This study reviewed all single experience of splenic injuries after colonoscopy in the last 40 years to define the possible risk factors and the management of this complication. A MEDLINE and a PubMed search was undertaken to identify articles in English, French, Spanish, and Italian from 1974 to 2012 using the key words: "splenic injury," "splenic rupture," and "colonoscopy." Data were analyzed using descriptive statistic. A total of 103 cases have been described in 75 reports. The majority of the patients were women (71.56%) and 6.85% underwent previous pelvic surgery. The mean age was 63 years (range, 29 to 90 y). About 61 of the 103 studies (59.2%) reported the presence or the absence of previous abdominal surgery and within these, only 31 of 61 patients (50.82%) underwent previous abdominal surgery. In this review, over half of the patients with splenic injury underwent colonoscopy for routine surveillance (62.75%), and only one third of the splenic injures were associated with biopsy or polypectomy. The majority of patients (78.57%) developed symptoms within the first 24 hours after colonoscopy and in a minority of cases (21.43%), there was a delayed presentation 24 hours after colonoscopy. Computed tomography was used as the primary modality to make the diagnosis in 69 of 98 cases (70.41%) and as a confirmatory test in many additional cases. Twenty-six of 102 patients (25.49%) were treated by conservative methods, whereas the majority of patients (69.61%) underwent splenectomy as a definitive treatment. Because of possible medicolegal implications, the endoscopists should consider mentioning splenic injury on the consent form of colonoscopy after bowel perforation and bleeding, particularly in higher risk patients.
Laparoscopic cholecystectomy does not affect survival if implemented properly. Reoperation should have two objectives: R0 resection and clearance of the lymph nodes.
The mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathway has a master control role in various cancer-related biological processes as cell growth, proliferation, differentiation, migration, and apoptosis. It also regulates many transcription factors that control microRNAs (miRNAs) and their biosynthetic machinery. To investigate on the still poorly characterised global involvement of miRNAs within the pathway, we profiled the expression of 745 miRNAs in three colorectal cancer (CRC) cell lines after blocking the pathway with three different inhibitors. This allowed the identification of two classes of post-treatment differentially expressed (DE) miRNAs: (1) common DE miRNAs in all CRC lines after treatment with a specific inhibitor (class A); (2) DE miRNAs in a single CRC line after treatment with all three inhibitors (class B). By determining the molecular targets, biological roles, network position of chosen miRNAs from class A (miR-372, miR-663b, miR-1226*) and class B (miR-92a-1*, miR-135b*, miR-720), we experimentally demonstrated that they are involved in cell proliferation, migration, apoptosis, and globally affect the regulation circuits centred on MAPK/ERK signaling. Interestingly, the levels of miR-92a-1*, miR-135b*, miR-372, miR-720 are significantly higher in biopsies from CRC patients than in normal controls; they also are significantly higher in CRC patients with mutated KRAS than in those with wild-type genotypes (Wilcoxon test, p < 0.05): the latter could be a downstream effect of ERK pathway overactivation, triggered by KRAS mutations. Finally, our functional data strongly suggest the following miRNA/target pairs: miR-92a-1*/PTEN-SOCS5; miR-135b*/LATS2; miR-372/TXNIP; miR-663b/CCND2. Altogether, these results contribute to deepen current knowledge on still uncharacterized features of MAPK/ERK pathway, pinpointing new oncomiRs in CRC and allowing their translation into clinical practice and CRC therapy.
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