Anorexia Nervosaの急性期管理は，救急・集中治療で対応するとよいのでしょう。
NICEガイドラインなども参照すると良いと思います。
より学術的に対応する必要があります。
文献1 Anorexia Nervosa
Nature. 2011 Aug 31.
Mirror extreme BMI phenotypes associated with gene dosage at the chromosome 16p11.2 locus.
Jacquemont S, Reymond A, Zufferey F, Harewood L, Walters RG, Kutalik Z, Martinet D, Shen Y, Valsesia A, Beckmann ND, Thorleifsson G, Belfiore M, Bouquillon S, Campion D, de Leeuw N, de Vries BB, Esko T, Fernandez BA, Fernández-Aranda F, Fernández-Real JM, Gratacòs M, Guilmatre A, Hoyer J, Jarvelin MR, Frank Kooy R, Kurg A, Le Caignec C, Männik K, Platt OS, Sanlaville D, Van Haelst MM, Villatoro Gomez S, Walha F, Wu BL, Yu Y, Aboura A, Addor MC, Alembik Y, Antonarakis SE, Arveiler B, Barth M, Bednarek N, Béna F, Bergmann S, Beri M, Bernardini L, Blaumeiser B, Bonneau D, Bottani A, Boute O, Brunner HG, Cailley D, Callier P, Chiesa J, Chrast J, Coin L, Coutton C, Cuisset JM, Cuvellier JC, David A, de Freminville B, Delobel B, Delrue MA, Demeer B, Descamps D, Didelot G, Dieterich K, Disciglio V, Doco-Fenzy M, Drunat S, Duban-Bedu B, Dubourg C, El-Sayed Moustafa JS, Elliott P, Faas BH, Faivre L, Faudet A, Fellmann F, Ferrarini A, Fisher R, Flori E, Forer L, Gaillard D, Gerard M, Gieger C, Gimelli S, Gimelli G, Grabe HJ, Guichet A, Guillin O, Hartikainen AL, Heron D, Hippolyte L, Holder M, Homuth G, Isidor B, Jaillard S, Jaros Z, Jiménez-Murcia S, Joly Helas G, Jonveaux P, Kaksonen S, Keren B, Kloss-Brandstätter A, Knoers NV, Koolen DA, Kroisel PM, Kronenberg F, Labalme A, Landais E, Lapi E, Layet V, Legallic S, Leheup B, Leube B, Lewis S, Lucas J, Macdermot KD, Magnusson P, Marshall C, Mathieu-Dramard M, McCarthy MI, Meitinger T, Antonietta Mencarelli M, Merla G, Moerman A, Mooser V, Morice-Picard F, Mucciolo M, Nauck M, Coumba Ndiaye N, Nordgren A, Pasquier L, Petit F, Pfundt R, Plessis G, Rajcan-Separovic E, Paolo Ramelli G, Rauch A, Ravazzolo R, Reis A, Renieri A, Richart C, Ried JS, Rieubland C, Roberts W, Roetzer KM, Rooryck C, Rossi M, Saemundsen E, Satre V, Schurmann C, Sigurdsson E, Stavropoulos DJ, Stefansson H, Tengström C, Thorsteinsdóttir U, Tinahones FJ, Touraine R, Vallée L, van Binsbergen E, Van der Aa N, Vincent-Delorme C, Visvikis-Siest S, Vollenweider P, Völzke H, Vulto-van Silfhout AT, Waeber G, Wallgren-Pettersson C, Witwicki RM, Zwolinksi S, Andrieux J, Estivill X, Gusella JF, Gustafsson O, Metspalu A, Scherer SW, Stefansson K, Blakemore AI, Beckmann JS, Froguel P.
Abstract
Both obesity and being underweight have been associated with increased mortality. Underweight, defined as a body mass index (BMI) ≤ 18.5 kg per m(2) in adults and ≤ -2 standard deviations from the mean in children, is the main sign of a series of heterogeneous clinical conditions including failure to thrive, feeding and eating disorder and/or anorexia nervosa. In contrast to obesity, few genetic variants underlying these clinical conditions have been reported. We previously showed that hemizygosity of a ∼600-kilobase (kb) region on the short arm of chromosome 16 causes a highly penetrant form of obesity that is often associated with hyperphagia and intellectual disabilities. Here we show that the corresponding reciprocal duplication is associated with being underweight. We identified 138 duplication carriers (including 132 novel cases and 108 unrelated carriers) from individuals clinically referred for developmental or intellectual disabilities (DD/ID) or psychiatric disorders, or recruited from population-based cohorts. These carriers show significantly reduced postnatal weight and BMI. Half of the boys younger than five years are underweight with a probable diagnosis of failure to thrive, whereas adult duplication carriers have an 8.3-fold increased risk of being clinically underweight. We observe a trend towards increased severity in males, as well as a depletion of male carriers among non-medically ascertained cases. These features are associated with an unusually high frequency of selective and restrictive eating behaviours and a significant reduction in head circumference. Each of the observed phenotypes is the converse of one reported in carriers of deletions at this locus. The phenotypes correlate with changes in transcript levels for genes mapping within the duplication but not in flanking regions. The reciprocal impact of these 16p11.2 copy-number variants indicates that severe obesity and being underweight could have mirror aetiologies, possibly through contrasting effects on energy balance.
文献2 Anorexia Nervosa
Eur Psychiatry. 2011 Aug 29.
Repetitive transcranial magnetic stimulation in anorexia nervosa: A pilot study.
Van den Eynde F, Guillaume S, Broadbent H, Campbell IC, Schmidt U.
Source
King's College London, Institute of Psychiatry, Section of Eating Disorders, De Crespigny Park, London, SE5 8AF, United Kingdom.
