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«Educational grants have been provided from: Programme 8:30 Registration and Coffee 9:15 Welcome and Introduction Dr Stephanie E Baldeweg & Mr Michael ...»

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Educational grants have been provided from:


8:30 Registration and Coffee

9:15 Welcome and Introduction

Dr Stephanie E Baldeweg & Mr Michael Powell

9:20 Three Cases

Case 1: Cushing‟s?

Author(s): Chioma Otti, N.M. Martin, N. Mendoza, F. Roncaroli,

A. Mehta, K. Wynne, K. Meeran.

Imperial Centre for Endocrinology, Imperial College Healthcare

NHS Trust, London.

Case 2: It pays to be NOSEY: A case of ACTH-producing nasal ectopic pituitary adenoma Author(s): K Gurazada1, A Ihuoma1, C Rennie2, J Kisalu1, B Khoo1, N Dorward3, T Wilhelm4, M Galloway5, Professor P Bouloux1.

Royal Free Hospital, London Case 3: A severely ill patient with Cushing‟s disease that escaped medical control Author(s): C T Lim, G Tharakan, N Mendoza, F Roncaroli, A Mehta, N M Martin, K Meeran, T Tan Imperial Centre for Endocrinology, Imperial College London 9:50 Keynote lecture:

Cushing‟s Disease – 100 years on Professor John Newell – Price University of Sheffield 10:35 Forum 1: Challenges during and after pregnancy Chairs: Dr mark Vanderpump & Miss Joan Grieve Case 4: Optimal management of a proposed pregnancy in a patient with acromegaly.

Author(s): C. Otti, N.M Martin, D. Papadopoulou, N. Mendoza, F.

Roncaroli, A. Falconer, A. Mehta, K. Wynne, K. Meeran.

Imperial Centre for Endocrinology, Imperial College Healthcare NHS Trust, London.

Case 5: An Unusual Case of Pituitary Apoplexy Occurring During Pregnancy.

Author(s): Tharakan G, Kadiyala R, Damani N, Clements MR and Ostberg JE Watford General Hospital Case 6: TSHoma and pregnancy – a management dilemma Author(s): C. Otti, A. Mehta, N.M. Martin, D. Papadopoulou, K.

Wynne, K. Meeran.

Imperial Centre for Endocrinology, Imperial College Healthcare NHS Trust, London.

11:25 Coffee and Posters 11:45 Forum 2: Apoplexy Chairs: Dr Stephanie Baldeweg & Mr Michael Powell Case 7: Pituitary Apoplexy post mitral valve replacement-“The mechanism may be different and is there any role for staged surgery, pituitary surgery first followed by cardiac surgery?” Author(s): G Mlawa1,M Silveira2.Royal Hampshire County Hospital (Winchester). 2.Southampton Hospital.

Case 8: Pituitary Apoplexy in an 88 year old man presenting as acute hyponatraemia with rapid recovery of hypopituitarism following conservative management Author(s): A Falinska, T Htay, M McEwan, M Pelly, D Morganstein, A Wren Best Cell Centre, Chelsea and Westminster Hospital Foundation Trust Case 9: Pituitary Apoplexy Guidelines – We‟re seeing better!

Author(s): F Olubajo, A Jesurasa, J Newell-Price, R Ross, S Mirza, Saurabh Sinha.

Royal Hallamshire Hospital, Sheffield 12:30 Reassessing cortisol requirements after pituitary surgery Dr Tricia Tan Imperial College London 13:00 Pituitary Foundation: Joy Ginn (LAPPS) 13:10 Lunch and Posters 14:00 Forum 3: Aggressive pituitary tumours Chairs: Dr James Ahlquist and Mr Michael Powell Case 10: Histological markers of an unusually aggressive acidophil stem cell pituitary adenoma Author(s): F Talbot1, N Stojanovic2, J Pollock2, F Roncaroli3 & James Ahlquist1,2 Southend Hospital, Westcliff on Sea, Essex, 2 Queen‟s Hospital, Romford, 3Neuropathology, Imperial College London.

Case 11: Acromegaly due to a massive, invasive pituitary macroadenoma: Management Options Author(s): O‟Toole SM, Srirangalingam U, Drake WM, Barts and The London Case 12: 'Refractory thyrotoxicosis' - TSHoma or not?

Author(s): O Koulouri1, N Kandasamy1, C Moran1, N Schoenmakers1, G Boran2, DJ Halsall1, N Antoun1, VK Chatterjee1 & M Gurnell1 University of Cambridge & Addenbrooke‟s Hospital, Cambridge, UK1 Department of Clinical Chemistry2, AMNCH, Dublin, Ireland Case 13: An unusually aggressive GH producing pituitary tumour Author(s): J Kisalu1; M Murphy1; N Dorward1 ; M Galloway1;

N Fersht2 ; P-M Bouloux1 Royal Free Hospital, London, UK. 2UCLH, London, UK Case 14: Diagnosis and Management of Pituitary Germinoma: an unusual cause of sellar mass Author(s) Dr A Garg; Dr S Baldeweg; Dr N Fersht; Miss J Grieve, UCLH, London

–  –  –

Author(s): M Horridge, A Jesurasa, F Olubajo, J Newell-Price, S Mirza, S Sinha Royal Hallamshire Hospital, Sheffield 17:05 Presentation and poster prizes Dr Stephanie E Baldeweg 17:15 Close Case 1: Cushing’s?

