IntroductionOne of the most severe complications of repair surgery for abdominal aortic aneurysms (AAA) is acute kidney injury (AKI). Acute kidney injury is an inflammatory process whose pathogenesis involves endothelial cells (EC). The aim of this study was to assess the dynamics of endothelium injury markers measured during elective AAA surgery which might confirm the inflammatory character of AKI.Material and methodsThe study group consisted of 14 patients with AAA. We measured plasma soluble forms of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, P-selectin as well as the levels of von Willebrand factor (vWF) before, during (including intra-abdominal vein levels before and after aortic clamp removal) and within 2 days after surgery.ResultsWe have found a biphasic response of ICAM-1, VCAM-1 and P-selectin with an initial fall and subsequent rise. However, only VCAM-1 changes were significant compared to its baseline value. The maximum decrease of VCAM-1 was observed in the renal vein 5 min after aortic clamp removal (335.42 ±129.63 ng/ml vs. 488.90 ±169.80 ng/ml baseline value, p < 0.05), and the highest rise 48 h after aortic clamp removal (721.46 ±333.99 vs. baseline, p < 0.05).ConclusionsVascular cell adhesion molecule-1 turned out to be the most sensitive indicator of EC injury and inflammatory status after AAA surgery. During AAA surgery, soluble forms of P-selectin, ICAM-1 and VCAM-1 demonstrate a biphasic response with an initial fall and subsequent rise. These soluble forms could have a modulatory effect on the development of inflammation.
INTROduCTION One of the most severe complications of repair surgery for abdominal aortic aneurysms (AAA) is acute kidney injury (AKI). Even small rises in serum creatinine after surgery are associated with increased mortality. ObjECTIvEs The aim of the study was to assess the dynamics of AKI after elective AAA surgery using novel markers. PATIENTs ANd mEThOds The study group consisted of 14 patients with AAA. We measured serum neutrophil gelatinase-associated lipocalin (NGAL) before, during (including intra-abdominal vein levels before and after removal of aortic clamp), and within 2 days after surgery. Moreover, we assessed urinary NGAL, interleukin 18 (IL-18), and liver-type fatty acid-binding protein (L-FABP) before, during, and within 3 days after surgery. REsuLTs We observed a marked but nonsignificant increase in serum NGAL directly after clamp removal (75.21 ±55.83 vs. 46.37 ±21.60 ng/ml baseline value, P >0.05) and significantly elevated plasma NGAL at 2 hours (91.54 ±76.54 vs. baseline, P <0.05), 12 hours (100.78 ±44.92 vs. baseline, P <0.05) and 24 hours (89.46 ±94.18 vs. baseline, P <0.05) after clamp release. There was also significant elevation of urinary IL-18 at 2 hours (51.60 [12.12-527.16] vs. 25.99 [9.34-187.80] pg/ml at baseline, P <0.05); L-FABP at 2 hours (47.10 [5.40-500.00] vs. 5.50 (2.20-27.20) ng/ml at baseline, P <0.05) and 12 hours (39.00 [5.20-500.00] vs. baseline, P <0.05); NGAL at 12 hours (20.75 [5.00-176.10] vs. 5.85 [1.40-16.00] ng/ml at baseline, P <0.05) and 24 hours (13.95 [3.90-163.30] vs. baseline, P <0.05) after clamp release. CONCLusIONs Elective AAA surgery may induce AKI. Novel markers can facilitate early detection of AKI, thus allowing to start therapy at an appropriate time point.
