Surgical management of recto-vaginal fistula (about 6 cases).

INTRODUCTION: Recto-vaginal fistula (RVF) is defined as a pathological epithelialized communication between the posterior wall of the vagina and the anterior wall of the rectum through the recto-vaginal septum. RVFs are rare and represent less than 5% of rectal fistulas. Occurring after childbirth or during a proctological pathology, they create a deep distress for the patients. The aim of our work is to analyze the epidemiological particularities and the risk factors of occurrence of RVF as well as the modalities and results of our therapeutic management. MATERIALS AND METHODS: Our work is retrospective analytic and comparative concerning 6 cases operated in the department of general surgery 3 of the UHC Ibn Rochd of Casablanca for recto vaginal fistula or recidive over a period of 7 years from 2012 to 2018. RESULTS: The analysis of the results of our study allowed us to note: A frequency of occurrence of RVF of about 0.48%. The average age at diagnosis was 55 in our patients. The etiologies were dominated by post-radiation (33.33%) and post-operative (16.66%) RVFs. The predominant mode of delivery in our study was vaginal delivery (83.33%). The antecedents were dominated by pelvic irradiation in 50% of patients, and pelvic surgery for cervical cancer and/or rectal cancer (50%). The diagnosis was revealed by a vaginal stool output in all patients. Surgical treatment was performed in all our patients. The surgical technique of choice in our series was drainage by Stenon, in 83.33% of patients. A protective stoma was performed in all our patients studied, a colostomy in 66.66%, and an ileostomy in 33.33% of patients. The immediate postoperative evolution was excellent in all our patients, while the short- and medium-term evolution revealed the occurrence of recurrence in one third of the patients (33.33%). The treatment of choice for recurrence was the interposition of a pedicled fat flap of the labia majora, known as the modified Martius technique. The morbidity, represented mainly by recurrence, was 25%, with a mortality rate of 0%. DISCUSSION: The occurrence of RVF in all its etiologies seems to be infrequent. However, its real incidence remains poorly documented in the literature, it varies between 0.3% and 15.3%. RVFs are considered simple or complex depending on their size, location and etiology. The high or low location and the etiology of the RVF determine the choice of the approach during surgical management. The diagnosis is most often clinical. The examination will try to find the cause of the RVF and the associated lesions. RVF can be asymptomatic. The importance of the symptoms depends on the topography of the fistula, the diameter of the orifice, and the quality of the intestinal transit. No additional investigations are required to confirm the diagnosis of RVF, since the positive diagnosis is essentially clinical. However, in the case of a high or complex fistula, the clinician can support his or her pre-therapeutic assessment with the exploration of imaging data, especially those of the digestive opacification, MRI and pelvic CT. The causes of RVFs are multiple. However, their proportions are difficult to establish. Post-obstetrical RVFs, those due to Crohn's disease, and post-op are probably the most frequent. The literature describes a variety of surgical approaches and treatment options for RVF. However, there are no treatment recommendations. The available data are vague and do not define an optimal treatment. Medical treatment with antibiotics and sitz baths is often necessary to control the local infection. The surgical management of RVFs is complex and follows several principles. The therapeutic arsenal is very varied and constitutes a real "escalation", ranging from simple drainage by suture to the radical treatment represented by abdominal-pelvic amputation. The results of the treatment of simple VF are excellent in all studies. The healing rate varies from 75 to 100% depending on the authors. CONCLUSION: The results of this study confirm the low incidence of RVF, and show that vaginal delivery and a history of pelvic surgery (for rectal or cervical cancer) are the most frequent predictors of RVF. Thus, from a therapeutic point of view, medical treatment is always required, it allows the flow of the fistula to be reduced, which facilitates preparation for the surgical procedure.

Retrorectal cystic hamartoma: A case report.

