Co-secreting thyrotropin/growth hormone (GH) pituitary adenomas are rare; their clinical presentation and long-term management are challenging. There is also a paucity of long-term data. Due to the cell of origin, these can behave as aggressive tumours. We report a case of a pituitary plurihormonal pit-1-derived macroadenoma, with overt clinical hyperthyroidism and minimalGHexcesssymptoms.ThediagnosiswasconfirmedbypathologyshowingelevatedthyroidandGHaxeswithfailureof physiologicalGHsuppression,elevatedpituitaryglycoproteinhormonealphasubunit(αGSU)andmacroadenomaonimaging. Pre-operatively the patient was rendered euthyroid with carbimazole and underwent successful transphenoidal adenomectomy (TSA) with surgical cure. Histopathology displayed an elevated Ki-67 of 5.2%, necessitating long-term follow-up. Correspondence should be addressed to V PredaLearning points:• Thyrotropinomas are rare and likely under-diagnosed due to under-recognition of secondary hyperthyroidism.• Thyrotropinomas and other plurihormonal pit-1-derived adenomas are more aggressive adenomas according to WHO guidelines.• Co-secretion occurs in 30% of thyrotropinomas, requiring diligent investigation and long-term follow-up of complications.H Y Ng and others TSH/GH pituitary adenoma

Summary Thyrotropinomas are an uncommon cause of hyperthyroidism and are exceedingly rarely identified during pregnancy, with limited evidence to guide management. Most commonly they present as macroadenomas and may cause symptoms of mass effect including headache, visual field defects and hypopituitarism. We present a case of a 35-year-old woman investigated for headaches in whom a 13 mm thyrotropinoma was found. In the lead-up to planned trans-sphenoidal surgery (TSS), she spontaneously conceived and surgery was deferred, as was pharmacotherapy, at her request. The patient was closely monitored through her pregnancy by a multi-disciplinary team and delivered without complication. Pituitary surgery was performed 6 months post-partum. Isolated secondary hypothyroidism was diagnosed postoperatively and replacement thyroxine was commenced. Histopathology showed a double lesion with predominant pituitary transcription factor-1 positive, steroidogenic factor negative plurihormonal adenoma and co-existent mixed thyroid-stimulating hormone, growth hormone, lactotroph and follicle-stimulating hormone staining with a Ki-67 of 1%. This case demonstrates a conservative approach to thyrotropinoma in pregnancy with a successful outcome. This highlights the need to consider the timing of intervention with careful consideration of risks to mother and fetus. Learning points Thyrotropinomas are a rare cause of secondary hyperthyroidism. Patients may present with hyperthyroidism or symptoms of mass effect, including headaches or visual disturbance. Thyrotropinoma in pregnancy presents a number of pituitary-related risks including pituitary apoplexy and compression of local structures. Hyperthyroidism in pregnancy raises the risk of complications including spontaneous abortion, preeclampsia, low birthweight and premature labour. Timing of medical and surgical therapies must be carefully considered. A conservative approach requires careful monitoring in case emergent intervention is required.

Thyrotropinomas (TSHomas) are rare pituitary tumours, comprising 1-2% of all pituitary adenomas. Thyrotropinomas in pregnancy are exceedingly rare and management of these in pregnancy can be challenging due to the potential for maternal and foetal harm. We report the case of a 35 year old woman who was found to have a pituitary macroadenoma on imaging whilst being evaluated for headaches and sinusitis. She had felt more stressed than usual but no other overt thyrotoxic symptoms. There were no visual field abnormalities or symptoms to suggest other endocrine hypo or hypersecretion. Pituitary MRI revealed a macroadenoma and biochemistry demonstrated raised free T4 24 pmol/L and free T3 6.8 pmol/L and inappropriately elevated TSH of 4.2 mIU/L, in keeping with secondary hyperthyroidism. She was scheduled for transsphenoidal (TSA) pituitary surgery, however on review she had naturally fallen pregnant. After a multi-disciplinary discussion, it was decided that surgery should be deferred and close observation be undertaken under the care of a multidisciplinary team. During the first half of pregnancy she suffered hyperemesis gravidarum with ongoing thyrotoxicosis but declined carbimazole. Her visual fields were normal throughout pregnancy. She delivered vaginally at 38 weeks, weight 3.395kg and had no malformations. Post birth was complicated by post-partum haemorrhage requiring multiple blood transfusions and intensive care. One week later after recovering, she was able to commence breastfeeding. She went on to TSA at 6months post partum with complete tumour resection. This case demonstrates the complexity of managing TSHomas in pregnancy and the potential cross reactivity of the early hCG rises with the already elevated TSH levels, likely exacerbating her hyperemesis gravidarum.

Gonadotropinoma in Klinefelter syndrome (KS) is uncommon and may be a result of protracted stimulation of gonadotrophs from lack of androgen feedback. Associations of white matter changes and increased venous thromboembolic risk have been reported and need to be considered in patients with KS.

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