[Indications for the decision of surgery].
Explore the source record for details and available documents.
Humans↗
Biomedical subjects
J C Givel
Publications and source records attributed to J C Givel.
[Surgery].
The evolution of visceral surgery is characterized by defining with ever increasing precision the real role of new techniques. Hernia repair, abdominal compartment syndrome, pancreatic and colorectal cancers, as well as haemorrhoids, confirm this reality. Although laparoscopy has clear indications in hernia repairs, many still prefer open approach. The abdominal compartment syndrome, now better understood thanks to laparoscopy, is increasingly important in intensive care. The role of laparoscopy for pancreatic and colorectal cancers is still limited. The development of minimally invasive techniques has led to a reduced morbidity of surgery for haemorrhoids and better results. The economic impact of new technologies must remain a primary concern.
Compartment Syndromes↗
Pilonidal sinus: how to choose between excision and open granulation versus excision and primary closure? Study of a series of 141 patients operated on from 1991 to 1995.
AIMS: The purpose of this study was to evaluate excision and open granulation versus excision and primary closure as treatments for pilonidal sinus. SUBJECTS AND METHODS: We evaluated a group of 141 patients operated on for a pilonidal sinus between 1991 and 1995. Ninety patients were treated by excision and open granulation, 34 patients by excision and primary closure and 17 patients by incision and drainage, as a unique treatment of an infected pilonidal sinus. RESULTS: The first group, receiving treatment of excision and open granulation, experienced the following outcomes: average length of hospital stay, four days; average healing time; 72 days; average number of post-operative ambulatory visits, 40; average off-work delay, 38 days; and average follow-up time, 43 months. There were five recurrences (6%) in this group during the follow-up period. For the second group treated by excision and primary closure, the corresponding outcome measurements were as follows: average length of hospital stay, four days; average healing time, 23 days; primary healing failure rate, 9%; average number of post-operative ambulatory visits, 6; average off-work delay, 21 days. The average follow-up time was 34 months, and two recurrences (6%) were observed during the follow-up period. In the third group, seventeen patients benefited from an incision and drainage as unique treatment. The mean follow-up was 37 months. Five recurrences (29%) were noticed, requiring a new operation in all the cases. DISCUSSION AND CONCLUSION: This series of 141 patients is too limited to permit final conclusions to be drawn concerning significant advantages of one form of treatment compared to the other. Nevertheless, primary closure offers the advantages of quicker healing time, fewer post-operative visits and shorter time off work. When a primary closure can be carried out, it should be routinely considered for socioeconomical and comfort reasons.
Adolescent↗
Dukes B colorectal cancer: distinct genetic categories and clinical outcome based on proximal or distal tumor location.
PURPOSE: The aim of this study was to determine whether tumor location proximal or distal to the splenic flexure is associated with distinct molecular patterns and can predict clinical outcome in a homogeneous group of patients with Dukes B (T3-T4, N0, M0) colorectal cancer. It has been hypothesized that proximal and distal colorectal cancer may arise through different pathogenetic mechanisms. Although p53 and Ki-ras gene mutations occur frequently in distal tumors, another form of genomic instability associated with defective DNA mismatch repair has been predominantly identified in the proximal colon. To date, however, the clinical usefulness of these molecular characteristics remains unproven. METHODS: A total of 126 patients with a lymph node-negative sporadic colon or rectum adenocarcinoma were prospectively assessed with the endpoint of death by cancer. No patient received either radiotherapy or chemotherapy. p53 protein was studied by immunohistochemistry using DO-7 monoclonal antibody, and p53 and Ki-ras gene mutations were detected by single strand conformation polymorphism assay. RESULTS: During a mean follow-up of 67 months, the overall five-year survival was 70 percent. Nuclear p53 staining was found in 57 tumors (47 percent), and was more frequent in distal than in proximal tumors (55 vs. 21 percent; chi-squared test, P < 0.001). For the whole group, p53 protein expression correlated with poor survival in univariate and multivariate analysis (log-rank test, P = 0.01; hazard ratio = 2.16; 95 percent confidence interval = 1.12-4.11, P = 0.02). Distal colon tumors and rectal tumors exhibited similar molecular patterns and showed no difference in clinical outcome. In comparison with distal colorectal cancer, proximal tumors were found to be statistically significantly different on the following factors: mucinous content (P = 0.008), degree of histologic differentiation (P = 0.012), p53 protein expression, and gene mutation (P = 0.001 and 0.01 respectively). Finally, patients with proximal tumors had a marginally better survival than those with distal colon or rectal cancers (log-rank test, P = 0.045). CONCLUSION: In this series of Dukes B colorectal cancers, p53 protein expression was an independent factor for survival, which also correlated with tumor location. Eighty-six percent of p53-positive tumors were located in the distal colon and rectum. Distal colon and rectum tumors had similar molecular and clinical characteristics. In contrast, proximal neoplasms seem to represent a distinct entity, with specific histopathologic characteristics, molecular patterns, and clinical outcome. Location of the neoplasm in reference to the splenic flexure should be considered before group stratification in future trials of adjuvant chemotherapy in patients with Dukes B tumors.
