Tumor lysis syndrome (TLS) is a potentially deadly complication of tumors or their treatment. This syndrome consists of a constellation of laboratory findings such as hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia, known as laboratory TLS. When clinical complications such as seizures, acute renal failure, and cardiac dysrhythmias occur in patients with laboratory TLS, the syndrome is called clinical TLS. TLS is especially common in patients with hematological malignancies with rapid cellular turnover rates such as acute lymphocytic leukemia and Burkitt lymphoma, but is very rare in patients with solid tumors. Nevertheless, there are multiple reports in the literature on the occurrence of TLS in patients with solid tumors. In this review article, we summarize the current data on the occurrence of TLS in patients with solid tumors. We propose an algorithm of risk stratification and prevention of TLS in patients with solid cancers.

Purpose We examined the frequency, tumor characteristics, and prognostic impact of HER2 protein expression and gene amplification in patients with curatively resected esophageal adenocarcinoma (EAC). Experimental Design HER2 expression was analyzed by immunohistochemistry (IHC) in surgical EAC specimens (n=713). Gene amplification was examined by fluorescence in situ hybridization (FISH) in a large subset (n=344). Most tumors were T3–4 (66%) or node-positive (72%); 95% were located in the esophagus or gastroesophageal junction. No patient received neoadjuvant therapy. Cox models were used. Results Overall, 17% of EACs were HER2-positive (ie, IHC3+ or IHC2+ with amplification), with strong agreement between HER2 amplification (HER2/CEP17 ratio ≥2) and expression (κ=.83). HER2-positivity was significantly associated with lower tumor grade, less invasiveness, fewer malignant nodes, and the presence of adjacent Barrett’s esophagus (BE). EACs with BE had higher odds of HER2-positivity compared to EACs without BE, independent of pathologic features (odds ratio 1.8 [95% confidence interval (CI) 1.1–2.8], p=.014). Among all cases, HER2-positivity was significantly associated with disease-specific survival (DSS) in a manner that differed by the presence or absence of BE (p for interaction=.0047). In EACs with BE, HER2-positivity was significantly associated with improved DSS (hazard ratio 0.54 [95% CI 0.35–0.84], p=.0065) and overall survival (p=.0022) independent of pathologic features, but was not prognostic among EACs without BE. Conclusions HER2-positivity was demonstrated in 17% of resected EACs and associated with reduced tumor aggressiveness. EACs with BE had nearly twice the odds of being HER2-positive and, within this subgroup, HER2-positivity was independently associated with improved survival.

Propofol infusion syndrome is a rare but extremely dangerous complication of propofol administration. Certain risk factors for the development of propofol infusion syndrome are described, such as appropriate propofol doses and durations of administration, carbohydrate depletion, severe illness, and concomitant administration of catecholamines and glucocorticosteroids. The pathophysiology of this condition includes impairment of mitochondrial beta-oxidation of fatty acids, disruption of the electron transport chain, and blockage of beta-adrenoreceptors and cardiac calcium channels. The disease commonly presents as an otherwise unexplained high anion gap metabolic acidosis, rhabdomyolysis, hyperkalemia, acute kidney injury, elevated liver enzymes, and cardiac dysfunction. Management of overt propofol infusion syndrome requires immediate discontinuation of propofol infusion and supportive management, including hemodialysis, hemodynamic support, and extracorporeal membrane oxygenation in refractory cases. However, we must emphasize that given the high mortality of propofol infusion syndrome, the best management is prevention. Clinicians should consider alternative sedative regimes to prolonged propofol infusions and remain within recommended maximal dose limits.

