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PubMed2004

Testosterone administration in women with anorexia nervosa.

Anorexia nervosa (AN) is complicated by severe bone loss, cognitive function deficits, and a high prevalence of major depression. We hypothesized that bone formation would increase and depressive symptoms and spatial cognition would improve with short-term physiological testosterone administration. We randomized 33 women with AN and relative testosterone deficiency to transdermal testosterone (Intrinsa, Procter and Gamble Pharmaceuticals, Cincinnati, OH), 150 mug, 300 mug, or placebo, for 3 wk. At baseline, free testosterone correlated with L4 bone density (r = 0.51, P < 0.001), body mass index (r = 0.39, P = 0.02), depressive symptoms (r = -0.44, P = 0.02), and spatial cognition (r = 0.45, P = 0.04). C-terminal propeptide of type 1 collagen levels were higher during testosterone administration than placebo (P = 0.03). The change in propeptide of type 1 collagen correlated with change in free testosterone over 3 wk (r = 0.50, P = 0.02). Osteocalcin and bone-specific alkaline phosphatase did not change. Depressed patients receiving testosterone improved from severely depressed to moderately depressed; the placebo group was unchanged (P = 0.02). Spatial cognition improved in the testosterone group, compared with placebo (P = 0.0015). Therefore, short-term low-dose testosterone may improve depressive symptoms and spatial cognition in women with AN. Low-dose testosterone may also prevent decreased bone formation in AN, but because testosterone did not affect all markers of bone formation studied, further data are needed.

Administration, Cutaneous↗
PubMed1986

Changes in insulin sensitivity and clearance in anorexia nervosa.

Anorexia nervosa (AN) is a state of self-induced malnutrition characterized by a marked pursuit of thinness and the fear of obesity. Although low fasting blood glucose and insulin have been demonstrated, there is contradictory data on insulin sensitivity and a lack of information about insulin metabolism and its metabolic effects in AN. Insulin sensitivity, kinetics, and metabolic effects were measured using the euglycemic clamp in nine females with AN (age 25.2 +/- 1.9 years and 70.6 +/- 2.2% ideal body weight), and the results compared with seven female normal controls (NC) (age 23.6 +/- 1.0 years and 92.7 +/- 2.5% ideal body weight). Fasting plasma glucose (FPG), immunoreactive insulin (IRI), and C-peptide were significantly lower in AN as compared to NC (84.3 +/- 1.5 v 91.5 +/- 1.7 mg dL-1, 9.3 +/- 1.0 v 13.5 +/- 1.4 microU mL-1, and 0.26 +/- 0.03 v 0.41 +/- 0.02 pmol mL-1) (P less than 0.05). During the glucose clamp, the glucose metabolized (M), the metabolic clearance rate of glucose (MCRg), and the glucose metabolized per unit of insulin (M/I ratio) were all higher in AN as compared to NC (M, 8.7 +/- 1.2 v 6.9 +/- 0.6 mg min-1 kg-1; MCRg, 9.9 +/- 1.5 v 7.4 +/- 0.6 mL min-1 kg-1; M/I ratio, 8.6 +/- 1.6 v 5.0 +/- 0.3 mg min-1 kg-1/microU mL-1 X 100), but only the M/I ratio attained statistical significance (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxybutyric Acid↗
PubMed1989

Growth hormone and prolactin response to growth hormone-releasing in anorexia nervosa.

Anorexia nervosa (AN) is associated with several endocrine disorders. In order to investigate the role of these alterations, growth hormone-releasing hormone (GHRH) was administered in a group of 9 AN patients and in 9 healthy normal-weight women as control. Growth hormone (GH) and prolactin (PRL) levels were evaluated in both groups after GHRH and saline solution administration. In the AN group, luteinizing hormone (LH), follicle-stimulating hormone (FSH), thyrotropin (TSH) and cortisol serum levels were evaluated during GHRH administration; somatomedin-C (Sm-C) basal levels were also determined. In both groups, GHRH induced a prompt GH increase, which was significantly higher in AN patients (55.3 +/- 2.9 ng/ml, mean +/- SE) than in normal subjects (9.8 +/- 2.6 ng/ml: p less than 0.01). A significant positive correlation between mean GH basal values and GH peak after GHRH was observed only in the control group (R = 0.82, p less than 0.01). No significant relationship between GH mean peak and body mass index (BMI) or Sm-C, estradiol (E2) and glucose serum levels was found in AN patients. However, a positive significant correlation with triiodothyronine (T3) basal values was observed in this group (R = 0.80, p less than 0.01). Both groups showed no variation in PRL serum levels after GHRH infusion. Our data suggest the presence of a central derangement in hypothalamic control of pituitary function in patients with AN, which is not necessarily due to weight loss alone.

