Psychosomatics 47:175-177, March-April
doi: 10.1176/appi.psy.47.2.175
© 2006 Academy of Psychosomatic Medicine
An Adrenal Adenoma Presenting With Psychosis
Michael Nugent, M.D., and
G. Scott Waterman, M.D.
Received July 9, 2004; revised November 15, 2004; accepted November 23, 2004. From the Dept. of Psychiatry, University of Vermont College of Medicine, Burlington, VT. Send correspondence and reprint requests to Michael Nugent, M.D., Dept. of Psychiatry, Univ. of Vermont College of Medicine, 1 South Prospect St., Burlington, VT 05401. e-mail: michael.nugent{at}vtmednet.org
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INTRODUCTION
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The use of synthetic anabolic steroids by athletes—body-builders and football players, most commonly—has been studied in its association with aggression and psychosis.1–4 Corticosteroids have long been known to cause psychosis both in iatrogenic states as well as in medical conditions that are associated with endogenous hypercorticosteroid states, such as Cushing's disease or congenital adrenal hyperplasia.5 However, no cases have been reported of endogenously-derived excessive anabolic-androgenic hormones causing or contributing to psychosis. This report is of a woman, who previously enjoyed good mental health, who rapidly developed a psychotic disorder and was subsequently discovered to have a hyperfunctioning adrenal adenoma.
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Case Report
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Initial Presentation and History of Presenting Illness
Ms. C was a 40-year-old woman who was seen in the emergency room of a teaching hospital with a 3-month history of paranoia. Her father and mother were present and had encouraged her to come to the emergency room under the pretense of having her skin changes evaluated. She had been living with her parents for 1 month after losing her job as a nursing assistant. She indicated that she thought her skin had been changing because of food allergies, and she had been changing her diet to try to correct this hypothesized allergy. She also stated that her neighbors had been spying on her, using cameras that they had planted in her house. One was said to be in the TV, and another in a bathroom mirror. She believed that they had made changes to the light switches that indicated there had been listening devices implanted in them. She resigned from her job as a nursing assistant and explained that people were verbally harassing her and laughing at her. She noted that she had been feeling "low" for several months and that she had "mood swings." Her sleep had also been disturbed.
Evaluation findings in the ER included normal electrolyte, B12, and folate levels, and head CT scan without contrast. Urine drug screen and RPR were negative. Hemoglobin was 16.0 g/dl (reference range: 11.6–15.2), hematocrit was 47.7% (reference range: 35–44.4), and WBC was 15.75 k/cm3 (reference range: 4.0–12.4). Urine drug screen was negative. Vital signs were normal. Urinalysis revealed trace blood and trace leukocyte esterase. She was started on an antibiotic for a suspected urinary tract infection and was admitted to the psychiatric inpatient unit for further evaluation. She refused to allow a physical exam to be performed but consented to show the examiner what looked like acne on her forearms.
Additional History
Ms. C was raised as an only child. She described herself as an "Army brat" who moved all over the United States. She received good grades in school and graduated from high school. She went to college briefly and worked in various entry-level jobs in auto mechanics, housekeeping, and, most recently, as a nursing assistant. She had had an abortion at age 14. She had never been married and had had few long-term relationships.
Mental Status Exam
Ms. C appeared as a short, stocky female with coarse facial features. She wore a baseball cap, jeans, sneakers, and a winter coat she would not take off, despite the summer weather. She was cooperative in answering direct questions, but was hesitant to speak freely and was guarded. Her eyes were downcast. She appeared psychomotorically retarded. Her voice was soft. Her mood was "sad." Her affect was congruent with that report. She denied suicidal or homicidal ideation. She was alert and fully oriented. Her thought content included paranoia about cameras and bugging devices that she believed had been planted, perhaps by the neighbors. She did not know of anyone who would harm her, but she thought the people at her former job did not like her and had treated her with contempt. She described herself as very religious and spiritual, though there were no religious delusions voiced. Her thought processes were slow but not impoverished. Her ideas regarding her skin changes being caused by food allergies were odd but were not held with delusional conviction. She denied perceptual disturbances.
