Lyme-Associated Pericarditis: A Case Report and Literature Review.

Lyme disease is caused by Borrelia burgdorferi (B. burgdorferi), which is a spirochete transmitted by ticks of the genus Ixodes. Complications related to the cardiovascular system usually occur in the early phase of infection, and the most common cardiovascular complication of Lyme disease is atrioventricular block, especially third-degree heart block. We report a case of a young Caucasian male patient who presented to the emergency department (ED) with complaints of chest pain and shortness of breath. Initial investigations, including chest X-ray, were negative. An EKG revealed ST elevation and PR depression with troponin elevation. The echocardiogram showed a normal ejection fraction with no pericardial effusion. Skin examination was positive for erythema migrans concerning Lyme. Initial Lyme testing was negative in the patient and it should be repeated after four to six weeks, according to the guidelines. This case report highlights the importance of keeping the differentials broad in these patients even if the initial testing is negative, especially since misdiagnosis or delayed diagnosis can cause cardiac complications.

Angiotensin-Converting Enzyme Inhibitor-Induced Angioedema: A Case Report With a Review of Management Options.

Angiotensin-converting enzyme inhibitors (ACEIs) are widely used for heart failure, renal failure, diabetic nephropathy, stroke, arterial hypertension, and a number of other cardiovascular or related conditions. ACEI-induced angioedema is a rare entity but can result in life-threatening emergencies. It mainly occurs in patients starting on ACEI as an antihypertensive. We present a case of lisinopril-induced angioedema in an African American patient managed in the emergency department. After appropriate evaluation, the patient was declared safe to be observed in the emergency department. Intubation was not performed. Early identification of angioedema is paramount, and emergency physicians should maintain airways or intubate such patients if indicated. There should be a high level of suspicion of angioedema in patients taking ACEIs if they present with symptoms of respiratory compromise.

The Rationale for Using Corticosteroids in COVID-19 Encephalopathy: Lessons From a Case Report With Evidence From Literature.

The coronavirus disease 2019 (COVID-19) virus primarily affects the pulmonary system, but neurological manifestations and complication of COVID-19 has been reported in abundance in the literature. We present a case of a middle-aged Caucasian male who was brought to the emergency department for altered mental status. His chief complaints were neurological rather than respiratory. A positive severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) reverse transcription polymerase chain reaction (RT-PCR) nasal swab confirmed the diagnosis. Brain imaging showed mildly dilated ventricles with no other acute findings. As the patient did not require oxygen, he was treated with remdesivir alone without corticosteroids, which is also a precipitating factor of psychosis but, unfortunately, thickly used in practice. That led to remarkable results in full recovery without exposing the patient to steroid therapy. We strongly believe that remdesivir alone is sufficient in treating COVID-19-induced encephalopathy in a patient who does not require oxygen, and evidence supports this practice.

The middle lipin domain adopts a membrane-binding dimeric protein fold.

Phospholipid synthesis and fat storage as triglycerides are regulated by lipin phosphatidic acid phosphatases (PAPs), whose enzymatic PAP function requires association with cellular membranes. Using hydrogen deuterium exchange mass spectrometry, we find mouse lipin 1 binds membranes through an N-terminal amphipathic helix, the Ig-like domain and HAD phosphatase catalytic core, and a middle lipin (M-Lip) domain that is conserved in mammalian and mammalian-like lipins. Crystal structures of the M-Lip domain reveal a previously unrecognized protein fold that dimerizes. The isolated M-Lip domain binds membranes both in vitro and in cells through conserved basic and hydrophobic residues. Deletion of the M-Lip domain in lipin 1 reduces PAP activity, membrane association, and oligomerization, alters subcellular localization, diminishes acceleration of adipocyte differentiation, but does not affect transcriptional co-activation. This establishes the M-Lip domain as a dimeric protein fold that binds membranes and is critical for full functionality of mammalian lipins.