Adenocarcinoma↗
Esophageal cancer as second primary tumor after breast cancer radiotherapy.
BACKGROUND: An increased risk of esophageal cancer has been reported in survivors of breast cancer treated with radiotherapy. This study further characterizes this association. METHODS: Through hospital databases, 118 patients (109 men, 9 women) treated for esophageal cancer between 1985 and 1993 were identified, of whom 37 had 60 synchronous or metachronous cancers. 5 women had primary esophageal cancer after having breast cancer, and are the subjects of this case-control study. RESULTS: All 5 women had been treated with radical mastectomy and adjuvant radiotherapy; none received chemotherapy. Their ages at the time of breast cancer ranged from 36 to 82 years; at esophageal cancer, 61 to 95 years. Time between radiotherapy and esophageal cancer varied from 13 to 31 years. All esophageal cancers were squamous cell carcinomas. Mean survival after esophageal cancer was 14.2 months. CONCLUSIONS: Radio-induced esophageal cancer can occur as a second primary cancer in women who survive at least 1 decade after mastectomy and adjuvant radiotherapy.
Adult↗
p53 and Ki-ras as prognostic factors for Dukes' stage B colorectal cancer.
Mutations of the TP53 and Ki-ras genes have been reported to be of prognostic importance in colorectal carcinomas. An increased intracellular concentration of the p53 protein, although not identical to, is sometimes seen in tumours with TP53 mutation and has been correlated with poor prognosis in some tumour types. Previous colorectal cancer studies, addressing the prognostic importance of Ki-ras mutation and TP53 aberrations, yielded contradictory results. The aim of this study was to determine in a clinically and therapeutically homogeneous group of 122 sporadic Dukes' B colorectal carcinomas with a median follow-up of 67 months (3-144 months) whether or not p53 protein expression, TP53 mutation and K-ras mutation correlated with prognosis. p53 staining was performed by immunohistochemistry, using the monoclonal antibody DO7 on paraffin-embedded tissue. Mutations in exons 5-8 of the TP53 gene and in codons 12 and 13 of the K-ras gene were assayed in paraffin-embedded tissue by the single-strand conformation polymorphism (SSCP) assay. Nuclear p53 staining was found in 57 (47%) tumours. Aberrant migration patterns indicating mutation of the TP53 gene were found in 39 (32%) tumours. Forty-six carcinomas (38%) showed a mutation of the Ki-ras codons 12 or 13. In a univariate analysis, patients with wild-type TP53 status showed a trend towards better survival, compared with those with mutated TP53 (log-rank test, P = 0.051). Likewise, tumours immunohistochemically positive for p53 showed a worse prognosis than p53-negative tumours (P = 0.010). The presence or absence of mutations in Ki-ras did not correlate with prognosis (P = 0.703). In multivariate analysis, only p53 immunoreactivity emerged as an independent marker for prognosis hazard ratio (HR) = 2.16, 95% confidence interval (CI) 1.12-4.11, P = 0.02). Assessment of p53 protein expression is more discriminative than TP53 mutation to predict the outcome of Dukes' stage B tumours and could be a useful tool to identify patients who might benefit from adjuvant therapy.
Adenocarcinoma↗
Prognosis in Duke's B colorectal carcinoma: the Jass classification revisited.
