A Case of COVID-19-Induced Immune Thrombocytopenia (ITP) in an Adult Female: An Under-Recognized Emerging Phenomenon.

Coronavirus disease 2019 (COVID-19) follows a mild course in majority of cases, but some patients may develop non-pulmonary yet life-threatening complications. A Pandora's box had been opened when multisystem hyper-inflammatory syndromes and autoimmune diseases that had been described previously in children and young adults, that are associated with COVID-19, have now emerged in adults. They need to be recognized as important sequelae of severe COVID-19 disease. Immune thrombocytopenia (ITP) or thrombocytopenic purpura is an autoantibody and T-cell-mediated autoimmune disorder characterized by isolated thrombocytopenia, which can be triggered by different infections. First-line treatment of severe ITP includes platelet transfusions in life-threatening cases, followed by corticosteroids and intravenous immunoglobulins (IVIG). Since the beginning of the pandemic, more and more cases of COVID-19-associated ITP have been reported. We report a case of acquired ITP in a young woman that could only be attributed to her COVID-19 infection and was refractory to platelet transfusion, requiring further treatments. The aim of this report is to review some of the etiologies and purposed molecular mechanisms of the autoimmune nature of the disease and to focus on diagnosis and treatment. We will review the current literature surrounding this non-pulmonary manifestation of COVID-19 and current treatment options for this uncommon presentation of ITP.

Failure of Guidelines and Consensus Statements to Recommend Follow-up for Chronic Cardiovascular Conditions.

BACKGROUND: Many cardiac conditions require long-term clinical follow-up to monitor progression of disease and tolerance and adherence to therapies. Providers are often unsure as to the frequency of clinical follow-up and who should provide the follow-up. In the absence of formal guidance, patients may be seen more frequently than necessary - thereby limiting clinic space for other patients, or not frequently enough, potentially leading to undetected progression of disease. OBJECTIVES: To determine the extent to which guidelines (GL)/consensus statements (CS) provide guidance about appropriate follow-up for common cardiovascular conditions. METHODS: We identified 31 chronic cardiovascular disease conditions for which long-term (beyond 1 year) follow-up is indicated and used PubMed and professional society websites to identify all relevant GL/CS (n = 33) regarding these chronic cardiac conditions. RESULTS: Of the 31 cardiac conditions reviewed, GL/CS contained no recommendation or vague recommendation for long-term follow-up for 7 of the conditions. Of the 24 conditions with recommendations for follow-up, 3 had recommendations for imaging follow-up only without mention of clinical follow-up. Of the 33 GL/CS reviewed, 17 made any recommendations about long-term follow-up. When recommendations were made regarding follow-up, they were often vague, using terminology such as "as needed". CONCLUSIONS: Half of GL/CS fail to provide recommendations for clinical follow-up of common cardiovascular conditions. Writing groups for GL/CS should adopt a standard of routinely including recommendations for follow-up including specific advice about level of expertise needed (eg, primary care physician, cardiologist), need for imaging or testing, and frequency of follow-up.

Acute Pancreatitis and Myocardial Infarction: A Narrative Review.

BACKGROUND: Acute pancreatitis can rarely present with electrocardiographic changes that imitate myocardial ischemia. Even rarer is for acute pancreatitis to present with ST segment elevation in contiguous leads, suggestive of an acute coronary syndrome. In this comprehensive review article, we highlight diagnostic challenges and examine possible pathophysiological causes as seen through 34 total cases in which acute pancreatitis has been found to mimic an acute myocardial infarction. SUMMARY: It has been shown that regardless of the severity of acute pancreatitis, it can be associated with myocardial injury of varying presentation. Thus far, there have been 34 total cases where acute pancreatitis presented with electrocardiographic changes consistent with acute myocardial infarction without true coronary artery thrombosis. An inferior wall ST-elevation myocardial infarction pattern was the most frequently demonstrated. Many hypotheses have been proposed as to the mechanism of injury including decreased coronary perfusion, direct myocyte damage by pancreatic proteolytic enzymes, indirect parasympathetic injury, electrolyte derangements, and coronary vasospasms. Given the complexity of the clinical presentation, thorough subjective and objective evaluation can be vital in guiding to diagnosis and possibly more invasive testing. KEY MESSAGES: It is imperative that clinicians are aware that acute pancreatitis can mimic an acute myocardial infarction. Although we have started to better understand the pathological mechanisms for this phenomenon, further research focused on specific molecular target areas is needed.

Gender Parity in High Impact Cardiology Journals.

