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Levothyroxine Abuse and Bulimia Nervosa
Levothyroxine Abuse and Bulimia Nervosa SCorrCROW, M.D. JAMES MITCHELL, M.D. DAVID KENDALL, M.D.
B
ulimia nervosa is a fairly common disorder primarily affecting adolescent and young adult women. The illness is characterized by recurrent eating binges with compensatory behaviors in an attempt to prevent weight gain. The classic compensatory behavior is self-induced vomiting, but the use of diet pills, diuretics and laxatives, extreme fasting, and compulsive exercise have been described. We report a case of hyperthyroidism induced by self-administration of excessive levothyroxine in a woman with bulimia nervosa.
Case Report A 30-year-old woman was referred to a psychiatrist after reporting to her therapist that she had been selfadministering levothyroxine to induce weight loss. She stated that 10 months prior she had presented to her physician with cold intolerance, easy bruising, dry skin, coarse bair, and hair loss. At that time, she was told that her thyroid function tests were "low" and that the cause was "extreme dieting." She was begun on levothyroxine 100 (J.l.g1day). She began to increase the dose on her own after about I week on the medication in hopes of losing weight. Subsequent thyroid function tests were "high," and the prescribed dose was diminished to 88 Ilglday. However, she continued to increase the dose gradually, and for several months she bad been taking 1,000 Ilg of levothyroxine per day. During this period, she lost 30 Ibs. and developed a coarse tremor of her upper extremities, insomnia, and tachycardia She denied beat intolerance. She said that she had had delayed menstrual periods on 2 occasions in the preceding 5 months. Her dry skin and coarse hair had resolved after starting the levothyroxine. Her heart rate on examination was 116; there was no VOLUME 38. NUMBER 2. MARCH - APRIL 1m
goiter, exophthalmos. or lid lag. She had a fine, rapid tremor of her extremities. Past medical history included migraine headaches. for which she received cafergot and nortriptyline; an esophageal tear secondary to self-induced vomiting; parotid hypertrophy; a tonsillectomy; and prior knee surgery. Her medications were levothyroxine as noted before, plus buspirone (10 mg tid). fluoxetine (80 mg per day). nortriptyline (100 mg per day). and cephalexin for cellulitis in an extremity. Thyroid function studies performed at her initial evaluation revealed thyroxine 23.71lgldL (normal: 5-11). thyroid index 37.91lgldL (normal: 5-11), thyroid hormone binding ratio 1.6 (normal 0.85-1.15). and thyrotropin 0.02 mUlL (normal: 0.5-6.2). She was instructed to discontinue levothyroxine. Repeat thyroid function testing 5 weeks later revealed thyroxine 1.4, triiodothyronine (T3) uptake 21 (normal: 22-35). thyroid index 0.3. and thyrotropin 24.5. While off the thyroid hormone, she again developed easy bruising, dry hair and skin, and mild cold intolerance. She also regained much of the weight she had previously lost. The tachycardia, anxiety symptoms, frequent sweating. and tremor all resolved. Synthroid was resumed at 100 Ilglper day. and I month later she reported using it as prescribed.
Discussion Extensive literature exists reviewing thyroid function and thyroid disease in connection with
Received January 26. 1996; revised March 20. 1996; accepted April 19. 1996. From the Department of Psychiatry and the Department of Medicine, University of Minnesota, Minneapolis. Address reprint requests to Dr. Crow. University of Minnesota. Department of Psychiatry. Box 393 UMHC, Minneapolis. MN 55455. Copyright 0 1997 The Academy of Psychosonwic Medicine.