Adolescent↗
PubMed2001

Association between an agouti-related protein gene polymorphism and anorexia nervosa.

Anorexia nervosa (AN) is a life threatening disorder affecting mostly adolescent women. It is a dramatic psychiatric syndrome accompanied by severe weight loss, hyperactivity and neuroendocrine changes (reviewed in Refs 1 and 2). Several studies have shown a strong genetic component in AN (reviewed in Ref 3). Recent advances in unraveling the mechanisms of weight control point to a crucial role of the melanocortin-4 receptor (MC4-r) system in regulating body weight. The orexigenic neuropeptide agouti-related protein (AGRP), a MC4-r antagonist, plays a crucial role in maintaining body weight, by inducing food intake. The sequence of the coding region of the human AGRP gene (AGRP) was determined and the AGRP of 100 patients with AN was screened for variations. Three single nucleotide polymorphisms (SNPs) were identified and screened in a further 45 patients and 244 controls. Two alleles were in complete linkage disequilibrium and were significantly enriched in anorectic patients (11%; P = 0.015) compared to controls (4.5%). These data indicate that variations of AGRP are associated with susceptibility for AN. This is possibly caused by defective suppression of the MC4-r by the variant AGRP, leading to a decreased feeding signal, increasing the risk of developing AN. These results implicate that antagonism of the MC4-r might be considered as pharmacotherapy for patients with AN.

Adolescent↗
PubMed2003

Endocrine abnormalities in Anorexia Nervosa.

Anorexia Nervosa (AN) is a psychiatric disorder characterized by the classic triad: amenorrhea, weight loss, and behavioral changes. It is generally seen in young, white women under 25 and is particularly common in adolescence. The mortality of the disease varies between 5.1% and 13%. The endocrine changes associated with AN have been studied in depth and provide strong evidence for hypothalamic dysfunction. All are secondary and reverse with weight gain. In general, gonadotropin (FSH, LH) levels are decreased in patients with AN, as well as the response to Gonadotropin releasing hormone (GnRH). Fasting growth hormone levels are elevated, but the stimulated response of Growth hormone (GH) to Growth hormone releasing hormone (GHRH) is normal and inversely correlated to body weight. Serum Growth hormone binding protein (GHBP), insulin growth factor I (IGF-I) and IGF binding protein (IGFBP) - 3 levels are all significantly decreased in patients with AN and return to normal with refeeding. IGFBP-1 and 2 are increased and return also to normal with weight gain. Serum IGF-II is decreased but not significantly. The IGFBP-3 proteolytic activity is normal. Thyroxine (T4) and Triiodothyronine (T3) while reverse T3 (rT3) is elevated. Thyrotropin stimulating hormone (TSH). TSH levels are normal with a delayed response to thyrotropin releasing hormone (TRH). Cortisol levels are normal or elevated as well as urinary free cortisol. Corticotropin (ACTH) levels are normal with decreased response to Corticotropin releasing hormone (CRH). Dexamethasone suppression test is abnormal. Sex steroids are decreased. Finally leptin levels are decreased in patients with AN while ghrelin levels are elevated. Both leptin and ghrelin levels return to control values after renutrition.

Anorexia Nervosa↗
PubMed2004

Effects of risedronate on bone density in anorexia nervosa.