Despite increased female representation in medical training, women physicians continue to be under-represented in academic cardiology, particularly in senior roles of authorship and leadership. We analyzed the top 20 most-cited cardiology journals (31,540 total articles) between January 1, 2018 and October 31, 2021 for gender distribution of editorial staff and authorship. Our data demonstrated that only 27% of articles had women as first authors and 20% as senior authors. Women constituted 23% of editorial staff. There is a statistically significant negative correlation (R = 0.67, P = 0.0011) between the percentage of women as first authors and the percentage of men on editorial boards. Overall, female authorship increased from 26% first and 19% senior authors in 2018, to 29% first and 22% senior authors in 2021. Women authors are significantly under-represented in academic cardiology publications, and additional work is needed to identify and address barriers to publishing and academic advancement for women in cardiology.

Endogenous Retroviral Envelope Syncytin Induces HIV-1 Spreading and Establishes HIV Reservoirs in Placenta.

Radical cure of HIV-1 (HIV) is hampered by the establishment of HIV reservoirs and persistent infection in deep tissues despite suppressive antiretroviral therapy (ART). Here, we show that among HIV-positive women receiving suppressive ART, cells from placental tissues including trophoblasts contain HIV RNA and DNA. These viruses can be reactivated by latency reversal agents. We find that syncytin, the envelope glycoprotein of human endogenous retrovirus family W1 expressed on placental trophoblasts, triggers cell fusion with HIV-infected T cells. This results in cell-to-cell spread of HIV to placental trophoblasts. Such cell-to-cell spread of HIV is less sensitive to ART than free virus. Replication in syncytin-expressing cells can also produce syncytin-pseudotyped HIV, further expanding its ability to infect non-CD4 cells. These previously unrecognized mechanisms of HIV entry enable the virus to bypass receptor restriction to infect host barrier cells, thereby facilitating viral transmission and persistent infection in deep tissues.

Pseudotyping of HIV-1 with Human T-Lymphotropic Virus 1 (HTLV-1) Envelope Glycoprotein during HIV-1-HTLV-1 Coinfection Facilitates Direct HIV-1 Infection of Female Genital Epithelial Cells: Implications for Sexual Transmission of HIV-1.

Female genital epithelial cells cover the genital tract and provide the first line of protection against infection with sexually transmitted pathogenic viruses. These cells normally are impervious to HIV-1. We report that coinfection of cells by HIV-1 and another sexually transmitted virus, human T-lymphotropic virus 1 (HTLV-1), led to production of HIV-1 that had expanded cell tropism and was able to directly infect primary vaginal and cervical epithelial cells. HIV-1 infection of epithelial cells was blocked by neutralizing antibodies against the HTLV-1 envelope (Env) protein, indicating that the infection was mediated through HTLV-1 Env pseudotyping of HIV-1. Active replication of HIV-1 in epithelial cells was demonstrated by inhibition with anti-HIV-1 drugs. We demonstrated that HIV-1 derived from peripheral blood of HIV-1-HTLV-1-coinfected subjects could infect primary epithelial cells in an HTLV-1 Env-dependent manner. HIV-1 from subjects infected with HIV-1 alone was not able to infect epithelial cells. These results indicate that pseudotyping of HIV-1 with HTLV-1 Env can occur in vivo Our data further reveal that active replication of both HTLV-1 and HIV-1 is required for production of pseudotyped HIV-1. Our findings indicate that pseudotyping of HIV-1 with HTLV-1 Env in coinfected cells enabled HIV-1 to directly infect nonpermissive female genital epithelial cells. This phenomenon may represent a risk factor for enhanced sexual transmission of HIV-1 in regions where virus coinfection is common.IMPORTANCE Young women in certain regions of the world are at very high risk of acquiring HIV-1, and there is an urgent need to identify the factors that promote HIV-1 transmission. HIV-1 infection is frequently accompanied by infection with other pathogenic viruses. We demonstrate that coinfection of cells by HIV-1 and HTLV-1 can lead to production of HIV-1 pseudotyped with HTLV-1 Env that is able to directly infect female genital epithelial cells both in vitro and ex vivo Given the function of these epithelial cells as genital mucosal barriers to pathogenic virus transmission, the ability of HIV-1 pseudotyped with HTLV-1 Env to directly infect female genital epithelial cells represents a possible factor for increased risk of sexual transmission of HIV-1. This mechanism could be especially impactful in settings such as Sub-Saharan Africa and South America, where HIV-1 and HTLV-1 are both highly prevalent.