The dexamethasone suppression test in anorexia nervosa: the influence of weight, depression, adrenocorticotrophic hormone and dexamethasone

Article Abstract:

Research has demonstrated abnormalities in the hormonal balance of the hypothalamic-pituitary adrenal (HPA) axis in the low-weight phase of anorexia nervosa and has linked HPA-axis hyperactivity and depression. To further investigate relationships between weight change, HPA-axis function, and depression, 20 hospitalized female anorexic patients (average age 21.1 years) were weighed weekly, and given weekly dexamethasone suppression tests (DSTs); dexamethasone is an anti-inflammation steroid. The DST determines the ability of dexamethasone to suppress HPA-axis production of cortisol (an adrenal hormone that plays a role in fat and water metabolism) for 24 hours. Anorexics tend toward high cortisol production rates, and tend not to suppress cortisol production after the DST. Eighteen female volunteers (average age of 27 years), served as study controls, and also had weekly DSTs. At initial DST, all controls were found to be cortisol suppressors, while only half of the anorexic patients were. No relationship was found between severity of weight loss and HPA-axis dysfunction. Weight gain had no effect on normalization of the DST response. Of the 10 anorexic patients who were initially non-suppressors, seven became suppressors before hospital discharge. Seventeen of the 20 anorexic patients scored in the depressed range on a depression rating scale; 10 of the 17 scored in the severely depressed range. However, no relationships were found between depression and suppressor status, or between depression and weight status. There was a significant inverse relationship found between pre- and post-DST plasma cortisol and dexamethasone concentrations. Overall results indicate that more than one mechanism is responsible for an abnormal DST in anorexia and that further exploration is required. (Consumer Summary produced by Reliance Medical Information, Inc.)

Adrenocortical hormones, Dexamethasone

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The effects of loss of taste and smell in a case of anorexia nervosa and bulimia nervosa

Article Abstract:

Acase report is presented of a 43-year-old female executive with a 20-year history of eating disorder, alcohol abuse, and obsessive-compulsive behavior. From age 20 to 25 she was anorectic. After age 25, she maintained anorectic symptoms, characterized by fear of weight gain, poor body image, low weight, and lack of menstrual cycles, and also became bulimic and would indulge in binge eating followed by laxative abuse. When she was 40 she was assaulted on the street, receiving a blow to the head with an iron bar. This caused an occipital bone fracture, which resulted in the loss of smell and she retained the ability to taste only very sweet or very salty stimuli. The woman began to add a great deal of salt, saccharin, and spice to her foods. Obsessive-compulsive rituals involving handwashing and the preparation of food became more time consuming. She was admitted to a general psychiatric ward, but was unable to adhere to a supervised behavioral program aimed at stabilizing her weight and establishing normal eating patterns. After transfer to an eating disorders unit, her eating habits improved, she gained weight, and was discharged. During a three-month follow-up she reported episodes of sleep-walking and occasional food binges, but managed to abstain from laxative and alcohol abuse. The inability to taste or smell food did not protect this patient from binge eating. Alterations in sucrose sensitivity have been demonstrated among anorectics with a low-calorie intake. Since this patient remained both anorectic and bulimic in spite of an almost complete taste loss, it seems unlikely that taste sensitivity plays a major role in eating disorders. (Consumer Summary produced by Reliance Medical Information, Inc.)

Psychological aspects, Case studies, Bulimia, Taste, Taste (Sense), Smell

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Absence of peripheral blood T cell responses to 'shared epitope' containing peptides in recent onset rheumatoid arthritis

Article Abstract:

Specific HLA DRbeta1 antigens that are produced in 90% of patients with rheumatoid arthritis (RA) do not appear to be involved in the development of the disease. Because these antigens are shared by so many patients, they are called shared epitopes. Researchers took blood samples from 20 patients with recent onset RA and 20 healthy volunteers and measured T cell reactivity to these shared epitopes. RA patients did not have significantly greater T cell reactivity to the shared epitopes than the healthy group.

Rheumatoid arthritis, T cells, Antigenic determinants

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