Retrorectal tumors are a rare group of tumors that can be of benign or malignant origin, the differential diagnosis concerns all retrorectal tumors. We report a case of a huge retrorectal cystic hamartoma in which surgical excision was performed. A 58 years-old female presented with a low back pain and constipation. Digital rectal examination found a renitent cystic mass compressing the posterior wall of the rectum. Colonoscopy showed a tumor compressing the rectum. Magnetic resonance imaging (MRI) scan showed a presacral cystic formation. Surgical resection using laparotomy was performed. The patient made a full recovery and was released eight days after the surgery. Histological examination of the mass revealed a retrorectal cystic hamartoma.

[Evaluation of preoperative nutritional status in visceral surgery Correlational study]. / Evaluation de l'etat nutritionnel préopératoire en chirurgie viscérale Etude corrélationnelle.

Objective Is to evaluate the nutritional status of preoperative patients in the visceral surgery department III of CHU Ibn Rushd of Casablanca and to correlate to postoperative length of stay. Patients and methods Prospective observational study of six months from February 2015 to late July 2015, in patients from being operated in the visceral surgery department II1. The nutritional status of 151 patients preoperatively was evaluated the correlation between the various diagnostic tests and clinical and biological parameters was investigated and postoperative length of stay was calculated. Results 151 patients predominantly female (72.84%1, reporting their consent, were selected for this study. 51.56% of patients had risk factors for undernutrition. The cholelithiasis was the most responded diagnosis (57.61%). The Nutritional Risk Index (NRII allowed to identify 13 low nutritional risk patients, 7 moderate-risk and 3 major risk. According to the Mini Nutritional Assessment (MNA two elderly people [over 70 years] were at risk of undernutrition and one person had a bad nutritional status. Nutritional risk stratification identified 19 patients with postoperative nutritional grade 3. The average length of stay was variable; it was not correlated with the nutritional status of patients against it is based on the type of surgery. Conclusion The risk of undernutrition was high; however, a single parameter is insufficient for the diagnosis of preoperative undernutrition, a combination of different parameters would be a more reliable method.

[Primary leiomyosarcoma of the pancreas]. / Léiomyosarcome primitif du pancréas.

Primary leiomyosarcoma (LMS) of the pancreas is a rare mesenchymal neoplasm (0.1% of pancreatic tumors) with only 35 cases reported in the world literature. We describe a 36th case. This tumor affects adults in the fifth decade of life, especially men. Its diagnosis is difficult and is based on immunohistochemical analyses that reveal smooth muscle cell markers. We report the case of a patient with primary LMS in the head of the pancreas. He underwent a pancreaticoduodenectomy for both diagnosis and treatment after imaging was unable to provide a precise diagnosis. The discussion covers the clinical, diagnostic, immunohistochemical, and therapeutic characteristics of this neoplasm.

Primary retroperitoneal mucinous cystadenoma.

Primary retroperitoneal mucinous cystic tumors are extremely rare, and although their histopathogenesis is still uncertain, several theories have been proposed. Traditionally, transabdominal laparotomy and enucleation of the cyst is the treatment of choice. The anatomopathological examination of the mass is imperative in the fact to eliminate malignant lesions. We report the case of a 43-year-old woman, with primary retroperitoneal mucinous cystic tumor, revealed by an abdomino-pelvic mass. During laparotomy, a totality of the tumor was removed. The anatomopathologic study permitted the diagnosis.

Hyperleptinemia precipitates diet-induced obesity in transgenic mice overexpressing leptin.

Transgenic mice overexpressing leptin backcrossed to the C57BL/6J genetic background (LepTg) have a lean phenotype, characterized by a 95% reduction in adipose mass; reduced plasma levels of glucose, triglycerides, insulin, and IGF-1; and a 75% decrease in adipocyte size. High-fat diet treatment for 20 wk revealed that, compared with normal mice, the LepTg mice had an increased susceptibility to diet-induced obesity, as demonstrated by their rate of weight gain, higher accumulation of sc white adipose tissue mass, hypertrophy of adipocytes, and normalization of their reduced metabolic parameters. The stromal vascular fraction of white adipose tissue from the LepTg mice was highly cellular and contained cells capable of rapid lipid accumulation in primary cultures. The precipitous diet-induced obesity of the LepTg mice was accompanied with 10-fold and 1.6-fold elevations in insulin and IGF-1, respectively, suggesting that the trophic action of insulin and IGF-1 on the preadipocytes and small adipocytes may have caused them to rapidly differentiate and accumulate triacylglycerol stores. Other contributing factors may involve a shift in insulin sensitivity triggered by hyperleptinemia and a decrease in energy expenditure. These studies demonstrate that a chronic response to hyperleptinemia as in the LepTg mice is a predisposing factor to diet-induced obesity and suggest that individuals who are particularly lean because of increased leptin secretion may develop rapid obesity under conditions of a high-fat diet.