Anorexia nervosa (AN), a psychiatric disease characterized by chronic starvation, is complicated by severe bone loss (1), for which there is no effective, available therapy. Although bone resorption is markedly increased in these patients, estrogen is an ineffective anti-resorptive therapy in the setting of undernutrition. We hypothesized bisphosphonate administration would result in a decrease in bone resorption and an increase in bone density in women with AN and bone loss, despite undernutrition. We therefore administered risedronate 5 mg daily for nine months to 10 women with AN, all of whom had osteopenia (mean AP spine T score: -2.7 +/- 2) and compared NTX and bone density with baseline values and with those from available control data prospectively followed for the same time period. Bone density increased significantly in patients who received risedronate compared with controls and compared with baseline, despite lack of significant weight gain, for an increase of AP spine bone density of 4.1 +/- 1.6% at six months and 4.9 +/- 1.0% at nine months. Bone resorption, as measured by NTX, decreased 23.8% at one month and 29.6% at three months, from the high-normal to mid-normal range of young women. Our data suggest that risedronate 5 mg daily administered to women with AN and osteopenia may increase in bone density at the AP spine despite low weight. This is the first study to demonstrate marked increases in bone density in women with AN. Because of the lack of data regarding the safety of such medications in women of reproductive age, bisphosphonates are not approved in the U.S. for premenopausal women other than those receiving glucocorticoids. Further studies are needed to establish the efficacy and safety of bisphosphonate therapy in this population.

Adult↗
PubMed2002

Heritability, genetics and association findings in anorexia nervosa.

Anorexia nervosa (AN) is a severe psychiatric disorder, characterized by a combination of abnormal eating behavior and weight regulation with disturbances of attitudes toward body weight and shape. Prevalence is estimated at 1/1000, but with a high prevalence of the partial syndrome and a 10% mortality rate. This article reviews the findings concerning the heritability and the contributing genes of the disorder, with a focus on candidate genes. In family studies, a higher frequency of AN and BN was found among relatives of AN probands. The heritability rate was estimated at 0.71, similar to twin studies, which estimate 0.58-0.76. The search for genes responsible for the disorder focuses on the monoaminergic and peptidergic systems that are related to appetite and weight regulation. So far, for serotonin and dopamine there are no consistent findings in association studies of AN. However, in an Israeli study, an association was found between susceptibility for AN and the COMT gene, which is involved in monoamine metabolism. Another Israeli study found a relation between AN and the gene encoding for the potassium channel (hSKCa3), which is involved in regulation of neuronal activity. In the endocrine system an unequivocal finding was described of an association to the gene encoding the receptor for beta-estrogen. In the appetite and weight regulation system an association was described between AN and a marker of the uncoupling protein-2 and -3 chromosomal region, raising the likelihood that the mutation within the gene is close to a positive marker. To conclude, although there is a strong familial component in AN, so far the search for candidate genes has not been fruitful and further large scale prospective and adoption studies are needed to confirm genetic factors. We hope that relative studies using a wide genome scan, as well as subtyping the different types of AN, will bring us closer to understanding of the heritability of AN and enable the development of improved means of prevention and treatment.

Adolescent↗
PubMed2004

Gonadotropin response to clomiphene and plasma leptin levels in weight recovered but amenorrhoeic patients with anorexia nervosa.

Anorexia nervosa (AN) is a state of leptin and gonadotropin deficiency. Leptin levels are decreased in normal weight women with hypothalamic amenorrhea and leptin may be a sensitive marker of overall nutritional status. The aim of the study is to provide additional information on plasma leptin levels and on gonadotropin responses after clomiphene testing in patients with AN who recovered weight but were still amenorrheic. We evaluated 17 patients with AN, female age 20+/-1.2 yr who reached goal weight [body mass index (BMI) 14.9+/-0.5 to 19.3+/-0.4 kg/m2]. At diagnosis serum leptin levels were 2.2+/-0.1 microg/l while after behavioural therapy and hypercaloric diet for 6-12 months serum leptin levels rose to 6.4+/-1.4 microg/l significantly lower compared with those in the control (no.=10, age 28+/-6.2 yr, BMI 21.1+/-0.3 kg/m2, leptin 9.3+/-0.7 pg/l; p<0.05). None of the patients resumed spontaneous menstrual cycles after weight gain. They were tested with a 10-day administration of clomiphene citrate. All had a significant rise in LH secretion (from 1.7+/-0.3 IU/l to 8.3+/-0.9 IU/l, p<0.01) and serum estradiol levels (from 19.0+/-5.4 to 937.7+/-241.2 pg/ml, p<0.03). Nine out of 17 patients menstruated after clomiphene. Serum leptin levels were not different in those who menstruated from those who did not (6.4+/-1.4 to 6.8+/-1.4 microg/l, p>0.05). Body compositon was studied in 12 additional carefully matched patients with AN who recovered weight. Six of them resumed spontaneous menstrual cycles. Neither BMI, body fat, nor leptin appeared as significant determinants of menstrual status. In conclusion, relative hypoleptinemia persists, independent of fat mass, in weight recovered patients with AN. A normal response to clomiphene in weight-recovered yet still amenorrhoeic patients with AN, offers reassurance that the axis is intact and that the problem lies in the hypothalamus. It is reasonable to believe that nutritional disturbances, fat intake and persisting psychological factors still affect plasma leptin levels and reproductive functions in weight-recovered patients with amenorrhea.