151
Case Reports
eating disorders. However, relatively little is known about the prevalence of eating disorders in populations with thyroid disease or about the frequency of the abuse ofthyroid medications for weight control purposes. Several investigators have examined thyroid function in bulimic persons. TJlevels have been found to be low l- J or normal4.5 when compared to reference values or control subjects. Basal thyroid-stimulating hormone (TSH) levels were found to be lower than normal subjects.s Additional studies have examined TSH response to a thyrotropin-releasing hormone (TRH) stimulation test. Gwirtsman et al. (1983) reported blunted TSH responses in 80% of their bulimia nervosa subjects, but most reports have found limited or no blunting.~10 A more consistent finding has been a delayed rise in TSH following TRH stimulation, with TSH values ultimately reaching a magnitude similar to control subjects. Frank hyperthyroidism has been reported in the setting of anorexia nervosa ll - 1J and bulimia nervosa.IJ-16 It is of note that in two of these cases (those of Woodside et aI. and Rolla and colleagues) the patients described refused treatment despite clinically obvious thyrotoxicosis for 1 and over 18 years, respectively. A third report, by Fonseca et aI., included a patient who appeared to be purposefully vomiting carbimazole to avoid effective treatment of her hyperthyroidism. Abuse of thyroid supplementation as a compensatory behavior in bulimia nervosa has been reported only rarely. Two separate reports, those of Schmidt and O'Donoghue '7 and Fornari and colleagues 'S detail single cases of subjects with bulimia nervosa who as a manifestation of their illness self-administered extra thyroid medication. The former case involved a patient who self-administered excessive doses of prescribed thyroid hormone, while the person reported by Fornari's group self-administered thyroid hormone that had been prescribed for someone else. It is important to note that hyperthyroidism, like eating disorders, occurs primarily in women and the ages of greatest risk are similar. Tiller and colleagues '9 surveyed the frequency of eating disorders of various types in a clinic for patients for thyroid disease. In a survey of73 patients, 4% IS2
were diagnosed with bulimia nervosa and 4% met criteria for eating disorder not otherwise specified. However, only 69% of the subject group returned their questionnaires, raising the possibility that a number of persons with eating disorders could conceivably have opted not to complete the questionnaire; thus, the true incidence in that group may have been higher. In Tiller's group, 7% of the respondents admitted to misusing thyroxine to control their weight. Excess thyroid hormone supplementation possesses the same significant medical risks as endogenous thyroid hormone overproduction. 20 While hyperthyroidism affects most organ systems, constitutional symptoms are the most common. Specific manifestations of the cardiovascular and neuromuscular symptoms are present in many patients. Increased basal metabolic rate, polyphagia, weight loss, heat intolerance, and sweating are commonly seen in thyrotoxicosis and would be expected in any person ingesting excess thyroid hormone. Cardiovascular manifestations include resting sinus tachycardia and supraventricular arrhythmias, with atrial fibrillation estimated to occur in up to 10% of cases. Atrial fibrillation, in turn, increases the risk of left-atrial thrombi and embolic cerebrovascular events. The spontaneous resolution of atrial fibrillation is likely once the thyroid hormone excess is alleviated. Hyperthyroidism also increases cardiac contractility and cardiac output that, in rare instances, can result in high output cardiac failure. Neuromuscular complications of hyperthyroidism range from simple tremors to severe myopathy. Many of these effects can be ascribed to the increase in catecholamine sensitivity, which results from thyroid hormone excess. In particular, superior eyelid lag, proptosis, and tremors are the result of such effects. Hyperthyroid myopathy can manifest as simple fatigue, muscle weakness, or profound muscle wasting, most commonly affecting proximal musculature. Neurologic manifestations include delirium, stupor, and rarely, coma. It appears that self-administration of excessive thyroid hormone is a weight control strategy used by some eating disorder patients. Clinicians should be cognizant of signs and symptoms of PSYCHOSOMATICS
Case Reports
hyperthyroidism, and may wish to inquire about these behaviors in eating disordered patients. Self-administration of excessive thyroid hor-
mone should be included in the differential diagnosis of hyperthyroidism.