Abstract
The search for new treatments to improve outcome in people with anorexia nervosa continues. This pilot study investigated whether one session of high frequency repetitive transcranial magnetic stimulation (rTMS) delivered to the left dorsolateral prefrontal cortex reduces eating disorder related symptoms following exposure to visual and real food stimuli. Safety and tolerability were also assessed. Ten right-handed people with anorexia nervosa underwent one session of rTMS. Subjective experiences related to the eating disorder (e.g. urge to restrict, feeling full etc.) were assessed before and after rTMS. Non-parametric repeated measures tests were used. rTMS was safe and well-tolerated, and resulted in reduced levels of feeling full, feeling fat and feeling anxious. Thus, rTMS may reduce core symptoms of anorexia nervosa. Future research should establish the therapeutic potential of rTMS in anorexia nervosa. PMID: 21880470
文献3 Anorexia Nervosa
J Am Acad Child Adolesc Psychiatry. 2011 Sep;50(9):915-24.
A double-blind, placebo-controlled study of risperidone for the treatment of adolescents and young adults with anorexia nervosa: a pilot study.
Hagman J, Gralla J, Sigel E, Ellert S, Dodge M, Gardner R, O'Lonergan T, Frank G, Wamboldt MZ.
Source
University of Colorado School of Medicine and Children's Hospital Colorado.
Abstract
OBJECTIVE:
The purpose of this double-blind, placebo-controlled exploratory pilot study was to evaluate the safety and efficacy of risperidone for the treatment of anorexia nervosa.
METHOD:
Forty female subjects 12 to 21 years of age (mean, 16 years) with primary anorexia nervosa in an eating disorders program were randomized to receive risperidone (n = 18) or placebo (n = 22). Subjects completed the Eating Disorder Inventory 2, Color-A-Person Test, Body Image Software, and Multidimensional Anxiety Scale for Children at baseline and regular intervals. Weight, laboratory values, and electrocardiograms were monitored. Study medication was started at 0.5 mg daily and titrated upward weekly in 0.5-mg increments to a maximum dose of 4 mg until the subject reached a study endpoint.
RESULTS:
The mean dose for the risperidone group was 2.5 mg and for the placebo group was 3 mg for a mean duration of 9 weeks. Subjects taking risperidone had a significant decrease on the Eating Disorder Inventory 2 Drive for Thinness subscale over the first 7 weeks (effect size, 0.88; p = .002), but this difference was not sustained to the end of the study (p = .13). The Eating Disorder Inventory 2 Interpersonal Distrust subscale decreased significantly more in subjects taking risperidone (effect size, 0.60; p = .03). Subjects taking risperidone had increased prolactin levels (week 7; p = .001). There were no significant differences between groups at baseline or the end of the study for the other rating scales, change in weight, or laboratory measurements.
CONCLUSIONS:
This study does not demonstrate a benefit for the addition of risperidone in adolescents with anorexia nervosa during the weight-restoration phase of care. Clinical trial registration information-A Double-Blind, Placebo-Controlled Study of Risperidone for the Treatment of Anorexia Nervosa, http://www.clinicaltrials.gov, NCT00140426.
文献4 Anorexia Nervosa
Nutrition. 2011 Aug 24.
Ghrelin and anorexia nervosa: A psychosomatic perspective.
Ogiso K, Asakawa A, Amitani H, Inui A.
Source
Department of Psychosomatic Internal Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Sakuragaoka, Kagoshima, Japan.
Abstract
Anorexia nervosa (AN) is a serious medical illness associated with gastrointestinal, metabolic, and psychological complications, and there are no effective pharmacologic treatments for the condition. Recent studies have suggested that the regulatory peptides, including ghrelin, are involved in the pathologic feeding behavior of AN. Previous studies have indicated that plasma total ghrelin and acyl ghrelin levels in patients with AN are higher than in controls, and the ratio of des-acyl ghrelin to acyl ghrelin in AN tend to be higher than in controls. In addition, ghrelin has been reported to stimulate appetite and food intake in various diseases, including chronic heart failure, chronic obstructive pulmonary disease, and cancer. Because it is speculated that difficulties in resolving the underlying psychological condition preclude reversal of the pathologic feeding behavior in AN, ghrelin is expected to be applied in a clinical setting as a new treatment. In this review, we describe the role of ghrelin in the pathophysiology and potential treatment of AN along the gut-brain axis.
文献5 Anorexia Nervosa
Pharmacol Rev. 2009 Dec;61(4):430-81.
Ghrelin gene products and the regulation of food intake and gut motility.
Chen CY, Asakawa A, Fujimiya M, Lee SD, Inui A.
Source
Faculty of Medicine, National Yang-Ming University School of Medicine, Taipei, Japan.
Abstract
A breakthrough using "reverse pharmacology" identified and characterized acyl ghrelin from the stomach as the endogenous cognate ligand for the growth hormone (GH) secretagogue receptor (GHS-R) 1a. The unique post-translational modification of O-n-octanoylation at serine 3 is the first in peptide discovery history and is essential for GH-releasing ability. Des-acyl ghrelin, lacking O-n-octanoylation at serine 3, is also produced in the stomach and remains the major molecular form secreted into the circulation. The third ghrelin gene product, obestatin, a novel 23-amino acid peptide identified from rat stomach, was found by comparative genomic analysis. Three ghrelin gene products actively participate in modulating appetite, adipogenesis, gut motility, glucose metabolism, cell proliferation, immune, sleep, memory, anxiety, cognition, and stress. Knockdown or knockout of acyl ghrelin and/or GHS-R1a, and overexpression of des-acyl ghrelin show benefits in the therapy of obesity and metabolic syndrome. By contrast, agonism of acyl ghrelin and/or GHS-R1a could combat human anorexia-cachexia, including anorexia nervosa, chronic heart failure, chronic obstructive pulmonary disease, liver cirrhosis, chronic kidney disease, burn, and postsurgery recovery, as well as restore gut dysmotility, such as diabetic or neurogenic gastroparesis, and postoperative ileus. The ghrelin acyl-modifying enzyme, ghrelin O-Acyltransferase (GOAT), which attaches octanoate to serine-3 of ghrelin, has been identified and characterized also from the stomach. To date, ghrelin is the only protein to be octanylated, and inhibition of GOAT may have effects only on the stomach and is unlikely to affect the synthesis of other proteins. GOAT may provide a critical molecular target in developing novel therapeutics for obesity and type 2 diabetes.