Adolescent↗
PubMed1997

Hexarelin is a stronger GH-releasing peptide than GHRH in normal cycling women but not in anorexia nervosa.

Anorexia nervosa (AN) is a chronic disease in which an enhanced GH response to GHRH, a paradoxic increase after TRH and LHRH, and low IGF1 levels may be present according to the patient's clinical state. It is well known that the GH hypersecretory state commonly found in the "acute phase" of AN is restored with weight gain. The new synthetic hexapeptide, Hexarelin (HEX), which is chemically similar to GH-releasing peptide 6, has recently been shown to possess a stronger GH-releasing activity than GHRH in humans and to share a synergistic effect with GHRH when administered intravenously. Indeed, HEX shows a slight cortisol and PRL-releasing activity. The aim of the study was to evaluate the effect of i.v. administration of old (GHRH) and new (HEX) GH-releasing peptides on GH, PRL and cortisol secretion in 9 AN patients in the "recovery phase" of the disease, after partial but significant weight gain. For controls we studied 7 normal cycling women. No significant difference in GH secretion after GHRH was found between AN and controls. GHRH was not able to release cortisol or PRL either in AN or controls. HEX produced a significantly (p < 0.05) higher GH peak in controls than in AN, while GH AUC was slightly but not significantly higher. Indeed, only in controls, HEX was a stronger GH-releasing peptide than GHRH. These findings could be explained by the fact that, in AN, GH secretion is already stimulated both by reduced IGF1 levels and by increased GHRH/somatostatin ratio. As reported in the literature, the action of HEX action is only slightly influenced by variations in somatostatin tone. It therefore appears likely that the absolute or relative GHRH increase present in AN could partially mimic the unknown hypothalamic factor necessary for HEX action on the hypophisis and that, following a structural modification of pituitary HEX receptors, GHRH would become able to bind to HEX receptors on somatotropic cells. Consequently, the pituitary cells would already be over-activated and so unable to respond maximally to HEX stimulation. Indeed, in AN, GHRH might play a role of negative modulation in the control of HEX action. Finally, in our study HEX was able to produce a persistent PRL release in controls but not in AN, thus suggesting that its action could be partially dependent on the estrogen milieu, while it stimulated cortisol secretion only transiently in the patients studied.

Adolescent↗
PubMed1999

A variation in Bone Alkaline Phosphatase levels that correlates positively with bone loss and normal levels of aminoterminal propeptide of collagen I in girls with anorexia nervosa.