Purpose Given that smoking affects body mass index (BMI) and survival, stratification by smoking status may be required to determine the true prognostic impact of BMI. Although obesity increases risk for developing esophageal adenocarcinoma (EAC), the prognostic influence of obesity and its potential modification by smoking status is unknown in this disease. Patients and Methods All patients (N = 778) underwent potentially curative esophagectomy. BMI was calculated using measured height and weight at surgery and categorized as obese (≥ 30 kg/m2), overweight (25 to 29.9 kg/m2), or normal (18.5 to 24.9 kg/m2). Cigarette smoking was categorized as never or ever. The association of BMI with disease-specific survival (DSS), disease-free survival (DFS), and overall survival (OS) was determined by Cox regression. Results Excess BMI was significantly associated with DSS in a manner that differed substantially by smoking status (P for interaction = .023). Among never smokers, obesity was significantly associated with adverse DSS (hazard ratio [HR] = 2.11; 95% CI, 1.31 to 3.43; P = .002), DFS (HR = 2.03; 95% CI, 1.30 to 3.18; P = .002), and OS (HR = 1.97; 95% CI, 1.24 to 3.14; P = .004), as compared with normal weight, after adjusting for covariates. By contrast, among ever smokers, obesity was not prognostic, and overweight status was significantly associated with favorable survival in univariate, but not multivariate, analysis. Conclusion Obesity among never smokers was independently associated with two-fold worsening of DSS, DFS, and OS after surgery for EAC, after adjusting for known prognostic factors. These data, in one of the largest reported resected EAC cohorts, are the first to show an adverse prognostic impact of obesity in EAC.

OBJECTIVE: To identify and describe clinicopathologic prognostic factors in patients with esophageal adenocarcinoma who underwent surgical resection with curative intent. PATIENTS AND METHODS:The study cohort consisted of 796 patients with adenocarcinoma of the esophagus, gastroesophageal junction, or gastric cardia who underwent complete tumor resection at Mayo Clinic from January 1, 1980, to December 31, 1997. We reviewed individual patient medical records and abstracted demographic, pathologic, perioperative, and cancer outcome data. Median follow-up for vital status and disease recurrence was 12.8 and 5.8 years, respectively. RESULTS:Univariate analysis revealed the following factors to be statistically associated with worse 5-year disease-specific survival: higher N and T status, higher tumor grade, age older than 76 years, and the presence of extracapsular lymph node extension and signet ring cells. The following factors remained significantly linked with worse 5-year disease-specific survival on multivariate analysis: higher N and T status, grade, and age and the absence of preoperative chemotherapy or radiotherapy. Anatomic location of tumor was not associated with differential prognosis. Lymph node metastases were found in 25 (27%) of 93 T1b tumors, 397 (85%) of 468 T3 tumors, and 22 (67%) of 33 T4a tumors. Diseasespecific survival was better in T3-4N0 than in T1bN1-3 carcinomas (hazard ratio, 0.50; 95% confidence interval, 0.28-0.89, adjusted for grade and age; P=.02). CONCLUSION:Our results confirm the importance of T and N status and tumor grade and suggest that age may affect prognosis. In addition, we show that a significant proportion of superficial esophageal adenocarcinomas exhibit regional metastases and have worse prognosis than more invasive nonmetastatic tumors. Proc. 2010;85(12):1080-1089 AIC = Akaike information criterion; AJCC = American Joint Committee on Cancer; CI = confidence interval; DFS = disease-free survival; DSS = disease-specific survival; EAC = esophageal adenocarcinoma; ESCC = esophageal squamous cell carcinoma; GEJ = gastroesophageal junction; HR = hazard ratio; LN = lymph node; OS = overall survival Mayo Clin © 2010 Mayo Foundation for Medical Education and ResearchT he increase in the incidence of adenocarcinoma of the esophagus, gastroesophageal junction (GEJ), and gastric cardia in recent decades has been among the highest for any cancer in Western countries. 1 This triad of adenocarcinomas (designated esophageal adenocarcinoma [EAC] in this article) has grown more than 400% in incidence in the past 40 years, paralleling the increase in obesity and gastroesophageal reflux. 2 It is lethal in most cases, yet its degree of aggressiveness also varies from person to person. 3 These statistics signal a need for a better understanding of not only EAC etiology, but its progression and long-term clinical behavior. Understanding and exploiting the heterogeneity in prognosis are critical to improving outcomes in EAC patients and require the study of large cohorts with well-descri...