文献6 Anorexia Nervosa
Eur Eat Disord Rev. 2011 Jul 21.
Association of Candidate Genes with Phenotypic Traits Relevant to Anorexia Nervosa.
Root TL, Szatkiewicz JP, Jonassaint CR, Thornton LM, Pinheiro AP, Strober M, Bloss C, Berrettini W, Schork NJ, Kaye WH, Bergen AW, Magistretti P, Brandt H, Crawford S, Crow S, Fichter MM, Goldman D, Halmi KA, Johnson C, Kaplan AS, Keel PK, Klump KL, La Via M, Mitchell JE, Rotondo A, Treasure J, Woodside DB, Bulik CM.
Source
Johns Hopkins University School of Medicine, Division of General Internal Medicine, Baltimore MD.
Abstract
This analysis is a follow-up to an earlier investigation of 182 genes selected as likely candidate genetic variations conferring susceptibility to anorexia nervosa (AN). As those initial case-control results revealed no statistically significant differences in single nucleotide polymorphisms, herein, we investigate alternative phenotypes associated with AN. In 1762 females, using regression analyses, we examined the following: (i) lowest illness-related attained body mass index; (ii) age at menarche; (iii) drive for thinness; (iv) body dissatisfaction; (v) trait anxiety; (vi) concern over mistakes; and (vii) the anticipatory worry and pessimism versus uninhibited optimism subscale of the harm avoidance scale. After controlling for multiple comparisons, no statistically significant results emerged. Although results must be viewed in the context of limitations of statistical power, the approach illustrates a means of potentially identifying genetic variants conferring susceptibility to AN because less complex phenotypes associated with AN are more proximal to the genotype and may be influenced by fewer genes. Copyright © 2011 John Wiley & Sons, Ltd and Eating Disorders Association.
文献7 Anorexia Nervosa
Pharmacogenomics. 2008 Oct;9(10):1487-520.
Genetic susceptibility to eating disorders: associated polymorphisms and pharmacogenetic suggestions.
Monteleone P, Maj M.
Source
Department of Psychiatry, University of Naples SUN, Largo Madonna delle Grazie, 80138 Naples, Italy. monteri@tin.it
Abstract
Anorexia nervosa (AN), bulimia nervosa (BN) and binge-eating disorder (BED) are characterized by abnormal eating behaviors often resulting in dramatic physical consequences for the patients. The etiology of eating disorders (EDs) is currently unknown; however, a strong genetic contribution is likely to be involved. To date, the majority of genetic studies have focused on candidate genes, and polymorphic variants of genes coding for substances likely to be involved in the etiopathogenesis of EDs have been assessed for association with AN, BN, BED and/or ED-related phenotypic traits. Results have been generally inconsistent and cannot be considered conclusive because of several methodological flaws and differences, such as small sample sizes, ethnic heterogeneity of studied populations, lack of statistical correction for multiple testing, adoption of different diagnostic criteria and population stratification. Although, at present, no convincing evidence for associations of candidate genes with EDs has been provided, the 5-HT(2A) receptor gene and the BDNF gene seem to be promising candidates for genetic influences on AN, since polymorphic variants of these genes have been found quite consistently, although not specifically, linked to AN restricting subtype in large sample studies. Moreover, pharmacogenetic investigations have suggested a possible role of some gene polymorphisms in predicting the response to treatment with selective serotonin reuptake inhibitors in BN, but results are still preliminary. The heterogeneity of ED phenotypes is believed to represent the most relevant variable responsible for contradictory and not conclusive results. Future studies should focus on more homogeneous subgroups, either relying on specific ED traits or identifying endophenotypes. This will be useful also for prevention and treatment of EDs.
文献8 Anorexia Nervosa
Whitelaw M, Gilbertson H, Lam PY, Sawyer SM. J Adolesc Health 2010;46:577-82.
Does aggressive refeeding in hospitalized adolescents with anorexia nervosa result in increased hypophosphatemia?
Department of Nutrition and Food Services, Royal Children's Hospital, Victoria, Australia. melissa.whitelaw@rch.org.au
Abstract
PURPOSE:
Concerns about refeeding syndrome have led to relatively conservative nutritional rehabilitation in malnourished inpatients with anorexia nervosa (AN), which delays weight gain. Compared to other programs, we aggressively refed hospitalized adolescents. We sought to determine the incidence of hypophosphatemia (HP) in 12-18-year-old inpatients in order to inform nutritional guidelines in this group.
METHODS:
A 1-year retrospective chart review was undertaken of 46 admissions (29 adolescents) with AN admitted to the adolescent ward of a tertiary children's hospital. Data collected over the initial 2 weeks included number of past admissions, nutritional intake, weight, height, body mass index, and weight change at 2 weeks. Serum phosphorus levels and oral phosphate supplementation was recorded.
RESULTS:
The mean (SD) age was 15.7 years (1.4). The mean (SD) ideal body weight was 72.9% (9.1). Sixty-one percent of admissions were commenced on 1,900 kcal (8,000 kJ), and 28% on 2,200 kcal (9,300 kJ). Four patients were deemed at high risk of refeeding syndrome; of these patients, three were commenced on rehydration therapy and one on 1,400 kcal (6,000 kJ). All patients were graded up to 2,700 kcal (11,400 kJ) with further increments of 300 kcal (1,260 kJ) as required. Thirty-seven percent developed mild HP; no patient developed moderate or severe HP. Percent ideal body weight at admission was significantly associated with the subsequent development of HP (p = .007).
