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Objectives: To identify clinical and radiological signs of the post-cesarean Ogilvie's syndrome in order to establish the appropriate treatment., Patients and Methods: Based on the Medline research, we listed 41 cases of Ogilvie's syndrome after cesarean section. We analyzed the patient's age, the clinical and radiological signs, the time to diagnosis, and the treatments and their efficiency., Results: The clinical signs generally appear in the first 72 h after cesarean. Diagnosis of Ogilvie's syndrome is based on a clinical picture of acute obstruction of the large bowel and by X-ray showing a large caecum without pathological lesion. If the caecal diameter is under 12 cm, conservative treatment is done with colonoscopic decompression when necessary, however if there are signs of peritonitis surgery is recommended., Conclusion: Ogilvie's syndrome after cesarean section is uncommon. Diagnosis must be fast in order to avoid the caecum to burst causing faecal peritonitis, which carries slight mortality rate., (Copyright © 2011 Elsevier Masson SAS. All rights reserved.)

The development of renal cell carcinoma (RCC) has been associated with both genetic and environmental factors, with somatic and germline mutations in the von Hippel-Lindau (VHL) tumor suppressor gene and with tobacco smoking, obesity, long term exposure to some nutrients, pollutants, and industrial solvents such as trichloroethylene. Intra and interfamilial variability of expression of germline mutations in the VHL gene and variable susceptibility to carcinogens in the sporadic forms strongly suggest the involvement of conditional modifier genes. In order to identify sub groups of individuals at increased risk because of susceptibility genotypes, we have collected a series of 460 patients who developed an RCC and 79 families with the von Hippel Lindau disease. To collect clinical and mutational data for correlation analysis we have developed a unique tool the Universal Mutation Database. Comparison of the spectrum of germline and somatic mutations in the VHL gene showed that: 1) in sporadic RCC mutations lead more often to truncated proteins (83%), while the remaining mutations (17%), include 3/4 of transversions and 1/4 of transitions. This high proportion of transversions supports the involvement of carcinogens the impact of which is conditioned by the genetic variability of xenobiotic metabolizing enzymes; 2) whereas in familial cases missense mutations are more common; this difference allowed us to define a prognostic factor for the occurrence of RCC in a VHL context. In order to look for genotypes conferring a higher risk we genotyped the RCC patients for 8 different genes (50 genotypes). A significant relationship was observed for several combinations of alleles including CYP1A1 ("variant"), NAT2 and NAT1 (slow) and GSTM1 (null allele). Associations between specific mutational profiles and at risk genotypes at different tumoral stages should allow us to: 1) define more precisely the nature of specific patterns of mutations in relation with the deficiency or overexpression of such or such enzymes in presence of particular carcinogens; 2) demonstrate that certain combinations of genotypes confer a particular risk to develop a specific type of tumor in VHL patients. Thus tracking of potentially carcinogenic substances, through their footprints and through identification of conditionally detrimental genotypes of genes participating in their detoxification should permit a better prevention through an appropriate nutrition adapted to each individual.