| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
LETTERS TO THE EDITOR |
Rudolf Magnus Institute of Neuroscience, Department of Child and Adolescent Psychiatry, University Medical Centre Utrecht, Utrecht, The Netherlands (Hoeven, Duyx)
Netherlands Pharmacovigilance Centre, Den Bosch, The Netherlands (Langen)
Department of Pediatric Immunology, Wilhelmina Children’s Hospital, University Medical Centre Utrecht, Utrecht, The Netherlands (Royen)
A 13-year-old boy with Wegener’s granulomatosis, a primary systemic vasculitis, was admitted to our outpatient child and adolescent psychiatry clinic because of incapacitating obsessive-compulsive symptoms and severe panic attacks. The onset of Wegener’s granulomatosis had been 9 months before with involvement of the central nervous system, resulting in serious symptoms, like aphonia. He had responded well to the standard treatment regimen consisting of high-dose prednisolone and cyclophosphamide. Residual symptoms, like disturbances of coordination, ataxia, mild dysarthria, diplopia, muscular atrophy, fatigue, cognitive impairment, and unexplained headache, all had improved gradually. Four weeks before admission, the cyclophosphamide had been replaced by azathioprine and the corticosteroids were tapered (1).
On psychiatric examination, we saw a 13-year-old boy who had never had psychiatric symptoms before. The family history was negative for psychiatric diagnoses. He had endured the described symptoms surprisingly well, but as he started making progress in physical rehabilitation, the following symptoms developed: obsessions about dying, committing suicide, harming others, and obsessive negative thoughts about himself and others; compulsive behavior; severe panic attacks more than once a day and sleep disturbances, all leading to a "symbiotic" interaction between mother and child.
We diagnosed an obsessive-compulsive disorder and panic attacks, etiologic factors being mainly psychosocial. We started treatment with fluvoxamine up to 100 mg daily and cognitive behavioral therapy, which was ineffective in the face of many crisis situations, and was replaced by supportive behavioral family therapy, which was hardly more effective.
Eighteen months after admission, the symptoms suddenly disappeared, 3 weeks after switching his immunosuppression from azathioprine to methotrexate. In the ensuing 4 years, no relapses of anxiety disorders were noted. There had been two relapses of the systemic vasculitis, treated with increases in prednisolone dosage and methotrexate, without psychiatric symptoms occurring.
The overall literature does not report psychiatric side effects from azathioprine. Neither does the database of the WHO Uppsala Monitoring Centre mention obsessive-compulsive symptoms or panic attacks as possible adverse drug reaction of azathioprine.
However, the described coincidence and the absence of symptoms before and after this period suggest a causal relation. Probably the combination of subtle cerebral dysfunction as a result of the vasculitis and the use of azathioprine may have caused the symptoms in this patient.
There is a body of knowledge on the neurobiology of obsessive-compulsive symptoms (2). Unfortunately, the effect of azathioprine on cerebral functioning is unknown, so it is difficult to hypothesize on a pathophysiological explanation.
In case of psychiatric symptoms in a patient with cerebrovascular pathology using azathioprine, the possibility of an adverse drug reaction, and therefore an early switch to other immunosuppressive drugs, should be considered.
DOI:10.1097/01.psy.0000160473.31162.4d
REFERENCES
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