Anorexia nervosa (AN) is a very extended pathology among adolescent girls nowadays. These patients show a high degree of osteopenia; hence, study of their bone remodelling is of great interest. Serum bone alkaline phosphatase (bAP) and aminoterminal propeptide of procollagen I (PINP) provide good sensitivity in the analysis of bone alterations in postmenopausal osteoporosis. The aim of this study was to compare the usefulness of bAP and PINP in the study of bone remodelling in AN, and their possible correlation with the degree of osteopenia in this pathology. In order to help in the interpretation of the results, levels of the beta-isomer of urinary carboxyterminal propeptide of collagen I (beta-CTX) have also been included. Serum bAP (IRMA) Tandem R-Ostase, Hybritech), PINP (RIA, Orion Diagnostica) and CTX (CrossLaps ELISA, Osteometer) were determined in 41 girls with AN, aged 18.5+/-2.2 years (mean+/-SD) and in 31 healthy control women, aged 19+/-2.3 years. Bone mineral density (BMD) in lumbar spine was measured by DEXA in the AN group. We found that 41 of the 43 patients had BMD z-scores under -2. No significant differences were found in the levels of serum bAP nor in PINP and beta-CTX levels between controls and patients, although values in the AN group were highly variable. All the BMD z-score values were negative, and their absolute value correlates positively with bAP (P = 0.0279) and almost with beta-CTX (P = 0.0921) but not with PINP (P = 0.4627). Bone AP correlates with PINP in control girls (P = 0.017), but not in the AN group (P = 0.3573). Patients with AN were divided into three groups according to their levels of bAP: low (I), normal (II) or high (III). Patients with the highest bAP levels also presented the highest increase in bone resorption, according to their beta-CTX levels, and the highest degree of osteopenia. However, values of PINP were similar in the three groups of patients. The bAP/beta-CTX ratios in subgroups I, II and III of AN patients were 0.035, 0.065 and 0.073, a finding that suggests that bAP is not indicating the real degree of bone mineralization in these patients, because it is a contradiction that the formation/resorption ratio should be higher in the patients who have the highest bone loss. These results could suggest that bone loss in AN is produced by an increase in bone resorption (beta-CTX), without variations in bone matrix formation (PINP); bAP levels are a good marker in the follow-up of osteopenia degree, but not a real indicator of bone mineralization, a similar situation to that of osteomalacia.

Adolescent↗
PubMed2005

A prospective study of changes in bone turnover and bone density associated with regaining weight in women with anorexia nervosa.

Anorexia nervosa (AN) is a condition of self-induced weight loss, associated with an intense fear of gaining weight. Previous studies have shown that bone density may increase with regaining and maintaining normal weight; however, relatively little is known about the changes in bone metabolism that occur during weight restoration. We describe the effect of weight restoration and maintenance of weight over 1 year on bone mineral density (BMD) and bone turnover. We recruited women from the eating disorders services at the South West London and St George's Mental Health NHS Trust, and the Priory and Charter Nightingale Hospitals in London, UK. Details of their AN, fracture history, menstrual history and exercise were obtained by interview and case note review. Morning samples of blood and second void urine were taken for biochemical analysis. BMD was measured by DXA at the lumbar spine (LS), femoral neck (FN), distal radius (RD) and total body bone mineral content (BMC). Patients then entered the treatment program, which includes re-feeding, dietary education and psychotherapy. Over a period of 42 months, we recruited 55 women who agreed to participate in this study and underwent baseline investigations. Of these, 15 (27%) subjects achieved and then maintained their target weight for the duration of the study. At baseline for all subjects (n=55) estradiol levels were lower than the normal reference ranges (both follicular and luteal phases) in 91% of the women. Bone specific alkaline phosphatase (BSAP) concentrations were lower than the premenopausal reference range in 55% of women, and urinary deoxypyridinoline (DPD) was above the premenopausal reference range in 78% of women. Baseline lumbar spine BMD was positively related to BMI (Pearson's r=0.29, P=0.04) and inversely related to bone turnover markers: urinary DPD (Pearson's r=-0.39, P=0.01 and serum BSAP (Pearson's r=-0.3, P=0.06). The 15 patients who regained and maintained weight were followed-up for a mean duration of 69 weeks (SD 7.3, range 54 to 84 weeks). Mean BMI increased from 14.2 (1.7) to 20.2 (0.77) kg/m2 and remained stable throughout follow-up. Menstruation resumed in 8 of the 15 women. Total body BMC and LS BMD increased significantly over the duration of follow-up (by 4.3% each), but FN BMD and distal radius remained stable. Lumbar spine bone area also increased significantly, whereas FN and distal radius did not. These changes were associated with a significant increase in BSAP (P=0.01), and a non-significant trend for a decrease in DPD (P=0.10). Our findings suggest that when women are at low body weight they are in a hypo-estrogenic state, which is associated with imbalance of bone turnover (high bone resorption and low bone formation). This is reversed with weight gain and persists as target weight is maintained and is associated with increases in BMC and BMD.

