Specific behaviour, mood and personality traits may contribute to obesity in patients with craniopharyngioma.

INTRODUCTION: Patients with craniopharyngioma (CP) often suffer from obesity, but the underlying causes are still not fully understood. We compared CP to patients with nonfunctioning pituitary adenoma (NFPA) and to a control group (CG) using standardized questionnaires to investigate whether behavioural, mood or personality traits contribute to obesity. METHODS: We compared 31 patients with CP (42% male, 53 ± 15·1 years) to 26 patients with NFPA (71% male, 63·2 ± 10·3 years) and to age- and gender-matched local CG (ratio 2:1). Normative data from the literature are included for reference. Patients were asked to complete eleven standardized questionnaires. Two questionnaires were used to evaluate eating disorders (FEV, EDE-Q), one depression (BDI), one anxiety (STAI), three health-related quality of life (SF-36, EuroQoL, QoL-AGHDA), one sleepiness (Epworth Sleepiness Scale), two personality (EPQ-RK, TPQ) and one body image (FKB-20). RESULTS: Patients with CP scored significantly higher in conscious hunger perception (FEV, CP 5·8 ± 3·2 scores, NFPA 3·6 ± 3·3 scores, CG 3·0 ± 2·5, P < 0·001). They had similar scores for BDI compared with NFPA, but higher scores to CG (P < 0·001, CP 10·6 ± 8·3, NFPA 7·5 ± 5·7, CG 4·96 ± 4·2). CP and NFPA scored higher than CG for anxiety and personality traits such as harm avoidance, fatigability and asthenia and slightly higher for neuroticism. No differences were seen for EDE-Q, quality of life, daytime sleepiness and body image between CP and NFPA. However, differences could be observed to normative data from the literature. CONCLUSION: Obesity in patients with CP might be influenced by eating disorders, negative mood alterations and increased anxiety-related personality traits.

Food intake regulating hormones in adult craniopharyngioma patients.

INTRODUCTION: Patients with craniopharyngioma (CP) have disturbances of the hypothalamic-pituitary axis and serious comorbidities such as obesity. We hypothesized that the secretion of hormones regulating the nutritional status is altered in adult patients with CP compared with patients with non-functioning pituitary adenoma (NFPA). METHODS: WE INCLUDED 40 CP (50% MALES, MEAN AGE: 49.6±14.3 years) and 40 NFPA (72.5% males, mean age: 63.4±9.8 years) patients. We measured glucose, insulin, leptin, total ghrelin, peptide-YY (PYY) and cholecystokinin (CCK) during oral glucose tolerance test (OGTT). Fat mass (FM) was determined by dual X-ray absorptiometry. RESULTS: Gender distribution was not significantly different, but CP patients were significantly younger (P<0.001). CP patients had significantly higher BMI and FM than NFPA patients (BMI 32±8 vs 28±4 kg/m(2), P=0.009 and FM 37±9 vs 33±9%, P=0.02). Fasting glucose level (84±12 vs 78±11 mg/dl, P=0.03), leptin (27.9±34.2 vs 11.9±11.6 µg/l, P=0.008) and leptin levels corrected for percentage FM (0.66±0.67 vs 0.32±0.25 µg/l%, P=0.005) were significantly higher in CP than in NFPA patients, whereas ghrelin was significantly lower (131±129 vs 191±119 ng/l, P=0.035). Insulin, PYY and CCK did not differ significantly between groups. After glucose load, leptin decreased significantly in CP patients (P=0.019). In both groups, ghrelin decreased significantly during OGTT (both P<0.001). The percentage decline was significantly smaller for CP. PYY and CCK increased equally after glucose in both groups. CONCLUSION: Our patients with CP have more metabolic complications than our patients with NFPA. The levels of leptin and ghrelin at fasting status and after glucose seem to be altered in CP, whereas changes in insulin, PYY and CCK do not seem to be responsible for the metabolic changes in these patients.