Individuals with human immunodeficiency virus (HIV) disease frequently suffer from anemia. The causes include anemia of chronic disease, vitamin B12 and iron deficiency, opportunistic infections (Mycobacterium tuberculosis, Pneumocystis jiroveci), HIV-related bone marrow suppression, AIDS-associated malignancies, and antiretroviral therapy (ART), specifically zidovudine. In HIV patients with advanced immunodeficiency, failure to produce neutralizing antibodies can lead to chronic parvovirus B19 (B19) infection. Normally, in persons with intact immunity, the progression of B19 is self-limited. However, in chronic B19 infection, it can lead to pure red cell aplasia (PRCA) and chronic anemia. In human immunodeficiency virus (HIV)-infected patients, B19-related anemia is rare and underdiagnosed. It has a great response to intravenous immunoglobulin (IVIG) therapy. Hence, early diagnosis and prompt treatment can significantly reduce mortality. In this article, we described the case of a 25-year-old male with HIV infection who presented with a headache. He had severe normocytic anemia with a low reticulocyte count. The workup for blood loss, hemolysis, hemoglobinopathy, and iron deficiency was negative. Because of extremely low reticulocytopenia with severe anemia, the investigations favored multiple myeloma, parvovirus infection, and bone marrow aspiration biopsy. He was tested for parvovirus B19 deoxyribonucleic acid (DNA) polymerase chain reaction (PCR) test due to insufficient seroconversion. It turned out to be positive and he was treated with IVIG therapy.

In the past decade, percutaneous endovenous stenting has emerged as the primary procedure for treating symptomatic venous outflow obstruction. Stent migration is a rare but serious and well-recognized complication of venous stenting. Cardiopulmonary complications following stent migration can manifest in a number of ways, including damage to the valves, arrhythmias, endocarditis, tamponade, and acute heart failure. Both extracardiac and intracardiac dislodgement of stents may be treated with catheter-directed extraction, stent redeployment, or surgical extraction. The decision on the type of procedure depends on multiple factors including the location of the stent, the size and accessibility of the stent, the symptoms, the extent of damage to the vital structures, and the overall health of the patient. We present the case of a 68year-old male who presented with tachycardia. On further evaluation and workup, he was found to have an iliac venous stent that had migrated to the right atrium.

Hyperammonemic encephalopathy (HE) can be broadly defined as an alteration in the level of consciousness due to elevated blood ammonia level. While hepatic cirrhosis is the most common cause of HE, non-hepatic causes like drugs, infections, and porto-systemic shunts can also lead to the presentation. In this case, we highlight an unusual occurrence of recurrent non-cirrhotic HE from obstructive urinary tract infection (UTI) with urea-splitting micro-organisms in an elderly male patient. The patient exhibited altered mentation, and elevated ammonia levels with normal hepatic function at presentation. Urine culture revealed Proteus mirabilis resistant to extended spectrum beta-lactamases (ESBL). Successful management of obstructive UTI was achieved through Foley’s catheterization and intravenous (IV) antibiotics, resulting in the resolution of HE. This outcome further supports the significance of UTI as a potential cause of hyperammonemia. Thus, UTI as one of the non-hepatic causes of hyperammonemia should always be explored among elderly patients presenting with altered mentation.

Amiodarone, a class III antiarrhythmic drug, is commonly used for the management of life-threatening ventricular arrhythmias, atrial fibrillation, and other refractory supra-ventricular arrhythmias. Factors like a large volume of distribution, lipophilic property, deposition in tissues in large amounts, etc. have led to the development of amiodarone-induced multisystem adverse events. We report a case of amiodarone-induced hepatic attenuation on computed tomography (CT) of the abdomen in an elderly female patient. Amiodarone with a composition of 40% iodine by weight deposits in the liver, leading to characteristically increased radiodensity reported as increased attenuation on CT scan. Surprisingly, the severity and extent of hepatic attenuation on CT scans do not necessarily correlate with the total exposure to amiodarone over time. Individual factors may influence the liver's response to the drug, leading to varying degrees of hepatic changes. To minimize the risk of adverse events associated with amiodarone, clinicians should carefully adjust the dosage to the lowest effective level and regularly monitor liver function tests in patients. This proactive approach enables early detection of liver dysfunction and facilitates timely adjustments or discontinuation of amiodarone, thereby reducing potential harm.

Introduction: Women with Polycystic Ovary Syndrome (PCOS) have classic risk factors for cardiovascular disease such as obesity, hypertension, hypercholesterolemia, insulin resistance, and metabolic syndrome. Studies have demonstrated that they have increased markers of cardiovascular disease, including endothelial dysfunction, coronary artery calcification, and increased arterial stiffness leading to myocardial infarction, angina, stroke, and rarely coronary artery dissection. We present a case of a young female with PCOS without any other major classic cardiovascular risk factors except hypertension who presented with chest pain, later found to have myocardial infarction due to dissection of the right coronary artery. Case: A 33year old female presented with lightheadedness and intermittent dull mid-sternal chest pain. It became progressively worse in 5-6 hours. Past medical history was relevant for hypertension, insulin resistance, PCOS, and overweight. She was noncompliant with her medications. Family history was significant for hypertension, diabetes, coronary artery disease, and negative for any connective tissue disorders. Electrocardiogram showed ST-T elevation in leads II, III, and aVF and depression in leads I and aVL. Troponin level was significantly high at 0.378 ng/ml. Dual antiplatelet therapy was initiated. The patient underwent an emergency cardiac catheterization that revealed focal 85% flow limiting dissection in the proximal right coronary artery with a long 35% lesion in the mid right coronary artery and 40% focal lesion in the right posterior descending artery. Percutaneous intervention with a drug-eluting stent was placed successfully. She was discharged later with dual antiplatelet therapy, beta-blocker, angiotensin receptor blocker, and statin. Conclusion: Spontaneous coronary artery dissection in young females is usually associated with hormonal therapy or in the postpartum state. However, our case report highlights that physicians should have a high index of suspicion for spontaneous coronary artery dissection in a young female with PCOS.