Absorptiometry, Photon↗
PubMed2002

Abnormal bone mineral accrual in adolescent girls with anorexia nervosa.

Anorexia nervosa (AN) is increasingly common in adolescent girls and occurs at a time of peak bone mass formation. Osteopenia is common in adolescent girls with AN, and in a cross-sectional study, we have reported low bone formation markers in such girls. To determine the impact of chronic undernutrition on bone mineral accrual in contrast to healthy controls, we prospectively measured bone mineral density (BMD) and body composition by dual energy x-ray absorptiometry, bone metabolism markers, and nutritional and hormonal status at baseline, 6 months, and 12 months in 19 adolescent girls with AN (mean +/- SEM, 15.4 +/- 0.4 yr) and 19 controls of comparable chronological and skeletal age. Overall, nutritional status in subjects with AN improved (mean percentage increase in body mass index from baseline, 9.2 +/- 1.9% and 15.2 +/- 2.6% at 6 and 12 months, respectively), with 11 subjects having recovered weight at 12 months. However, lumbar BMD at 12 months (AN, 0.88 +/- 0.02 g/cm(2), vs. control, 0.98 +/- 0.03 g/cm(2); P = 0.008) remained significantly reduced in AN compared with controls, even in recovered subjects. This was due to significant increases in lumbar BMD in controls vs. no change in AN subjects over the year (0.003 +/- 0.001 g/cm(2).month vs. 0.000 +/- 0.001 g/cm(2).month, respectively; P = 0.04). The most significant determinant of change in lumbar BMD at 12 months was change in lean body mass in both AN (r = 0.62; P = 0.008) and control (r = 0.80; P = 0.0006) groups. There were significant increases in surrogate markers of bone turnover in subjects with AN compared with controls as assessed by osteocalcin (AN, 0.9 +/- 0.4 micro g/liter.month, vs. control, -1.1 +/- 0.4 micro g/liter.month; P = 0.0007), bone-specific alkaline phosphatase (AN, 0.6 +/- 0.5 U/liter.month, vs. control, -1.5 +/- 0.4 U/liter.month; P = 0.002), deoxypyridinoline [AN, 0.1 +/- 0.1 nmol/mmol creatinine (cr).month, vs. control, -0.4 +/- 0.1 nmol/mmol cr.month; P = 0.005], and N-telopeptide (AN, 4 +/- 4 nmol BCE/mmol cr/month, vs. control, -9 +/- 4 nmol BCE/mmol cr/month; P = 0.01). Changes in IGF-I levels over the year were highly correlated with changes in bone turnover over the same period in AN (osteocalcin, r = 0.77; P = 0.001; deoxypyridinoline, r = 0.66; P = 0.01). A rise in N-telopeptide over the year was correlated with an increase in all bone mineral measures, including lumbar bone mineral content (r = 0.58; P = 0.03) and BMD (r = 0.53; P = 0.05) and total bone mineral content (r = 0.69; P = 0.006) and BMD (r = 0.69; P = 0.006) in the AN group. Therefore, despite recovery over 1 yr, poor bone mineral accrual persists in adolescent girls with AN in contrast to rapid bone accrual in healthy girls. Normalization of bone turnover markers occurs in association with nutritional recovery and an increase in the nutritionally dependent bone trophic factor IGF-I. A rise in bone turnover markers may be an early indicator of increase in BMD in recovering girls with AN.

Adipose Tissue↗
PubMed1997

Research update on serotonin function in bulimia nervosa and anorexia nervosa.

The extent to which dysregulation of serotonin function in the central nervous system may contribute to core symptoms in patients with bulimia nervosa and anorexia nervosa is currently an area of intensive psychobiological investigation. Preclinical and clinical studies have demonstrated the involvement of the neurotransmitter serotonin in the regulation of food intake, suggesting that impaired serotonin-mediated satiety signals could contribute to patterns of recurrent binge eating. Other symptom patterns in patients with eating disorders, including mood dysregulation, impulsivity, and obsessionality, as well as therapeutic response to serotonergic agents, suggest involvement of serotonergic pathways. With a primary focus on serotonin function, this article reviews clinical studies of neuroendocrine and behavioral response to pharmacological challenges, levels of neurotransmitter metabolite in cerebrospinal fluid, and platelet studies. Controlled clinical trials involving pharmacological treatment with serotonergic medications are summarized. Considerations for future research are discussed.

