Escitalopram induced thrombocytopenia reversed after shifting to bupropion in a depressive patient

To the Editor

A previous retrospective study reported that antidepressant treatment with escitalopram, a selective serotonin re-uptake inhibitor (SSRI), significantly reduced the platelet count, whereas bupropion, a noradrenalin and dopamine re-uptake inhibitor (NDRI) had no such effect (Song et al., 2012). Whether escitalopram-related thrombocytopenia can be reversed without discontinuing anti-depressant therapy, such as by using bupropion as an alternative drug, is unclear.

Herein, we describe the case of a 31-year-old physically healthy and drug-naïve Taiwanese male who received anti-depressants for depressed mood (initial Hamilton Depression Rating Scale [HAM-D] score 28). Before treatment, his haematological findings were all within normal ranges, including a platelet count of 159,000/µL (reference range: 150,000–400,000/µL). However, after 1 month of monotherapy with escitalopram (10 mg/day), his platelet count decreased to 106,000/µL despite other haematological profiles remaining normal. Neither medical disease nor traumatic injuries were noted during the treatment period. Inflammatory, liver and thyroid functions were all within normal limits, as were coagulator parameters including pro-thrombin time and partial pro-thrombin time. In addition, no increased bleeding tendency signs such as unexplained bruising or petechiae were noted. Due to concerns over the possible side effects of escitalopram, treatment was shifted to bupropion monotherapy (150 mg/day). After 2 weeks of bupropion treatment, follow-up haematological studies showed an increase in platelet count to 136,000/µL, which increased to 157,000/µL after 1 month of treatment. His depressed mood improved (HAM-D score 13), and other haematological profiles remained normal throughout.

By excluding the presence of other aetiological factors that may have contributed to thrombocytopenia, the cause of the adverse haematological effect seems attributable to escitalopram. A previous case series of fluoxetine, another SSRI, reported that thrombocytopenia associated with treatment reversed after the agent was switched to reboxetine, a noradrenalin re-uptake inhibitor (NRI) (Yucel et al., 2015). This is consistent with our patient in that escitalopram-related thrombocytopenia was reversed after shifting the anti-depressant to the non-SSRI bupropion. Although the definite biological mechanism for this phenomenon is unclear, drug-induced immune thrombocytopenia has been demonstrated with a probable level of evidence (Aster and Bougie, 2007).

Taken together with our findings, both NRIs and NDRIs can be considered as alterative agents for SSRI-related thrombocytopenia if ongoing anti-depressant therapy is needed. Our findings provide clinicians with a potential treatment strategy if SSRI-related thrombocytopenia occurs. Further clinical and pharmacological studies should be considered to validate our findings.