[Non-functional retroperitoneal paraganglioma]. / Paragangliome rétropéritonéal non fonctionnel.

Non functional retroperitoneal paragangliomas are rare tumors: less than 50 cases are reported in the literature. They are usually asymptomatic and can attain big dimensions. The authors report a case diagnosed by histological examination of the operative specimen. Malignant tumors more frequent than the benign tumors present with a regional extension and delayed metastases. The treatment is completed by surgical excision. Radiotherapy and chemotherapy can be used for palliation of symptoms.

Leptin-deficient mice backcrossed to the BALB/cJ genetic background have reduced adiposity, enhanced fertility, normal body temperature, and severe diabetes.

A deficiency of leptin synthesis in mice results in a complex phenotype characterized by morbid obesity, diabetes, sterility, and defective thermogenesis. To determine whether the genetic background could alter the pleiotropic effects of leptin deficiency, we backcrossed the ob mutation for 10 generations from the C57BL/6J to the BALB/cJ genetic background. Compared with C57BL/6J ob/ob mice, BALB/cJ ob/ob mice showed at 27 wk of age a 35-40% reduction in body weight attributed to a 60% decrease in white adipose tissue mass. Food intake was not significantly different between the two obese strains, suggesting distinct utilization of energy intake. In the fed state, BALB/cJ ob/ob mice had elevated insulin and triglycerides levels, demonstrating a worsening effect on diabetes. At the reproductive level and in contrast to sterile C57BL/6J ob/ob mice, male and female BALB/cJ ob/ob mice were capable of reproducing after a mating period of 16 and 32 wk, respectively. At thermoneutrality, the body temperature of BALB/cJ ob/ob mice was 2.9 C higher than that of C57BL/6J ob/ob mice, whereas exposure of both groups to 4 C demonstrated a prolonged cold tolerance of BALB/cJ ob/ob mice. These studies show that the abnormalities caused by leptin deficiency can be genetically dissected and separated from each other, suggesting discrete pathways controlled by leptin modifier genes.

Transgenic mice overexpressing leptin accumulate adipose mass at an older, but not younger, age.

Sensitivity to leptin is associated with a normal regulation of the adipose mass, whereas decreased leptin sensitivity results in elevated adipose tissue stores. To address whether the effects of chronic hyperleptinemia are sustained with age, we generated transgenic mice that overexpress leptin under the control of the fat specific aP2 promoter/enhancer. At 6-9 weeks of age, transgenic mice overexpressed 5-fold more human leptin than endogenous mouse levels and had consistently low body weights, with reduced brown and white fat depots characterized by adipocytes either devoid of or containing minute lipid droplets. However, at 33-37 weeks, despite continuous secretion of human leptin, the transgenic mice showed a rebound effect characterized by an increase in body weight, accumulation of adipose mass, and lipid-filled adipocytes. Thus, this mouse model exhibits a two-stage phenotype, with respect to fat accumulation. In addition, plasma glucose, triglycerides, and cholesterol levels were markedly depressed in young, but not older, transgenic mice. A detrimental consequence of early hyperleptinemia was a failure of the transgenic mice to acclimatize to the cold, as a result of depleted fat stores within their brown adipocytes. Cold exposure was tolerated after a 2-week high-fat diet or at an older age when fat depots had naturally accumulated. Treatment of the older transgenic mice with large doses of leptin stimulated weight loss, demonstrating that the leptin pathway still responds to pharmacological levels of leptin. Overall, these studies show that moderate hyperleptinemia in normal mice results in a sensitivity of the adipose mass to leptin at a younger (but not older) age. The mechanisms that lead to the accumulation of fat at an older age remain largely unknown, and this hyperleptinemic mouse model will allow the uncovering of at least some of these mechanisms.