OBJECTIVE: To assess whether Jass staging enhances prognostic prediction in Dukes' B colorectal carcinoma. DESIGN: A historical cohort observational study. SETTING: A university tertiary care centre, Switzerland. SUBJECTS: 108 consecutive patients. INTERVENTIONS: Curative resection of Dukes' B colorectal carcinoma between January 1985 and December 1988, Patients with familial adenomatous polyposis; hereditary non-polyposis colorectal cancer; Crohns' disease; ulcerative colitis and synchronous and recurrent tumours were excluded. A comparable group of 155 consecutive patients with Dukes' C carcinoma were included for reference purposes. MAIN OUTCOME MEASURES: Disease free and overall survival for Dukes' B and overall survival for Dukes' C tumours. RESULTS: Dukes' B tumours in Jass group III or with an infiltrated margin had a significantly worse disease-free survival (p = 0.001 and 0.0001, respectively) and those with infiltrated margins had a significantly worse overall survival (p = 0.002). Overall survival among those with Dukes' B Jass III and Dukes' B with infiltrated margins was no better than overall survival among all patients with Dukes' C tumours. CONCLUSION: Jass staging and the nature of the margin of invasion allow patients undergoing curative surgery for Dukes' B colorectal carcinoma to be separated into prognostic groups. A group of patients with Dukes' B tumours whose prognosis is inseparable from those with Dukes' C tumours can be identified, the nature of the margin of invasion being used to classify a larger number of patients.
Aged↗
For patients with Dukes' B (TNM Stage II) colorectal carcinoma, examination of six or fewer lymph nodes is related to poor prognosis.
BACKGROUND: Lymph node status is pivotal to the staging of colorectal carcinoma. The diagnosis of a lymph node negative tumor should imply a good prognosis; however, the outcomes for Dukes' B (TNM Stage II) patients remain variable, possibly in part due to understaging. The aim of this study was to determine whether examining a specified minimum number of lymph nodes using conventional techniques would eliminate the risk of understaging and thus have an effect on prognosis. METHODS: Data on patients who underwent surgery for colorectal carcinoma at a single institution between 1985 and 1990 were reviewed. Patients with Dukes' B (TNM Stage II) or C (TNM Stage III) tumors and histologically confirmed disease-free resection margins who were treated with curative intent were included. Correlations among variables were assessed using the chi-square test, and survival comparisons were made using Kaplan-Meier curves and the log rank test. Multivariate analysis was performed using a Cox regression model. RESULTS: Dukes' B (TNM Stage II) patients with < or =6 lymph nodes examined had significantly poorer overall survival than those with > or =7 lymph nodes examined (P = 0.0014). Such a significant difference was not observed among Dukes' C (TNM Stage III) patients (P = 0.7). Survival of Dukes' C patients was significantly worse compared with that of Dukes' B patients overall and Dukes' B patients with > or =7 lymph nodes examined (P < 0.0001). There was no significant difference in survival between Dukes' C and Dukes' B patients with < or =6 lymph nodes examined (P = 0.02). The number of examined lymph nodes was the only significant parameter correlated with survival in the multivariate analysis (P = 0.002). CONCLUSIONS: Because Dukes' B patients with < or =6 examined lymph nodes have poorer outcomes than those with a higher number examined (probably due to understaging), the total number of examined lymph nodes should always be reported.
Adult↗
The type of K-ras mutation determines prognosis in colorectal cancer.
BACKGROUND: Mutations involving the oncogene K-ras in colorectal cancer may be related to tumor aggressiveness. However, the value of K-ras gene determination as a prognostic marker has not been clearly established. PATIENTS AND METHODS: The results from 98 patients recruited in a prospective study analyzing the effect of a K-ras mutation as a prognostic factor in colorectal cancer are reported. RESULTS: Disease-free (P = 0.02) and overall survival (P = 0.03) were significantly reduced for patients harboring a K-ras mutation. Two specific mutations demonstrated a significantly increased risk of disease recurrence, namely, 12-TGT (P = 0.04) and 13-GAC substitutions (P = 0.002). Patients with either of these substitutions had a 2-year disease-free survival rate of 37% compared with that of 67% for the group of patients harboring any other mutation type or a wild-type status (P = 0.01). CONCLUSIONS: The results herein presented suggest that K-ras acts as a prognostic factor in colorectal cancer and that this effect is probably related to a limited number of defined mutations.