Author(s): Chioma Otti, N.M. Martin, N. Mendoza, F. Roncaroli, A. Mehta, K.

Wynne, K. Meeran.

Imperial Centre for Endocrinology, Imperial College Healthcare NHS Trust, London.

A 29-year-old woman was referred in 2008 with oligomenorrhea and hypertension. She described a tendency to bruise easily for 3 years, weight gain, a 5 year history of hirsutism that improved with Dianette and subsequent laser therapy, and mood swings. Examination findings included a BMI of 24.6, blood pressure of 130/80 mmHg, central adiposity, but no evidence of proximal myopathy, bruising or striae. Midnight sleeping cortisol was 546 nmol/l and 9AM ACTH was 27 ng/l. Results of low dose dexamethasone suppression tests (LDDSTs) and cortisol day curves are shown in the table below. Pituitary MRI scan in 2008 was normal, whilst in August 2009 a repeat scan was reported as showing a 5mm discrete region of reduced enhancement. Due to persistent failure to suppress cortisol following LDDST, a diagnosis of ACTHdependent Cushing‟s syndrome was made. IPSS in June 2009 revealed a basal central/peripheral ACTH gradient of 0.95 on the left and 1.4 on the right, and peak central/peripheral ACTH of 9.1 on the left and 42 on the right. Due to the biochemical findings (but without progression of symptoms) she underwent trans-sphenoidal surgery in November 2009. However no corticotroph adenoma was identified on post-operative histology. Other causes of hypertension (and congenital adrenal hyperplasia) were sought and excluded. Regular menses commenced post-operatively, with subsequent natural conception and delivery in March 2011. Currently, she is treated solely with amlodipine.

–  –  –

Questions for the expert panel:

- Did this patient ever have Cushing‟s disease?

- Would you have managed her differently?

- Should we perform repeat dynamic function tests and if so when?

Case 2: It pays to be NOSEY: A case of ACTH-producing nasal ectopic pituitary adenoma


Kalyan Gurazada1, Ajibola Ihuoma1, Catherine Rennie2, Judith Kisalu1, Bernard Khoo1, Neil Dorward3, Thomas Wilhelm4, Malcolm Galloway5, Professor Pierre Bouloux1.

Royal Free Hospital, London A 19 year old male was diagnosed with Cushing‟s syndrome in Beirut (2000).

Initial investigations suggested a pituitary adenoma, for which he underwent Trans-sphenoidal surgery (TSS); histology however revealed normal pituitary tissue only. Because of the persistence of his disease, a bilateral adrenalectomy soon ensued.

He was then referred to us from Beirut, for further investigations. MRI in 2003 showed a 3mm nodule on the right side of the pituitary. Bilateral inferior petrosal sinus sampling (BIPSS) suggested a pituitary origin of ACTH with right sided preponderance. Trans-sphenoidal resection of the nodule again revealed normal pituitary tissue only. Two years later, with a progressive, though glucocorticoid suppressible rise in ACTH, the patient received radiotherapy to the pituitary bed. Despite this, ACTH continued to rise (5000ng/L) and the patient became excessively pigmented. A repeat MRI in 2009 showed a mass below the sella turcica in the clivus, resection of which revealed a benign squamous cyst, again with no pituitary tissue.

The following year, after extensive review of previous scans, an abnormal mass was identified in the nasal cavity adjacent to the cribriform plate along the proximal and mid-ethmoidal cells on the left. A designated MRI of the region suggested that this mass was enlarging. Repeat investigations including BIPPS, CRH test and High dose dexamethasone suppression test, however continued to suggest a pituitary origin of the ACTH. Nasal exploration of this abnormal tissue, finally confirmed a pituitary adenoma, with strong immunoreactivity to ACTH. Post-operatively the ACTH fell precipitously to

6.2ng/L, and the excess pigmentation rapidly cleared.

Nasal ectopic pituitary adenomas are rare. Pituitary tissue has been found along the developmental pathway of Rathke‟s Pouch, which includes the sphenoid sinus, clivus, cavernous sinus and suprasellar region. In our case, the etiology could be an ectopic ACTH pituitary adenoma or an inadvertently implanted pituitary tissue during the initial exploration.

Case 3: A severely ill patient with Cushing’s disease that escaped medical control Author(s): Chung Thong Lim, George Tharakan, Nigel Mendoza, Federico Roncaroli, Amrish Mehta, Niamh M Martin, Karim Meeran, Tricia Tan Imperial Centre for Endocrinology, Imperial College London, London Hypercortisolism that escapes from control with medical therapies presents particular challenges in severely-ill patients. We present a 57-year old female with severe Cushing‟s syndrome (CS), characterised by new onset type 2 diabetes mellitus, hypokalaemia, hypertension, weight gain, easy bruising, proximal myopathy, severe depression and slow-healing cellulitic leg ulcers.