Differential Diagnosis
Her hirsutism and history of progressive virilization that would later emerge during the hospital course did not factor into the initial differential diagnosis. The paranoid delusions in the context of some depressive symptoms—social withdrawal, psychomotor retardation—suggested a major depressive episode with psychotic features. Schizophrenia was considered remotely possible because of the psychotic symptoms, although no previous history consistent with that possibility was elicited. There was no evidence suggestive of delirium.
Hospital Course
The patient was admitted to the unlocked inpatient psychiatric unit. She immediately attempted to leave and was transferred to a secure unit. It was found that her sneakers held several thousand dollars.
In the morning, she submitted to an exam. Her father produced a picture from high school that, in comparison, revealed the change in her facial features—prominent brow, strong jawline, and male pattern balding. Her father believed the changes had occurred over 2 years' time. A staff member elicited the history that the patient's menstrual flow had been low in volume and less frequent than previously. She had an increased libido, with increased frequency of masturbation, and had been shaving her face daily for several months. She had not been to a physician, but had been modifying her diet, thinking that she suffered from a food allergy. She had noticed that she could lift furniture she previously could not, despite not working out. The possibility of an endocrine-based etiology of the patient's psychosis and masculinization prompted an endocrinology consultation. Their more complete physical exam noted Grade 4 hirsutism (facial and chest hair), clitoromegaly, and café-au-lait spots.
Laboratory values subsequently obtained included a serum testosterone concentration of 200 ng/dl (reference range: 14–76), a serum DHEA concentration of 16.5 µg/ml (reference range: 0–1.88), and a serum estrogen concentration of 26 pg/ml (but it was not known where in her menstrual cycle she was at that time). Serum 17-hydroxyprogesterone, luteinizing hormone, and prolactin were normal. Urine catecholamines were essentially normal. Urine metanephrine, cortisol, and aldosterone were normal. Abdominal CT scan was done first without contrast on Hospital Day 5 because Ms. C did not wish to cooperate with procedures involving the use of contrast material. A 4.3-cm x 4.2-cm mass was reported as adjacent and "likely contiguous" with the left adrenal gland, and consistent with adrenal adenoma or carcinoma. A CT scan with contrast (to which she consented at that point) of chest, abdomen, and pelvis was done on Hospital Day 7 at the behest of surgery consultants, in order to delineate further the mass and to rule out metastasis in preparation for surgery. Findings indicated a mass that was circumscribed, with no metastasis and no adenopathy. The adrenal mass was thought to be either an adrenocortical adenocarcinoma or a hyperfunctioning adrenal adenoma.
The patient reluctantly began taking quetiapine 25 mg bid on Hospital Day 3. She noted that she was already feeling less stressed before taking quetiapine, although she still believed there were cameras in her father's house. On Hospital Day 5, during the night, she had abrupt onset of left arm weakness and numbness. She declined an ECG and blood-drawing for cardiac enzymes, and, in the morning, it had resolved.
A family meeting was held on Hospital Day 6 with Ms. C, her father, the internist who worked on the psychiatric unit who had been involved in her care, the psychiatry resident, and a medical student. The results of the diagnostic tests were explained as a mass that was potentially malignant and needed to be removed. Ms. C. appeared to understand her condition and the likelihood that it could worsen if not treated aggressively. She consented the next day to surgery.
The patient was discharged from the Psychiatry Service on quetiapine 25 mg bid with her psychosis having resolved, and she was scheduled for surgery 1 week later. The surgeon found a circumscribed mass grossly consistent with an adrenal adenoma. It was thought to have been fully excised. Pathology later confirmed that it was an adrenal-cortical adenoma.
She returned to visit the psychiatric unit 2 months later, having recovered fully and wishing to thank the staff. Six months postoperatively, her testosterone level had fallen to 12 ng/dl (reference range: 14–76), and, 1 year later, it was 21 ng/dl. She did not follow up with recommended psychiatric care. Limited history from her father 2 years later indicated that she had not returned to work and that the left arm weakness had returned intermittently.
