To the Editor: A 34-year old woman presented with fever, confusion, disorientation and gum bleeding. Laboratory workup revealed a hemoglobin 7.7 g/dL, platelet count 3x10⁹/L, normal WBC with normal differential, many fragmented RBCs on peripheral blood film, normal coagulation profile, lactate dehydrogenase (LDH) 1443 U/L (reference range, 100-190) and serum creatinine of 103 μmol/L (reference range, 53-88). Her previous medical and surgical history was unremarkable with no reports of drug intake within the last month. Her HIV status was negative. The picture was consistent with classical thrombotic thrombocytopenic purpura (TTP) and the patient was treated with plasma exchange (40 mL/kg daily) in combination with prednisolone (60 mg/day) and pulses of vincristine injections (four doses were given on days 1, 2, 7 and 10).

Her improvement was gradual and a complete remission was achieved after eight days of treatment with full recovery of neurological and renal function along with normalization of the hematological parameters. On routine visits to the hematology clinic (twenty five days post discharge), the platelet count dropped to 88 x 10⁹/L with normal hemoglobin and LDH levels. The patient was hospitalized with presumed early relapse of TTP. During the first 72 hours in hospital the patient was transfused with fresh frozen plasma but despite this the platelet count continued to drop reaching 40 x 10⁹ /L. Plasma exchange was started, but after eight days of intensive treatment the platelet count did not improve. LDH values were constantly within the normal limit and peripheral smears showed no evidence of RBC s fragmentation.

As a result, the diagnosis of idiopathic thrombocytopenic purpura (ITP) was considered since all secondary causes of immune thrombocytopenia were ruled out (Anti-DNA, ANA, HIV, hepatitis B were negative, bone marrow aspirate and biopsy, CT of the chest, abdomen and pelvis were also within normal limits). The patient was started on prednisolone 100 mg daily. The response was remarkable, with an increase in the platelet count to 150 x 10⁹ /L after four days. The steroid was tapered accordingly but the patient experienced several relapses of thrombocytopenia, all of which responded to restarting the steroid. Nonetheless, a splenectomy was eventually performed twelve months later because of recurrent ITP. The patient had full platelet recovery after splenectomy and was in complete remission after two years follow up.

Recent investigations have found that both TTP and ITP are autoimmune processes that could overlap in an immunocompromized patient. We found no predisposing factors in this case. There are two reports of 3 cases of ITP developing during remission of TTP.^1-3 Therefore it is important to bear in mind that ITP may occur during TTP remission. Inappropriate or unnecessary use of therapeutic tools may have a negative impact on the patient. We must continue to look for predisposing factors for TTP and ITP.