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Anorexia Nervosa


A 30-year-old woman was brought to the hospital with syncope, bradycardia, and hypotension. For the past 6 years, she had vomited after eating meals and after occasional episodes of binge eating.

A 30-year-old woman was brought to the hospital with syncope, bradycardia, and hypotension. For the past 6 years, she had vomited after eating meals and after occasional episodes of binge eating.

Despite profound weight loss, the patient denied hunger, thinness, and fatigue. She was emaciated and amenorrheic; body fat was undetectable, and the bones protruded through the skin. Drs Demetrios Papaioannides, S. N. Nikas, and E. Athanassiou of Arta, Greece, and Dr N. Akritides of Ioannina, Greece, diagnosed anorexia nervosa; they admitted the patient for nutritional support and further studies.

This chronic disorder is characterized behaviorally by self-induced weight loss; psychologically by distorted body image and other perceptual disturbances; and biologically by physiologic alterations-such as amenorrhea-that result from nutritional depletion. Ninety-five percent of patients with anorexia nervosa are young, affluent white women.1 Estimates of prevalence range from 0.4 to 1.5 per 100,000 population. Rates as high as 1 per 100 adolescent girls from middle- or upper-class white families have been reported.2

The cause of anorexia nervosa is unknown. A psychiatric origin is likely, but its nature is unclear. One view holds that this disorder begins in response to inadequate or destructive interpersonal relationships in goal-oriented and high-achieving families.

A triad of clinical disturbances provides the essential criteria for diagnosing anorexia nervosa in its typical form:

  • The patient's weight is markedly below normal. Considerable weight loss results mainly from self-deprivation of foods the patient considers “fattening” (ie, rich in carbohydrates). Weight loss may be accentuated by additional behaviors, such as self-induced vomiting or purging or excessive exercise.
  • A specific psychopathology is present: the patient clings tenaciously to the idea that “fatness” is to be avoided at all costs. Her definition of fatness is uncommonly harsh, and she sets a weight threshold that she will not exceed.
  • Hypothalamic dysfunction is manifested by partial diabetes insipidus, abnormal thermoregulation, and hypogonadotropic hypogonadism with secondary amenorrhea. Male patients experience a loss of sexual interest and potency. Menses usually return with weight gain.

Other endocrine changes include low levels of thyroxine and triiodothyronine and increased cortisol secretion. Osteoporosis may lead to vertebral compression fractures and stress fractures. Parotid gland enlargement and edema may be accompanied by anemia, leukopenia, hypokalemia, and hypoalbuminemia. Be sure to rule out organic disease that can cause weight loss (eg, malignancy, malabsorption, or hyperthyroidism) and primary psychiatric illness that might account for the failure to eat.

Physical examination reveals severe or gross wasting that involves mainly subcutaneous fat and results in hollow cheeks, stick-like limbs, shrunken breasts, a flat belly, and wasted thighs and buttocks. Bone points stand out sharply. The hands and feet are blue and cold, especially during cool weather. The skin is dry with an excess of downy hair (lanugo) over the nape of the neck, cheeks, forearms, and legs. The heart rate is slow (50 to 60 beats per minute); the blood pressure is low (eg, 90/60 mm Hg).

In a severely malnourished patient, virtually every major organ system may malfunction, but cardiac and fluid and electrolyte disorders are the most dangerous. Cardiac muscle mass, chamber size, and output decrease. Sudden death-most likely caused by ventricular tachyarrhythmias-may occur. Electrolyte disturbances heighten the risk of tachyarrhythmia in those patients who have prolonged QT intervals. Hypokalemic hypochloremic alkalosis is the most frequently occurring electrolyte abnormality. Renal abnormalities largely reflect dehydration and reduced glomerular filtration rate.

Patients may suffer from GI motility problems. Abdominal pain, bloating, postprandial distress, and constipation are very common. Depression often accompanies anorexia nervosa.

There is no specific therapy. Supportive treatment involves a combination of psychotherapy and family counseling. If severe malnutrition, hypotension, prerenal azotemia, or hypokalemia is present, hospitalize the patient for nutritional support. Antidepressants, such as fluoxetine, have been somewhat effective. Other selective serotonin reuptake inhibitors as well as chlorpromazine, amitriptyline, and lithium carbonate may be used.2 Treatment is long-term, often unsuccessful, and requires perseverance by patient, family, and physician.

REFERENCES:1. Drossman DA. The eating disorders. In: Bennett JC, Plum F, eds. Cecil Textbook of Medicine. 20th ed. Philadelphia: WB Saunders Co; 1996:1158-1160.
2. Foster DW. Anorexia nervosa and bulimia. In: Isselbacher KJ, Braunwald E, Wilson JD, et al, eds. Harrison's Principles of Internal Medicine. 13th ed. New York: McGraw-Hill; 1994:452-455.

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