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Background: Denosumab and abiraterone were approved by the United States Food and Drug Administration in 2011 for the treatment of metastatic castration-resistant prostate cancer. Neither denosumab nor abiraterone is known to cause rhabdomyolysis., Case Presentation: A 76-year-old Caucasian man with metastatic prostate cancer presented with non-oliguric severe acute kidney injury (AKI) 3 weeks after receiving simultaneous therapy with denosumab and abiraterone. The patient had been on statin therapy for more than 1 year with no recent dose adjustments. His physical exam was unremarkable. Blood work on admission revealed hyperkalemia, mild metabolic acidosis, hypocalcemia, and elevated creatine kinase (CK) at 44,476 IU/L. Kidney biopsy confirmed the diagnosis of rhabdomyolysis-induced AKI. The patient responded well to intravenous isotonic fluids and discontinuation of denosumab, abiraterone, and rosuvastatin, with normalization of CK and recovery of kidney function., Conclusion: We report the first case of biopsy-proven rhabdomyolysis-induced AKI in a cancer patient acutely exposed to denosumab and abiraterone. Whether one of these drugs individually, or the combination, was the bona fide culprit of muscle breakdown is unknown. Nonetheless, our report is hypothesis-generating for further investigations on the effect of these drugs on muscle cells.

A case is reported of a 50-year-old woman with a history of small-cell lung cancer admitted with pancreatic head lesions, discovered during investigation for obstructive jaundice. Endoscopic ultrasound assisted fine needle aspiration of the pancreatic mass was consistent with small cell carcinoma, presenting as an isolated metastasis from the previously diagnosed lung cancer. Endoscopic retrograde cholangiopancreatography (ERCP) showed extrinsic compression and a bile duct stricture, requiring sphincterotomy and stent insertion. This case highlights that acute pancreatitis and biliary obstruction can occur as a manifestation of small cell lung cancer metastasizing to the pancreas. EUS is a safe, low risk and rapid diagnostic tool in such cases, and ERCP with stenting offers a safe and effective treatment option.

Chronic kidney disease is associated with an increased left ventricular (LV) mass. Few data are available regarding the effect of renal transplantation on LV mass regression or the clinical factors associated with LV mass regression. Patients with ≥1 year of chronic kidney disease followed by successful renal transplantation were identified. All patients underwent echocardiography ≥6 months before transplantation with repeat echocardiography ≥1 year after transplantation. An experienced echocardiographer, who was unaware of the clinical data, performed all linear measurements in the parasternal long-axis projection, including systolic and diastolic LV chamber dimensions and LV wall thickness. The LV mass was calculated as follows: 0.8 × {1.04 [(LV internal dimension at end diastole + posterior wall thickness at end diastole + LV wall thickness at the cardiac base for the anteroseptum)(3) - (LV internal dimension at end diastole)(3)]} + 0.6 g. Candidate clinical variables for an association with LV mass regression were assembled, including age, gender, race, donor type, renal disease etiology, medications (insulin, oral hypoglycemics, antihypertensives, statins, and antirejection medications), and co-morbidities. Patients were separated into 2 groups according to presence and absence of LV mass regression. A total of 105 patients (mean age 54 years; 58 men) were included in the study with a mean follow-up of 1.7 years. Of the 105 patients, 57 had significant LV mass regression (mean difference -37.2 ± 31.3 g/m(2)) and 48 had no significant regression (mean difference 15.7 ± 17.1 g/m(2)). The extent of the LV mass before transplantation was the only predictor of mass regression after transplantation (odds ratio 1.50, 95% confidence interval 1.26 to 1.80). In conclusion, significant LV mass regression is present in most patients after renal transplantation. The extent of the LV mass before transplantation was the only clinical predictor of regression., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Background: Patients who undergo percutaneous endoscopic gastrostomy (PEG) placement are often on anticoagulation and/or antiplatelet therapy with a potential thromboembolic risk if these medications are discontinued. Data on the safety of peri-procedural use of these drugs is limited., Aims: To assess the risk and to identify any predictive factors for post-PEG bleeding, and to determine if clopidogrel increases the risk of bleeding following PEG., Methods: A retrospective chart audit was conducted from January 1, 2002 to June 30, 2011., Results: A total of 1,541 patients underwent PEG placement during this period. Gastrointestinal bleeding after PEG placement occurred in 51 cases (3.3%) and bleeding directly attributed to PEG was noted in six patients (0.4%). Multivariate logistic regression analysis of variables (age, gender, length of hospitalization, indication for PEG, antiplatelet or anticoagulant medications) showed that heparin infusion (P = 0.018) and length of hospitalization (P = 0.029) were statistically significant predictors of bleeding. The mean period for cessation and resumption of clopidogrel with PEG placement were 2.2 and 1.3 days, respectively., Conclusion: Although PEG is classified as a high-risk endoscopic procedure, bleeding with PEG placement was rare, even with use of anticoagulation and antiplatelet medications. In selected patients on heparin infusion undergoing PEG, delaying the procedure, alternative use of low-molecular-weight heparin or close monitoring and frequent assessments should be considered. Clopidogrel did not contribute to an increase in bleeding risk, despite being held for a much shorter peri-procedural period as recommended by expert consensus.

A 68-year-old Caucasian female with a past medical history of a deceased donor kidney transplant four months prior was admitted with a two-day history of anuria and acute kidney injury. A renal ultrasound demonstrated thrombus in the transplanted kidney's renal vein that extended into the left iliac vein as well as into the left femoral venous system. Catheter-guided tissue thrombolytics were infused directly into the clot. Within twelve hours of initiating thrombolytic infusion, there was brisk urine output. Interval venography demonstrated decreasing clot burden. At the time of discharge her creatinine was 0.78 mg/dL, similar to her baseline value prior to presentation. The patient was noted to have May-Thurner syndrome on intravascular ultrasound (IVUS). Angioplasty followed by stent placement was done. Unique to our case report was the timing of the presentation of renal vein thrombosis (four months after transplant) and the predisposing anatomy consistent with May-Thurner syndrome, which was diagnosed with IVUS and successfully treated with local thrombolytics.

A 78-year-old woman presented with progressive dyspnea and atrial flutter and was found to have a right atrial mass. Multimodality cardiac imaging was useful in further characterizing this mass, which was ultimately diagnosed after biopsy as a low-grade angiosarcoma., (Copyright (c) 2010 American Society of Echocardiography. Published by Mosby, Inc. All rights reserved.)