Black Hairy Tongue Associated With Lorazepam Treatment of a Male Smoker With Major Depression

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To the Editors
Black hairy tongue syndrome (BHT) is a relatively common (prevalence rates between 1% and 11% in various dental outpatient populations) and harmless coating of the tongue resulting from hyperkeratosis of elongated filiform lingual papillae (“hairs”).1–3 This condition can allow debris to accumulate and may drive an overgrow of chromogenic bacteria of the normal oral flora (and sometimes yeast). Black, brown, yellow, blue, and green discolorations have been described in the centrum of the dorsal tongue.1–3 Black hairy tongue syndrome is usually asymptomatic, but it may be rarely associated with nausea, gagging, xerostomia, metallic taste, halitosis, burning mouth syndrome, and sensation of fullness in the back of the mouth.1–3 The exact pathogenesis of BHT is unknown. Predisposing factors include advanced age, male sex, smoking, excessive coffee or black tea drinking, poor oral hygiene, xerostomia, or general debilitation.1–3 Remarkably, BHT was described to be a cutaneous manifestation of a graft-versus-host disease that occurred as a complication of allogenic stem cell transplantation.4 Furthermore, BHT was found to be associated with the administration of various medications, most of which being effective modulators of the immune defense, such as antibiotics1,5 and interferon therapy.6 In addition, there are a few reports of BHT occurring under treatment with psychiatric medications, such as phenothiazines, olanzapine, and fluoxetine.1,3,7 Regarding benzodiazepines, there is only one article reporting BHT under clonazepam treatment.3 However, a “coated tongue” is listed as an adverse reaction in the patient information of clonazepam. In the following, the first BHT is presented being probably caused by lorazepam treatment.
A 62-year-old male Caucasian cigarette smoker showed an asymptomatic black discoloration of his tongue he had never noticed before and which was located distal of the circumvallate papillae in the central part of his dorsal tongue (Fig. 1). A BHT was diagnosed by dermatological examination including microscopy. The discoloration (Fig. 1) occurred 2 weeks after starting an inpatient lorazepam treatment (1 mg q.i.d., no sublingual or intravenous preparation) of the patient who had major depression with anxious features. He smoked less than 1 pack of cigarettes per day since his adolescence and did not neglect oral hygiene during his severe depression (Hamilton Depression Scale [HAMD], 28 points),8 which remitted (HAMD, 5 points) within 3 months of treatment with mirtazapine (45 mg/d), bupropion (300 mg/d), and venlafaxine (150 mg/d). The BHT resolved within 8 weeks after inpatient lorazepam taper (Fig. 1). Two euthymic years later, the bupropion treatment was terminated, and 2 months later, the patient relapsed with anxious depression (HAMD, 25 points). He was readmitted, and, again, BHT occurred 2 weeks after inducing relaxation with lorazepam (0.5 mg q.i.d.) and vanished about 8 weeks after the lorazepam taper (Fig. 1). Because the BHT was asymptomatic again, it was not treated. The depression remitted (HAMD, 2 points) after reinstating bupropion (300 mg/d) and augmentation with pregabalin (150 mg/d) within 2 months of inpatient treatment. Unlike the lorazepam treatment (Fig. 1), there was no timely relationship between BHT and the severity of the depression. The patient had reported less appetite at the peak of his depressive episodes but no relevant dietary and smoking changes, xerostomia, or mouthwashes. Medical workups revealed no neurological or internal symptoms with the exception of a mild chronic obstructive pulmonary disease according to spirometry. Routine laboratory and serum levels of thiamine, riboflavin, niacin, pyridoxine, folate, holotranscobalamin, and 25-hydroxyvitamin D were unremarkable. HIV and lues were excluded. A gastroscopy showed an asymptomatic and mild (Helicobacter pylori–negative and nonatrophic) gastritis. Brain computed tomography, electroencephalography, electrocardiogram, abdominal ultrasonography, echocardiography, and chest X-ray were normal. Irrespective of nicotine, the addiction history was negative. Although all applied medications (Fig.
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