A History of Coagulopathy in Liver Disease: Legends and Myths
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ABSTRACT:
SUBMITTER: Northup P
PROVIDER: S-EPMC7538927 | biostudies-literature | 2020 Oct
REPOSITORIES: biostudies-literature
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Project description:Bismuth subsalicylate (BSS) is the active ingredient in over-the-counter antacid and antidiarrheal medications. Coagulopathy in the setting of acetylsalicylic acid toxicity is well documented but not in setting of bismuth subsalicylate overuse. We present a case report of coagulopathy from BSS poisoning in a patient with underlying cirrhosis. The patient's high prothrombin time suggests inhibition of vitamin K-dependent coagulation factors. The patient had decreased factor V activity, which is responsible for converting prothrombin to thrombin. Patients with cirrhosis often have hypoprothrombinemia which may be exacerbated by salicylate-induced coagulopathy. Given the widespread use of BSS products, physicians should recognize coagulopathy as a possible manifestation of toxicity especially in patients with underlying liver disease.
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Project description:Based on the assumption that characterizing the history of a disease will help in improving practice while offering a clue to research, this article aims at reviewing the history of nonalcoholic fatty liver disease (NAFLD) in adults and children. To this end, we address the history of NAFLD histopathology, which begins in 1980 with Ludwig's seminal studies, although previous studies date back to the 19th century. Moreover, the principal milestones in the definition of genetic NAFLD are summarized. Next, a specific account is given of the evolution, over time, of our understanding of the association of NAFLD with metabolic syndrome, spanning from the outdated concept of "NAFLD as a manifestation of the Metabolic Syndrome", to the more appropriate consideration that NAFLD has, with metabolic syndrome, a mutual and bi-directional relationship. In addition, we also report on the evolution from first intuitions to more recent studies, supporting NAFLD as an independent risk factor for cardiovascular disease. This association probably has deep roots, going back to ancient Middle Eastern cultures, wherein the liver had a significance similar to that which the heart holds in contemporary society. Conversely, the notions that NAFLD is a forerunner of hepatocellular carcinoma and extra-hepatic cancers is definitely more modern. Interestingly, guidelines issued by hepatological societies have lagged behind the identification of NAFLD by decades. A comparative analysis of these documents defines both shared attitudes (e.g., ultrasonography and lifestyle changes as the first approaches) and diverging key points (e.g., the threshold of alcohol consumption, screening methods, optimal non-invasive assessment of liver fibrosis and drug treatment options). Finally, the principal historical steps in the general, cellular and molecular pathogenesis of NAFLD are reviewed. We conclude that an in-depth understanding of the history of the disease permits us to better comprehend the disease itself, as well as to anticipate the lines of development of future NAFLD research.
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Project description:Patients with liver disease frequently develop coagulopathy, and fresh frozen plasma is traditionally used for correction of coagulopathy to manage and prevent bleeding. Prothrombin complex concentrates (PCCs) offer an attractive alternative because they are more readily available and avoid large-volume transfusion. This retrospective, single-center study reviewed clinical use of PCC in patients with acute/chronic liver disease. A total of 105 patients with 194 episodes of PCC administration were reviewed. Data pertaining to indication, dosing, effectiveness, and safety were collected. The effect of PCC on coagulation was analyzed in patients for whom coagulation results were available 7 hours before and after PCC. Data on thromboembolic events and mortality within 4 weeks of PCC administration were captured. Most patients (77%) had chronic liver disease; the remainder had acute liver failure. Indications for PCC were preprocedure prophylaxis and treatment for active/recent bleeding in 48% and 52% of 194 treatment episodes, respectively. The median dose of PCC administered was 22 IU/kg (interquartile range, 16-29 IU/kg). Before PCC administration, 45% of patients had an international normalized ratio (INR) greater than 2.0, and 36% had fibrinogen levels of at least 1.5 g/L. PCC produced statistically significant reductions in prothrombin time and INR (coadministration with fibrinogen or cryoprecipitate: 3.1 versus 1.9; P < 0.001; no coadministration: 2.3 versus 1.8; P < 0.001). Three patients with multiple risk factors developed thrombotic events (hepatic artery thrombosis, incidental bilateral pulmonary embolism, nonocclusive portal vein thrombosis); there were no cardiovascular or cerebrovascular adverse events. Overall, 46 patients died of causes unrelated to PCC treatment. Conclusion: In patients with liver disease, PCC therapy was effective in improving coagulation test results without an excess of thrombotic events. Further assessment of PCC as hemostatic therapy in this setting is required.
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Project description:Patients with the severe form of coronavirus disease 2019 (COVID-19) have been frequently found to suffer from both arterial and venous thrombotic events due to the perpetuation of a hypercoagulable state. This phenomenon, termed COVID-19-associated coagulopathy, is now considered a major component of the pathophysiology of this novel infectious disease, leading to widespread thrombosis. While at first, the vascular insults may be limited to the pulmonary microvasculature, as the disease progresses, systemic involvement occurs, culminating in distant organ thrombosis and multiorgan dysfunction syndrome. In this review article, we discuss recent insights into the pathophysiologic mechanisms of COVID-19-associated coagulopathy and review the clinical, histopathologic, and laboratory evidence, which leads us to conclude that COVID-19 is both a pulmonary and vascular disorder.