Leptin as a regulator of adipose mass and reproduction.

Leptin, an adipocyte-derived hormone, informs neuroendocrine pathways about the status of energy stores in adipose tissue. The integration of this peripheral signal in hypothalamic networks results in activation of peripheral metabolic pathways that control energy build-up and expenditure. Firing of the reproductive cascade of hormones at puberty and its regulation in adults is tightly associated with energy metabolism and is thus regulated by leptin. This article provides an update of past and present theories that link nutrition and reproduction in light of new research.

Effect of the genetic background on the reproduction of leptin-deficient obese mice.

Obesity is often associated with an impairment of the hypothalamic-pituitary-gonadal axis. The leptin-deficient ob/ob mouse model is characterized by a morbid obesity with a sterility in males and females that is corrected by continuous leptin treatment. Since ob/ob mice are maintained on the C57BL/6J inbred genetic background, we sought to determine whether their infertility can be corrected without leptin treatment but via the effect of modifier genes brought into the obese-sterile phenotype by a different genetic background. Thus, we generated via an F2 intercross ob/ob mice on a mixed C57BL/6J-BALB/cJ genetic background and assayed them for fertility by mating with wild-type C57BL/6J mice. Whereas genetically heterogeneous F2 obese females remained sterile like male and female C57BL/6J ob/ob mice, 41% of F2 C57BL/6J-BALB/cJ obese males were capable of reproducing despite a morbidly obese state. Therefore, the sterility of the original C57BL/6J ob/ob mouse model was genetically corrected independently of its obese state via the effects of modifier genes. Unlike testosterone levels, triglyceride levels, and testes weight-to-body weight ratios, which were all higher in fertile vs. sterile mice, glucose levels were similar in both groups, indicating that the underlying hyperglycemia of ob/ob mice was not an impediment to the onset of fertility. A genome-wide scan in F2 ob/ob males resulted in the localization of four modifier loci on chromosomes 1, 3, 5, and 14 with respective quantitative traits consisting of number of pregnancies, testes weights normalized to body weights, body weight at 8 weeks of age, and circulating testosterone. We conclude that the inheritance of modifier genes at the identified loci acts to promote fertility of otherwise sterile leptin-deficient obese male mice.

Leptin is not necessary for gestation and parturition but regulates maternal nutrition via a leptin resistance state.

Leptin levels are significantly elevated in pregnant mice, rats and humans suggesting a critical role for leptin during gestation. To address whether leptin plays a putative role in the physiology of pregnancy, we asked whether a mouse pregnancy would be affected by the complete absence of leptin from both the mother and fetuses. Thus, leptin-deficient ob/ob females were first treated with exogenous leptin and then mated to similarly treated ob/ob males. All resulting fetuses have an ob/ob genotype and lack like their mothers any endogenous leptin production. Withdrawal of leptin treatment at 0.5, 6.5, 10.5 and 19.5 days p.c. did not affect any stage of the pregnancy despite a gradual return of the mothers to an obese state. However, some mice had delayed gestation periods of 21-23 days which were associated with prolonged parturition. The pups were normally delivered with no obvious signs of deformities although none survived beyond a day after delivery due to failure of lactation. Monitoring daily food intake of pregnant ob/ob females treated throughout gestation with leptin revealed significantly elevated levels of food intake from day 10 p.c. and onward demonstrating an attenuation of a leptin response during pregnancy and a leptin resistance effect. These studies demonstrate that in the mouse, leptin is not a critical molecule for implantation, gestation, fetal growth and parturition but that the leptin resistance effect at mid-gestation aims to stimulate food intake thus providing sustained energy resources for pregnancy.