Anorexia Nervosa↗
PubMed1990

Gastric emptying in patients with bulimia nervosa and anorexia nervosa.

A dual radioisotope technique was used to measure gastric emptying of a mixed liquid and solid meal in 11 patients with bulimia nervosa, and was compared with 10 patients with anorexia nervosa and a sex-matched control population. The relationship of body weight and gastrointestinal symptoms to gastric emptying was also examined. Gastric emptying of solids in patients with bulimia nervosa was similar to that in controls (gastric T1/2 131 +/- 15 min vs 119 +/- 7 min; mean +/- SEM). In contrast, patients with anorexia nervosa had overall delayed emptying (182 +/- 31 min; p less than 0.05); six patients had normal emptying of the solid components of the meal and four had markedly delayed emptying. Gastric emptying of liquids was similar in the bulimics and controls (gastric T1/2 48 +/- 5 min and 49 +/- 4 min, respectively), whereas the anorexics tended to have prolonged gastric emptying (65 +/- 11 min, p = NS). There was no correlation between body weight, gastrointestinal symptoms, and gastric emptying in either group. These findings suggest that gastrointestinal symptoms are unreliable indicators of gastric emptying in patients with eating disorders, and that gastric emptying studies should be performed in such patients before treatment with prokinetic agents is considered.

Adolescent↗
PubMed2001

Medication response in the treatment of patients with anorexia nervosa.

Anorexia nervosa (AN) is a serious mental disorder, characterized by severely low weight and cognitive distortions about body shape and weight. AN is generally associated with a constellation of psychological symptoms, including depression, anxiety, obsessionality, and ritualistic behaviors. The presence of these associated symptoms, together with the great challenge of treating patients with AN, has led clinicians to try many psychopharmacologic agents in the treatment of these patients, usually to no avail. Investigators have studied a range of agents, but have found little, if any, utility in treating underweight patients with medication. In this article, the authors review the literature regarding medication treatment for patients with AN, propose a theoretical basis for the poor response of these patients to the agents that have been tried, and conclude with recommendations for treatment strategies and additional research that should be pursued to further our understanding of this difficult illness.

Journal Article↗
PubMed2003

[Osteoporosis in anorexia nervosa].

Anorexia nervosa (AN) has recently become one of common disorders in adolescent girls. A chronic course of AN is related to morbidity, with one of the most serious medical complications being severe osteopenia. The prevalence of osteoporosis is estimated to be 40 % in AN during the follow up. The incidence of bone fracture in AN after the recovery of body weight is reported to be two to seven higher than that in healthy age-matched controls. Because adolescence is a critical time in terms of acquisition of peak bone mass, osteopenia during this time may be permanent. Adult woman with adolescence-onset AN has lower bone mineral density than that with adult-onset AN. In addition, bone mineral density (BMD) of AN has been shown to be influenced by several factors, including reduced body weight due to malnutrition, intake of calcium and vitamin D, and duration of estrogen deficiency. Among them, body weight is known to be the most important prognostic factor, both in a short and long period of years. Thus, medical doctor should monitor BMD in patients with AN throughout their life.

English Abstract↗
PubMed2005

The Maudsley family-based treatment for adolescent anorexia nervosa.

Anorexia nervosa (AN) usually onsets in mid-adolescence and presents with serious psychiatric and medical morbidities. Yet, few psychological treatments for this debilitating disorder have been studied. One intervention which involves the parents of the adolescent has proved to be promising, especially in patients with a short duration of illness, i.e., less than three years. The benefits of this family-based treatment have also been shown to be enduring at five-year follow-up. All available studies of psychological treatments for adolescent AN, both controlled trials and case series, are reviewed here. Almost all of them involve parents in treatment. These studies show that the majority of patients, even those who are severely ill, can be treated quite successfully as outpatients provided that the parents participate in treatment. In this family-based treatment, parents are viewed as a resource rather than a hindrance. Optimism regarding these encouraging findings should be tempered until larger scale randomized trials have been conducted.

Journal Article↗