Troponin Elevation in Sickle Cell Disease.

OBJECTIVE: Sickle cell disease is associated with cardiovascular abnormalities. Troponin is not typically measured in this population, and thus the significance of abnormal levels of troponin is unknown. We wanted to evaluate the use of troponin and factors that predispose troponin elevation in patients admitted with sickle cell pain crisis (SCPC). METHODS: We reviewed data of consecutive patients admitted to a tertiary care hospital between 2006 and 2011 with a diagnosis of SCPC. Subjects with elevated troponin (ET) (troponin I >0.04 ng/mL) were compared with those with normal troponin (NT) for demographics, risk factors, presence of echocardiography-derived tricuspid regurgitant jet velocity (TRV) ≥3 m/s suggesting pulmonary hypertension, and laboratory tests. The Mann-Whitney U test was used to compare groups. RESULTS: Two hundred eighty-three of 724 patients admitted with SCPC had chest pain. Troponin I was measured in 63 patients: 51 had NT and 12 had ET ranging from 0.06 to 3.42 ng/ml. ET was associated lower hemoglobin (p = 0.02), lower hematocrit (p = 0.02), lower platelet number (p < 0.001), higher LDH (p = 0.012), higher AST levels (p = 0.004), higher bilirubin levels (p = 0.006), and TRV ≥3 m/s (p = 0.028). CONCLUSIONS: Troponin was measured in <10% of patients with SCPC, and 1 out of 5 of them had ET. Troponin elevation was not associated with traditional cardiovascular risk factors but was associated with lower hematocrit, elevated LDH, bilirubin levels, and TRV ≥3 m/s.

Utility of routine pretreatment evaluation of left ventricular ejection fraction in breast cancer patients receiving anthracyclines.

Anthracycline-based chemotherapy is widely used in the management of breast cancer. Despite the lack of clinical evidence, obtaining prechemotherapy left ventricular ejection fraction (LVEF) by echocardiogram or multigated acquisition scan is a widely adopted practice throughout the world. We present here the results of a retrospective analysis of breast cancer patients who had LVEF measurements in anticipation of an anthracycline chemotherapy to determine whether predefined cardiac risk factors predicted for poor cardiac function. Retrospective data were analyzed from 482 female breast cancer patients in whom LVEF was measured before starting anthracycline-based chemotherapy. Baseline demographics and multiple risk factors associated with congestive heart failure were collected. Twenty-six possible risk factors for CHF were defined, and the frequency of finding an abnormal LVEF as a function of total risk factors was assessed. Statistical tests include chi-squared and logistic regression analysis. The median age of the study population was 52 years. The original chemotherapy plan was changed in 7 patients (1.45%) based on LVEF findings, all of which had asymptomatic LV dysfunction (LVEF ranging 40%-50%). In 32 patients, despite normal LVEF results, anthracyclines were omitted secondary to prior cardiac issues. In 17 patients where LVEF was reported normal, anthracyclines were skipped based on patient's preference, tumor characteristics, or upstaging of the cancer based on imaging studies. No patient with ≤2 risk factors had an abnormal LVEF (N = 350). The probability of finding an abnormal LVEF in patients without any cardiac risk factors is extremely rare. Skipping baseline LVEF assessment may be an option in some patients with no cardiac risk factors undergoing anthracycline-based chemotherapy.

Use of Eltrombopag in Improving Poor Graft Function after Allogeneic Hematopoietic Stem Cell Transplantation.

Eltrombopag is a thrombopoietin agonist and has been used in aplastic anemia and post-transplantation thrombocytopenia. The c-MPL receptor is present on hematopoietic stem cells. There are no reports of eltrombopag utilization for improving poor graft function in the post-transplant setting. Here were report a case of a young female with post-transplant poor graft function as evident from the low absolute neutrophil count, anemia, and thrombocytopenia on day 60. Eltrombopag was started on day 72 and resulted in improvement in all 3 cell lines. The counts continued to be stable even after eltrombopag was discontinued. The patient tolerated the drug without significant side effects for 1 year.

Excellent response to chemotherapy post immunotherapy.

INTRODUCTION: Immunotherapy in the form of immune checkpoint inhibitors has changed the landscape of cancer treatment. Newer monoclonal antibodies are coming up and are being tested in various cancers during different stages of treatment. With the increasing use of immune checkpoint inhibitors in the management of various types of cancers, the question is raised as to what next can be offered to a patient who has progressed on this newer treatment. Does Sequence matter? There have been reports of improved responses to chemotherapy after immunotherapy in the form of vaccines. Here we present a case series of 6 patients who progressed on immunotherapy with immune checkpoint inhibitors after initial modality of treatment (chemotherapy/radiation), subsequently received chemotherapy with excellent response. METHODS: We have a cohort of six patients who had disease progression on second line Immunotherapy for solid or hematological malignancies and had ECOG < 2. All these patients received third line salvage chemotherapy. Three patients had metastatic head and neck cancer, 2 had non-small cell lung cancer (NSCLC), and one had T -cell rich B- cell lymphoma. Prior review and approval were obtained from our institutional review board. RESULTS: All patients had an excellent response to chemotherapy in third line setting, after immune checkpoint inhibitors and most of them achieved a complete response. CONCLUSION: Targeting cancer with chemotherapy after failure of immunotherapy is a valid option and can lead to better response rates and PFS which may lead to OS. This effect may be secondary to immunotherapy removing the inhibition exerted by tumor cells or other immune cells initially followed by cytotoxic chemotherapy mediated killing of tumor cells.

Cocaine use does not affect mean platelet volume.

Increased mean platelet volume (MPV) is a marker of platelet activation. Platelet activation with cocaine use is not well studied. We wanted to investigate MPV levels in patients with cocaine-associated chest pain (CACP) as a marker of platelet activation. Retrospectively, MPV of 82 consecutive patients with CACP (group 1) with positive urine drug screen (UDS), without acute myocardial infarction (AMI) (group 1A) and with AMI with elevated troponin (group 1B), were included in the study. The control group (group 2) consisted of 89 consecutive patients admitted during the same time period with acute chest pain (ACP) who had negative UDS and negative cardiac markers with a normal cardiac stress test or normal coronary angiogram. Analysis showed no statistically significant difference of MPV between group 1, 8.46 ± 1.06 fL, versus group 2, 8.7 ± 1.07 fL; p = 0.142; and between group 1A, 8.46 ± 1.05 fL, and group 1B, 8.46 ± 1.09 fL; p = 0.983. By multiple linear regression analysis, MPV was not influenced by cocaine abuse (R = 0.269, R (2) = 0.072, adjusted R (2) = -0.009, p = 0.562). MPV is not elevated in patients with cocaine use even when they had AMI. Further studies may be necessary to investigate the role of platelet activation in patients with cocaine use and chest pain.