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Pituitary Hyperplasia

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This topic has come up several times, so I dug out the article I'd read before. If you look at the references at the end, there are obviously other articles out there. I'll see if I can find some of them.

 

Article: Pituitary Hyperplasia (click here)

 

Hugs,

Robin

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Thanks so much for finding this article, Robin. I read it over but I want to take my time and read it again later tonight. Thanks!!!

Kate G

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I wish I had the patience to really read these articles thoroughly and in-depth. Most of the time, though, my eyes just glaze over! ;)

 

This did jump out at me:

 

Pituitary cell hyperplasia can be a source of hyperprolactinemia, gigantism, and Cushing's disease. Indeed, up to 18% of Cushing's disease and some of the nonremissions following successful removal of corticotroph ademona could be attributable to corticotroph hyperplasia.

 

Thanks for the link, Robin!

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Robin, thanks again for looking for this article. I printed the whole article and read it a few times. I found it very informative ( as informative as it can be when they know so little about hyperplasia). There seems to be lots of speculation about hyperplasia since they don't know why this happens. I found it interesting when they said estogen was a trigger that might cause hyperplasia.

Thanks.

Kate G

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Thanks for the info. I'll add it to my blog.

 

I already have two tumors showing (IMCC thinks it is one), but I worry about hyperplasia already.

 

You always come through Robin. We thank you!

Melissa

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Thanks for posting this. I was already familiar with it as researched the topic since Dr. Mc said my path. report stated I had it. Unfortunately, according to Dr. Mc it makes a cure for Cushing's unlikely which is another reason I had a BLA after my two pit surgeries. The pituitary surgeries remain important to remove any tumors that can be found.

 

Take care, Robin dear! Big hugs!

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Thanks, Robin.

 

And, ew. I don't like this stuff. I am kind of assuming I have hyperplasia, because of the multiple spots found through my endocrine system.

 

But, here is my question: if excess hormones are causing hyperplasia, and one has certain glands removed to try to stop the hormones, and permanant hormone replacement is necessary - won't the hyperplasia keep getting worse??

 

Love,

Katie

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Hi, y'all...did you read where some of the hyperplasia is reversible once the source of high hormone is removed? I'll try to post later about it. I'm heading out to the doctor with a bad sinus infection and just don't feel like it right now.

 

Hugs

Robin

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Thanks Robin. I did read it. I am just bugging, as usual...

 

Yuck - I'm sorry to hear about your sinus infection. Good luck at the doc.

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Robin.

This is the first time (beside my path report) that I found anything about rare corticotroph and Crooke's hyaline changes and rare basophils. All this was part of my pathology report. So in other words it was some kind of rare hyperplasia? Anyone else have this kind? Thanks, Robin

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Hmmm... but my ovaries are gone, my thyroid is gone - I am hypo hypo hypo this and that... yet my ACTH keeps going up and up, and my path was hyperplasia. Am I an exception (*cough*) or is something else going on... they keep reading my MRIs as post op, normal... but trust is lacking.

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Robin,

 

I hope that you are feeling better soon. Thanks for the article!

 

Hugs,

Mar

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Sorry you are feeling so yucky, Robin. Hopefully you are able to get some well needed rest this weekend.

I did read that some hyperplasia can be treated if the source is taken away. For instance, if someone is breast feeding, they might have more prolactin cells that are hyperplasia and once they stop feeding, the hyperplasia will cease. There seem to be some hyperplasia that can be treated once the source is removed. At the end of the article it did mention that some ACTH hyperplasia can not be treated.

Someone mentioned Crooke's, that was mentioned in the artilce too. The pathologist in Canada that will be reviewing my pathology basis a fair amount on Crooke's. Dr. F. passed this along this info, that Dr. Asa does base a fair amount of Crooke's. Dr.F. feels that Crooke's does not happen with mild Cushing's, he believes it happens with advanced Cushing's. I was trying to find info on Crooke's and I found a little bit. I still don't totally understand what Crooke's is. This article mentioned Crooke's and someone who replied to this thread mentioned they had Crooke's.

