Post-Coronavirus disease 2019 (COVID-19) development of polymyositis is rare, with very few cases documented in the literature. In patients developing vague symptoms after recovery from COVID-19, it is important to investigate all avenues, including the possibility of polymyositis. Polymyositis is typically characterized as symmetrical muscle weakness and histological, electrical, and chemical evidence of muscle injury. Patients identified can be treated with immunosuppressants to return some quality of life and prevent disease progression. In this report, we describe a 58-year-old Caucasian male who presented with symptoms of weakness, myalgias, and arthralgias, six months after recovering from flu-like symptoms of COVID-19. The patient was tested for other autoimmune etiologies and myopathies without positive results. He was treated with prednisone and reported moderate improvement in symptoms. Unfortunately, the patient declined a muscle biopsy or electromyographic testing. According to the criteria for polymyositis set by the Myositis Association and the response to therapy, the patient's symptoms pointed to a likely diagnosis of post-COVID-19 polymyositis.
Follicular dendritic cells help advance B-Cells in becoming memory B-Cells or antibody-producing plasma cells in the light zone, or undergo additional affinity maturation in the dark zone. Follicular dendritic cell sarcoma (FDCS) is an extremely rare soft tissue malignancy derived from follicular dendritic cells. Autoimmune disease increases the risks for the development of hematological malignancies. To the best of our knowledge, there are few cases of FDCS development in the setting of underlying Sjogren's syndrome (SS). Therefore, in this report, we present a novel case of FDCS associated with new-onset SS. In SS, the follicular dendritic cells are organized within germinal centers within the glands it infiltrates and is involved in B-Cell development. Because FDCS is derived from follicular dendritic cells, our report postulates that the unregulated follicular dendritic cell proliferation that may occur in SS could increase the risk for FDCS. Due to this possible connection observed in our patient, we highlight FDCS as a differential diagnosis when considering soft tissue cancers. We urge additional research to outline and explore the possible pathologic link between SS and FDCS.
Herpes simplex encephalitis is a rare disease presentation that is usually characterized by its temporal involvement and positive cerebrospinal fluid (CSF) polymerase chain reaction (PCR) for the herpes simplex virus (HSV). HSV PCR has a sensitivity of 96% and specificity of 99%. Even when the test is negative, if clinical suspicion is high, acyclovir therapy should be continued with a repeated PCR within a week. In this case, we report a 75-year-old female patient who presented with signs of hypertensive emergency with rapid deterioration to seizure-like activity on electroencephalogram (EEG) and signs of temporal encephalitis on magnetic resonance imaging (MRI). The patient did not respond to the initial regimen of antibiotics but did show significant clinical response to acyclovir though she had a negative CSF PCR for HSV ten days after the start of her neurological symptoms. In this case, we argue that alternative methods of diagnosis should be considered in cases of acute encephalitis. Our patient had negative PCR but her computerized tomography (CT), EEG, and MRI results pointed to temporal encephalitis caused by HSV.
Hyperparathyroidism (HPT) causes an elevation of parathyroid hormone (PTH). This can result in elevated calcium levels, which can cause bone, kidney, muscle, gastrointestinal, and neuropsychiatric symptoms, including psychosis. Our report presents a unique case of an elderly woman who presented to the emergency department in an unconscious state with a working diagnosis of metabolic encephalopathy secondary to sepsis and urinary tract infection. Despite fluids and antibiotic treatment, the patient showed hallucinations. The acuteness of her psychotic episodes prompted the medical team to further investigate the cause of her hallucinations. Additional labs revealed HPT, which she had never been diagnosed with prior to the hospital admission. Our patient's novel clinical presentation revealed elevated PTH and normal calcium levels as the cause of her psychosis. We determined that the normal calcium levels were due to the patient's calcium loss secondary to acute kidney injury. Cinacalcet administration showed resolution of the patients' hallucinations, highlighting the importance of PTH screening even in normocalcemic patients. In this report, we present a rare clinical presentation of acute psychosis in the setting of undiagnosed normocalcemic HPT.
Breakthrough hemolysis (BTH) is the return of hemolytic disease resulting in an overall increase in complement activation in a patient being treated for paroxysmal nocturnal hemoglobinuria (PNH) with complement inhibitors (CI). BTH after COVID-19 vaccination has only been reported in PNH patients treated with the traditional C5 CI eculizumab and ravulizumab. We report on a new association of BTH in a newly COVID-19 vaccinated, previously stable PNH patient treated with pegcetacoplan, a C3 CI.The patient is a 29-year-old female diagnosed with PNH in 2017 and was started on eculizumab but was switched to pegcetacoplan in 2021 after continuing to exhibit symptomatic hemolysis. Subsequently, the patient returned to PNH remission serologically and symptomatically until her first COVID-19 vaccination. Since then, her lactate dehydrogenase (LDH) and hemoglobin counts have not fully returned to previous baseline levels, with significant exacerbations after her second COVID-19 vaccine and de novo COVID-19 infection. As of May 2022, the patient requires packed red blood cell transfusions every two to three months and has undergone a bone marrow transplant evaluation. This case study suggests that the administration of the upstream C3 CI, pegcetacoplan, is associated with active extravascular hemolysis in the setting of COVID-19 vaccinations and active COVID-19 infection. The pathophysiology of this hemolysis is unclear as hemolysis could be related to the underlying complement factor deficiency or amplification of complement factors causing extravascular hemolysis. There are conflicting reports in the literature regarding the mechanism by which COVID-19 vaccination and infection cause BTH in PNH patients, regardless of the choice of CI treatment. Bringing awareness to this case of BTH secondary to COVID-19 in a PNH patient treated with pegcetacoplan can further warrant the investigation of the role of COVID-19 in complement disruption and its role in BTH.
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