Incidence and outcomes of heparin-induced thrombocytopenia in solid malignancy: an analysis of the National Inpatient Sample Database.

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.

An Unusual Case of Hemolytic Anemia Reversed with Liver Transplantation.

Spur cell anemia is acquired hemolytic anemia seen in patients with advanced liver disease, particularly in the setting of alcoholism, and warrants urgent liver transplant evaluation. We describe the case of a 58-year-old female with alcoholic cirrhosis who presented with worsening liver disease, profound anemia poorly responsive to blood transfusions, and multiple spur cells on the peripheral smear. She underwent a liver transplant, which led to the resolution of hematologic abnormalities and the need for transfusions. Our case highlights the significance of spur cell anemia as a harbinger of poor prognosis in patients with advanced liver disease and its reversibility with liver transplantation.

Polycythemia in a Patient With Atonic Bladder and Hydronephrosis.

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.

Endothelium injury and inflammatory state during abdominal aortic aneurysm surgery: scrutinizing the very early and minute injurious effects using endothelial markers - a pilot study.

INTRODUCTION: One 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 METHODS: The 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. RESULTS: We 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). CONCLUSIONS: Vascular 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.

Acute kidney injury after abdominal aortic aneurysm surgery: detailed assessment of early effects using novel markers.

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 gelatinase­associated lipocalin (NGAL) before, during (including intra­abdominal vein levels before and after removal of aortic clamp), and within 2 days after surgery.  Moreover, we assessed urinary NGAL, interleukin 18 (IL­18), and liver­type fatty acid­binding protein (L­FABP) 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 IL­18 at 2 hours (51.60 [12.12-527.16] vs. 25.99 [9.34-187.80] pg/ml at baseline, P <0.05); L­FABP 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.