Abstract
Karen Southall and Noel Fernando, Gisborne, New Zealand:
Clozapine has been reported to cause parotitis in some patients [1]. In a report by Brodkin [2], a suggested treatment for this was benztropine. We would like to present the first such documented case of clozapine-induced parotitis in New Zealand.
Ms Wis a 49-year-old woman with a 20-year history of bipolar disorder. Her manic and depressive relapses have been severe despite maintenance lithium treatment with therapeutic lithium levels. Her prominent mood congruent psychotic symptoms have responded poorly to classical antipsychotic medications. Therefore, a trial of clozapine was considered.
Routine blood investigations per the clozapine protocol showed a normal complete blood count with a white count of 9.8 and a neutrophil count of 6.66. The only aberrant value was an erythrocyte sedimentation rate of 12. This was not felt to be a contraindication to commencing clozapine treatment. Her renal and liver functions were all within normal limits. Free T4 (thyroxine) was 13 with the thyroid stimulating hormone raised at 9 (normal range = 0.3-7). Baseline electrocardiograph was normal. Following initiation of clozapine, the dose was increased to 300 mg daily over a 1-week period. Up until this point Ms W had noticed that she was feeling sedated and also complained of some increased salivation, although this was not problematic to the extent where it was pooling on her pillow at night.
On the day on which Ms W first received 300 mg of clozapine, she was noted to have developed a swelling on one side of her face. As she had been in contact with glandular fever, glandular fever serology was performed, with a negative result. She complained of pain in her right parotid gland although was not distressed by it. It was tender to palpation. A diagnosis was made of parotitis possibly secondary to her clozapine medication and she was commenced by the house surgeon on a 7-day course of oral penicillin. The following day her symptoms remained unchanged and she was prescribed 2 mg of cogentin. This brought about a significant improvement in her parotid-related symptoms. On physical examination 1 week later her parotid glands were not swollen and were non-tender. She had no further sialorrhoea, and in fact stated that at this point that her mouth felt dry.
Other causes of parotitis include mumps, sarcoidosis, tuberculosis, lymphoma and Sjögren's syndrome. Unilateral parotid swelling can result from tumours, cysts or ductal obstruction due to stones or strictures. She was not on medication besides clozapine to account for an iatrogenic cause. Mumps was considered unlikely in view of her age and the absence of known exposure. In sarcoidosis, clinically apparent parotitis involvement occurs in less than 10% of patients, bilateral involvement is the rule, the gland is usually non-tender and the lung is almost always involved whereas our patient did not have symptoms referable to the respiratory system. The only haematological parameter possibly compatible was her slightly raised ESR. Sjögren's syndrome does occur predominantly in middle-aged women but in view of the onset of symptoms occurring coincident with clozapine treatment and with no prior symptoms, this diagnosis was considered too unlikely to justify further eye and salivary tests and serology. She is on the waiting list for a non-urgent parotid ultrasound scan, but in view of the prompt response to benztropine, a stone or stricture is considered unlikely.