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Clinical Specialist Endocrinology and Metabolic Diseases Department Baskent University 5. Street, Bahcelievler Ankara, Turkey fax 90 312 4482335 drsahinmustafa{at}yahoo.com
Clinical Specialist Endocrinology and Metabolic Diseases Department Baskent University
Associate Professor, Director Endocrinology and Metabolic Diseases Department Baskent University
Published Online, June 14, 2005. www.theannals.com, DOI 10.1345/aph.1E517
Case Report. A 49-year-old man was admitted to our clinic in January
2004 with left breast enlargement. He had no remarkable medical history. The
enlargement was elastic and painful to palpation. He had no galactorrhea or
lymph node enlargement. Results of the rest of the physical examination were
normal. Results of all biochemical markers, including renal and liver function
tests, ruled out malnutrition and hepatic and renal diseases.
Follicle-stimulating hormone, luteinizing hormone, estradiol, human chorionic
ß-gonadotropin, 
-fetoprotein, prostate-specific antigen, total and
unbound testosterone levels, and results of thyroid function tests ruled out
gonadal insufficiency, testicular tumors, paraneoplastic syndromes, and
hyperthyroidism.
Ultrasound examination of the testes and computed tomography of the chest showed no signs of testicular or bronchogenic carcinoma. Breast examination, mammography, and ultrasonography confirmed the marked enlargement of the left breast, which showed a retroareloar glandular component. Multiple-site biopsies were performed, and cytologic analysis confirmed the absence of infectious or malignant cells. There was no traumatic (castration, trauma) etiology. The patient had not been taking any other drug or herbal product at the time of onset of gynecomastia except fluoxetine 20 mg/day for depression for 4 months, which was stopped after the onset of gynecomastia.
Discussion. There are 2 previous reports on gynecomastia in association with SSRIs, but as of this writing, none with fluoxetine alone. Although idiopathic gynecomastia could not be ruled out, fluoxetine treatment was considered the cause. Gynecomastia appeared after the onset of fluoxetine therapy and was still present but subsided 10 months after cessation of the drug. We did not readminister the drug or give a placebo to the patient. The patient had had no previous exposure to a similar drug. There are insufficient data about the relationship between fluoxetine blood levels and gynecomastia.
According to the Naranjo probability scale, it was possible that the gynecomastia was fluoxetine-related.4 Fluoxetine treatment has been reported to cause gynecomastia in combination with risperidone, but there was no clear relationship between prolactin levels and gynecomastia in our patient. Controlled studies are necessary to clarify this adverse effect of fluoxetine. As a result, physicians should take into account SSRIs as a possible cause of gynecomastia.
References
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