CONCLUSIONS:
These data support more aggressive approaches to nutritional rehabilitation for hospitalized adolescents with AN compared to current recommendations and practice.
文献9 Anorexia Nervosa
Lakartidningen. 2005 Sep 5-11;102(36):2464-7.
[Somatic complications of anorexia nervosa in children and adolescents. Prognosis is good if the patient achieves normal weight within a couple of years].
[Article in Swedish]
Ejderhamn J, Borgström B, Wentz E.
Source
Anorexicentrum, AB Mando, Huddinge, Sweden. jan.ejderhamn@neurotec.ki.se
Abstract
This article presents an overview of somatic complications in anorexia nervosa in children and adolescents. Cardiovascular-, gastrointestinal-, and endocrine- complications are often observed as a consequence of starvation in anorexia nervosa, Prolongation of QT interval can cause fatal arrhythmias. Checking levels of serum electrolytes, phosphate and magnesium daily during initial phase of refeeding is necessary to avoid the Refeeding syndrome. The activity of the thyroid gland and the gonads is depressed. The patients will remain or return to a prepubertal status with poor growth and low levels of sex hormones. This, in addition to low IGF-I, low adrenal androgens and lack of energy, may result in subnormal development of bone density. If anorexia nervosa starts early in life and continues for many years there will not be a full recovery, resulting in osteoporosis and a decrease of final height. The other complications however have a good prognosis when food intake is normalised.
文献10 Anorexia Nervosa
Arch Gen Psychiatry. 2011 Jul;68(7):724-31.
Mortality rates in patients with anorexia nervosa and other eating disorders: a meta-analysis of 36 studies.
Arcelus J, Mitchell AJ, Wales J, Nielsen S.
Source
Loughborough University Centre for Research into Eating Disorders, Loughborough University England. J.Arcelus@lboro.ac.uk
Abstract
CONTEXT:
Morbidity and mortality rates in patients with eating disorders are thought to be high, but exact rates remain to be clarified.
OBJECTIVE:
To systematically compile and analyze the mortality rates in individuals with anorexia nervosa (AN), bulimia nervosa (BN), and eating disorder not otherwise specified (EDNOS).
DATA SOURCES:
A systematic literature search, appraisal, and meta-analysis were conducted of the MEDLINE/PubMed, PsycINFO, and Embase databases and 4 full-text collections (ie, ScienceDirect, Ingenta Select, Ovid, and Wiley-Blackwell Interscience).
STUDY SELECTION:
English-language, peer-reviewed articles published between January 1, 1966, and September 30, 2010, that reported mortality rates in patients with eating disorders.
DATA EXTRACTION:
Primary data were extracted as raw numbers or confidence intervals and corrected for years of observation and sample size (ie, person-years of observation). Weighted proportion meta-analysis was used to adjust for study size using the DerSimonian-Laird model to allow for heterogeneity inclusion in the analysis.
DATA SYNTHESIS:
From 143 potentially relevant articles, we found 36 quantitative studies with sufficient data for extraction. The studies reported outcomes of AN during 166 642 person-years, BN during 32 798 person-years, and EDNOS during 22 644 person-years. The weighted mortality rates (ie, deaths per 1000 person-years) were 5.1 for AN, 1.7 for BN, and 3.3 for EDNOS. The standardized mortality ratios were 5.86 for AN, 1.93 for BN, and 1.92 for EDNOS. One in 5 individuals with AN who died had committed suicide.
CONCLUSIONS:
Individuals with eating disorders have significantly elevated mortality rates, with the highest rates occurring in those with AN. The mortality rates for BN and EDNOS are similar. The study found age at assessment to be a significant predictor of mortality for patients with AN. Further research is needed to identify predictors of mortality in patients with BN and EDNOS.
文献11 Anorexia Nervosa
Proc Nutr Soc. 2009 Aug;68(3):281-8.
Feeding size 0: the challenges of anorexia nervosa. Managing anorexia from a dietitian's perspective.
Cockfield A, Philpot U.
Source
The Retreat, York, UK. ACockfield@theretreatyork.org.uk
Abstract
Anorexia nervosa has the highest mortality rate of any psychiatric condition and its management is complex and multi-faceted, requiring a multidisciplinary team approach. Dietitians are an important part of the multidisciplinary team, offering objective nutritional advice with the aim of helping the patient to develop an improved relationship with food. Refeeding patients with a low body weight requires careful management; nonetheless, refeeding the low-weight patient with anorexia presents many additional complications, largely of a psychological nature. Treatment plans need to consider psychological, physical, behavioural and psycho-social factors relating to anorexia nervosa. Currently, there is no consistent approach and a paucity of evidence to support best practice for weight restoration in this group of patients. Tube feeding is utilised at varying BMI in anorexia nervosa, mainly in an inpatient setting. However, its use should be seen as a last resort and limited to a life-saving intervention. Weight restoration is best managed by an experienced dietitian within a specialist eating disorders team, using normal foods. This approach is ideal for nutrition rehabilitation, promoting skills for eating and normal behaviour and providing a longer-term solution by challenging unhelpful coping strategies from the onset. Dietitians have a unique mix of skills and knowledge in numerous areas including nutrition, physiology, psychology, sociology and behaviour change, which can be applied to support patients with thoughts and behaviours around food, weight and appetite. Further research is required into the effectiveness of dietetic interventions in eating disorders in order to establish an evidence base for best practice.
