Lupus-Induced Accelerated Heart Failure in a Young African American Female: Cardiovascular and Systemic Complications of Noncompliance to Maintenance Therapy and the Social Determinants of Cardiovascular Disease.

Systemic lupus erythematosus (SLE) is an autoimmune inflammatory disorder characterized by dysregulations of the immune system with intermittent and remitting symptoms. SLE affects multiple organs and systems, including the cardiovascular system. This condition is associated with an increased risk of cardiovascular disease, particularly in younger patients. Our case report describes a patient who rapidly developed structural, functional, and electrophysiological cardiac abnormalities due to lupus-induced cardiomyopathy. The accelerating cardiac events were the result of medication noncompliance. Myocarditis and other potentially fatal cardiac complications associated with SLE have been the subject of numerous studies. This presentation appears to be the first to emphasize the rarity of lupus-induced cardiomyopathy, the importance of treatment adherence, the adverse cardiac effects of targeted therapeutic interventions, and the influence of social determinants of cardiovascular health on a patient's prognosis.

Molecular Mimicry: An Uncommon Occurrence of Vitamin B12 Deficiency Imitating Thrombotic Thrombocytopenic Purpura in an African American Male.

Thrombotic thrombocytopenic purpura (TTP) and vitamin B12 deficiency can share similar symptoms but require different treatment approaches. TTP is a blood disorder with a high mortality rate requiring immediate plasmapheresis treatment. On the other hand, vitamin B12 deficiency usually presents with anemia, low platelet counts, jaundice, and signs of disrupted red blood cell breakdown, resembling a condition called microangiopathic hemolytic anemia. Vitamin B12 deficiency can sometimes lead to or mimic pseudo-thrombotic microangiopathy (pseudo-TMA), a rare occurrence. Pseudo-TMA manifests as microangiopathic hemolytic anemia and thrombocytopenia and is characterized by schistocytes in a peripheral blood smear. Differentiating TTP cases from pseudo-TMA cases is essential and should be done promptly. The etiology, treatments, and prognosis of these two conditions differ and can be fatal if not identified and managed. We present a case that emphasizes the need for familiarity with TTP-like conditions, the use of ADAMTS13 as a diagnostic tool, prompt and accurate treatment decision-making, the complexities of therapeutic plasma exchange, and the importance of excluding an enzyme inhibitor or mutator as the cause of TTP or TTP-like cases. Lack of knowledge can lead to erroneous diagnoses, resulting in unnecessary treatments or delayed life-saving interventions.