Adult↗
Selective suppression of cytokine secretion in whole blood cell cultures of patients with colorectal cancer.
We have investigated the secretion of interferon alpha (IFN-alpha), IFN-gamma, interleukin-1alpha (IL-1alpha), IL-1beta, IL-2 and tumour necrosis factor alpha (TNF-alpha) in whole blood cell cultures (WBCCs) of colorectal cancer patients upon mitogen stimulation. Whereas the values for IL-1beta and TNF-alpha remained virtually unchanged in comparison with healthy control subjects, WBCCs of colorectal cancer patients secreted significantly lower amounts of IFN-alpha (P < 0.005), IFN-gamma (P < 0.0001), IL-1alpha (P < 0.0001) and IL-2 (P < 0.05). This reduction correlated with the progression of the disease. The total leucocyte and monocyte population were almost identical in both groups. In contrast, a dramatic depletion of lymphocytes was observed in colorectal cancer patients, which affected both lymphocyte counts (P < 0.0005) and their distribution (P < 0.0001). Our results suggest a selective suppression of cytokines in colorectal cancer patients that is related to tumour burden. Several mechanisms might account for this phenomenon, one of which might be lymphocyte depletion.
Adult↗
[Hereditary nonpolyposis colorectal cancers].
Hereditary non-polyposis colorectal cancer (HNPCC) is an autosomal, dominantly inherited disease leading to a marked increase in cancer susceptibility, notably colorectal cancer, affecting up to one in 400 individuals in the Western world. Four genes responsible for the majority of cases have been identified. Colorectal cancer in affected people tends to be right sided, occur at an earlier age, and there is a propensity for synchronous or metachronous lesions. Extra-colonic tumours may occur with an elevated frequency, most importantly cancer of the endometrium, but also stomach, hepatobiliary system, small bowel, proximal ureter and renal pelvis, and ovary. On account of these features, management guidelines for members of HNPCC kindreds require modification from those generally advised for patients with sporadic tumours. The cardinal feature for the identification of affected families is the family history. All clinicians have a duty to identify such patients under their care as appropriate screening and surgery should lead to an improved prognosis for such patients and their families.
Adult↗
[Familial adenomatous polyposis].
Familial adenomatous polyposis (FAP) is an autosomal dominant disease characterized by the development of numerous adenomatous polyps in the colon and rectum with diverse extracolonic manifestations. Recent genetic advances have lead to the sequencing of the FAP gene, with important implications for screening, diagnosis and follow-up. Appropriate management of probands and at-risk patients is of the utmost importance, as untreated carriers will develop colorectal cancer. Identification of FAP families and tracing of pedigrees represent the most important steps. To this end registries are essential, allowing a comprehensive multidisciplinary approach. They have justified their place by decreasing related morbidity and mortality. An overview and discussion of clinical features and management are presented.
Adenomatous Polyposis Coli↗
p53 mutations as a possible predictor of response to chemotherapy in metastatic colorectal carcinomas.
Although intrahepatic infusion therapy with 5-fluorouracil for unresectable colorectal liver metastases may lead to improved overall survival for some patients, it is not clear why a response is not observed in others. Gene alterations in oncogenes or tumor-suppressor genes are critical events in tumor formation, and some of them could play a role in the process of drug resistance. The tumor-suppressor gene p53, which is known to trigger cell arrest or apoptosis in response to DNA damage, is found to be mutated in a wide range of human tumors. The aim of this work is to establish whether a relationship is found between p53 mutations and survival in patients undergoing adjuvant chemotherapy for advanced Dukes' D colorectal cancers. Seventeen tumors from patients treated with 5-fluorouracil regimen via intrahepatic infusion for unresectable colorectal hepatic metastasis were considered. p53 mutations from tumor DNA were detected, after amplification by PCR of exons 5 to 8, by non-radioactive single-strand conformation polymorphism and direct DNA sequencing. Patients with mutated p53 colorectal tumors had short survival, whereas prolonged survival was associated with the presence of wild-type p53 (p = 0.019). Our data suggest that mutated p53 colorectal tumors had a weak response, or even no response, to chemotherapeutic treatment. Routine assessment of p53 status would be helpful in selecting patients with only wild-type p53 gene who have a predictably better response to chemotherapy.