松任谷さんぐらいの元気で行きましょう。
救急・集中治療の皆さんは，病院内をニコニコと元気よく歩きましょう！
NICEガイドラインなども参照すると良いと思います。
より学術的に対応する必要があります。
文献1 Anorexia Nervosa
Nature. 2011 Aug 31.
Mirror extreme BMI phenotypes associated with gene dosage at the chromosome 16p11.2 locus.
Jacquemont S, Reymond A, Zufferey F, Harewood L, Walters RG, Kutalik Z, Martinet D, Shen Y, Valsesia A, Beckmann ND, Thorleifsson G, Belfiore M, Bouquillon S, Campion D, de Leeuw N, de Vries BB, Esko T, Fernandez BA, Fernández-Aranda F, Fernández-Real JM, Gratacòs M, Guilmatre A, Hoyer J, Jarvelin MR, Frank Kooy R, Kurg A, Le Caignec C, Männik K, Platt OS, Sanlaville D, Van Haelst MM, Villatoro Gomez S, Walha F, Wu BL, Yu Y, Aboura A, Addor MC, Alembik Y, Antonarakis SE, Arveiler B, Barth M, Bednarek N, Béna F, Bergmann S, Beri M, Bernardini L, Blaumeiser B, Bonneau D, Bottani A, Boute O, Brunner HG, Cailley D, Callier P, Chiesa J, Chrast J, Coin L, Coutton C, Cuisset JM, Cuvellier JC, David A, de Freminville B, Delobel B, Delrue MA, Demeer B, Descamps D, Didelot G, Dieterich K, Disciglio V, Doco-Fenzy M, Drunat S, Duban-Bedu B, Dubourg C, El-Sayed Moustafa JS, Elliott P, Faas BH, Faivre L, Faudet A, Fellmann F, Ferrarini A, Fisher R, Flori E, Forer L, Gaillard D, Gerard M, Gieger C, Gimelli S, Gimelli G, Grabe HJ, Guichet A, Guillin O, Hartikainen AL, Heron D, Hippolyte L, Holder M, Homuth G, Isidor B, Jaillard S, Jaros Z, Jiménez-Murcia S, Joly Helas G, Jonveaux P, Kaksonen S, Keren B, Kloss-Brandstätter A, Knoers NV, Koolen DA, Kroisel PM, Kronenberg F, Labalme A, Landais E, Lapi E, Layet V, Legallic S, Leheup B, Leube B, Lewis S, Lucas J, Macdermot KD, Magnusson P, Marshall C, Mathieu-Dramard M, McCarthy MI, Meitinger T, Antonietta Mencarelli M, Merla G, Moerman A, Mooser V, Morice-Picard F, Mucciolo M, Nauck M, Coumba Ndiaye N, Nordgren A, Pasquier L, Petit F, Pfundt R, Plessis G, Rajcan-Separovic E, Paolo Ramelli G, Rauch A, Ravazzolo R, Reis A, Renieri A, Richart C, Ried JS, Rieubland C, Roberts W, Roetzer KM, Rooryck C, Rossi M, Saemundsen E, Satre V, Schurmann C, Sigurdsson E, Stavropoulos DJ, Stefansson H, Tengström C, Thorsteinsdóttir U, Tinahones FJ, Touraine R, Vallée L, van Binsbergen E, Van der Aa N, Vincent-Delorme C, Visvikis-Siest S, Vollenweider P, Völzke H, Vulto-van Silfhout AT, Waeber G, Wallgren-Pettersson C, Witwicki RM, Zwolinksi S, Andrieux J, Estivill X, Gusella JF, Gustafsson O, Metspalu A, Scherer SW, Stefansson K, Blakemore AI, Beckmann JS, Froguel P.
Abstract
Both obesity and being underweight have been associated with increased mortality. Underweight, defined as a body mass index (BMI) ≤ 18.5 kg per m(2) in adults and ≤ -2 standard deviations from the mean in children, is the main sign of a series of heterogeneous clinical conditions including failure to thrive, feeding and eating disorder and/or anorexia nervosa. In contrast to obesity, few genetic variants underlying these clinical conditions have been reported. We previously showed that hemizygosity of a ∼600-kilobase (kb) region on the short arm of chromosome 16 causes a highly penetrant form of obesity that is often associated with hyperphagia and intellectual disabilities. Here we show that the corresponding reciprocal duplication is associated with being underweight. We identified 138 duplication carriers (including 132 novel cases and 108 unrelated carriers) from individuals clinically referred for developmental or intellectual disabilities (DD/ID) or psychiatric disorders, or recruited from population-based cohorts. These carriers show significantly reduced postnatal weight and BMI. Half of the boys younger than five years are underweight with a probable diagnosis of failure to thrive, whereas adult duplication carriers have an 8.3-fold increased risk of being clinically underweight. We observe a trend towards increased severity in males, as well as a depletion of male carriers among non-medically ascertained cases. These features are associated with an unusually high frequency of selective and restrictive eating behaviours and a significant reduction in head circumference. Each of the observed phenotypes is the converse of one reported in carriers of deletions at this locus. The phenotypes correlate with changes in transcript levels for genes mapping within the duplication but not in flanking regions. The reciprocal impact of these 16p11.2 copy-number variants indicates that severe obesity and being underweight could have mirror aetiologies, possibly through contrasting effects on energy balance.
文献2 Anorexia Nervosa
Eur Psychiatry. 2011 Aug 29.
Repetitive transcranial magnetic stimulation in anorexia nervosa: A pilot study.
Van den Eynde F, Guillaume S, Broadbent H, Campbell IC, Schmidt U.
Source
King's College London, Institute of Psychiatry, Section of Eating Disorders, De Crespigny Park, London, SE5 8AF, United Kingdom.
