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.

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.