Yolk Sac Tumor in the Anterior Mediastinum Presenting as Acute Pericarditis.

BACKGROUND Mediastinal masses can originate from anatomical structures normally located in the mediastinum, or from structures that travel through the mediastinum during embryogenesis. Initial presenting symptoms usually vary from shortness of breath, cough, chest pain, and superior vena cava syndrome to nonspecific constitutional symptoms (eg, fever, weight loss, fatigue). However, the initial presentation of a mediastinal mass with acute pericarditis has not been reported in the literature as far as we know. CASE REPORT A 20-year-old man presented to the Cardiology Clinic with chest pain and new pericardial effusion on echocardiography, both fulfilling the diagnostic criteria of acute pericarditis. The patient also had venous engorgement on the neck, and a chest X-ray followed by computed tomography imaging showed a large mediastinal mass. The serum tumor marker a-fetoprotein (AFP) was markedly elevated. The biopsy and immunohistochemistry revealed a high-grade malignant neoplasm - yolk sac tumor, which is a type of non-seminomatous germ cell tumor. The acute pericarditis resolved after administration of NSAID and colchicine. The patient was then started on chemotherapy. CONCLUSIONS The discussed case shows the rare presentation of an anterior mediastinal mass with acute pericarditis. This emphasizes the importance of a thorough review of systems and critical analysis of every sign and symptom at the time of initial presentation, which helps the physician to obtain appropriate imaging studies early in the course, leading to an early diagnosis and treatment of the disease, such as in this case of an extremely rare germ cell tumor.

Observational Study of Thrombotic Events in a Random Cohort of Hospitalized COVID-19 Patients at a Community-Based Hospital of New York City During the Beginning of the 2020 Pandemic.

Coronavirus disease 2019 (COVID-19) continues to pose an unprecedented challenge for the entire world and the healthcare system. Different theories have been proposed elucidating the pathophysiological mechanisms attributing to high mortality and morbidity in COVID-19 infection. Out of them, thrombosis and procoagulant state have managed to earn the maximum limelight. We conducted an observational study based on data from randomly selected 349 hospitalized patients with COVID-19 infection in a community-based hospital in New York City during the first wave of the COVID-19 viral surge in March 2020. The main objective of our study was to assess the risk and occurrence of thrombotic events (both venous and arterial) among the hospitalized patients including the intensive care unit (ICU) and non-ICU admissions with confirmed COVID-19 infection. The primary outcome in our study was defined as the thrombotic events that included myocardial infarction (MI), deep venous thrombosis (DVT), cerebrovascular accidents (CVA), and pulmonary embolism (PE). The study correlated the association of thrombotic events with the level of biomarkers of interest: D-dimer >1000 ng/ml, troponin-I >1 ng/ml, or both. The association of D-dimers and troponin-I with thrombotic events was measured using both univariate and multivariate Cox proportional hazard (PH) regression analysis. Out of a total of 349 patients, 78 patients (22.35%) were found to have elevated biomarkers (D-dimer >1000 ng/ml and/or troponin-I >1 ng/ml) and were categorized as a high-risk group. Eighty-nine patients developed thrombotic complications (evidence of more than one thrombotic event was found in several patients). Two-hundred seventy-one (77.65%) patients had no documentation of thrombosis. The incidence of thrombotic events included myocardial infarction (MI; N=45; 12.8%), cerebrovascular accidents (CVA; N=16; 4.5%), deep venous thrombosis (DVT; N=16; 4.5%), and pulmonary embolism (PE; N=9; 2.57%).

Treatment-Refractory, Primary Immune Thrombocytopenic Purpura in a Patient with Celiac Disease.

BACKGROUND Immune thrombocytopenic purpura (ITP) is primarily caused by antibody-mediated destruction of platelets. Alterations in immune homeostasis can induce loss of peripheral tolerance and promote the development of self-reactive antibodies. Primary ITP is the diagnosis of exclusion made after the extensive work-up rules out other possible causes of thrombocytopenia. The association between the ITP and other autoimmune disorders is well-established. In recent years, increasing attention has been directed toward the association between celiac disease (CD) and ITP. CASE REPORT A 27-year-old man with a history of primary ITP presented with an occasional nosebleed, 1 episode of rectal bleeding, and easy bruising. The patient was later found to have high titers of TTG-IGA and endomysial IGA levels consistent with CD. Our patient not only failed to improve with the gluten-free diet, but also failed multiple lines of treatment including steroids, IVIG, rituximab, eltrombopag, and even a non-traditional treatment for ITP (azathioprine and plasma exchange). The patient's CD-related antibody titers remained elevated. CONCLUSIONS It is possible that in certain cases the alteration of immune response caused by CD with a concurrent elevation of CD-related antibodies can make ITP refractory to all medical management. Whether or not this refractoriness to treatment is related to the persistently elevated antibody titers of CD or unknown genetic relationship between ITP and CD remains not entirely clear and warrants further molecular, immunologic, and genetic analysis.