Abstract
The search for new treatments to improve outcome in people with anorexia nervosa continues. This pilot study investigated whether one session of high frequency repetitive transcranial magnetic stimulation (rTMS) delivered to the left dorsolateral prefrontal cortex reduces eating disorder related symptoms following exposure to visual and real food stimuli. Safety and tolerability were also assessed. Ten right-handed people with anorexia nervosa underwent one session of rTMS. Subjective experiences related to the eating disorder (e.g. urge to restrict, feeling full etc.) were assessed before and after rTMS. Non-parametric repeated measures tests were used. rTMS was safe and well-tolerated, and resulted in reduced levels of feeling full, feeling fat and feeling anxious. Thus, rTMS may reduce core symptoms of anorexia nervosa. Future research should establish the therapeutic potential of rTMS in anorexia nervosa. PMID: 21880470
文献3 Anorexia Nervosa
J Am Acad Child Adolesc Psychiatry. 2011 Sep;50(9):915-24.
A double-blind, placebo-controlled study of risperidone for the treatment of adolescents and young adults with anorexia nervosa: a pilot study.
Hagman J, Gralla J, Sigel E, Ellert S, Dodge M, Gardner R, O'Lonergan T, Frank G, Wamboldt MZ.
Source
University of Colorado School of Medicine and Children's Hospital Colorado.
Abstract
OBJECTIVE:
The purpose of this double-blind, placebo-controlled exploratory pilot study was to evaluate the safety and efficacy of risperidone for the treatment of anorexia nervosa.
METHOD:
Forty female subjects 12 to 21 years of age (mean, 16 years) with primary anorexia nervosa in an eating disorders program were randomized to receive risperidone (n = 18) or placebo (n = 22). Subjects completed the Eating Disorder Inventory 2, Color-A-Person Test, Body Image Software, and Multidimensional Anxiety Scale for Children at baseline and regular intervals. Weight, laboratory values, and electrocardiograms were monitored. Study medication was started at 0.5 mg daily and titrated upward weekly in 0.5-mg increments to a maximum dose of 4 mg until the subject reached a study endpoint.
RESULTS:
The mean dose for the risperidone group was 2.5 mg and for the placebo group was 3 mg for a mean duration of 9 weeks. Subjects taking risperidone had a significant decrease on the Eating Disorder Inventory 2 Drive for Thinness subscale over the first 7 weeks (effect size, 0.88; p = .002), but this difference was not sustained to the end of the study (p = .13). The Eating Disorder Inventory 2 Interpersonal Distrust subscale decreased significantly more in subjects taking risperidone (effect size, 0.60; p = .03). Subjects taking risperidone had increased prolactin levels (week 7; p = .001). There were no significant differences between groups at baseline or the end of the study for the other rating scales, change in weight, or laboratory measurements.
CONCLUSIONS:
This study does not demonstrate a benefit for the addition of risperidone in adolescents with anorexia nervosa during the weight-restoration phase of care. Clinical trial registration information-A Double-Blind, Placebo-Controlled Study of Risperidone for the Treatment of Anorexia Nervosa, http://www.clinicaltrials.gov, NCT00140426.
文献4 Anorexia Nervosa
Nutrition. 2011 Aug 24.
Ghrelin and anorexia nervosa: A psychosomatic perspective.
Ogiso K, Asakawa A, Amitani H, Inui A.
Source
Department of Psychosomatic Internal Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Sakuragaoka, Kagoshima, Japan.
Abstract
Anorexia nervosa (AN) is a serious medical illness associated with gastrointestinal, metabolic, and psychological complications, and there are no effective pharmacologic treatments for the condition. Recent studies have suggested that the regulatory peptides, including ghrelin, are involved in the pathologic feeding behavior of AN. Previous studies have indicated that plasma total ghrelin and acyl ghrelin levels in patients with AN are higher than in controls, and the ratio of des-acyl ghrelin to acyl ghrelin in AN tend to be higher than in controls. In addition, ghrelin has been reported to stimulate appetite and food intake in various diseases, including chronic heart failure, chronic obstructive pulmonary disease, and cancer. Because it is speculated that difficulties in resolving the underlying psychological condition preclude reversal of the pathologic feeding behavior in AN, ghrelin is expected to be applied in a clinical setting as a new treatment. In this review, we describe the role of ghrelin in the pathophysiology and potential treatment of AN along the gut-brain axis.
文献5 Anorexia Nervosa
Pharmacol Rev. 2009 Dec;61(4):430-81.
Ghrelin gene products and the regulation of food intake and gut motility.
Chen CY, Asakawa A, Fujimiya M, Lee SD, Inui A.
Source
Faculty of Medicine, National Yang-Ming University School of Medicine, Taipei, Japan.
Abstract
A breakthrough using "reverse pharmacology" identified and characterized acyl ghrelin from the stomach as the endogenous cognate ligand for the growth hormone (GH) secretagogue receptor (GHS-R) 1a. The unique post-translational modification of O-n-octanoylation at serine 3 is the first in peptide discovery history and is essential for GH-releasing ability. Des-acyl ghrelin, lacking O-n-octanoylation at serine 3, is also produced in the stomach and remains the major molecular form secreted into the circulation. The third ghrelin gene product, obestatin, a novel 23-amino acid peptide identified from rat stomach, was found by comparative genomic analysis. Three ghrelin gene products actively participate in modulating appetite, adipogenesis, gut motility, glucose metabolism, cell proliferation, immune, sleep, memory, anxiety, cognition, and stress. Knockdown or knockout of acyl ghrelin and/or GHS-R1a, and overexpression of des-acyl ghrelin show benefits in the therapy of obesity and metabolic syndrome. By contrast, agonism of acyl ghrelin and/or GHS-R1a could combat human anorexia-cachexia, including anorexia nervosa, chronic heart failure, chronic obstructive pulmonary disease, liver cirrhosis, chronic kidney disease, burn, and postsurgery recovery, as well as restore gut dysmotility, such as diabetic or neurogenic gastroparesis, and postoperative ileus. The ghrelin acyl-modifying enzyme, ghrelin O-Acyltransferase (GOAT), which attaches octanoate to serine-3 of ghrelin, has been identified and characterized also from the stomach. To date, ghrelin is the only protein to be octanylated, and inhibition of GOAT may have effects only on the stomach and is unlikely to affect the synthesis of other proteins. GOAT may provide a critical molecular target in developing novel therapeutics for obesity and type 2 diabetes.
