Enhanced-view totally extraperitoneal repair in a morbidly obese patient with epigastric and umbilical hernias in combination with rectus diastasis: A case report.

INTRODUCTION: The use of enhanced-view totally extraperitoneal (eTEP) repair for patients with ventral hernias has become more widespread due to its ability to prevent mesh-and-tacker-related complications by placing the mesh in the retrorectus space. However, the efficacy of eTEP repair in obese patients remains unknown. Herein, we report a case of a morbidly obese patient with epigastric and umbilical hernias in combination with a rectus diastasis repaired using the eTEP technique. PRESENTATION OF CASE: A 42-year-old man with a history of spontaneously reduced incarcerated epigastric hernia two weeks previously was referred to our hospital. His body mass index (BMI) was 42.9 kg/m2. Abdominal computed tomography revealed a small epigastric hernia, an umbilical hernia, and a rectus diastasis. We performed eTEP repair. The postoperative course was uneventful, and the patient was discharged on postoperative day 3. There has been no evidence of hernia recurrence after a follow-up period of 2 years. DISCUSSION: We consider that the eTEP technique is rarely affected by intra-abdominal fat because endoscopic manipulation is performed in the bilateral retrorectus and preperitoneal spaces. Moreover, the eTEP allows the epigastric artery perforator to be spared. Therefore, eTEP repair is considered the best surgical option for morbidly obese patients with ventral hernias in combination with rectus diastasis. CONCLUSIONS: This case provides support for the efficacy of eTEP repair in morbidly obese patients with epigastric and umbilical hernias in combination with a rectus diastasis.

Laparoscopic repair for interparietal hernia after enhanced-view totally extraperitoneal hernia repair: A case report.

INTRODUCTION: The enhanced-view totally extraperitoneal (eTEP) technique, an endoscopically performed Rives-Stoppa method, has been used extensively for ventral hernia repairs. However, in this technique, the necessity of posterior rectus sheath re-approximation and mesh fixation remains unclear. There are a few reports of post-eTEP interparietal hernias (IHs) occurring because of dehiscence of the re-approximated posterior rectus sheath; however, IH secondary to mesh migration is rare. Herein, we report a rare case of IH due to mesh migration after eTEP repair for an incisional hernia. PRESENTATION OF CASE: A 70-year-old man underwent eTEP repair for an incisional hernia using a self-gripping mesh without mesh fixation and posterior rectus sheath re-approximation one year previously, developed an IH. An elective laparoscopic surgery revealed an orifice to the retrorectus space as though the IH sac between the retrorectus muscle and the posterior layer including the bilateral posterior rectus sheaths, peritoneum, and mesh. We placed eight transmural sutures with 0 nylon thread and closed the orifice. The patient was then discharged on postoperative day two and was asymptomatic at 24 months without evidence of ventral hernia recurrence. DISCUSSION: We consider that strenuous activity and deep bending may cause mesh migration or dislocation. If that occurs in the early post-eTEP period without posterior rectus sheaths closure, the vulnerable peritoneal area will be exposed, which consider to be an IH orifice. CONCLUSIONS: Even after using the self-gripping mesh in eTEP repair, mesh fixation remains the best option to prevent postoperative complications, including IH.

Relationship between peroxisome proliferator-activated receptor-gamma expression and differentiation of human esophageal squamous cell carcinoma.

Peroxisome proliferator-activated receptor-gamma (PPAR-gamma), a member of the nuclear hormone receptor superfamily, is involved in suppressing the growth of several tumors. We showed that PPAR-gamma is expressed in Barrett's adenocarcinoma cell lines and inhibited the growth of these lines through the induction of G1 cell cycle arrest and apoptosis. We examined PPAR-gamma expression in human esophageal squamous cell carcinoma (SCC) in vitro and in vivo and investigated whether PPAR-gamma ligands affect the proliferation and apoptosis of human SCC cell lines. Biopsy specimens (n=46) obtained from human SCC of the esophagus were stained using a monoclonal antibody against human PPAR-gamma. We assessed the effects of PPAR-gamma ligands on the growth of SCC cells by adding 15-deoxy prostaglandin J2 (15d-PGJ2), or troglitazone to six human esophageal SCC cell lines (TE-1, TE-2, TE-3, TE-5, TE-8, and TE-9). Immunohistochemical staining showed that 34 of 46 (73.9%) SCC of the esophagus expressed PPAR-gamma. All SCC cell lines expressed PPAR-gamma mRNA and protein, especially when poorly differentiated (TE-2, TE-5, and TE-9). The PPAR-gamma ligands significantly and dose-dependently inhibited the proliferation of SCC lines, except for well-differentiated TE-1 and TE-3. Apoptosis was induced by 15d-PGJ2 (10 microM) in all tested SCC lines except TE-1, whereas troglitazone (50 microM) was marginally effective in only the TE-2 and TE-3 cell lines. The present findings suggest that PPAR-gamma could be a therapeutic target for treating squamous cell carcinoma of the esophagus, possibly through the induction of apoptosis.

