Hypercholesterolaemia is a common finding in patients with anorexia nervosa (AN). To investigate the type, frequency and pathophysiological mechanisms of changes in lipoprotein metabolism in AN we performed a cross-sectional study in fifty-eight female patients (mean age 24·2 years, BMI 15·3 (SD 1·5) kg/m 2 ) and fifty-eight healthy age-matched controls (CO; BMI 22·2 (SD 1·7) kg/m 2 ). Total cholesterol and LDL-cholesterol were higher in AN (5·5 (SD 1·3) v. 5·0 (SD 0·8) mmol/l, P¼0·023; 3·6 (SD 1·1) v. 3·2 (SD 0·7) mmol/l, P¼0·025 respectively). LDL particles were significantly more enriched in cholesterol and triacylglycerol in AN. In multiple regression analysis with LDL-cholesterol as the dependent and BMI, total body fat ( %), lathosterol:cholesterol ratio (endogenous cholesterol synthesis), 7a-hydroxy-4-cholesten-3-one (bile acid synthesis), non-esterified glycerol, free triiodothyronine and free thyroxine as independent variables, BMI was the only significant predictor in CO (R 2 0·36, overall P¼0·001). In AN the variability of LDL-cholesterol was significantly predicted by total body fat, free thyroxine, BMI, free triiodothyronine and non-esterified glycerol (R 2 0·55, overall P,0·001). Subgroup analysis between restricting (AN-R) and binge-eating -purging patients (AN-B) indicated that in AN-R changes in lipoproteins, BMI and total body fat were more pronounced. AN-R patients had lower bile acid synthesis than AN-B (P¼0·02). We conclude that elevated cholesterol concentrations in AN are generally due to an increase in LDL-cholesterol, which is mostly determined by the severe loss of body fat and the resulting changes in thyroid hormones, increased lipolysis and decreased endogenous cholesterol synthesis with resulting decrease in LDL removal. The clinical subtype of AN plays a major role in the mechanisms leading to hypercholesterolaemia.Anorexia nervosa: Lipoprotein metabolism: Hypercholesterolaemia
Objective: To study the longitudinal changes in plasma levels of leptin, insulin and cortisol during the transition from the state of starvation to the state of refeeding focussing on diurnal secretion characteristics and their temporal relationships. Design: Leptin, insulin and cortisol were measured every 2 h for 24 h during acute starvation (T1). Sampling was repeated after reaching half the target-body mass index (BMI) (T2) and again at target-BMI (17.5 kg/m 2 ; T3). The temporal relationships between the diurnal secretion patterns were assessed by cross-correlation analysis. Results: Although BMIs at T1 were uniformly low, leptin levels varied widely within a range clearly below normal levels (0.03-1.7 mg/l). With increasing body fat during the course of refeeding, mean leptin levels increased from 0.64 mg/l (range: 0.27-1.73 mg/l) (T1) to 1.61 mg/l (range: 0.36-4.2 mg/l) (T2) and to 3.67 mg/l (range: 0.7-9.8 mg/l) (T3). Circadian leptin secretion patterns showed maximal values uniformly around 0200 h and minimal values around 0800 h at all stages of the study. At all three weight levels, plasma leptin levels were highest between midnight and the early morning hours and lowest around the late morning hours. Refeeding neither profoundly changed secretion patterns of leptin nor did it change the positive, time-delayed relationship between leptin and insulin with increments in insulin secretion preceding those of leptin by 6 h. A temporal relationship between leptin and cortisol could not be demonstrated in the state of semistarvation but emerged after a substantial weight gain; at that time, leptin increases preceded cortisol increases by 8 h. Conclusions: Absolute leptin, insulin and cortisol levels are profoundly changed during starvation in anorectic patients, while refeeding, paralleled by a BMI gain, reverses these changes. During refeeding the relationship between leptin and cortisol changed profoundly, showing no significant correlation in the state of starvation, whereas at T3 after refeeding a strong inverse relationship could be observed. Leptin and insulin did not correlate significantly at any of the three stages studied.
There is still great need of specialist services at university hospitals in Germany for adults with ASD, although more services have been established over the past few years. Over half of the patients with ASD had other psychiatric comorbid disorders, which were mostly mental retardation and affective disorders. The most common differential diagnosis for patients presenting at the clinics were personality disorders and depression.
The classification of personality disorders (PD) according to ICD-10 and DSM-IV has been critisized for several reasons. For example, those who have attempted to validate the presence of a non-arbitrary distinction between normal and abnormal personality functioning have suggested that no such distinction exists. Furthermore, PDs frequently co-occur with a number of Axis-I conditions and other Axis-II disorders leading to multiple diagnoses. Therefore, many have suggested classifying PDs dimensionally, rather than categorically. However, there are only a few studies that have investigated the applicability of these models with respect to PDs, and most of these studies used the Big Five. In this study we investigated the applicability of the Seven-Factor model of temperament and character for the classification of PDs. Our results show that the Seven-Factor model discriminates well between PDs and healthy controls, as well as between PDs and Axis-I disorders. We discuss our findings and present a modified scheme to diagnose PDs.
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