Reprinted from Eating Disorders Review
May/June Volume 27, Number 3
©2016 iaedp
Q. I have a new adolescent patient who has many of the characteristics of anorexia nervosa (AN) but also some symptoms that seem unusual, including a craving for salt. Also, although her body mass index is 12.7 kg/m2, she is not amenorrheic. Do you have any suggestions? (DP, Detroit)
A. Your patient’s profile is very similar to that of a case just reported in the British Medical Journal Case Reports (BMJ Case Rep. 2016. doi:10.1136/bcr-2015-214058). Dr. Katie Nicholls and pediatricians at the Maidstone and Tunbridge Wells NHS Trust, Kent, Aylesford, UK, have shared the case of a 15-year-old girl whose history suggested an eating disorder and whose body mass index (BMI) below the 0.4th percentile seemed to back this up.
The girl was referred to the pediatric outpatient clinic by her general practitioner, who reported that she had a 6-month history of fatigue and slow recovery from a series of viral illnesses. The girl had intermittent vomiting episodes and very low weight and poor appetite. She had been seen by her GP at least four times for extreme fatigue, vomiting, and shortness of breath.
When Dr. Nicholls and her colleagues met with the patient and her family, her parents offered one singular clue—their daughter’s extreme craving for salt. They described how she had eaten jars of olives and pints of salty gravy over the preceding months; this was a new and unusual pattern of eating for the girl. Also, unlike most AN patients, the girl had an accurate perception of her body image, and did not purposely limit her food intake.
Physical examination revealed other clues to the true diagnosis. For example, the girl appeared very tanned compared to her older sister and mother, with hyperpigmentation in her skin creases and in the skin overlying her spine and breast nipples. Electrolyte studies showed hyponatremia (129 mEq/L) but normal potassium and glucose levels. Results of a short ACTH tetracosactide (Synacthen®) test were grossly abnormal and a diagnosis of Addison’s disease was made.
Steroid treatment was begun with hydrocortisone, 10 mg in the morning and at lunch and 5 mg in the evening, for a total daily dosage of 20 mg/m2. Fludrococortisone, 100 mcg once a day, was started after 24 hours of hydrocortisone. A follow-up 2 months later showed the girl had responded well to the steroid therapy and her fludrocortisone dosage was increased to 150 mcg/day. Her weight and BMI increased, and the hyperpigmentation had greatly improved.
The authors also reported a second case, this time involving a 20-year-old man who presented with anorexia, vomiting, and significant weight loss. The first diagnosis was AN but this was changed a month later when the man developed severe dehydration and hyponatremia—and once more a diagnosis of Addison’s disease was made (Postgrad Med J. 1988; 64:953). After a course of steroids, the patient began to eat normally and regained weight.
These cases point out that one aspect of the medical evaluation for AN can be ruling out medical mimics of AN. In addition to Addison’s, these can include celiac disease, Crohn’s disease, and eosinophilic esophagitis.
— SC