Introduction Anticoagulant therapy in individuals with cirrhosis is challenging, as their risk of hemorrhage is significant due to concomitant alterations in primary hemostasis, secondary hemostasis and fibrinolysis. For many years, warfarin and heparin (including low molecular weight heparin) were the only treatment options for patients with thrombosis. Since 2010, novel, direct-acting oral anticoagulants (DOAC) that inhibit either thrombin (dabigatran) or factor Xa (e.g., rivaroxaban, apixaban, edoxaban, and betrixaban) are available. These direct-acting oral anticoagulants do not require laboratory monitoring and have minimal food and drug interactions, which makes them appealing to use for many patients. Unfortunately, there is inadequate data about efficacy and safety of these direct oral anticoagulants in cirrhotic patients as this group was commonly excluded from clinical trials evaluating these medications. In our study we aim to describe a large single institution experience with use of DOACs in patients with cirrhosis and explore clinical characteristics as potential predictors for bleeding and thrombosis. Methods: We conducted a retrospective cohort study of patients with cirrhosis who were seen in our institution between September 1, 2010 and June 30, 2017 and were treated with a DOAC utilizing a database search tool, called the Advanced Cohort Explorer that allows electronic records to be reviewed in a time efficient manner through text search or code search functionality. Only patients with cirrhosis diagnosed by histopathologic evaluation or with clinical presentation consistent with cirrhosis and confirmed by a gastroenterologist or by radiologic imaging (MRI, CT) were included in the study. Results: In our study, 106 individuals (male=72) met the inclusion criteria. Ninety three (88%) patients were treated with an anti-Xa inhibitor (rivaroxaban or apixaban), and remaining 13 (12%) with direct thrombin inhibitor (dabigatran). Median age at starting anticoagulant was 66 (range 24-89) years. The most common indication for anticoagulation was atrial fibrillation/flutter (54%), followed by pulmonary embolism/deep vein thrombosis (19%) and splanchnic vein thrombosis (15%). At the time of DOAC initiation, the median Charlson comorbidity index (CCI) was 7 (range 3-15); MELD score was 10 (range 6-24); and platelet count 150,000/ul (range 50,000-432,000). Thirty six (34%) patients had objectively diagnosed varices. Median follow up was 563 days (range: 7-2646). Bleeding requiring medical evaluation occurred in 32 (30.2%) patients. Major bleeding as defined by ISTH was experienced by 12 (11.3%) individuals. The most common source of bleeding was gastrointestinal tract (21.7%); other organs were less commonly affected (table 1). Hemorrhagic complication usually occurred early after starting anticoagulation (median 101 days; range 4-1356), and was the most common reason for discontinuation of anticoagulant treatment (14%), followed by completion of treatment (10%). On Cox proportional hazard modeling, rising BMI (HR: 1.032 per unit increase in BMI; p<0.05) and elevated bilirubin (HR: 1.223 per 1 mg/dL increase) were associated with increased risk of bleeding. Other clinical factors, including sex, type of anticoagulant used, platelet count, PT/INR, albumin, MELD score, varices, portal hypertension, concomitant aspirin use, and Charlson comorbidity index were not associated with bleeding risk. Thrombotic events while on DOAC affected 7 (6.7%) individuals, which included venous thrombosis in 4 (3.8%) and arterial thrombosis in 3 (2.9%) patients. No clinical factors were associated with increased risk of thrombosis. Conclusions: Our study is the largest series of patients with cirrhosis treated with DOACs. Bleeding complications with DOAC use in this population is high. Providers considering starting DOACs in patients with cirrhosis should consider the risk of bleeding in this population. Disclosures No relevant conflicts of interest to declare.
Kidneys influence the production of red blood cells by secreting most of the erythropoietin (EPO) in adults. Consequently, renal diseases often impact erythropoiesis and hemoglobin levels. Chronic kidney diseases lead to anemia due to EPO deficiency. However, erythrocytosis can occur in patients with cystic diseases of the kidney and renal artery stenosis due to upregulation of hypoxia-inducible factors (HIFs) and increased EPO production. Here, we present a patient with secondary polycythemia who was found to have atonic bladder and hydronephrosis. Resolution of hydronephrosis led to the reversal of erythrocytosis, highlighting the intricate regulation of red cell production.
Summary Heparin‐induced thrombocytopenia (HIT) is an immune‐mediated adverse reaction to heparin products characterized by thrombocytopenia with or without thrombosis. This study aimed to determine the incidence, morbidity, mortality and economic burden of HIT in solid‐malignancy‐related hospitalizations. We analyzed the National Inpatient Sample Database (NIS), the largest public database of hospital admissions in the United States, from January 2012 to September 2015. The primary outcome of the study was the incidence of HIT. Secondary outcomes included incidence of venous thrombosis (acute deep venous thrombosis and pulmonary embolism), arterial thrombosis (thrombotic stroke, myocardial infarctions and other arterial thromboembolism), mortality associated with HIT, length of stay, total hospital charges and disposition. During the study period, 7 437 049 hospitalizations had an associated diagnosis of solid malignancy. Approximately 0·08% (n = 6225) hospitalizations had a secondary diagnosis of HIT in this population. The standardized incidence of total thrombotic events was higher in the solid malignancy with HIT compared to the solid malignancy without HIT group (24·7% vs. 6·8%, P < 0·001). The standardized mortality rate was 4·8% in solid malignancy with HIT compared to 3·4% in the without HIT group (OR, 1·53; 95% CI, 1·25–1·89; P < 0·001). HIT in solid malignancy is a rare condition but associated with increased morbidity and mortality.