Kate G

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Robin,

 

I found your article fascinating! Of course having hyperplasia, it is a concern of mine. I did find it particularly interesting that estrogen excess can be a cause of hyperplasia, and especially the fact that it can sometimes be reversed! Wow! I started looking up some info on path reports because some of the terminology I am not familiar with. (I was just looking for the words "positive for ACTH staining") :) So I looked up some histology info. It shows some great slides of what normal tissue looks like, vs hyperplasia (expanded acini) and adnenoma tissue.

 

Also Violet, I found some info on Crooke's cells. Rare & related to cyclical Cushing's. Interesting. Check it out.

 

Hugs,

Cindy

 

P.S. Hope you feel better soon Robin. Thanks for sharing this info. Even when you don't feel well, you always put yourself out there to help us. You're a gem!

 

HYPERPLASIA

Hyperplasia is an increase in the number of cells of an organ or tissue in response to a stimulus. Any cell population within the pituitary gland can undergo hyperplasia. This process can be physiological or pathological (3;95;96) and when prolonged may progress to adenoma formation (97-102).

 

Somatotroph hyperplasia is seen in patients with ectopic production of GH-releasing hormone (GRH) by pheochromocytomas, endocrine tumors of lung, pancreas or other elements of the dispersed endocrine system (97;103;104). Rarely, it may be associated with a gangliocytoma of the hypothalamus (105). Mammosomatotroph hyperplasia is the characteristic pituitary lesion in McCune-Albright syndrome (106;107); rarely, it may be due to GRH excess or it may be idiopathic (108). Lactotroph hyperplasia is physiologic during pregnancy or other conditions of estrogen excess, but pathological idiopathic lactotroph hyperplasia is a rare cause of hyperprolactinemia (109;110). Corticotroph hyperplasia is a cause of Cushing's disease that may be associated with a corticotroph adenoma (98-100). In rare patients, it is attributed to ectopic or eutopic excess of corticotropin-releasing hormone (CRH). It is also physiological in patients with untreated Addison's disease. Thyrotroph hyperplasia develops in patients with prolonged primary hypothyroidism(111-113). Gonadotroph hyperplasia is seen in patients with prolonged primary hypogonadism (101;102).

 

Radiologic evaluation of patents with hyperplasia usually reveals diffuse sellar enlargement without enhancing normal tissue on contrast administration. Hyperplasia is usually reversible if the underlying condition is appropriately treated. However, in patients with idiopathic hyperplasia, the underlying stimulus is not known. Patients with lactotroph hyperplasia can be treated with dopaminergic agonists. Those with Cushing's syndrome may require total hypophysectomy to achieve clinical control.

 

The key to distinguishing adenohypophysial hyperplasia from adenoma lies in the reticulin stain (Figure 14). Hyperplasia is characterized by expanded acini with an intact reticulin framework whereas adenomas have breakdown of the reticulin fiber network. Immunohistochemistry shows predominance of the hyperplastic cell type with other hormone-containing cells interspersed. Ultrastructural examination is not a reliable method to distinguish hyperplasia from adenoma, however, it was the method used to describe the cell enlargement that defines "thyroidectomy" cells (Figure 15) in patients with primary hypothyroidism, and "gonadectomy" cells in patients with primary hypogonadism. In both situations, the target cells develop abundant vacuolated cytoplasm that is occupied almost entirely by dilated rough endoplasmic reticulum with secretory material.

 

Figure 14. The reticulin stain is the most valuable tool to distinguish normal acinar architecture (a) from the expanded acini of hyperplasia (:wtg: and to confirm total breakdown of the reticulin fiber network in adenomas ©.

 

Hyperplasiacystology.jpg

 

Crooke's cell adenomas are rare tumors that exhibit Crooke's hyaline change (142;143). Usually, Crooke's hyalinization is restricted to nontumorous corticotrophs, but rarely this marker of feedback suppression by glucocorticoids is seen in adenomas. These tumors can be associated with Cushing's disease, but it is generally an unusual form of the disease, such as cyclical Cushing's. The tumor cells can exhibit marked cytologic and nuclear atypia (Figure 21). The perinuclear ring of pale hyaline material represents the accumulation of low molecular weight cytokeratin filaments that are intermediate filaments on electron microscopy (144). The cells exhibit a rim of peripheral positivity when stained with PAS, and this is due to immunohistochemically detectable ACTH in secretory granules located either at the periphery of the cell or in the perinuclear region.

