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Clinical Reasoning and Diagnostic Errors
Published in Paul Cerrato, John Halamka, Reinventing Clinical Decision Support, 2020
Suppose Mr. Jones, 59 years old, with a history of hypertension, stroke, and elevated lipid levels arrives in the ED complaining of sudden-onset intense sub-sternal chest pain that radiates to his left leg but does not affect his left arm or jaw.22 An experienced clinician would likely begin to think intuitively about this patient’s diagnosis. Mr. Jones’ symptoms suggest coronary ischemia, that is, a loss of blood to the heart tissue. Naturally, the attending physician will want to do a detailed physical examination to look for more clues to help refine the list of differential diagnoses, as well as appropriate lab tests. One finding that stands out in Mr. Jones’ lab readings is an elevated troponin I level. Troponin is a muscle protein that can escape from heart tissue that has been damaged by an MI.
Physiological, biochemical, and hormonal changes in rats exposed to bottled water left in a hot car and the freezer
Published in International Journal of Environmental Health Research, 2022
The measurement of total cholesterol (TC), triglyceride (TG), and high-density lipoprotein cholesterol (HDL-C) are performed on a COBAS INTEGRA 400 plus system analyzer, which is serviced by Roche Diagnostics (Deutschland). Low-density lipoprotein cholesterol (LDL-C) was calculated using the Friedewald equation (Friedewald et al. 1972), as shown in the following: LDL-C = TC − (HDL-C + total TG/5) mg/100 ml. Glucose (FBS), urea, and creatinine activity of serum were assayed by using a commercial kit (BIOLABO, France). The activity of alkaline phosphatase (ALP), alanine (ALT) and aspartate (AST) aminotransferase of serum was assayed by the commercial kits (NS, BIOTECH Co., Egypt). Serum cardiac troponin I (cTnI) levels were estimated using a Cobas-e411 analyzer (Roche Diagnostics, Mannheim, Germany). C-reactive protein (CRP) levels in blood serum were quantified by hsCRP ELISA kit (BioVendor Co., Czech Republic).
Blood biochemical parameters for assessment of COVID-19 in diabetic and non-diabetic subjects: a cross-sectional study
Published in International Journal of Environmental Health Research, 2022
Syeda Umme Fahmida Malik, Parveen Afroz Chowdhury, Al Hakim, Mohammad Shahidul Islam, Md Jahangir Alam, Abul Kalam Azad
Troponin-I represents an important biomarker of disease progression and prognosis in cardiac injury, and elevation of this marker has been hypothesized in COVID-19 (Shah et al. 2020). Results in the present study showed pretty higher but little bit insignificant level (p< 0.0555) of Troponin-I in patients with COVID-19 than in patients without COVID-19 (Table 2). The higher trend of the Troponin-I level indicates that it might be a predictor of clinical outcomes and its higher values would be associated with the severity of COVID-19. However, elevated level of Troponin-I was only in 22 (22.45%) of the COVID-19 patients [males 14 (63.64%), females 8 (36.36%)], particularly in those who died. This result indicates that the Troponin-I could be the predictor only for severity assessment of COVID-19 or poor prognosis. Higher levels of cardiac Troponin-I have been suggested in severe COVID-19 patients (Lippi et al. 2020).
Potential adverse cardiac remodelling in highly trained athletes: still unknown clinical significance
Published in European Journal of Sport Science, 2018
Luigi Gabrielli, Marta Sitges, Mario Chiong, Jorge Jalil, María Ocaranza, Silvana Llevaneras, Sebastian Herrera, Rodrigo Fernandez, Rodrigo Saavedra, Fernando Yañez, Luis Vergara, Alexis Diaz, Sergio Lavandero, Pablo Castro
The repetitive cycle of oxidative stress increase and heart muscle mechanical deformation during extreme exercise (Krip, Gledhill, Jamnik, & Warburton, 1997) might induce cardiomyocyte cell membrane damage that correlates with an elevation of multiple cardiac injury biomarkers such as myoglobin, cardiac troponin-I, creatine kinase MB and B-type natriuretic peptide (Fortescue et al., 2007). These biomarkers could stimulate immune cells recruitment – including lymphocytes, macrophages and mast cells – toward the damage area (Scherr et al., 2011). Then, immune cells would secrete pro-inflammatory cytokines, such as interleukin-6, which work as extracellular signals to induce fibroblast to myofibroblast differentiation with the subsequent secretion of procollagen (Benito et al., 2011). This phenomenon could be responsible for fibrosis deposited in patches in the myocardium and larges arteries (Figure 1(D)) (La Gerche et al., 2012). In fact, in rat models, prolonged strenuous exercise increased expression of transforming growth factor β-1 (TGF β-1) – the main mediator of fibroblast activation and cardiac fibrosis – in the right and left atria and right ventricle resulting in increased cardiac stiffness (Benito et al., 2011). Interestingly, this mechanism could be correlated with the elevation of galectin-3 plasma level and cardiac fibrosis in human (Hattasch et al., 2014).