Aim:Alzheimer's disease (AD) and other forms of dementia create a noncurable disease population in world's societies. To develop a blood-based biomarker is important so that the remedial or disease-altering therapeutic intervention for AD patients would be available at the early stage.Materials & methods:TDP-43 levels were analyzed in postmortem brain tissue and platelets of AD and control subjects.Results:We observed an increased TDP-43 (<60%) in postmortem AD brain regions and similar trends were also observed in patient's platelets.Conclusion:Platelet TDP-43 could be used as a surrogate biomarker that is measurable, reproducible and sensitive for screening the patients with some early clinical signs of AD and can be used to monitor disease prognosis.
Aim: Alzheimer’s disease (AD) and other forms of dementia create a non-curable disease population in World’s societies. To develop a blood-based biomarker is important so that the remedial or disease-altering therapeutic intervention for AD patients would be available at the early stage. Materials & Methods: TDP-43 levels were analyzed in post-mortem brain tissue and platelets of AD and control subjects. Results: We observed an increased TDP-43 (<60%) in post-mortem AD brain regions and similar trends were also observed in patient’s platelets. Conclusion: Platelet TDP-43 could be used as a surrogate biomarker that is measurable, reproducible, and sensitive for screening the patients with some early clinical signs of AD and can be used to monitor disease prognosis.Lay abstractIn this study, we explore to identify an Alzheimer’s disease-selective phospho-specific antibody that recognizes the diseased form of TDP-43 protein in patient’s blood-derived platelets. Our results suggest that selective anti-phosphorylated TDP-43 antibody discriminates Alzheimer’s disease from non-demented controls and patients with amyotrophic lateral sclerosis. Therefore, platelet screening with a selective antibody could potentially be a useful tool for diagnostic purposes for Alzheimer’s disease.
Vaping involves the use of a device to deliver aerosolized nicotine and tetrahydrocannabinol (THC) oils to the lungs. Vaping continues to increase in popularity; however, because it is a novel drug delivery system there is little evidence regarding its safety and long-term consequences. Here, we present a 22-year-old Caucasian male who was admitted with acute hypoxic respiratory failure and massive hemoptysis. Contrasted computed tomography of the chest demonstrated ground glass opacities throughout all lung fields and bilateral pulmonary emboli. Bronchoalveolar lavage revealed increased red blood cell counts in serial aliquots, consistent with the diagnosis of diffuse alveolar hemorrhage (DAH). An extensive workup did not reveal an etiology for the DAH. However, further history was obtained, and the patient divulged daily vaping of THC. E-cigarette, or vaping, product use associated lung injury (EVALI) consists of a myriad of different lung injury patterns. Our case illustrates an uncommon presentation of EVALI with DAH and multiple pulmonary emboli.
INTRODUCTION: E-cigarette or vaping product use-associated lung injury (EVALI) encompass a host of pulmonary complications including diffuse alveolar hemorrhage, lipoid pneumonia, hypersensitivity pneumonitis, and rarely, acute eosinophilic pneumonia (AEP) [1]. AEP presents as an acute febrile illness with hypoxemia, diffuse pulmonary infiltrates, and eosinophilia on bronchoalveolar lavage (BAL) without evidence of prior infection or atopic illness [2]. Presented is a young adult patient with a history of continuous vaping and extended exposure to kitchen smoke who developed acute hypoxemic respiratory failure later diagnosed as AEP.CASE PRESENTATION: An 18-year-old male with no significant past medical history presented to the emergency department with acute onset malaise, fever, non-productive cough, and shortness of breath over 12 hours. Social history revealed 3-week workplace exposure to smoke as a barbeque cook and a 5-year history of daily vaping with reported cessation 3 weeks prior. Vitals were notable for hypoxemia which was corrected with administration of 8L of oxygen via nasal cannula. Quickly after admission, he had worsening respiratory status: tachypnea, increased oxygen requirement, use of accessory muscles, and bilaterally diminished breath sounds. He was transferred to the medical intensive care unit for emergent endotracheal intubation. Laboratory testing revealed a neutrophil predominant leukocytosis of 19.3x109/L. COVID-19, rapid influenza A and B, and urine antigens for streptococcus and legionella were negative as were autoimmune serologies. A computed tomography (CT) scan of the chest revealed diffuse bilateral consolidative opacities [Figure 1] with worsening over the next 24 hours [Figure 2]. Further investigation was undertaken with bronchoscopy. A BAL was obtained, and cell count and cultures were sent. BAL cell count was remarkable for 33% eosinophilia. The diagnosis of AEP was made, and the patient was started on systemic glucocorticoids, with significant improvement within 24 hours. DISCUSSION:The modified Philit criteria is used to make the diagnosis of AEP, which the patient satisfied [3]. Although a 5year vaping history was present, no previous significant respiratory symptoms were reported. Prior studies have demonstrated a relationship between workplace smoke exposure and AEP [3]. Based on the modified Philit criteria, we suspect that the patient had acute respiratory failure from AEP as a result of chronic EVALI acutely exacerbated by workplace smoke exposure. The treatment of AEP treatment involves high-dose intravenous glucocorticoids followed by a prolonged oral steroid taper. CONCLUSIONS:Obtaining occupation history as well as smoke exposure is as important as obtaining vaping history in an otherwise healthy young patient who presents with acute hypoxemic respiratory failure with bilateral diffuse opacities on imaging.
Pneumocystis pneumonia (PCP) is an opportunistic fungal infection associated with human immunodeficiency virus (HIV) infection as an acquired immunodeficiency syndrome (AIDS)-defining illness. The PCP incidence in patients with HIV has declined over the last few decades due to effective antiretroviral therapy and prophylaxis. The PCP incidence in HIV-negative patients has increased due to the increasing use of a wide array of immunosuppressants in cancer and autoimmune disease. PCP clinical course varies from patients with HIV in their clinical features, the severity of clinical presentation, and mortality. PCP in autoimmune diseases is rare, especially in rheumatoid arthritis (RA) in the United States of America (USA). Here, we describe an elderly Caucasian female with rheumatoid arthritis and left lung mucinous adenocarcinoma status post recent resection with no chemotherapy on a low dose of methotrexate (MTX) and prednisone presenting with acute hypoxic respiratory failure due to PCP from absolute lymphopenia.
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