Caroline Steele

Presentation, management and outcomes in acute pituitary apoplexy: a large single-centre experience from the United Kingdom

To study the presentation, management and outcomes and to apply retrospectively the Pituitary Apoplexy Score (PAS) (United Kingdom (UK) guidelines for management of apoplexy) to a large, single‐centre series of patients with acute pituitary apoplexy.

Pituitary adenomas in childhood, adolescence and young adulthood: presentation, management, endocrine and metabolic outcomes

OBJECTIVE To elucidate the long-term outcomes of pituitary adenomas diagnosed in childhood and adolescence, knowledge of which remains sparse. DESIGN AND METHODS A retrospective review of patients aged ≤21 years at diagnosis of pituitary adenoma, attending a neuroendocrine service in Liverpool, UK, between 1984-2009. RESULTS There were 41 patients (33 female), mean age at diagnosis 17.3 years (range 11-21) and mean follow-up 9.6 years; 29 patients had prolactinomas (15 macroprolactinomas), 6 non-functioning pituitary adenomas (NFPAs), 5 Cushings disease (CD) and 1 acromegaly. All prolactinoma patients received dopamine agonists (DAs) and three also underwent pituitary surgery. Furthermore, ten patients underwent surgery: five with CD, one with acromegaly and four with NFPA. Four received radiotherapy after surgery. Another ten patients received hormone replacement: nine hydrocortisone, five thyroxine, seven sex steroids and five GH; another seven had severe asymptomatic GH deficiency. Three female patients were treated for infertility (two successfully). Thirteen patients gained significant weight (body mass index (BMI) increase >2 kg/m(2)) since diagnosis and 16 in total are now obese (BMI>30 kg/m(2)). Five were treated with orlistat and one attended a weight management service. Two received antihypertensive medications, two had type 2 diabetes and four were treated for dyslipidaemia. CONCLUSIONS This is one of the largest reviews of patients aged 21 or younger at diagnosis of pituitary adenoma followed up by a single service. Two-thirds had prolactinomas, all were treated with DAs and three underwent surgery. Increased cardiovascular risk factors (obesity and dyslipidaemia) and infertility are important sequelae and active identification and treatment are necessary.

Hypothalamic Obesity: Prevalence, Associations and Longitudinal Trends in Weight in a Specialist Adult Neuroendocrine Clinic

OBJECTIVE Obesity is highly prevalent among adults with acquired, structural hypothalamic damage. We aimed to determine hormonal and neuroanatomical variables associated with weight gain and obesity in patients following hypothalamic damage and to evaluate the impact of early instigation of weight loss measures to prevent or limit the severity of obesity in these patients. DESIGN Retrospective study of 110 adults with hypothalamic tumours attending a specialist neuroendocrine clinic. BMI was calculated at diagnosis and at last follow-up clinic visit. Endocrine data, procedures, treatments and weight loss measures were recorded and all available brain imaging reviewed. RESULTS At last follow-up, 82.7% of patients were overweight or heavier (BMI≥25 kg/m(2)), 57.2% were obese (BMI≥30 kg/m(2)) and 14.5% were morbidly obese (BMI≥40 kg/m(2)). Multivariate analysis revealed that use of desmopressin (odds ratio (OR)=3.5; P=0.026), GH (OR=2.7; P=0.031) and thyroxine (OR=3.0; P=0.03) was associated with development of new or worsened obesity. Neuroimaging features were not associated with weight gain. Despite proactive treatments offered in clinic in recent years (counselling, dietetic and physical activity advice, and anti-obesity medications), patients have continued to gain weight. CONCLUSIONS Despite increased awareness, hypothalamic obesity is difficult to prevent and to treat. Improved understanding of the underlying pathophysiologies and multicentre collaboration to examine efficacy of novel obesity interventions are warranted.

Cerebral activations during viewing of food stimuli in adult patients with acquired structural hypothalamic damage: a functional neuroimaging study

Background/Objectives:Obesity is common following hypothalamic damage due to tumours. Homeostatic and non-homeostatic brain centres control appetite and energy balance but their interaction in the presence of hypothalamic damage remains unknown. We hypothesized that abnormal appetite in obese patients with hypothalamic damage results from aberrant brain processing of food stimuli. We sought to establish differences in activation of brain food motivation and reward neurocircuitry in patients with hypothalamic obesity (HO) compared with patients with hypothalamic damage whose weight had remained stable.Subjects/Methods:In a cross-sectional study at a University Clinical Research Centre, we studied 9 patients with HO, 10 age-matched obese controls, 7 patients who remained weight-stable following hypothalamic insult (HWS) and 10 non-obese controls. Functional magnetic resonance imaging was performed in the fasted state, 1 h and 3 h after a test meal, while subjects were presented with images of high-calorie foods, low-calorie foods and non-food objects. Insulin, glucagon-like peptide-1, Peptide YY and ghrelin were measured throughout the experiment, and appetite ratings were recorded.Results:Mean neural activation in the posterior insula and lingual gyrus (brain areas linked to food motivation and reward value of food) in HWS were significantly lower than in the other three groups (P=0.001). A significant negative correlation was found between insulin levels and posterior insula activation (P=0.002).Conclusions:Neural pathways associated with food motivation and reward-related behaviour, and the influence of insulin on their activation may be involved in the pathophysiology of HO.