipocytes
- Urine culture: sent pending results

SDMA: normal
They did however recommend testing of Thyroid (not taken up at that time).

It will be illuminating to compare these test results (although they were taken in emergency care) with those on July 25th.

We'll see. But thanks for the heads-up on the Lantus cartridge. Since it was the last in the pack, it might have gone over to the dark side.

 

I'm glad JL mentioned the dental and reminded me that Eddie's on the list for that, provided he passes the cardio visit. Needing a dental, combined with IAA might be why you are seeing his numbers go up. The dental vet can bring in a carded anesthesiology vet for the procedure. I have a friend who does that every time her cat gets a dental there.

I thought Eddue was on levothyroxine since his hypophysectomy?

 

Yes, Eddie is on the list for a dental but it's Blue who is already booked. Right now, with Eddie, the current test is to compare his mid-April results with now and then we take it to echocardiogram. Boundary Bay is bringing in a carded anesthesiology vet for Blue. Eddie will be next up.

Also, yes, Eddie is on Levothryoxine (0.1mg/BiD) and perhaps that might need to be revisited.

 

One thing that occurs to me today (why today? who knows...): What makes Cab in Eddie's situation dangerous or as you say, "incredibly risky", in your view? Give me something to think about, please. I'm asking of course because Eddie's BG is skyrocketing...

 

Re-quoting my post -
If you end up in a situation where the cab starts working, another round of cells dies off, and IAA takes a break....that's an incredibly dangerous situation. July 2021 on my SS - you can see just how much I was having to test and feed to keep him safe - just from cab alone.

I don't think anyone has done cab in a post SRT cat? So we'd really just be winging it in terms of giving dose advice in the event Eddie nosedives from a combo of factors listed above. The nice thing about the depot insulins is the depot itself...but that's also a downside in a nosedive, even if you skip shots the depot is still there and you have to fight it.

 

At least not here. Maybe someone else? Of course, doing cabergoline at all the first time here meant the caregiver had to be a testaholic. It was uncharted ground. That would be my main worry, cab in a post SRT cat would mean being very vigilant in testing and potentially lost sleep.