Risk of Bias and Quality of Reporting in Colon and Rectal Cancer Systematic Reviews Cited by National Comprehensive Cancer Network Guidelines.

INTRODUCTION: Given the changing landscape of colorectal cancer, systematic reviews are likely to play a key role in advancing the understanding of prevention, diagnosis, and treatment. METHODS: We conducted a cross-sectional investigation of the risk of bias and reporting quality of systematic reviews referenced by colon and rectal cancer National Comprehensive Cancer Network (NCCN) guidelines. We used two widely accepted tools: Risk of Bias in Systematic reviews (ROBIS) and Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). RESULTS: Using ROBIS, only 3 (4.8%) systematic reviews were judged with low risk of bias, 35 (55.6%) systematic reviews were judged with unclear risk of bias, and 25 (39.7%) systematic reviews were judged with high risk of bias. Across all systematic reviews, the individual bias domains at the highest risk of bias were domains 1 (protocol and eligibility criteria) and 2 (methods to identify and select studies). Across all studies, the median adherence to PRISMA was 74.1% (IQR 69.2-80.0%), corresponding to approximately 20 of 27 items. CONCLUSIONS: Systematic reviews cited in NCCN guidelines for colon and rectal cancer are frequently at unclear or high risk of bias and do not report key systematic review items that are important for the critical appraisal of results.

Pneumococcal Induced T-activation with Resultant Thrombotic Microangiopathy.

Thrombotic microangiopathies are disorders resulting from platelet thromboses forming in the microvasculature with resultant schistocyte forms. Hemolytic uremic syndrome (HUS) is a microangiopathic hemolytic anemia often complicated by acute renal failure in children. HUS is typically caused by bacterial infection, most commonly enterohemorrhagic Escherichia coli. Neuraminidase-producing organisms, such as Streptococcus pneumoniae have also been reported as potential etiologies. The pathogenesis in these cases involves cleavage of sialic acid residues from the surfaces of erythrocytes, platelets, and glomerular capillary endothelial cells, exposing the Thomsen-Friedenreich antigen, a process known as T-activation. We describe a 2-year-old girl who presented with pneumococcal pneumonia and sepsis ultimately resulting in a thrombotic microangiopathy with acute renal failure, most consistent with HUS. The patient's direct antiglobulin test was positive. Polyagglutination was observed with human adult serum, but not with umbilical cord serum. Her red blood cells (RBCs) were reactive against peanut and soybean lectins, but not Salvia sclarea or Salvia horminum lectins. These findings are consistent with T-activation. Clinicians should be cognizant of the possibility of T-activation with resultant HUS in patients infected with neuraminidase-producing bacteria. Such patients may be difficult to identify using monoclonal typing antisera, as these typically do not have anti-T antibodies. Whether such patients are at risk for transfusion-associated hemolysis is debatable.