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Abstract: Between 1990 and 1996, we treated nine HIV-positive patients with a clinical diagnosis of thrombotic thrombocytopenic purpura (TTP) with therapeutic plasma exchange (TPE). Response to TPE was seen in all but three of these patients. The nonresponders were subsequently diagnosed with disseminated Mycobacterium avium intracellulare (MAI) infection. Their anemia and platelet counts improved only after a 3- to 4-week course of appropriate anti-mycobacterial agents. A fourth patient with MAI infection had a transient response to TPE; this patient was also treated with anti-mycobacterial agents. The list of differential diagnoses in patients who appear to have TTP is longer in this patient population. Mycobacterial infection may mimic TTP in a substantial number of cases. On the basis of our experience, we recommend working up and considering empiric therapy for mycobacterial infection along with other possible diagnoses in Hill-positive patients.
Thrombotic thrombocytopenic purpura (TTP) is a disease characterized by fluctuating neurological signs, a Coombs' negative microangiopathic hemolytic anemia, thrombocytopenia, fever and renal dysfunction.  The clinical manifestations of TTP result from abnormal adherence of platelets to endothelium, producing platelet-fibrin thrombi in small arterioles with resultant end-organ damage. Before plasma exchange was available, the prognosis for these patients was very poor with high mortality. Most patients died of thrombotic complications. Fortunately, the availability of total plasma exchange (TPE) therapy has changed this. According to more recent studies, 70% to 90% of TTP patients respond to plasma exchange. 
The risk factors for development of TTP are many. They include bacterial infections such as pneumococcal bacteremia  and E. coil 0157:H7 infections.  More recently, HIV has also become recognized as a major risk factor contributing to a significant increase in the incidence of TTP. [7-9]
With the addition of HIV infection as a risk factor, a new dimension in evaluation of TTP appears to have become necessary. Multiple pathophysiological processes in HIV mimic TTP. Clinically, the presentation and course of HIV-associated TTP may be similar to that in HIV-negative patients with TTP.  However, in HIV-positive patients, current criteria for the diagnosis of TTP may not be adequate, because often these patients are on multiple medications and/or have confounding factors such as opportunistic infections that may affect their clinical and hematologic presentation. In fact, thrombocytopenia alone affects up to 10% of HIV-positive patients  and can be associated with multiple factors varying from ganciclovir therapy to myelophthisis.  Also, seizures and acute mental status changes may be seen in HIV-positive patients due to AIDS encephalopathy, CXS lymphoma …