 

Crookescelladenomas.jpg

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I wanted to add something about this article. I was thinking and it might not work but they mentioned if you change something that triggers the hyperplasia it can die off. So, when people who are breast feeding, they might have hyperplasia cells to do with prolactin but when they stop breast feeding, those cells go back to the way they should have been. People who have thyroid stimulating hyperplasia and they add thyroid meds. that hyperplasia could die off.

For ACTH they said that there is too much estrogen to begin with. Dopamine is lowered for some reason. They feel that the combination could trigger ACTH hyperplasia. So, what is you took some estrogen lowering drugs or natural products that lower estrogen ( like DMI). Plus someone takes a dopamine supplement or something that raises dopamine like St. Johns Wart. Could the two combinations kill off ACTH hyperplasia? It probably wouldn't work but what if they tried to cut off the chain of events that cause hyperplasia, could the tumor die off? I know that this is just speculation since they don't know exactly what causes hyperplasia but they do feel that certain triggers cause it and can possibly correct the problem.

Mind you, at the end of the article it did mention that Cushing's hyperplasia is still harder to treat and remission isn't always possible after surgery.

Kate G

P.S. Cindy, those photos are from a doctor here in Canada. I have seen that same article she wrote. Her name is Dr. Asa. My pathology is being sent to her. She is a leading pathologist and happens to be married to Dr. Ezzat, an endo in Canada. Thanks for adding those photos!

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I was just re-reading this, because Paula told me my path report came back noting hyperplasia (acini). How did I know? Ew - this sends shivers up my spine. I hate when my predictions or suspicions are right, but they almost always are! AAAAAH.

 

Anyway, I don't have the whole report yet, so I don't know about staining or whatever. I just know there was hyperplasia.

 

It seems to me there is no way to eliminate the stimulus if you don't know what it is. The whole estrogen thing makes sense for me, I guess, because I took OCs for a very long time, starting very young. At the same time, I took some psych meds for a while that may have affected my dopamine, so it seems I may have had a ACTH hyperplasia-inducing cocktail going on. Then, when I took progesterone last year, I went into my longest, highest cycle to date. So, there are definitely stimuli. BUT, how can I eliminate the stimuli. Apparently, now that my pit is dang-near shot, I HAVE to take estrogen and progesterone for a variety of reasons, both current and preventative, as well as thyroid hormone.

 

Any thoughts? I'm stuck, right?

 

Anyhow, my plan for now is to hang in there fir as long as possible without another surgery. I am not ready to start thinking about pit surgery #2 or BLA. But, I am sure my body will tell me when it needs it...

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Hi, Robin. thanks for posting ---- I believe that I posted this article before. It was the best that I had at the time of my hyperplasia diagnosis.

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Aww Katie,

I am sorry to hear this. It will be interesting to see your full path report. Didn't you have an acro diagnosis as well? Was the hyperplasis ACTH or GH hyperplasia? Alex's pathology was ACTH hyperplasia. Her surgeon was interested in figuring out the stimuli, but wants "someone else" to do the figuring. Dr. F doesn't seem to think there is much that can be done about it. Dont' blame yourself sweetie, if it makes you feel any better Alex started on this Cushing's ride as a toddler... she wasn't on any kind of meds and here we are anyway.

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Rene - I can hardly bear to think about Alex and all of the other kids dealing with this, so, in that way, it doesn't make me feel any better. But, I do need to hear that I shouldn't blame myself. It's more about - if I knew then what I know now - kind of thing.

 

I don't have the full report yet, so I don't know about staining. But, yes, I was DXed with acromegaly and Cushing's. I am facing the reality that someday I may be without a pituitary and without adrenals. I am pretty sure Dr. F would be down for a full removal of the pit, but I really want better testing of my adrenals. Because, of course, what if the hyperplasia is being caused by cortisol from my adrenals.

 

I will let you know when I have more info. I should get my path report in the mail tomorrow and I am set to talk to Dr. F tonight. I may just keep testing until I get to the point where the next step is in my hands.

 

Hugs for you and Alex.

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