Was my pituitary tumour surgery a success

So this week i was back at The Christie for baseline blood tests along with the Glucose tolerance test.

The results from the baseline tests (which they took and sent straight up/down to the lab) were fantastic. My prolactin level was down from post op 1800-2000 down to a fabulous 88, my cortisol level was within normal range and testosterone was up from post op less that 1 up to just over 6! Fantastic results.

Yesterday, i was due to get the all important MRI results back along with the Glucose tolerance test results. In the morning i phoned The Christie and spoke to a cracking registrar Dr W who confirmed that I and my results were being discussed later in the day at the group meeting that takes place between the Doctors, Specialists and nurses etc.

So i waited all day for the call but it never came. At 6pm i was pretty low and if it wasn’t for Amy getting the call that she had been successful in a recent interview with her job, Neil getting the all clear from Cancer then I’d have had to go for a Maccies :)

Anyway, at about 8pm just as I was leaving the flat the phone went and unbelievably it as my Surgeon Mr G from The Salford Royal. What a lovely chap he is!

He said that the MRI imagery was pretty good and he doesn’t think he can see any residual tumour but that if it invaded the cavernous sinus bone as he initially suspected then he wouldn’t be able see it until it grows further so no repeat surgery and he will see me in 3 months. Bang tidy!

He went on to say that the blood results from Tuesday had real positives that we already know about but the glucose tolerance test showed slightly higher GH levels (1.2 so less suppression than required) than those taken after surgery.

He said that Prof T is going to get me back into Christies and treat himself and see how we go on. He said that the increased gh could be caused by residual tumour but the that the risks of going back in were too high. Specifically, damaging the carotid artery or damaging normal pituitary function which he says he is not comfortable with at this stage.

So out of the woods to some extent and some work to do for Prof T and his team in treating the Acromegaly.

All in all I still feel a bit funny after surgery with ups/downs but I am much happier with the results, the feedback from Mr G and everything in general!

Thanks for reading and thanks to all the NHS staff who took part in the DickyMoo conference :)

7 Comments

  1. Great! Good to know things went smooth.
    Just a word of caution, I was asked to visit my surgeon every 6 months after my first surgery. I went in 4 months the first time, and things were clear. Next visit was after 8 months, and there was a tumor larger than before, due to which I had to get another surgery. Just make sure you stick to the 3-month-doctor-visit.

  2. A friend asked me earlier today what will happen at The Christie short term in terms of treating the remaining higher GH and IGF1 values.

    Well courtesy of http://www.acromegaly.org/about_acromegaly.aspx this is the likely course of action:

    Medical Therapy:

    For patients with persistent GH elevation after surgery (or those who decline to have surgery), Octreotide or stereotactic radiosurgery or both are generally indicated. Octreotide (given three times a day by injection or by one monthly injection) achieves long-acting suppression of GH in about 70% of patients. It causes some degree of tumor shrinkage in 30-50% of patients, and often improves symptoms of soft tissue swelling, headache, joint pains and sleep apnea. The preoperative use of Octreotide may facilitate tumor removal and lessen the risks of general anesthesia. Side effects may include loose stools, malabsorption, cholelithiasis (gall stones), local pain at the injection site. Bromocriptine (Parlodel) and Cabergoline (Dostinex) are “dopamine agonist” pills which lower GH secretion in about 15% of acromegalic patients. The major side effect is gastrointestinal upset. Growth hormone lowering and tumor shrinkage are seen in only 10 – 15% of patients with acromegaly.

    Pegvisomant (Somavert) is approved for the treatment of acromegaly. This drug is generally self-administered as a daily injection and blocks the actions of GH. Although it is very effective in lowering IGF-1 levels, it does not shrink the pituitary tumor. In rare cases, elevations of liver tests have been reported.

    Somatuline® Depot (lanreotide) is indicated for the long-term treatment of acromegaly in patients who have had an inadequate response to surgery and/or radiation, and for patients who cannot tolerate surgery or radiation. Somatuline® Depot is the latest advancement in acromegaly treatment and is the first somatostatin analogue available in a prefilled syringe that achieves effective and long-acting suppression of GH and IGF-1 levels in patients. Somatuline® Depot uses a shorter needle to deliver the injection deep subcutaneously, instead of into the muscle.
    Common side effects of Somatuline® Depot include diarrhea, cholelithiasis, abdominal pain, nausea, injection site reactions, flatulence, arthralgia, and loose stools. In clinical trials, Somatuline was well tolerated with only 1.9 % of patients discontinuing therapy due to treatment-related adverse events.

    Radio-therapy:

    For patients whose acromegaly is not controlled with surgery, both conventional (external beam) and stereotactic radiosurgery are relatively effective. However, the lowering of GH and IGF-1 levels takes significantly longer with external beam radiotherapy (average 7 years) compared to stereotactic radiotherapy (average 18 months). Also, external beam radiation reliably causes loss of normal pituitary function over 5 to 10 years. Neurologic complications such as visual loss, weakness, and memory impairment have rarely been reported with both external beam and stereotactic radiotherapy.