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Discussion
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No reports were found in the literature of psychosis associated with a hyperandrogenic state caused by a hyperfunctioning adrenal adenoma. Certainly, there are other well-documented clinical situations where hyperandrogenism is thought to cause psychosis and/or mania. The phenomenon of athletes using anabolic-androgenic steroids has been reviewed by Uzych1 and Pope,2 both of whom found evidence that anabolic-androgenic steroids can cause psychosis (paranoid delusions, auditory hallucinations), mania, or hypomania, as well as "withdrawal" major depression in athletes who take megadoses (10–100 times the amounts prescribed for patients) and then abruptly stop taking them. Dean3 reported a case of mania and psychosis in a previous healthy man who began using a DHEA-S supplement. There are numerous other case reports in the literature of anabolic-androgenic supplement abuse leading to psychosis and/or mania.3,4
Anabolic-androgenic steroid abuse may cause psychosis, but is there evidence that endogenous anabolic-androgenic steroids play a role in psychosis? Maayan et al.6 found that, among 17 patients with pharmacotherapy-resistant psychotic depression treated with ECT, there was an association between elevated basal DHEA-S levels and resistance to therapeutic effects of ECT. This association is a more indirect link between psychosis and hyperandrogenism than athletes abusing over-the-counter testosterone supplements and developing psychosis, but it does provide evidence that elevated endogenous androgen states may be related to treatment-resistance. Oades and Schepker7 measured serum gonadal hormone levels among 22 young schizophrenic patients and found that men showed elevated levels of DHEA when matched with normal and inpatient obsessive-compulsive-disorder control subjects. The authors caution against generalization because of the sample size. However, it is interesting that the hormone DHEA, which, in megadose supplements, can cause psychosis, was observed to be mildly elevated in those young schizophrenic patients. A recent investigation into the role of DHEA in first-episode schizophrenic subjects also found significantly elevated DHEA and DHEA-S levels. The authors speculate whether this is a biologically adaptive mechanism or a secondary response to a psychotic illness.8 Further studies are needed to elucidate the cause of elevated DHEA in schizophrenia.
A drawback to this case report is the limited follow-up data. Two years after presentation, the patient was not in psychiatric treatment. DHEA and testosterone levels had returned to normal, however. The patient's father had provided information that she had not returned to work for 2 years, and, although reportedly not psychotic since hospitalization, she had not returned to premorbid functioning as a nursing assistant and may have had a recurrence of left-arm weakness of unknown etiology.
In conclusion, we report a case of psychosis in a patient with a hyperfunctioning adrenal-cortical adenoma. This association has not been reported previously. A comparable state among athletes abusing high doses of anabolic-androgenic steroids allows us to speculate about the etiology of psychosis in this woman. Further studies are needed to elucidate how elevated levels of anabolic-androgenic steroids may cause or contribute to the persistence of psychosis.
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REFERENCES
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- Uzych L: Anabolic-androgenic steroids and psychiatric-related effects: a review. Can J Psychiatry 1992; 37:23–27[Medline]
- Pope HG, Katz DL: Affective and psychotic symptoms associated with anabolic steroid use. Am J Psychiatry 1988; 145:487–490[Abstract/Free Full Text]
- Dean CE: Praesterone (DHEA) and mania. Ann Pharmacother 2000; 34:1419–1422[Abstract]
- Porcerelli JH, Sandler BA: Anabolic-androgenic steroid abuse and psychopathology. Psychiatr Clin North Am 1998; 21:829–833[CrossRef][Medline]
- Soundy TJ, Black JL, Peterson GC, et al: Psychosis in a male pseudohermaphrodite with 17-hydroxylase deficiency. Psychosomatics 1992; 33:452–454[Free Full Text]
- Maayan R, Yagorowski Y, Grupper D, et al: Basal plasma DHEA-S: a possible predictor for response to electroconvulsive therapy in depressed psychotic inpatients. Biol Psychiatry 2000; 48:693–701[CrossRef][Medline]
- Oades RD, Schepker R: Serum gonadal steroid hormones in young schizophrenic patients. Psychoneuroendocrinology 1994; 19:373–385[CrossRef][Medline]
- Strous RD, Maayan R, Lapidus R, et al: Increased circulatory dehydroepiandrosterone and dehydroepiandrosterone-sulphate in first-episode schizophrenia: relationship to gender, aggression, and symptomatology. Schizophr Res 2004; 71:427–434[CrossRef][Medline]
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INTRODUCTION
Case Report
