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Metabolic Syndrome
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Metabolic syndrome involves inflammation and hypercoagulability, along with oxidative stress, endothelial dysfunction, and hyperinsulinemia. It is also referred to as MetSyn and Syndrome X. At least three of the following conditions must be present for metabolic syndrome to be diagnosed: Abdominal obesity, atherogenic dyslipidemia (decreased HDL cholesterol and increased triglycerides), hypertension, insulin resistance, increased plasminogen activator inhibitor, and a proinflammatory state. Fibrinogen increases in response to high levels of cytokines. It is an acute-phase reactant. Importantly, metabolic syndrome may predispose patients to even more serious complications, such as type 2 diabetes mellitus, heart attack, and stroke. The National Cholesterol Education Program Adult Treatment Panel III Report is summarized in Table 2.1.
Blood Coagulation and Fibrinolysis in TTP and HUS
Published in Pia Glas-Greenwalt, Fibrinolysis in Disease Molecular and Hemovascular Aspects of Fibrinolysis, 2019
Juan Monteagudo, Arturo Pereira
The routine laboratory tests of hemostasis are normal or near normal in most patients with TTP and HUS. In fact, marked prolongation of the prothrombin time (PT) or activated partial thromboplastin time (aPTT), abnormally decreased levels of fibrinogen, and/or the presence of fibrin/ogen split products should cast doubt upon the diagnosis of TTP/HUS. However, profound alterations of these laboratory tests can be found in patients with advanced disease and superimposed disseminated intravascular coagulation.11-14 In our series of 31 patients with TTP/HUS, the PT at diagnosis was abnormal (prothrombin ratio >1.2) in nine, but in no case was the ratio higher than 1.5. The fibrinogen concentration was 360 ±180 mg/dl (mean ± S.D.) with no value below 150 mg/dl. In fact, the fibrinogen levels were abnormally high in nearly half the patients, perhaps owing to its characteristics as an acute-phase reactant. The absence of consumptive coagulopathy was settled in studies with labeled fibrinogen, in which a normal turnover rate for this protein had been observed.15,16 The fibrin/ogen split products found in some patients with uncomplicated TTP/HUS have been ascribed to an enhanced release of plasminogen activator by the damaged endothelium rather than to an increased cleavage of fibrinogen by thrombin.8 Isolated prolongations of the aPTT have been reported in patients with thrombotic microangiopathy associated with the antiphospholipid syndrome.17
Coagulation Theory, Principles, and Concepts
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
The purpose of the blood-clotting enzymes is the conversion of fibrinogen to fibrin, the basis of clot formation. This event, which is so simple in concept, is one of the most fascinating processes in biology. Fibrinogen is a large, complex molecule that under normal circumstances is soluble. Minor proteolysis leads to the formation of a soluble product that polymerizes spontaneously to form an insoluble mesh composed of fibrils. The nature of this change is subtle. The basic structure is a fibrous molecule that shares many characteristics with other fibrous molecules. It has a molecular weight of 340,000 and consists of three pairs of nonidentical peptide chains denoted as α, β, and γ, which are covalently linked by a series of disulfide bonds. The structure has been well characterized. It is a long chain characterized by a “dumbbell shape,” with a central globular mass at its center. Thrombin cleaves two pairs of peptide chains releasing fibrinopeptides A and B yielding fibrin monomer (57,58).
LC-MS/MS: A sensitive and selective analytical technique to detect COVID-19 protein biomarkers in the early disease stage
Published in Expert Review of Proteomics, 2023
Siva Nageswara Rao Gajula, Ankita Sahebrao Khairnar, Pallavi Jock, Nikita Kumari, Kendre Pratima, Vijay Munjal, Pavan Kalan, Rajesh Sonti
In addition, elevated serum ferritin levels are observed due to the cytokine storm syndrome and secondary hemophagocytic lymphohistiocytosis (sHLH) [41]. Compared to mild COVID-19 infection, severely infected patients have lymphopenia with lower B cells, CD8 + T cells, CD4 + T cells, and natural killer (NK) cells, and a lower percentage of basophils, monocytes, and eosinophils [42]. It has been proposed that lymphopenia might be due to direct viral cytotoxic action associated with ACE-2 dependent or independent entry into the lymphocyte. The D-dimer level rises abnormally in the early stages of COVID-19 infection, and fibrinogen in the blood reflects severe inflammation. Elevated fibrinogen levels can also be caused by disseminated intravascular coagulation (DIC) in later stages [43].
Tigecycline-induced life-threatening coagulopathy in a patient with a Mycobacterium abscess: a case report and step-by-step diagnostic approach
Published in Acta Clinica Belgica, 2021
Sara Akalay, Thomas Vanassche, Paul De Munter
Some risk factors for developing this side effect have been mentioned. First, if we review the literature on tigecycline-associated coagulopathy it appears that all the reported cases had renal impairment [2–7]. In our case, the patient had a history of kidney transplantation 13 years ago with an actual estimated glomerular filtration rate (eGFR) of 30 ml/min/1.73 m2. Therefore, it has been suggested that renal insufficiency might be a risk factor for this side effect. However, two studies found no significant change in the tigecycline pharmacokinetics in patients with impaired renal function and tigecycline is not cleared by dialysis [11,12]. Therefore, current recommendations do not recommend adjusting the drug dose in patients with impaired renal function or in patients undergoing hemodialysis treatment. Possibly, the presence of a metabolite of tigecycline that accumulates in renal insufficiency might be causing the coagulopathy. Secondly, a retrospective analysis by Zhang et al. [9] found that patients with severe infections treated with tigecycline experienced a reduction in fibrinogen levels that was proportional to the dose. Their results suggest that dose increase and/or regimen prolongation may cause greater decreases in fibrinogen levels. There was no difference in fibrinogen decrease according to age.
Assessment of functional status by the Duke Activity Status Index in stable bronchiectasis
Published in Expert Review of Respiratory Medicine, 2021
Isabella Lomonaco, Amanda Souza Araújo, Mara Rúbia F. de Figueiredo, Marcelo A. Holanda, Eanes D. B. Pereira
The demographic data, history of childhood respiratory infections (pertussis, pneumonia, measles), investigation of infertility, past pulmonary tuberculosis, information of asthma, chronic obstructive pulmonary disease (COPD), connective tissue disorders, immune deficiencies, smoking status and sputum purulence were taken from each patient by the doctor of the institution.Others comorbidities, such as heart failure and GORD (gastro-esophageal reflux disease) were obtained in patients with a compatible medical history. Information about post-tuberculosis was based on patient-reported history and evaluation of lesions of old TB on chest CT. Blood samples were performed for differential count and serum levels of fibrinogen, a biomarker for which routine measurements are available in clinical practice. Masurement of IgG, IgA, IgM and total IgE were obtained in patients with a compatible medical history and extensive bilateral bronchiectasis.: