Maurice F. Rabb » Idiopathic Thrombocytopenis Purpura (ITP)

The patient, a 29 year old white female, developed idiopathic thrombocytopenis purpura (ITP) in 1964. She was treated with steroids but splenectomy was required to successfully induce remission. Around the time of the ITP, she had psoriatic-like lesions above her elbows. There were no clear precipitants to the episode in terms of either environmental or toxic exposures or infections. The patient is an active horse person and is often around farm animals; sometime between 1965 and 1998, she fell from a horse and injured her right rotator cuff. In 1996, she suffered the first recurrence of ITP, identified by the evelopment of spontaneous, easy bruisability. The episode was self-contained and required no treatment. A second recurrence of ITP occurred in 1998/1999, when the patient again developed spontaneous, easy bruising. This episode was treated with a short course of corticosteroids. The cause for the original or recurrent brief episodes of ITP was not found. The patient never received intravenous immunoglobulin for any of these episodes. In 1999, she delivered a healthy baby; however, post-partum she was febrile with a greatly elevated white cell count. No source of infection was found and the patient received no specific treatment. In February 2000, the patient suffered a major motor seizure, lost consciousness and was taken to the ER where a CT scan was performed. Two weeks later, she underwent craniotomy for a right frontal subcallosal mass diagnosed pathologically as non-tumorous inflammatory cells, being a mixture primarily of lymphcytes and some B cells. She recovered fully and went home within three days of the procedure. Following a period of sinusitis and upper respiratory infection in August 2000, a CT scan of the chest revealed bilateral nodular interstitial opacities and bulky mediastinal and hilar adenopathy. The working diagnosis was sarcordosis. The patient was referred to the Hermann Eye Center in September 2000. She had no visual complaints. The visual acuity with contact lenses was 20/30+3 OD and 20/25 OS. Intraocular pressures were 14mm Hg OD and 13mm Hg OS. Slit lamp examination showed 1+ cells in the aqueous and 1+ cells in the vitreous. The fundii showed widespread, discrete, subretinal lesions demonstrated in the photographs. The patient returned in two weeks with no change in the multifocal lesions and no change in vision. Systemic Prednisone was started at 10mg QD X 1 week, then raised to 40mg QD. Three weeks later there were no changes.