Case report: An unusual presentation of acute promyelocytic leukemia in a middle aged female mimicking dengue infection.

RATIONALE: Acute promyelocytic leukemia (APL) is an uncommon subtype of acute myeloid leukemia (AML). M3v phenotype is a less common presentation of APL and these patients usually present with leukocytosis and abnormal promyelocytes that are characterized by sparse granulation and are less likely to have faggot cells with multiple Auer rods. Distinguishing M3v phenotype from acute febrile illness can be challenging as the diagnosis relies on examination of peripheral smear. PATIENT CONCERNS: Fifty-seven-year-old female who presented after recent trip to Dominican Republic for high grade fever and gum bleeding. She was exposed to patients with Dengue fever during her stay. At presentation, patient had leukocytosis, thrombocytopenia, and urinalysis showing bacteria and white cell. She was started on treatment for urinary tract infection. Patient remained febrile and thrombocytopenia worsened. On day 2, flow cytometry of the peripheral smear showed 43% medium sized blasts. Fluorescence in situ hybridization was positive for promyelocytic leukemia/retinoic acid receptor alpha. DIAGNOSES: The patient was diagnosed with APL. INTERVENTIONS: Patient was started on treatment with all-trans retinoic acid and arsenic trioxide along with supportive care OUTCOMES:: Patient had a favorable clinical response and her symptoms subsided. LESSONS: Flow cytometry of the peripheral smear is key to diagnosis of suspected APL. One must maintain high suspicion for this life-threatening condition as early diagnosis saves lives.

Benazepril-Induced Agranulocytosis: A Case Report and Review of the Literature.

BACKGROUND: Angiotensin-converting enzyme inhibitors are widely used drugs, and in appropriately selected patients, serious side effects are infrequent. Commonly seen side effects include cough, rash, hyperkalemia, renal dysfunction, and angioedema. Historically, dose-related agranulocytosis has been associated with captopril. Benazepril, a relatively more potent angiotensin-converting enzyme inhibitor, is rarely associated with agranulocytosis. CASE REPORT: Here, we report a case of drug-induced agranulocytosis due to benazepril, with complete recovery of white blood cell count upon discontinuation of the drug. All tests for other causes of agranulocytosis were unremarkable. This report highlights a serious and rare side effect associated with benazepril. CONCLUSIONS: Benazepril is a commonly employed anti-hypertensive medication, and we report an unusual condition associated with this medication in order to increase vigilance among caregivers. In such cases, prompt recognition and discontinuation of the causative drug can make the difference between a recovery and a fatal outcome associated with drug-induced agranulocytosis.

Heparin-Induced Thrombocytopenia in a Patient with Essential Thrombocythemia: A Case Based Update.

Vascular thrombosis is a common clinical feature of both essential thrombocythemia (ET) and heparin-induced thrombocytopenia (HIT). The development of HIT in a patient with ET is rare and underrecognized. We report the case of a 77-year-old woman with preexisting ET, who was admitted with acute coronary syndrome, and IV heparin was started. She was exposed to unfractionated heparin (UFH) 5 days prior to this admission. Decrease in platelet count was noted, and HIT panel was sent. Heparin was discontinued. Patient developed atrial fibrillation, and Dabigatran was started. On day three, patient also developed multiple tiny cerebral infarctions and acute right popliteal DVT. On day ten of admission, HIT panel was positive, and Dabigatran was changed to Lepirudin. Two days later, Lepirudin was also discontinued because patient developed pseudoaneurysm on the right common femoral artery at the site of cardiac catheterization access. A progressive increase in the platelet count was noted after discontinuing heparin. Physicians should be aware of the coexistence of HIT and ET, accompanied challenges of the prompt diagnosis, and initiation of appropriate treatment.

Acquired factor VIII inhibitor in patients with hepatitis C virus infection and the role of interferon-alpha: a case report.

A patient with HIV and hepatitis C virus (HCV) co-infection developed an autoantibody to factor VIII after 8.7 months of treatment with pegylated interferon-alpha and ribavirin. Three previous cases of the development of factor VIII autoantibody in patients infected with the hepatitis C virus have been reported. Only one of these patients was treated with interferon-alpha, and this patient had hemophilia A, a condition prone to development of factor VIII autoantibody, even without interferon treatment. It is possible that chronic HCV infection itself, which has been associated with immunological disorders, is responsible for this phenomenon, but the immunomodulatory properties of interferon-alpha may also contribute to this rare occurrence. No previous case of factor VIII inhibitor in a patient infected with HIV has been reported.