References 1. Pirke KM, Pahl J, SchweigerU, et al: Metabolic and endocrine indices of starvatioo in bulimia: a comparison with lIIIOIexia nerv0S8. Psychiatty Research 1985; 15:33-39
2. Obarzanek E, Lesem MD, Goldstein OS, et al: Reduced resting metabolic rate in patients with bulimia nervosa. Arch Gen Psychiatry 1991; 48:456-462 3. Spalter AR, Gwinsman HE, Demitrack MA, et al: Thyroid function in bulimia nervosa. Bioi Psychiatry 1993; 33:408-414 4. Gwinsman HE, Roy-Byroe P, Yager J, et al: Neuroendocrine abnormalities in bulimia. Am J Psychiatry 1983; 140:559-563 5. Devlin MJ, Walsh BT. Kral JO. et al: Metabolic abnormalities in bulimia nervosa. Arch Oen Psychiatry 1990; 47:144-148 6. Mitchell JE, Bantle JP: Metabolic and endocrine investigations in women of normal weight with the bulimia syndrome. Bioi Psychiatry 1983; 18:355-365 7. Norris PO, O'Malley BP. Palmer RL: The TRH test in bulimia and anorexia nervosa: a controlled study. J Psychiatr Res 1985; 19:215-219 8. Kiriike N. Nishiwaki S, Izumiya Y, et al: Thyrotropin, prolactin, and growth hormone responses to thyrotropinreleasing hormone in anorexia nervosa and bulimia. Bioi Psychiatry 1987; 22:167-176 9. Levy AB, Dixon KN, Malarkey WB: Pituitary response to TRH in bulimia. Bioi Psychiatry 1988; 23:476-484 10. Kaplan AS. Garfinkel PE, Brown GM: The DST and TRH test in bulimia nervosa. Br J Psychiatry 1989; 154:86-92
VOLUME 38. NUMBER 2. MARCH - APRIL 1m
11. Rolla AR, El-Hajj GA, Goldstein HE: Untreated thyrotoxicosis as a manifestation of anorexia nervosa. Am J Med 1986; 81:163-165 12. Byerley B, Black OW, Grosser BI: Anorexia nervosa with hyperthyroidism: case report. J Clin Psychiatry 1983; 44:308-309
13. Fonseca V, Wakeling A. Havard CWH: Hyperthyroidism and eating disorders. BMJ 1990; 301:322-323 14. Krahn 0: Thyrotoxicosis and bulimia nervosa. Psychosomatics 1989; 31:222-224 15. Wong C, Birmingham CL, Tildesley lID: Hyperthyroidism and bulimia: case report. Int J Eat Disord 1987; 6:763-765 16. Woodside DB, Walfish P, Kaplan AS, el al: Graves' disease in a woman with thyroid hormone abuse, bulimia nervosa, and a history of anorexia nervosa. Int J Eat Disord 1991; 10:111-115 17. Schmidt U, O'Oonoghue G: Bulimia nervosa in thyroid disorder. Int J Eat Disord 1992; 12:93-96 18. Fomari V. Edleman R, Katz JL: Medication manipulation in bulimia nervosa: an additional diagnostic criterion? Int J Eat Disord 1990; 9:585-588 19. Tiller J. Macrae A, Schmidt U, et al: The prevalence of eating disorders in thyroid disease: a pilot study. J PsychosomRes 1994; 38:~16 20. Burman KD: Hyperthyroidism. in Principles and Practice of Endocrinology, edited by Becker KL. Philadelphia, PA,18 Lippincott. 1990, pp. 331-347
IS3
B
ulimia nervosa is a fairly common disorder primarily affecting adolescent and young adult women. The illness is characterized by recurrent eating binges with compensatory behaviors in an attempt to prevent weight gain. The classic compensatory behavior is self-induced vomiting, but the use of diet pills, diuretics and laxatives, extreme fasting, and compulsive exercise have been described. We report a case of hyperthyroidism induced by self-administration of excessive levothyroxine in a woman with bulimia nervosa.
Case Report A 30-year-old woman was referred to a psychiatrist after reporting to her therapist that she had been selfadministering levothyroxine to induce weight loss. She stated that 10 months prior she had presented to her physician with cold intolerance, easy bruising, dry skin, coarse bair, and hair loss. At that time, she was told that her thyroid function tests were "low" and that the cause was "extreme dieting." She was begun on levothyroxine 100 (J.l.g1day). She began to increase the dose on her own after about I week on the medication in hopes of losing weight. Subsequent thyroid function tests were "high," and the prescribed dose was diminished to 88 Ilglday. However, she continued to increase the dose gradually, and for several months she bad been taking 1,000 Ilg of levothyroxine per day. During this period, she lost 30 Ibs. and developed a coarse tremor of her upper extremities, insomnia, and tachycardia She denied beat intolerance. She said that she had had delayed menstrual periods on 2 occasions in the preceding 5 months. Her dry skin and coarse hair had resolved after starting the levothyroxine. Her heart rate on examination was 116; there was no VOLUME 38. NUMBER 2. MARCH - APRIL 1m
goiter, exophthalmos. or lid lag. She had a fine, rapid tremor of her extremities. Past medical history included migraine headaches. for which she received cafergot and nortriptyline; an esophageal tear secondary to self-induced vomiting; parotid hypertrophy; a tonsillectomy; and prior knee surgery. Her medications were levothyroxine as noted before, plus buspirone (10 mg tid). fluoxetine (80 mg per day). nortriptyline (100 mg per day). and cephalexin for cellulitis in an extremity. Thyroid function studies performed at her initial evaluation revealed thyroxine 23.71lgldL (normal: 5-11). thyroid index 37.91lgldL (normal: 5-11), thyroid hormone binding ratio 1.6 (normal 0.85-1.15). and thyrotropin 0.02 mUlL (normal: 0.5-6.2). She was instructed to discontinue levothyroxine. Repeat thyroid function testing 5 weeks later revealed thyroxine 1.4, triiodothyronine (T3) uptake 21 (normal: 22-35). thyroid index 0.3. and thyrotropin 24.5. While off the thyroid hormone, she again developed easy bruising, dry hair and skin, and mild cold intolerance. She also regained much of the weight she had previously lost. The tachycardia, anxiety symptoms, frequent sweating. and tremor all resolved. Synthroid was resumed at 100 Ilglper day. and I month later she reported using it as prescribed.
