Lymphadenopathy could represent a vast spectrum of etiologies including infectious and non-infectious diseases. Besides proper history taking, physical examination, and laboratory investigations, a tissue diagnosis is often necessary to unmask the cause of generalized lymphadenopathy. Here we present a 23-year-old woman who was admitted for diffuse generalized lymphadenopathy, fatigue, malaise, weight loss, nausea, and bilateral lower extremity edema. She reported a history of seizures as well as stroke 2 years prior with no other medical conditions present. Although malignant and infectious etiologies were initially the primary targets for workup, her history of seizures and stroke remained a dilemma. Extensive workup for malignant and infectious diseases was unrevealing; however, rheumatologic workup was eventually positive for systemic lupus erythematosus (SLE). This case illustrates that extensive generalized diffuse lymphadenopathy may be a presenting feature of SLE and should be considered in the differential diagnosis of patients presenting with diffuse lymphadenopathy and constitutional symptoms.
Small molecule tyrosine kinase inhibitors (TKIs) are potent anti-cancer targeted therapies. TKIs are considered safe and efficacious therapeutic modalities, and are generally tolerated well. However, they are associated with certain side effects including hematologic toxicities such as anemia, macrocytosis, neutropenia, thrombocytopenia, hemolytic anemia, bone marrow aplasia and necrosis. Thrombotic microangiopathy, arterial thromboembolism and splenic infarction can also occur following treatment with TKIs. Cytopenias are the most common adverse effects associated with these agents, and other hematologic toxicities are not frequent. It is essential for clinicians to monitor patients closely, and recognize those side effects as early as possible, in order to improve efficacy of small molecule TKIs and optimize outcomes. This article summarizes hematologic toxicities associated with the commonly used small molecule TKIs. It also provides practical strategies for the management of these toxicities.
Autoimmune neutropenia (AIN) is defined as a neutrophil count <1.5 × 10/L caused by increased peripheral destruction of neutrophils from an underlying autoimmune mechanism in which autoantibodies are directed against a patient's own neutrophils. AIN has a multifactorial etiology ranging from an idiopathic primary phenomenon to secondary disorders associated with established autoimmune diseases. Primary AIN is more prevalent in children, generally self-limited, and typically manifests as a sole hematologic abnormality. Secondary AIN is more common in adults and often occurs in the setting of concurrent autoimmune diseases, infections, malignancies, or medications. It may be seen posttransplantation or occasionally with neurological diseases. Various laboratory modalities are used to detect anti-neutrophil antibodies. Although biologic agents such as rituximab and alemtuzumab (Campath-1H) have been used in the management of AIN, granulocyte colony-stimulating factor remains the first-line therapy. In this article we provide a review of the pathogenesis of AIN, its clinical presentation, and the current treatment options.
Pericardial effusions are not uncommon in rheumatoid arthritis (RA); however, they are rarely the presenting symptom of the disease. We describe a 55-year-old female who presented to the emergency department with complaints of chest pain and dyspnea on exertion. Initial workup revealed a medium-sized pericardial effusion. The wide spectrum of etiologies, including infectious and non-infectious disease, was explored. Eventually, after ruling out an array of disease states, rheumatologic workup was positive for RA. The initial presentation in our case was atypical due to absence of small joint polyarthritis and other common symptoms of RA. In difficult cases, extensive workup including laboratory tests, electrocardiography, echocardiography and imaging studies can aid in narrowing the causes of pericardial effusion. This case demonstrates that pericardial effusion could be an early presenting feature of RA, even in the absence of more common symptoms, and should be considered in differential diagnosis.
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