Adenocarcinoma↗
Differential effect of interleukin-4 and transforming growth factor beta 1 on expression of proto-oncogenes and autocrine insulin-like growth factor II in colorectal carcinoma cells.
We have compared the effect of interleukin-4 and transforming growth factor beta 1 on proliferation and gene expression in two colorectal carcinoma cell lines, LS513 and LS1034. Transforming growth factor beta 1 was a potent inhibitor for both cells lines and virtually abolished de novo DNA synthesis. Interleukin-4 inhibited thymidine incorporation up to 60 and 45%, respectively. While both cytokines exerted a comparable cyto-inhibitory activity they displayed differential effects on proto-oncogene expression. Transforming growth factor beta 1 markedly down-regulated c-myc in LS1034 but not in LS513 cells. In contrast, expression of c-fos was induced by interleukin-4 in LS513 but not in LS1034 cells. Interestingly, in agreement with their cyto-inhibitory activity both cytokines suppressed the expression of insulin-like growth factor II in LS1034, which is an autocrine growth factor for these cells.
Cell Division↗
[Dynamic graciloplasty, an effective approach to anal incontinence].
Explore the source record for details and available documents.
Anal Canal↗
[Familial adenomatous polyposis (FAP): integration of clinical and genetic parameters in the screening of subjects at risk. A one-family example].
AIM OF THE STUDY: Amongst family members at risk of developing familial adenomatous polyposis (FAP) to distinguish between those who are affected by the disease and those who are not, in order to provide optimal treatment to those requiring it whilst excluding those without the disease from the endoscopic surveillance programme. MATERIAL AND METHODS: A programme of endoscopy, ophthalmologic examination for retinal pigment lesions associated with FAP and genetic analysis was proposed to a patient suffering from FAP and 3 of his children considered to be at risk. RESULTS: One person at risk eventually proved to have the disease. He had diffuse recto-colic polyposis as well as the typical retinal lesions found in his father and was treated by prophylactic proctocolectomy. He had inherited the mutated paternal allele. The other 2 children had neither polyposis nor retinal lesions and had inherited the normal allele from their father. DISCUSSION: Retinal lesions seen at fundoscopy allowed the diagnosis of FAP to be made before endoscopic confirmation in one patient at risk for FAP, but their absence did not exclude the diagnosis in the other 2. In these patients genetic analysis revealed that they had inherited the normal paternal allele and hence would not develop FAP. CONCLUSION: Systematic investigation of a family suffering from FAP allowed the members at risk to be identified. Two subjects at risk were able to be excluded from further follow-up and the remaining patient was able to be treated in an optimal fashion. An algorithm is proposed for the screening of patients at risk.
Adenomatous Polyposis Coli↗
Potential value of biliary CEA assay in early detection of colorectal adenocarcinoma liver metastases.
Elevation of the biliary CEA level in patients with liver metastases from colorectal carcinoma has been reported. The aim of this study is to determine the potential value of biliary CEA assay in the early detection of liver metastases. Biliary and serum CEA levels were determined in patients operated on for a colorectal cancer and in control groups. Among 13 patients with liver metastases from colorectal carcinomas, biliary CEA levels were markedly elevated (> 40 ng/ml) in nine, moderately elevated (5-40 ng/ml) in two and normal (arbitrarily defined as < 5 ng/ml) in two. Of 28 patients with primary colorectal carcinoma without detectable hepatic secondaries, three had marked CEA elevation in the bile, 10 had moderate CEA elevation and 15 had normal levels. Among nine patients with non-malignant hepatobiliary pathology, there was one marked biliary CEA elevation, one moderate elevation and seven normal levels. None of the 13 individuals with no identified hepatobiliary pathology had elevated biliary CEA levels. The follow-up of patients with a primary colorectal tumour, no evidence of hepatic secondaries and a biliary CEA elevation is of particular interest. If subsequent appearance of liver metastases is found in such cases, intra-operative biliary CEA assay could be considered a valuable diagnostic test. Further studies will then have to prove the possible benefit of a specific treatment for this group of patients.
Adenocarcinoma↗