Investigations confirmed ACTH-dependent CS. LDDST was performed:

baseline ACTH 85ng/L, baseline cortisol 907nmol/L, T=48h cortisol 807nmol/L.

HDDST showed failure of cortisol suppression to less than 50% baseline: T=0h cortisol 1372nmol/L, T=48h cortisol 825nmol/L. MRI pituitary revealed a leftsided microadenoma. CT chest, abdomen and pelvis did not reveal any potential ectopic source of ACTH. The patient was too unwell for petrosal sinus sampling.

Combined ketoconazole and metyrapone therapy was initiated. However, cortisol levels repeatedly escape from control (1000nmol/L) despite increases in the dose of both drugs. A subhypnotic infusion of etomidate (2.5mg/h) was therefore commenced but serum cortisol again escaped control despite increases in dose to 5mg/h. Patient also suffered from bowel perforation which was managed surgically but complicated by poor wound healing and dehiscence. The options of bilateral adrenalectomy and pituitary surgery were discussed and she eventually underwent trans-sphenoidal hypophysectomy.

Histology confirmed a corticotroph adenoma and post-operatively, she recovered well although her depression persisted despite long-term remission of her Cushing‟s disease.

Here we report the first case of escape from control with etomidate. Pituitary corticotroph adenomas are theoretically more likely to escape control with medical therapy. This could be due to reduced negative feedback from falling serum cortisol levels resulting in greater ACTH drive, sufficient to overcome pharmacological blockade of cortisol production. This case also raises

questions for the expert panel:

(1) Does HDDST have any place in the investigation of the source of ACTH in ACTH-dependent CS?;

(2) Has anyone experienced „escape‟ from etomidate control in acute emergency management of hypercortisolism?

Case 4: Optimal management of a proposed pregnancy in a patient with acromegaly.

Author(s): C. Otti, N.M Martin, D. Papadopoulou, N. Mendoza, F. Roncaroli, A.

Falconer, A. Mehta, K. Wynne, K. Meeran.

Imperial Centre for Endocrinology, Imperial College Healthcare NHS Trust, London.

We present a case of a woman who is now 29 years old who initially presented in 2007 with headaches and secondary amenorrhea. Random growth hormone was 780 mu/l (260 mcg/l) and pituitary MRI revealed a macroadenoma with hypothalamic extension and encroachment on the left internal carotid artery. After treatment with sandostatin LAR to attempt tumour shrinkage pre-operatively, she underwent transsphenoidal surgery to resect the pituitary macroadenoma twice in 2008. The second operation was complicated by meningitis, from which she made a full recovery.

She underwent radiotherapy in 2009 as her growth hormone (GH) levels remained elevated (GH nadir on OGTT 49.9mu/l [16.6 mcg/l], mean GH on a day curve 209 mu/l [70 mcg/l]), and high IGF-1 (132 nmol/l; normal range 13-64). Subsequently lanreotide (Somatuline Autogel) was commenced and her disease was well controlled on 120mg every 3 weeks. However, in November 2011, reassessment of her acromegaly off somatostatin analogues confirmed that her disease was still active (GH nadir on OGTT 7.21 mcg/l, mean GH on day curve 10.72 mcg/l, and IGF-1 62 nmol/l). Therefore lanreotide was continued. Currently, her pituitary axes are intact post-radiotherapy. The most recent MRI of her pituitary (performed in 2011) showed residual tumour with solid enhancement superiorly.

We plan to reassess her GH burden off lanreotide later this year. However she has expressed a desire to start trying to conceive in about 1 year's time.

Questions for the expert panel:

- What advice should she be given about planning for pregnancy?

- Should lanreotide be continued throughout pregnancy?

- Should lanreotide be stopped during pregnancy and if so at what point should it be stopped?

Case 5: An Unusual Case of Pituitary Apoplexy Occurring During Pregnancy.

Author(s): Tharakan G1, Kadiyala R1, Damani N2, Clements MR1 and Ostberg JE1.Department of Diabetes and Endocrinology, Watford General Hospital.Department of Radiology, Watford General Hospital We present a rare case of pituitary apoplexy occurring in pregnancy. A 34-year old woman was admitted to the obstetric ward with a severe headache in the 38th week of her second pregnancy.

In 2008 the patient was referred with an 8 month history of secondary amenorrhoea and galactorrhoea. Pituitary testing demonstrated a raised prolactin. The initial MRI was reported to show no pituitary tumour, although on later review there is evidence of a small adenoma. Initiation of cabergoline restored menstruation and in June 2010 she became pregnant again.

In the 38th week of her pregnancy she developed severe headaches resulting in an admission for investigation of her symptoms. Her prolactin level was 7131mU/l.

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