Increased expression of transforming growth factor-alpha and epidermal growth factor receptors in rat chronic reflux esophagitis.

BACKGROUND AND AIM: Transforming growth factor-alpha (TGF-alpha), which binds to epidermal growth factor receptors (EGF-R), stimulates esophageal epithelial cell proliferation, enabling rapid repair after mucosal injury. The aim of the present study was to examine epithelial proliferation and dynamics of TGF-alpha and EGF-R gene and protein expression in rat chronic acid reflux esophagitis. METHODS: Gastric acid reflux esophagitis was induced in Wistar rats by ligating the transitional region between the forestomach and the glandular portion, and by covering the duodenum near the pyloric ring with a small piece of an 18Fr Nélaton catheter. Epithelial cell proliferation was assessed by bromodeoxyuridine (BrdU) uptake. Expression of TGF-alpha and EGF-R mRNA and protein was assessed by reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry. RESULTS: Esophageal lesions were observed in the lower and middle esophagus. Histologically, a significant increase in mucosal thickening with elongation of lamina propria papillae and basal cell hyperplasia was observed. The BrdU labeling index was significantly increased from 2.7 +/- 1.0 in normal mucosa and 2.8 +/- 1.2 in background mucosa adjacent to the esophageal lesion, to 60.3 +/- 32.7 in the lesions of chronic esophagitis. Expression of TGF-alpha and EGF-R mRNA in the esophageal lesion significantly increased compared to those in the control and background tissue, whereas treatment with rabeprazole significantly inhibited increases in TGF-alpha and EGF-R mRNA expression. According to immunohistochemical study, TGF-alpha and EGF-R revealed strong expression in esophageal lesions compared with control and background mucosa. The superficial layer of the esophagus was strongly positive for TGF-alpha and most cells in regions of basal hyperplasia had a positive reaction for EGF-R in the esophagitis lesion. CONCLUSION: Epithelial proliferation and expression of TGF-alpha and EGF-R were significantly increased in rat chronic reflux esophagitis. Activation of TGF-alpha and EGF-R genes in response to acid reflux may facilitate rapid mucosal healing by stimulating epithelial proliferation. These results suggest that TGF-alpha and EGF-R play crucial roles in rat chronic reflux esophagitis.

Increased expression of cytokines and adhesion molecules in rat chronic esophagitis.

BACKGROUND/AIMS: Cytokines and adhesion molecules regulate many inflammatory processes in several gastrointestinal diseases. The dynamics of cytokines and adhesion molecules in reflux esophagitis are unknown in detail. We examined the expression and dynamics of interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), monocyte chemotactic protein-1 (MCP-1), macrophage inflammatory protein-1alpha (MIP-1alpha), MIP-2, GRO/cytokine-induced neutrophil chemoattractant-2alpha (CINC-2alpha), intercellular adhesion molecule-1 (ICAM-1), leukocyte function-associated antigen 1 (LFA-1; CD11a/CD18), and Mac-1 (CD11b/CD18) in rat chronic reflux esophagitis. METHODS: Chronic acid reflux esophagitis was induced in Wistar rats by ligating the transitional region between the forestomach and the glandular portion and wrapping the duodenum near the pylorus with a small piece of an 18-Fr Nélaton catheter. Rats were killed 3 or 21 days after operation. The levels of mRNA expression of cytokines and ICAM-1 were determined by real-time quantitative RT-PCR. Localization of adhesion molecules and cytokines was investigated by immunohistochemical staining, and numbers of LFA-1- or Mac-1-positive cells were quantified. RESULTS: IL-1beta, TNF-alpha, MCP-1, MIP-1alpha, MIP-2, CINC-2alpha, and ICAM-1 mRNA expression was significantly increased in esophageal lesions compared with normal esophagus. There were few these cytokines- or adhesion molecule-positive cells in normal esophagus. In regions of esophagitis, numerous inflammatory leukocytes in lamina propria and the submucosal layer exhibited positive reactions for these cytokines and endothelial cells were intensely stained for ICAM-1. Numbers of LFA-1- and Mac-1-positive cells were significantly increased in rat chronic esophagitis. Treatment with rabeprazole almost completely inhibited development of chronic acid reflux esophagitis and significantly decreased expression of cytokines and ICAM-1 mRNA in esophageal tissue compared with control. CONCLUSION: Cytokines and adhesion molecules play important roles in the pathogenesis of chronic reflux esophagitis in this rat model.