Discussion Extensive literature exists reviewing thyroid function and thyroid disease in connection with
Received January 26. 1996; revised March 20. 1996; accepted April 19. 1996. From the Department of Psychiatry and the Department of Medicine, University of Minnesota, Minneapolis. Address reprint requests to Dr. Crow. University of Minnesota. Department of Psychiatry. Box 393 UMHC, Minneapolis. MN 55455. Copyright 0 1997 The Academy of Psychosonwic Medicine.
151
Case Reports
eating disorders. However, relatively little is known about the prevalence of eating disorders in populations with thyroid disease or about the frequency of the abuse ofthyroid medications for weight control purposes. Several investigators have examined thyroid function in bulimic persons. TJlevels have been found to be low l- J or normal4.5 when compared to reference values or control subjects. Basal thyroid-stimulating hormone (TSH) levels were found to be lower than normal subjects.s Additional studies have examined TSH response to a thyrotropin-releasing hormone (TRH) stimulation test. Gwirtsman et al. (1983) reported blunted TSH responses in 80% of their bulimia nervosa subjects, but most reports have found limited or no blunting.~10 A more consistent finding has been a delayed rise in TSH following TRH stimulation, with TSH values ultimately reaching a magnitude similar to control subjects. Frank hyperthyroidism has been reported in the setting of anorexia nervosa ll - 1J and bulimia nervosa.IJ-16 It is of note that in two of these cases (those of Woodside et aI. and Rolla and colleagues) the patients described refused treatment despite clinically obvious thyrotoxicosis for 1 and over 18 years, respectively. A third report, by Fonseca et aI., included a patient who appeared to be purposefully vomiting carbimazole to avoid effective treatment of her hyperthyroidism. Abuse of thyroid supplementation as a compensatory behavior in bulimia nervosa has been reported only rarely. Two separate reports, those of Schmidt and O'Donoghue '7 and Fornari and colleagues 'S detail single cases of subjects with bulimia nervosa who as a manifestation of their illness self-administered extra thyroid medication. The former case involved a patient who self-administered excessive doses of prescribed thyroid hormone, while the person reported by Fornari's group self-administered thyroid hormone that had been prescribed for someone else. It is important to note that hyperthyroidism, like eating disorders, occurs primarily in women and the ages of greatest risk are similar. Tiller and colleagues '9 surveyed the frequency of eating disorders of various types in a clinic for patients for thyroid disease. In a survey of73 patients, 4% IS2
were diagnosed with bulimia nervosa and 4% met criteria for eating disorder not otherwise specified. However, only 69% of the subject group returned their questionnaires, raising the possibility that a number of persons with eating disorders could conceivably have opted not to complete the questionnaire; thus, the true incidence in that group may have been higher. In Tiller's group, 7% of the respondents admitted to misusing thyroxine to control their weight. Excess thyroid hormone supplementation possesses the same significant medical risks as endogenous thyroid hormone overproduction. 20 While hyperthyroidism affects most organ systems, constitutional symptoms are the most common. Specific manifestations of the cardiovascular and neuromuscular symptoms are present in many patients. Increased basal metabolic rate, polyphagia, weight loss, heat intolerance, and sweating are commonly seen in thyrotoxicosis and would be expected in any person ingesting excess thyroid hormone. Cardiovascular manifestations include resting sinus tachycardia and supraventricular arrhythmias, with atrial fibrillation estimated to occur in up to 10% of cases. Atrial fibrillation, in turn, increases the risk of left-atrial thrombi and embolic cerebrovascular events. The spontaneous resolution of atrial fibrillation is likely once the thyroid hormone excess is alleviated. Hyperthyroidism also increases cardiac contractility and cardiac output that, in rare instances, can result in high output cardiac failure. Neuromuscular complications of hyperthyroidism range from simple tremors to severe myopathy. Many of these effects can be ascribed to the increase in catecholamine sensitivity, which results from thyroid hormone excess. In particular, superior eyelid lag, proptosis, and tremors are the result of such effects. Hyperthyroid myopathy can manifest as simple fatigue, muscle weakness, or profound muscle wasting, most commonly affecting proximal musculature. Neurologic manifestations include delirium, stupor, and rarely, coma. It appears that self-administration of excessive thyroid hormone is a weight control strategy used by some eating disorder patients. Clinicians should be cognizant of signs and symptoms of PSYCHOSOMATICS
Case Reports
hyperthyroidism, and may wish to inquire about these behaviors in eating disordered patients. Self-administration of excessive thyroid hor-
mone should be included in the differential diagnosis of hyperthyroidism.
