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Murali K Sekar, Specialist Trainee Year 5 Leicestershire Partnership NHS Trust
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drmurali98{at}yahoo.com Murali K Sekar
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As a psychiatrist working in an eating disorder service, I am always intrigued by the stability of the eating disorder diagnosis over time. As Palmer(1) has quoted in his writing that “when long term prognosis is considered, the overlap between AN and BN becomes more striking”, We all know that patients diagnosed to have anorexia later switch over to other eating disorders and vice versa (2). Hence the article about long term outcome of anorexia nervosa attracted my attention without fail. The methodology of recruiting is vital in a population based study. The authors of this study have taken extreme steps to be as rigorous as possible. But I consider that they might have overlooked some of the aspects. The authors have described how the diagnosis of individual patients has changed over time from anorexia nervosa to bulimia nervosa to no eating disorders to EDNOS (Fig.1 of their article). This highlights the diagnostic instability these groups of illnesses. Authors have assessed individuals cross-sectionally and asserted them to have anorexia nervosa. The important information missing here is whether these individuals had symptoms of other eating disorders like EDNOS before having symptoms of anorexia. Since the study is about long term outcome of anorexia nervosa, they should have taken adequate care to ascertain the cohort they were following was in fact belonging to anorexia nervosa group. This drawback is further highlighted in the exclusion criteria of the study. Excluding patients at the initial stage (Study 1) of individuals with history of eating disturbances could have excluded potential patients who might have been suffering from non anorexic type of eating disorder. The authors asserts that in the subsequent study they did not exclude patients who crossed over to other eating disorders (thereby promptly registering changes prospectively) but what they did by excluding certain people is to exclude these potential participants who could have shown crossing over from other type of eating disorder to anorexia nervosa. There are other minor points that are worth mentioning. Comprehensive screening, that would have included patients of all severity of individuals, who were born in a particular year (1970) identified 24 cases of anorexia nervosa. Combining this with a less comprehensively assessed (thereby potentially picking up only very severe cases) group of individuals could have resulted in heterogeneous population being mixed. Instead of mixing these two cohorts with potential difference in their severity with a possible impact over their outcome including complications (3), the authors could have treated them as two groups. I was also wondering about the validity of making a personality disorder diagnosis in such young individuals. Overall, if anorexic could become bulimic, EDNOS or have no eating disorder diagnosis, the authors failed consider the reverse being true (with the relative exception of bulimia to anorexia), at the important initial stage of this study. References 1. Professor Bob Palmer, Handbook of eating disorders 2nd Ed, Page 2 2. Kamryn. T et al, Diagnostic Crossover in Anorexia Nervosa and Bulimia Nervosa: Implications for DSM-V;, Volume 165(2), February 2008, p 245–250 3. Bulik et al, Suicide Attempts in Anorexia Nervosa. Psychosomatic Medicine. 70(3):378-383, April 2008 |
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Elisabet Wentz, Associate professor M.D., PhD, I. Carina Gillberg, Henrik Anckarsäter, Christopher Gillberg, and Maria Råstam
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elisabet.wentz{at}vgregion.se Elisabet Wentz, et al.