Introduction Hemophilia A and B are hereditary genetic disorders caused by clotting factor deficiency, factors VIII and IX respectively. In the era of effective therapy with factor concentrates life expectancy of patients with hemophilia has significantly increased. With increasing age, these patients face the same medical problems as other aging groups, especially atherosclerosis and cardiovascular disease. Medications which affect the clotting process, like aspirin, clopidogrel or warfarin are usually central to the treatment of these conditions. Obviously, antiplatelet therapy and anticoagulants could be potentially dangerous for patients with baseline increased risk of bleeding. This is why emphasis on prevention of cardiovascular disease is that much more important in this patient group. Data about prevalence of atherosclerotic cardiovascular risk factors in this group of patients are still suboptimal. The aim of our study was to assess prevalence of modifiable cardiovascular risk factors like hypertension, diabetes, obesity and smoking in patients with hemophilia A and B at out treatment center. Methods We performed retrospective chart review of patients followed at a single hemophilia treatment center in the United States. We included 59 patients with factor VIII or IX deficiency, age 30 and older, followed in clinic between 2005 and 2014. Patients with acquired hemophilia were excluded from the study. Hypertension was defined as blood pressure over 140/90 mmHg and/or the use of antihypertensive medications; diabetes mellitus as HbA1c at least 6.5% and/or use of medications for treatment of diabetes; overweight as body mass index between 25 kg/m2 and 29.9 kg/m2 and obesity as body mass index (BMI) of 30 kg/m2 or more. Patient was considered a smoker if he smoked tobacco during the month preceding last clinic visit. We chose to address the other significant risk factor namely hyperlipidemia, in more detail in a separate abstract as the newest 2013 ACC/AHA Guideline have proposed a stepwise approach to hyperlipidemia treatment. Results 34 (57.6%) patients had hypertension [95% CI 0.44-0.70], 6 (10.2%) patients had diabetes treated with oral medications only [95% CI 0.04-0.21] , 3 (5.1%) patients had diabetes treated with insulin [95% CI 0.01-0.14], 20 (33.9%) patients were overweight [95% CI 0.22-0.47], 24 (40.7%) patients had obesity [95% CI 0.28-0.54], 23 (39%) patients were smokers [95% CI 0.27-0.53]. 3 (5.1%) patients experienced myocardial infarction and 1 (1.7%) of them died due to intracerebral hemorrhage during treatment with antiplatelet therapy. Conclusions Cardiovascular disease is the leading cause of death in developed countries. With increasing life expectancy of patients with hemophilia greater emphasis is needed on modifiable risk factors for prevention as treatment of cardiovascular events carries greater risk of adverse outcomes due to bleeding in these patients. Our study indicated that the prevalence of cardiovascular risk factors in hemophilia patients is high. There are only few existing publications about prevalence of hypertension, diabetes, obesity and smoking in hemophilia patients. This is an area that warrants more systematic study and a cooperative effort to generate such data at a national and even international level that in turn would assist with strategic planning and mitigation. Disclosures No relevant conflicts of interest to declare.
Background: Acute chest syndrome (ACS) frequently complicates sickle cell disease (SCD) and is a leading cause of hospitalization and mortality. Many factors have been implicated in ACS, including infections, thrombosis, fat and pulmonary emboli. However, a clear etiology is not defined in 50% of the cases and ACS is considered a clinical endpoint for different pathogenic processes (Vichinsky et al 2000). The non-specific nature of ACS makes diagnostic tests challenging, and there are no serum tests clinical used to aid diagnosis. Procalcitonin (PCT) is a prohormone of calcitonin and serum PCT rises within hours of an inflammatory stimulus. PCT has clinical utility as a marker of severe systemic inflammation, infection, and sepsis (Becker et al. 2008). Few studies have evaluated PCT as a biomarker for ACS in patients presenting with vaso-occlusive crises (VOC). Two studies have reported no difference in PCT (Biemond et al. 2018 and Stankovic et al 2011), while one study reported higher PCT between ACS and VOC (Patel et al 2014). Methods: We retrospectively reviewed 106 patients with SCD who presented to the emergency department with fever and painful crises during 2015-2019. The patients were divided into two categories based on discharge diagnoses - patients with VOC only (n=88) and patients with ACS (n=18). Inclusion criteria for both groups were patients with SCD, 17 years and older and PCT measurement on presentation. Exclusion criteria were defined as patients who had received empiric antibiotics prior to PCT testing. Data collected on presentation included genotype, age, gender, complete blood count, PCT, creatinine, total bilirubin and hydroxyurea use. Length of stay was recorded. Data was analyzed between the two groups using descriptive statistics and accounting for unequal variances, withp-value set at 0.05 for significance. Results: Demographics and clinical characteristics are summarized in Table 1 (Figure). The sample included primarily adult males (77%), with about two-thirds on hydroxyurea. Genotype HbSS (73.6%) was most prevalent followed by HbSC (22.6%) and HbSβ (3.8%). The ACS group had a higher percentage of HbSS, lower use of hydroxyurea and higher mean bilirubin. Mean PCT for the ACS group was 0.52 ng/mL (range, 0.05-2.04), compared to 0.31 ng/mL (range, 0.02-6.82) in the VOC group; withp=0.084. ROC analysis showed a PCT>0.5ng/mL had 39% sensitivity and 85% specificity for ACS in this sample. Conclusion: In this sample, PCT on presentation was higher in those with ACS compared to VOC, but this difference did not achieve statistical significance. Further study in a larger population would be useful to evaluate this finding. Disclosures No relevant conflicts of interest to declare.
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