References 1. Pirke KM, Pahl J, SchweigerU, et al: Metabolic and endocrine indices of starvatioo in bulimia: a comparison with lIIIOIexia nerv0S8. Psychiatty Research 1985; 15:33-39
2. Obarzanek E, Lesem MD, Goldstein OS, et al: Reduced resting metabolic rate in patients with bulimia nervosa. Arch Gen Psychiatry 1991; 48:456-462 3. Spalter AR, Gwinsman HE, Demitrack MA, et al: Thyroid function in bulimia nervosa. Bioi Psychiatry 1993; 33:408-414 4. Gwinsman HE, Roy-Byroe P, Yager J, et al: Neuroendocrine abnormalities in bulimia. Am J Psychiatry 1983; 140:559-563 5. Devlin MJ, Walsh BT. Kral JO. et al: Metabolic abnormalities in bulimia nervosa. Arch Oen Psychiatry 1990; 47:144-148 6. Mitchell JE, Bantle JP: Metabolic and endocrine investigations in women of normal weight with the bulimia syndrome. Bioi Psychiatry 1983; 18:355-365 7. Norris PO, O'Malley BP. Palmer RL: The TRH test in bulimia and anorexia nervosa: a controlled study. J Psychiatr Res 1985; 19:215-219 8. Kiriike N. Nishiwaki S, Izumiya Y, et al: Thyrotropin, prolactin, and growth hormone responses to thyrotropinreleasing hormone in anorexia nervosa and bulimia. Bioi Psychiatry 1987; 22:167-176 9. Levy AB, Dixon KN, Malarkey WB: Pituitary response to TRH in bulimia. Bioi Psychiatry 1988; 23:476-484 10. Kaplan AS. Garfinkel PE, Brown GM: The DST and TRH test in bulimia nervosa. Br J Psychiatry 1989; 154:86-92
VOLUME 38. NUMBER 2. MARCH - APRIL 1m
11. Rolla AR, El-Hajj GA, Goldstein HE: Untreated thyrotoxicosis as a manifestation of anorexia nervosa. Am J Med 1986; 81:163-165 12. Byerley B, Black OW, Grosser BI: Anorexia nervosa with hyperthyroidism: case report. J Clin Psychiatry 1983; 44:308-309
13. Fonseca V, Wakeling A. Havard CWH: Hyperthyroidism and eating disorders. BMJ 1990; 301:322-323 14. Krahn 0: Thyrotoxicosis and bulimia nervosa. Psychosomatics 1989; 31:222-224 15. Wong C, Birmingham CL, Tildesley lID: Hyperthyroidism and bulimia: case report. Int J Eat Disord 1987; 6:763-765 16. Woodside DB, Walfish P, Kaplan AS, el al: Graves' disease in a woman with thyroid hormone abuse, bulimia nervosa, and a history of anorexia nervosa. Int J Eat Disord 1991; 10:111-115 17. Schmidt U, O'Oonoghue G: Bulimia nervosa in thyroid disorder. Int J Eat Disord 1992; 12:93-96 18. Fomari V. Edleman R, Katz JL: Medication manipulation in bulimia nervosa: an additional diagnostic criterion? Int J Eat Disord 1990; 9:585-588 19. Tiller J. Macrae A, Schmidt U, et al: The prevalence of eating disorders in thyroid disease: a pilot study. J PsychosomRes 1994; 38:~16 20. Burman KD: Hyperthyroidism. in Principles and Practice of Endocrinology, edited by Becker KL. Philadelphia, PA,18 Lippincott. 1990, pp. 331-347
IS3