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ADOLESCENT-ONSET ANOREXIA NERVOSA: 18-YEAR OUTCOME. THE COMPLETE STORY. We appreciate that Dr. Sekar has written his thoughts about our paper as a letter to the British Journal of Psychiatry, so that we can further clarify methods and results in our studies on adolescent-onset anorexia nervosa (AN). Dr. Sekar has concerns that the individuals in our study had other eating disorders (EDs) before the onset of AN in adolescence. The aim of the original study, that took place in 1985, was to investigate the prevalence of adolescent-onset AN (and to examine background factors in this sample), not the prevalence of bulimia nervosa (BN) or ED not otherwise specified. The mothers of the individuals, who were diagnosed with AN at the time of the original study, were interviewed thoroughly regarding premorbid eating disturbances (1). Furthermore, the individuals themselves were interviewed regarding the same topic. No individual in the AN group (or the Comparison group) had another ED before the onset of AN. The school nurses at the schools in Göteborg continued to follow all pupils born in 1970 regarding weight and height until leaving school, usually after age 18 years. In the process, individuals with a later adolescent-onset of AN were also found. We believe that we have missed no cases of AN born in 1970 with AN onset before age 18 years. Since the original study focused on adolescent-onset AN we have not continued the screening of individuals born in 1970 after leaving school. Mean age of AN onset in our adolescent-onset sample was 14.3 years. BN typically presents during or after late adolescence and it is rare with BN onset before age 14 years (2, 3). The study has a prospective and not a cross-sectional design, i.e. we have examined all individuals at four occasions, but we have interviewed them both regarding current EDs (and other psychiatric disorders) as well as EDs during the follow-up period (4, 5). Data regarding EDs during the last follow-up period, between AN Study III and AN Study IV can be collected from the first author. Dr. Sekar is also worried about the two subgroups being too diverse; the birth cohort with individuals born in 1970 was pooled together with a group of individuals with adolescent onset AN born in adjacent years (in most cases 1971 to 1973). In the original study the two groups were compared using several hundred background parameters and found to be similar in virtually all key respects (1). The use of personality disorder diagnoses with teenagers is arguable, but we considered (and still consider) it justifiable in cases persistently (over a period of several years) showing the essential characteristics of a personality disorder described in the DSM-III-R (the diagnostic manual used at the time of the original study). This is explicitly suggested by the guidelines of the DSM-III-R. In the original study, apart from the age criterion, all criteria of the DSM-III-R had to be fulfilled for a diagnosis of personality disorder to be made. All cases receiving a diagnosis of personality disorder showed significant impairment in social functioning and/or subjective distress (1). To conclude, since the aim of the original study was to investigate prevalence of adolescent-onset AN, we did not screen for other EDs. Nevertheless, from the time of entering our study all participants (AN group and Comparison group) were examined in great detail regarding ED (past, present, and longitudinally at several follow-up occasions). We believe that we can safely say that there were no individuals who had crossed-over from another ED to AN before the onset of AN in adolescence. 1. Rastam M. Anorexia nervosa in 51 Swedish adolescents: premorbid problems and comorbidity. J Am Acad Child Adolesc Psychiatry. 1992 Sep;31(5):819-29. 2. Bryant-Waugh R, Lask B. Eating disorders in children. J Child Psychol Psychiatry. 1995 Feb;36(2):191-202. 3. Keski-Rahkonen A, Hoek HW, Linna MS, Raevuori A, Sihvola E, Bulik CM, et al. Incidence and outcomes of bulimia nervosa: a nationwide population- based study. Psychol Med. 2008 Sep 8:1-9. 4. Rastam M, Gillberg IC, Gillberg C. Anorexia nervosa 6 years after onset: Part II. Comorbid psychiatric problems. Compr Psychiatry. 1995 Jan- Feb;36(1):70-6. 5. Wentz E, Gillberg C, Gillberg IC, Rastam M. Ten-year follow-up of adolescent-onset anorexia nervosa: psychiatric disorders and overall functioning scales. J Child Psychol Psychiatry. 2001 Jul;42(5):613-22. Elisabet Wentz, Institute of Neuroscience and Physiology, Child and Adolescent Psychiatry, Göteborg University, Göteborg, Sweden, and The Vårdal Institute, The Swedish Institute for Health Sciences, Sweden, I. Carina Gillberg, Institute of Neuroscience and Physiology, Child and Adolescent Psychiatry, Göteborg University, Göteborg, Sweden, Henrik Anckarsäter, Institute of Neuroscience and Physiology, Forensic Psychiatry, Göteborg University, Göteborg, Sweden Christopher Gillberg, Institute of Neuroscience and Physiology, Child and Adolescent Psychiatry, Göteborg University, Göteborg, Sweden, and Department of Child and Adolescent Psychiatry, Strathclyde University, Yorkhill Hospital, Glasgow, UK, Maria Råstam, Institute of Clinical Sciences, Child and Adolescent Psychiatry, Lund University, Lund, Sweden, and Institute of Neuroscience and Physiology, Child and Adolescent Psychiatry, Göteborg University, Göteborg, Sweden Corresponding author: Elisabet Wentz, Institute of Neuroscience and Physiology, Child and Adolescent Psychiatry, Göteborg University, Otterhällegatan 12 B, SE-411 18 Göteborg, Sweden, e-mail: elisabet.wentz@vgregion.se, Phone: #46-31-3425958, Fax : #46-31-848932 Declaration of interest: The authors have no conflicts of interest including financial interests and relationships and affiliations relevant to the subject of this manuscript. |
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