文献6 Anorexia Nervosa
Eur Eat Disord Rev. 2011 Jul 21.
Association of Candidate Genes with Phenotypic Traits Relevant to Anorexia Nervosa.
Root TL, Szatkiewicz JP, Jonassaint CR, Thornton LM, Pinheiro AP, Strober M, Bloss C, Berrettini W, Schork NJ, Kaye WH, Bergen AW, Magistretti P, Brandt H, Crawford S, Crow S, Fichter MM, Goldman D, Halmi KA, Johnson C, Kaplan AS, Keel PK, Klump KL, La Via M, Mitchell JE, Rotondo A, Treasure J, Woodside DB, Bulik CM.
Source
Johns Hopkins University School of Medicine, Division of General Internal Medicine, Baltimore MD.
Abstract
This analysis is a follow-up to an earlier investigation of 182 genes selected as likely candidate genetic variations conferring susceptibility to anorexia nervosa (AN). As those initial case-control results revealed no statistically significant differences in single nucleotide polymorphisms, herein, we investigate alternative phenotypes associated with AN. In 1762 females, using regression analyses, we examined the following: (i) lowest illness-related attained body mass index; (ii) age at menarche; (iii) drive for thinness; (iv) body dissatisfaction; (v) trait anxiety; (vi) concern over mistakes; and (vii) the anticipatory worry and pessimism versus uninhibited optimism subscale of the harm avoidance scale. After controlling for multiple comparisons, no statistically significant results emerged. Although results must be viewed in the context of limitations of statistical power, the approach illustrates a means of potentially identifying genetic variants conferring susceptibility to AN because less complex phenotypes associated with AN are more proximal to the genotype and may be influenced by fewer genes. Copyright © 2011 John Wiley & Sons, Ltd and Eating Disorders Association.
文献7 Anorexia Nervosa
Pharmacogenomics. 2008 Oct;9(10):1487-520.
Genetic susceptibility to eating disorders: associated polymorphisms and pharmacogenetic suggestions.
Monteleone P, Maj M.
Source
Department of Psychiatry, University of Naples SUN, Largo Madonna delle Grazie, 80138 Naples, Italy. monteri@tin.it
Abstract
Anorexia nervosa (AN), bulimia nervosa (BN) and binge-eating disorder (BED) are characterized by abnormal eating behaviors often resulting in dramatic physical consequences for the patients. The etiology of eating disorders (EDs) is currently unknown; however, a strong genetic contribution is likely to be involved. To date, the majority of genetic studies have focused on candidate genes, and polymorphic variants of genes coding for substances likely to be involved in the etiopathogenesis of EDs have been assessed for association with AN, BN, BED and/or ED-related phenotypic traits. Results have been generally inconsistent and cannot be considered conclusive because of several methodological flaws and differences, such as small sample sizes, ethnic heterogeneity of studied populations, lack of statistical correction for multiple testing, adoption of different diagnostic criteria and population stratification. Although, at present, no convincing evidence for associations of candidate genes with EDs has been provided, the 5-HT(2A) receptor gene and the BDNF gene seem to be promising candidates for genetic influences on AN, since polymorphic variants of these genes have been found quite consistently, although not specifically, linked to AN restricting subtype in large sample studies. Moreover, pharmacogenetic investigations have suggested a possible role of some gene polymorphisms in predicting the response to treatment with selective serotonin reuptake inhibitors in BN, but results are still preliminary. The heterogeneity of ED phenotypes is believed to represent the most relevant variable responsible for contradictory and not conclusive results. Future studies should focus on more homogeneous subgroups, either relying on specific ED traits or identifying endophenotypes. This will be useful also for prevention and treatment of EDs.
文献8 Anorexia Nervosa
Whitelaw M, Gilbertson H, Lam PY, Sawyer SM. J Adolesc Health 2010;46:577-82.
Does aggressive refeeding in hospitalized adolescents with anorexia nervosa result in increased hypophosphatemia?
Department of Nutrition and Food Services, Royal Children's Hospital, Victoria, Australia. melissa.whitelaw@rch.org.au
Abstract
PURPOSE:
Concerns about refeeding syndrome have led to relatively conservative nutritional rehabilitation in malnourished inpatients with anorexia nervosa (AN), which delays weight gain. Compared to other programs, we aggressively refed hospitalized adolescents. We sought to determine the incidence of hypophosphatemia (HP) in 12-18-year-old inpatients in order to inform nutritional guidelines in this group.
METHODS:
A 1-year retrospective chart review was undertaken of 46 admissions (29 adolescents) with AN admitted to the adolescent ward of a tertiary children's hospital. Data collected over the initial 2 weeks included number of past admissions, nutritional intake, weight, height, body mass index, and weight change at 2 weeks. Serum phosphorus levels and oral phosphate supplementation was recorded.
RESULTS:
The mean (SD) age was 15.7 years (1.4). The mean (SD) ideal body weight was 72.9% (9.1). Sixty-one percent of admissions were commenced on 1,900 kcal (8,000 kJ), and 28% on 2,200 kcal (9,300 kJ). Four patients were deemed at high risk of refeeding syndrome; of these patients, three were commenced on rehydration therapy and one on 1,400 kcal (6,000 kJ). All patients were graded up to 2,700 kcal (11,400 kJ) with further increments of 300 kcal (1,260 kJ) as required. Thirty-seven percent developed mild HP; no patient developed moderate or severe HP. Percent ideal body weight at admission was significantly associated with the subsequent development of HP (p = .007).
