Natural history of non-functioning pituitary microadenomas: results from the UK non-functioning pituitary adenoma consortium.

OBJECTIVE: The optimal approach to the surveillance of non-functioning pituitary microadenomas (micro-NFPAs) is not clearly established. Our aim was to generate evidence on the natural history of micro-NFPAs to support patient care. DESIGN: Multi-centre, retrospective, cohort study involving 23 endocrine departments (UK NFPA consortium). METHODS: Clinical, imaging, and hormonal data of micro-NFPA cases between January, 1, 2008 and December, 21, 2021 were analysed. RESULTS: Data for 459 patients were retrieved [median age at detection 44 years (IQR 31-57)-152 males/307 females]. Four hundred and nineteen patients had more than two magnetic resonance imagings (MRIs) [median imaging monitoring 3.5 years (IQR 1.71-6.1)]. One case developed apoplexy. Cumulative probability of micro-NFPA growth was 7.8% (95% CI, 4.9%-8.1%) and 14.5% (95% CI, 10.2%-18.8%) at 3 and 5 years, respectively, and of reduction 14.1% (95% CI, 10.4%-17.8%) and 21.3% (95% CI, 16.4%-26.2%) at 3 and 5 years, respectively. Median tumour enlargement was 2 mm (IQR 1-3) and 49% of micro-NFPAs that grew became macroadenomas (nearly all >5 mm at detection). Eight (1.9%) patients received surgery (only one had visual compromise with surgery required >3 years after micro-NFPA detection). Sex, age, and size at baseline were not predictors of enlargement/reduction. At the time of detection, 7.2%, 1.7%, and 1.5% patients had secondary hypogonadism, hypothyroidism, and hypoadrenalism, respectively. Two (0.6%) developed hypopituitarism during follow-up (after progression to macroadenoma). CONCLUSIONS: Probability of micro-NFPA growth is low, and the development of new hypopituitarism is rare. Delaying the first follow-up MRI to 3 years and avoiding hormonal re-evaluation in the absence of tumour growth or clinical manifestations is a safe approach for micro-NFPA surveillance.

Recurrent Thyroid Storm Caused by a Complete Hydatidiform Mole in a Perimenopausal Woman.

BACKGROUND: Gestational trophoblastic disease (GTD) which includes hydatidiform mole, invasive mole, placental site trophoblastic tumor, and choriocarcinoma is a rare cause of hyperthyroidism due to excess production of placental human chorionic gonadotrophin hormone (hCG) by tumor cells. Molecular mimicry between hCG and thyroid stimulating hormone (TSH) leads to continuous stimulation of TSH receptor by extremely high levels of hCG seen in these tumors. Consequently, biochemical and clinical hyperthyroidism ensues and it is potentially complicated by thyrotoxic crisis which is fatal unless urgent therapeutic steps are undertaken. Case Description. We present a 49-year-old perimenopausal woman who presented with recurrent thyroid storm and high output cardiac failure. The initial workup revealed suppressed TSH, high-free thyroxine (FT4), and free triiodothyronine (FT3) levels with increased vascularity of the normal-sized thyroid on ultrasonography. She was managed with parenteral beta blockers, steroids, and high-dose carbimazole. Her lower abdominal tenderness led to further investigations which revealed tremendously elevated beta-hCG and a snow storm appearance on transabdominal ultrasound suggestive of GTD. She underwent curative surgery and was diagnosed with complete hydatidiform mole postoperatively by histology. CONCLUSION: Recurrent thyroid crisis in gestational trophoblastic disease is an exceedingly rare presentation and that is highly fatal. This case highlights the importance of early detection and treatment of the etiology of thyrotoxicosis to eliminate mortality.