| S-EPMC7604017 | biostudies-literature
Project description:BackgroundAlthough there is unequivocal evidence for progression of nonalcoholic steatohepatitis (NASH) to cirrhosis, there is uncertainty with regard to the progression to nonalcoholic fatty liver (NAFL) and NASH.AimsWe investigated the rate of progression to NASH and advanced fibrosis in patients with nonalcoholic fatty liver disease (NAFLD) and assessed the factors associated with such progression.MethodsHistological assessment was performed in 36 patients with NAFLD with paired liver biopsies (≥1 year apart; median, 3.8 years; range, 1-10.33 years). NASH Clinical Research Network (NASH CRN) criteria were used to assess NAFLD Activity Score (NAS).ResultsAt baseline, 26 (72%) patients had NAFL and 10 (28%) patients had NASH. At follow-up, 27% NAFL progressed to NASH (NAS score ≥5), and 50% of patients with NASH no longer met the criteria of NASH. Fibrosis progressed in 15 (42%), regressed in 9 (25%), and remained stable in 12 (33%) patients overall. Thirty-five percent of patients with NAFL had fibrosis progression. The incidence of type 2 diabetes mellitus (T2DM) was higher in patients with NASH versus NAFL (40% vs. 27%). Both at the time of baseline and follow-up, liver biopsies, composite models of noninvasive scores such as Fibrosis-4 (FIB-4) score and NAFLD fibrosis score, and ratio of aspartate aminotransferase (AST) to alanine aminotransferase (ALT) were all significantly higher in progressors than in nonprogressors.ConclusionsNAFLD is a dynamic liver disease with varying degrees of progression and regression. T2DM was strongly associated with fibrosis progression. Noninvasive fibrosis scores such as AST/ALT ratio, FIB-4 score, and NAFLD fibrosis score can identify those at risk of fibrosis progression.
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Project description:Conclusions about women's and girls' sexual history are made in some settings based on assumptions about the hymen, a small membranous tissue with no known biological function, which typically occupies a portion of the external vaginal opening in females. Clinicians, however, continue to refer to changes in the hymen to assess for a history of consensual or nonconsensual sexual intercourse. We reviewed published evidence to dispel commonly held myths about the hymen and its morphology, function, and use as evidence in cases of sexual violence.An examination of the hymen is not an accurate or reliable test of a previous history of sexual activity, including sexual assault. Clinicians tasked with performing forensic sexual assault examinations should avoid descriptions such as "intact hymen" or "broken hymen" in all cases, and describe specific findings using international standards and terminology of morphological features.We call on clinicians to consider the low predictive value of a hymen examination and to: 1) avoid relying solely on the status of the hymen in sexual assault examinations and reporting; 2) help raise awareness of this issue among their peers and counterparts in law enforcement and the judicial system; and 3) promote fact-based discussions about the limitations of hymenal examinations as part of clinical education for all specialties that address the sexual or reproductive health of women and girls.
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Project description:The long term outcome of drug related liver disease is unknown.To study the natural history of histologically proved drug induced hepatotoxicity.110 patients with liver biopsies coded either as drug induced liver disease or hepatitis/cholestasis of unknown aetiology were identified from hospital records 1978-1996. Review of case notes and histology identified 44 patients with definite drug induced hepatotoxicity. Forty surviving patients were invited to attend a follow up clinic. History, examination, full liver screen, and isotope and ultrasound liver scans were repeated in all patients. Repeat liver biopsies were offered to patients with abnormal liver tests.Presentation at index biopsy was jaundice in 24 patients, abnormal liver tests in 17, and hepatic failure in three. Antibiotics (n=13) and non-steroidal anti-inflammatory drugs (n=11) were the most common drugs implicated. Initial histology showed acute hepatitis in six, chronic hepatitis in 20, and cholestasis in 18. At 1-19 years (median 5 years) follow up, 13/33 (39%) patients had persistent significant abnormalities in their liver blood tests and/or scans. Three of the five repeat liver biopsies performed showed significant abnormalities. Factors predicting persistence or development of chronic liver disease were fibrosis and continued exposure to the drug.Drugs should be considered in the differential diagnosis of abnormal liver function and/or histology, as failure to withdraw the offending drug is associated with a high risk of persistent liver damage.
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Project description:BackgroundA significant proportion of patients with coronavirus disease 19 (COVID-19) suffer from excessive coagulation activation and coagulopathy which is associated with an increased risk of venous and arterial thromboembolism and adverse outcome. Our study investigates coagulation markers and the incidence of thromboembolic events in COVID-19 patients receiving recommended anticoagulation strategies.MethodsIn a retrospective single-center analysis at the University Hospital Zurich, Switzerland, we investigated 31 adult COVID-19 patients between April 6th and May 13th, 2020 and with at least one laboratory assessment of the coagulation markers prothrombin time/Quick, thrombin time, fibrinogen and D-dimers. For antithrombotic prophylaxis low-molecular-weight-heparin or unfractionated heparin was administered and two patients with heparin-induced thrombocytopenia received argatroban.ResultsWe analyzed 31 patients (68% male, mean age 60± SD 15 years). 22 (71%) of these required intensive care unit treatment, 5 (16%) were hospitalized in a ward, and 4 (13%) were outpatients. Mean fibrinogen levels were markedly elevated to 6.4± SD 1.8g/l, with a peak in the third week of the disease and no significant decrease over time. D-dimers were elevated to a mean value of 5.1±4.4mg/l with peak levels of 6.8±5.3mg/l in the fourth week of disease, and a subsequent decrease. Platelet count (308±136G/l) and PT/Quick (85±22%) showed no significant changes over time. Sensitivity analyses for patients treated in the ICU showed that D-dimer levels were higher in this group. The results of other sensitivity analyses were comparable. Thromboembolic events were diagnosed in 4 (13%) patients and 5 (16%) patients died during the observation period.ConclusionWe find coagulation alterations in COVID-19 patients indicating significant hypercoagulability. These alterations are visible despite antithrombotic treatment, and peak around week 3-4 of the disease.
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