Clinical pathology abstracts editor: Deborah Sesok-Pizzini, MD, MBA, associate professor, Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, and medical director, Blood Bank and Transfusion Medicine, Children’s Hospital of Philadelphia.
Predictive factors for blood transfusion in living donor pediatric liver transplantation
Patients undergoing liver transplantation, in particular pediatric liver transplantation, may receive massive transfusion. However, technical surgical improvements over the years have made it possible for many patients undergoing pediatric living donor liver transplantation (LDLT) to avoid transfusion. Yet a few patients will undergo massive blood transfusion to replace the loss of more than one estimated circulating blood volume, which is associated with increased perioperative morbidity and mortality. The authors conducted a study to identify the preoperative risk factors that can predict the requirement for massive transfusion in this population. They reviewed retrospectively the anesthesia charts of pediatric patients undergoing LDLT. The study involved 198 pediatric patients, 13 of whom met the definition for massive transfusion. The other patients were grouped accordingly with patients who did not require massive blood transfusion. The two groups were then compared. The authors concluded that the patients requiring massive transfusion were younger and had a smaller body size and prolonged international normalized ratio (INR). The only predictive factor for bleeding was the INR. Furthermore, each prolongation of 0.1 unit of INR elevated the risk of requiring a massive blood transfusion by 1.083-fold. The authors concluded that INR was the only predictive factor for massive transfusion during LDLT. They recommend increasing the ratio of fresh frozen plasma transfusion in patients with prolonged INR before or during pediatric LDLT.
Huang C-J, Kwok-Wai C, Chen C-L, et al. Predictive factors for pediatric patients requiring massive blood transfusion during living donor liver transplantation. Ann Transplant. 2013;18:443–447.
Correspondence: Chih-Hsien Wang at [email protected]
Role of the physician in laboratory medicine: a European perspective
The development of physicians who specialize in laboratory medicine evolved over the years as advances in diagnostics led to physicians acquiring distinct expertise in various subject areas. Now, however, with advances in medical technology, including the development of automated cross-disciplinary, single-platform analyzers, the boundaries between traditional specialties have blurred. The Union of European Medical Specialists commissioned a paper to examine the changing role of laboratory-based physicians by focusing on the added value laboratory physicians bring to improving the clinical outcomes of patients undergoing laboratory tests. The authors outlined the responsibilities of a laboratory-based physician, which include performing tests and determining the predictive value of laboratory tests and the probability of a test result influencing health status, resulting in a change in disease management. They also defined laboratory-related patient outcomes. The authors presented eight case histories and reviewed lessons from the cases, which showed laboratory physicians’ contributions to patient care. They concluded from these case histories that interpretation of laboratory results by an expert in laboratory medicine significantly influences patient outcomes. The authors also maintained that the need for expert advice regarding test selection and interpretation of results will increase as the complexity of clinical medicine and need for cost containment grows.
Misbah SA, Kokkinou V, Jeffery K, et al. The role of the physician in laboratory medicine: a European perspective. J Clin Pathol. 2013; 66:432–437.
Correspondence: Dr. Siraj A. Misbah at [email protected]
Cytokine genetic variations and fatigue among patients with breast cancer
Fatigue is a common adverse effect of cancer treatment and may last several years after therapy. The risk factors for fatigue have not been determined, though a number of studies have associated fatigue with circulating markers of inflammation, before and after treatment, in cancer patients. Given this association, it is possible that genetic factors that influence cytokine gene expression are plausible risk factors for cancer-related fatigue. These single nucleotide polymorphisms (SNPs) were identified in the promoter regions of several genes that encode proinflammatory cytokines. The authors conducted a study in which they examined, in women who recently completed treatment for early stage breast cancer, whether regulatory polymorphisms in three key proinflammatory cytokine genes were associated. The study also investigated the association between SNPs and other behavioral symptoms, including depression, memory complaints, and sleep disturbances. The authors studied 171 women with early stage breast cancer who completed a questionnaire to assess fatigue and other behavioral problems. The subjects then provided blood for genotyping within three months of primary treatment. The blood was assayed for SNPs in the promoter regions of ILB −511 C>T (rs16944), IL6 −174 G>C (rs1800795), and TNF −308 G>A (rs1800629). An additive genetic risk score was computed by summing the number of high-expression alleles across the three polymorphisms. The authors found that the genetic risk index was significantly associated with fatigue and that TNF −308 and IL6 −174 were independently associated with fatigue. Of interest, the genetic risk index was also associated with depressive symptoms and memory complaints. The authors concluded that these findings further implicate inflammatory processes as contributors to cancer-related fatigue. The results support a new strategy for identifying and treating patients at risk for fatigue based on genetic variants in proinflammatory cytokine genes.
Bower JE, Ganz PA, Irwin MR, et al. Cytokine genetic variations and fatigue among patients with breast cancer. J Clin Oncol. 2013;31(13): 1656–1661.
Correspondence: Julienne E. Bower at [email protected]