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Burton: The chronic eating disorder

As physicians we witness diseases in both their acute and chronic manifestations, but do we always treat the acute and chronic symptoms with equal vigour?

Eating disorders are examples of mental health conditions requiring both acute and chronic management. I believe we have become accomplished at caring for the acute physiological presentations and chronic psychological presentations of individuals suffering from eating disorders. We are all aware of how to address severely low weight, refeeding syndromes and, more specifically, manifestations of disordered potassium. We move on to arrange cognitive behavioural therapy, refer for psychiatric input and consider the use of appropriate medications to ensure that a patient’s long-term mental health is improved.

As yet, however, little consideration has been given to the long-term physical side-effects of those suffering from eating disorders. There are currently no standardized guidelines for the medical follow-up of such patients, despite the fact that physical abuse and starvation are often of long duration and may span significant developmental periods of a child and/or adolescent’s life.

It was not until the 1970s that eating disorders came to the attention of the public, and eating disorders now have the highest mortality rate of all mental illnesses.1 Over half of teenage girls and almost one-third of teenage boys exhibit unhealthy weight control behaviours such as skipping meals, fasting, vomiting, taking laxatives and smoking cigarettes.2 Therefore, as a relatively new but certainly burdensome disease, the long-term physical consequences are only starting to emerge.

In 2007, a ’27 year old female presented with a one year history of progressively worsening epigastric pain, reflux, and fatigue. She reported a remote history of bulimia nervosa of approximately one year duration at the age of 17 along with smoking 10 cigarettes per day since the age of 20.’3 Upper gastrointestinal endoscopy revealed a 10-mm ulcerated lesion with biopsies confirming a poorly differentiated adenocarcinoma.3 Metastases were later identified.

It can be argued that in this particular case the early onset of oesophageal adenocarcinoma was coincidental with the short history of bulimia. Smoking was a further risk factor but the pathophysiology was not consistent with smoking as the cause. If corrosive agents such as alcohol can result in oropharyngeal and oesophageal cancers, why have we not considered corrosive agents, such as gastric acid, as in Barrett’s oesophagus? Bulimics are known to vomit up to three or four times a day, 7 days a week, over lengthy periods of their life. Anorexia has an average duration of 7 years,4 but it is common for bulimia sufferers to conceal their illness for 8–10 years5 before seeking treatment.

Compounding this, forced vomiting following episodes of bingeing (quantities recorded up to three times the daily recommended calorific intake) has been known to cause hiatus hernias and significant ongoing gastro-oesophageal reflux disease (GORD) in women in their 20s. GORD presenting at such a young age increases the risk of Barrett’s oesophagus and therefore, again, increases the risk of oesophageal carcinoma.

This is just one example of the health risks surrounding sufferers of chronic eating disorders. The consequences of secondary amenorrhoea on fertility, bone health, endometrial cancer risk and general patient well-being should additionally be considered.

Furthermore, glucose intolerance following disordered eating, dental caries following vomiting, cathartic colon following laxative abuse, arrhythmias and thyroid dysfunction following the abuse of thyroxine or other diet pills need to be studied in more detail. The list of physical defects following eating disorders is long and not yet fully recognized within our field.

As primary care practitioners are predominantly the medical providers for chronic eating disorder sufferers, I feel emphasis should be placed on ensuring their confidence and awareness of emerging long-term physical side-effects of such a disease. The pro forma illustrated, see Suggested checklist for suspected eating disorder patients, is a suggested example of how we could try to standardize medical treatment in this situation and avoid patients ‘slipping through the net’, particularly because these patients, by the aetiology of their disease, attempt to be ‘invisible’ within our clinics.

References

1. 

Sullivan PF. Mortality in anorexia nervosa. Am J Psychiatry 1995; 15.2:1073–4.

2. 

Newmark-Sztainer D. I’m like so fat!! New York: The Guilford Press; 2005. p. 5.

3. 

Swisher-McClure S, Husson M, Sun W, Metz JM. Esophageal cancer in a young woman with bulimia nervosa: a case report. J Med Case Rep 2007; 1:160. http://dx.doi.org/10.1186/1752-1947-1-160

4. 

Steiner H, Kwan W, Shaffer TG, et al. Risk and protective factors for juvenile eating disorders. Eur Child Adolesc Psychiatry 2003; 12(Suppl. 1):20–4. http://dx.doi.org/10.1007/s00787-003-1106-8

5. 

Gaskill D, Sanders F. The Encultured Body: policy implications for healthy body image and disordered eating behaviours. Publications and Printing Unite, Queensland University of Technology, Brisbane,Australia; 2000.

Suggested checklist for suspected eating disorder patients





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