CONCLUSIONS:
These data support more aggressive approaches to nutritional rehabilitation for hospitalized adolescents with AN compared to current recommendations and practice.
文献9 Anorexia Nervosa
Lakartidningen. 2005 Sep 5-11;102(36):2464-7.
[Somatic complications of anorexia nervosa in children and adolescents. Prognosis is good if the patient achieves normal weight within a couple of years].
[Article in Swedish]
Ejderhamn J, Borgström B, Wentz E.
Source
Anorexicentrum, AB Mando, Huddinge, Sweden. jan.ejderhamn@neurotec.ki.se
Abstract
This article presents an overview of somatic complications in anorexia nervosa in children and adolescents. Cardiovascular-, gastrointestinal-, and endocrine- complications are often observed as a consequence of starvation in anorexia nervosa, Prolongation of QT interval can cause fatal arrhythmias. Checking levels of serum electrolytes, phosphate and magnesium daily during initial phase of refeeding is necessary to avoid the Refeeding syndrome. The activity of the thyroid gland and the gonads is depressed. The patients will remain or return to a prepubertal status with poor growth and low levels of sex hormones. This, in addition to low IGF-I, low adrenal androgens and lack of energy, may result in subnormal development of bone density. If anorexia nervosa starts early in life and continues for many years there will not be a full recovery, resulting in osteoporosis and a decrease of final height. The other complications however have a good prognosis when food intake is normalised.
文献10 Anorexia Nervosa
Arch Gen Psychiatry. 2011 Jul;68(7):724-31.
Mortality rates in patients with anorexia nervosa and other eating disorders: a meta-analysis of 36 studies.
Arcelus J, Mitchell AJ, Wales J, Nielsen S.
Source
Loughborough University Centre for Research into Eating Disorders, Loughborough University England. J.Arcelus@lboro.ac.uk
Abstract
CONTEXT:
Morbidity and mortality rates in patients with eating disorders are thought to be high, but exact rates remain to be clarified.
OBJECTIVE:
To systematically compile and analyze the mortality rates in individuals with anorexia nervosa (AN), bulimia nervosa (BN), and eating disorder not otherwise specified (EDNOS).
DATA SOURCES:
A systematic literature search, appraisal, and meta-analysis were conducted of the MEDLINE/PubMed, PsycINFO, and Embase databases and 4 full-text collections (ie, ScienceDirect, Ingenta Select, Ovid, and Wiley-Blackwell Interscience).
STUDY SELECTION:
English-language, peer-reviewed articles published between January 1, 1966, and September 30, 2010, that reported mortality rates in patients with eating disorders.
DATA EXTRACTION:
Primary data were extracted as raw numbers or confidence intervals and corrected for years of observation and sample size (ie, person-years of observation). Weighted proportion meta-analysis was used to adjust for study size using the DerSimonian-Laird model to allow for heterogeneity inclusion in the analysis.
DATA SYNTHESIS:
From 143 potentially relevant articles, we found 36 quantitative studies with sufficient data for extraction. The studies reported outcomes of AN during 166 642 person-years, BN during 32 798 person-years, and EDNOS during 22 644 person-years. The weighted mortality rates (ie, deaths per 1000 person-years) were 5.1 for AN, 1.7 for BN, and 3.3 for EDNOS. The standardized mortality ratios were 5.86 for AN, 1.93 for BN, and 1.92 for EDNOS. One in 5 individuals with AN who died had committed suicide.
CONCLUSIONS:
Individuals with eating disorders have significantly elevated mortality rates, with the highest rates occurring in those with AN. The mortality rates for BN and EDNOS are similar. The study found age at assessment to be a significant predictor of mortality for patients with AN. Further research is needed to identify predictors of mortality in patients with BN and EDNOS.
文献11 Anorexia Nervosa
Proc Nutr Soc. 2009 Aug;68(3):281-8.
Feeding size 0: the challenges of anorexia nervosa. Managing anorexia from a dietitian's perspective.
Cockfield A, Philpot U.
Source
The Retreat, York, UK. ACockfield@theretreatyork.org.uk
Abstract
Anorexia nervosa has the highest mortality rate of any psychiatric condition and its management is complex and multi-faceted, requiring a multidisciplinary team approach. Dietitians are an important part of the multidisciplinary team, offering objective nutritional advice with the aim of helping the patient to develop an improved relationship with food. Refeeding patients with a low body weight requires careful management; nonetheless, refeeding the low-weight patient with anorexia presents many additional complications, largely of a psychological nature. Treatment plans need to consider psychological, physical, behavioural and psycho-social factors relating to anorexia nervosa. Currently, there is no consistent approach and a paucity of evidence to support best practice for weight restoration in this group of patients. Tube feeding is utilised at varying BMI in anorexia nervosa, mainly in an inpatient setting. However, its use should be seen as a last resort and limited to a life-saving intervention. Weight restoration is best managed by an experienced dietitian within a specialist eating disorders team, using normal foods. This approach is ideal for nutrition rehabilitation, promoting skills for eating and normal behaviour and providing a longer-term solution by challenging unhelpful coping strategies from the onset. Dietitians have a unique mix of skills and knowledge in numerous areas including nutrition, physiology, psychology, sociology and behaviour change, which can be applied to support patients with thoughts and behaviours around food, weight and appetite. Further research is required into the effectiveness of dietetic interventions in eating disorders in order to establish an evidence base for best practice.
松任谷さんぐらいの元気で行きましょう。
救急・集中治療の皆さんは，病院内をニコニコと元気よく歩きましょう！
アクセス
トータル
ランキング
