A 62-year-old woman with a previous history of bone tuberculosis in childhood presented with lymph node tuberculosis reactivation. She initiated therapy (isoniazid, pyrazinamide, rifampicin, and ethambutol), but after ten months treatment was interrupted due to pancytopenia. Drug toxicity was suspected, but pancytopenia persisted after stopping the treatment. A first bone marrow biopsy was inconclusive. The patient's hematologic cell counts continue to drop (Table 2) and a new medullar evaluation was compatible with a myelodysplastic syndrome with complex karyotype (chromosomes 5 and 7 deletions). Treatment with azacitidine was started and soon interrupted due to the presence of fever with absent signs of infection. The patient was admitted to hospital. The fever was refractory to antibiotics (imipenem, vancomycin) and fluconazole. The bacteriologic studies of urine, respiratory secretions, and blood cultures were negative. A high ferritin value of 19000 mug/L made the suspicion of HPS. Further tests revealed elevated alpha-chain IL-2 soluble receptor and low fibrinogen levels (Table 2). A new bone marrow biopsy revealed signs of hemophagocytosis (Figure 1). At this point, the diagnosis of HPS was made. Even though the patient did not present neurologic symptoms, a lumbar puncture was performed revealing high protein levels, indicating probable central nervous system (CNS) involvement. The patient began treatment with etoposide and dexamethasone and intrathecal methotrexate according to protocol HLH-94 with clinical improvement, resolution of fever, and continuous recovery of blood count (Table 2). She completed 8 weeks of therapy. Despite an initial clinical improvement, she was readmitted to hospital and died with septic shock due to a severe respiratory infection 2 months after completion of initial therapy.