ABSTRACT
As a chronic autoimmune disease, systemic lupus erythematosus (SLE) primarily affects young women and does not discriminate against any particular organs. In December 2019, coronavirus disease 2019 (COVID-19) spread worldwide, with many speculations of cardiac involvement in the pathogenesis of infection. Moreover, in cases where cardiac symptoms were described, they consisted solely of chest pain or a general deterioration in health if the patient presented with pleural effusion or pericardial effusion. Our patient, a 25-year-old Hispanic woman, initially complained of chest pain, cough, and shortness of breath. After being admitted, she noticed growing dyspnea and mild discomfort on the right side of her chest. The patient had both SLE and COVID-19 and had developed pleural and pericardial effusions. After two days in culture, nothing had grown from the fluid samples. In addition, measures of brain natriuretic peptide and total creatine kinase fell within the normal range. Considering the investigational findings, pericardiocentesis was performed. After the procedure, the patient's condition improved, and she was discharged. The patient continued taking CellCept® 1,500 mg and Plaquenil 200 mg and started taking colchicine. Her daily prednisone dose was increased to 40 milligrams. She felt well initially; however, after two weeks of follow-up, the pericardial effusion recurred, and pericardiocentesis was performed again. The patient was discharged in stable condition after a two-day hospital stay. After treatment of both initial and recurrent effusions, the patient's cardiac symptoms were resolved, and blood pressure became stable. We hypothesize that there may be other unreported cases of COVID-19-related viral pericarditis, pericardial effusion, and pericardial tamponade that could be caused by a combination of COVID-19 and a pre-existing condition, mainly autoimmune disorders. Due to the lack of clarity surrounding typical COVID-19 manifestations, it is crucial to record all cases of this unique illness and analyze any increased incidence of pericarditis, pericardial effusion, and pericardial tamponade in the public.
ABSTRACT
Arising from the external and internal iliac veins, the common iliac veins (CIVs) carry blood from the lower extremities and pelvic region into the inferior vena cava at the level of the fifth lumbar vertebra. It is sometimes common to observe slight anomalies in vascular anatomy in patients; however, anomalies of the CIVs are rare. We present a case of a patient with significant edema of the left lower extremity due to extrinsic compression (May-Thurner syndrome [MTS]) involving a duplicated left CIV found during vascular angiography. Anomalies in pelvic vasculature are well documented in the medical literature; however, documented cases of a duplicated CIV remain few and far between. These anomalies in pelvic vascular anatomy are essential to be aware of to avoid surgical complications and understand their implications in associated pathologies.
ABSTRACT
Ehlers-Danlos syndrome (EDS) is a hereditary disorder caused by a mutation in the COL gene, which leads to the faulty synthesis of the collagen protein. EDS can present with a wide array of manifestations depending upon which COL gene is mutated. Birt-Hogg-Dubé (BHD) syndrome is a rare hereditary disorder currently identified in 200 families worldwide. It presents clinically with cutaneous, renal, and pulmonary manifestations due to an autosomal dominant mutation in a tumor suppressor gene, FLCN, on chromosome 17p11.2. We present a case of a 22-year-old male with Birt-Hogg-Dubé syndrome, showing typical features consistent with the classical type of EDS, with genetic testing revealing a COL5A1 mutation of "uncertain clinical significance", not yet reported in clinical literature. We discuss the treatment of this patient and describe the presentations of the two pathologies. Lastly, we put forth guidelines for the management of a dilated ascending aorta, with which this patient presents, for future patients who may present with this novel EDS mutation.
