Feasibility of laparoscopic surgery after stent insertion for obstructive colorectal cancer

Introduction

A growing number of patients with obstructive colorectal cancer are being treated with self‐expanding metallic stents (SEMS) followed by laparoscopic resection. The aim of this study was to assess the feasibility of stent insertion and laparoscopic surgery for obstructive colorectal cancer and to compare these outcomes to regular laparoscopic surgery for non‐obstructive colorectal cancer.

Methods

We retrospectively analyzed the outcomes of patients with a malignant colonic obstruction who underwent SEMS placement followed by elective laparoscopic resection. The comparison was made between stent‐laparoscopy and laparoscopy alone for non‐obstructive colorectal cancer.

Results

Colonic stenting as a bridge to surgery was successful in 97.1% of all cases. Fifteen patients underwent an elective laparoscopic surgery for left‐sided colon and rectal cancer after SEMS. The mean interval from SEMS insertion to laparoscopic surgery was 21.5 days. There was no conversion to open surgery and no need for a diverting stoma. One patient (6.7%) experienced paralytic ileus. Our comparison of stent‐laparoscopy to regular laparoscopy for non‐obstructive colorectal cancer treatment showed comparable short‐term postoperative outcomes with the exception of blood loss, which was greater in the stent‐laparoscopy group.

Conclusion

Elective laparoscopic surgery after colonic stenting is a safe and feasible strategy for the treatment of an acute malignant colonic obstruction.     

Intracranial hemorrhage in neuro-Behçet's syndrome

OBJECTIVE: Most cerebrovascular disturbances in Beh?et's syndrome are occlusive in nature, while hemorrhage is rare. In this paper, we report three cases of neuro-Beh?et's syndrome presenting with intracerebral hemorrhaging, and discuss the possible causes as they relate to cyclosporine treatment. PATIENTS: Three cases of neuro-Beh?et's syndrome presented with intracranial hemorrhage. One patient had been taking cyclosporine, and the other two patients had never taking cyclosporine. RESULTS: Together with previous reports, these cases suggest that there are two types of intracranial hemorrhage in neuro-Beh?et's syndrome. One type occurs in the center of a lesion and during the acute phase of the disease, while the other occurs in the peripheral lesion and during the subacute phase. CONCLUSIONS: It appears that the intracranial hemorrhages in neuro-Beh?et's syndrome can be divided into two groups. It is possible that the vascular pathologies caused by Beh?et's syndrome and by cyclosporine conspire to induce CNS hemorrhaging in some cases.     

Endogenous nitric oxide inhibits growth hormone secretion through cyclic guanosine monophosphate-dependent mechanisms in GH3 cells

Constitutive nitric oxide synthase (NOS) is expressed in rat adenohypophysis and clonal GH3 cells. The mechanisms of action of nitric oxide (NO) to inhibit hormone secretion and the possible role of (6R)-5, 6, 7, 8-tetrahydro-L-biopterin (THB) in the action of endogenous NO were studied in GH3 cells. Inhibiting NOS with N(G)-nitro-L-arginine or trapping NO with oxyhemoglobin enhanced both the basal and TRH-stimulated rat GH release. Sodium nitroprusside did not further decrease either the basal or the TRH-stimulated GH secretion, suggesting that endogenous NO exerted the maximal inhibitory effect. Inhibition of de novo synthesis of THB increased GH secretion. A cyclic guanosine-monophosphate (cGMP) antagonist did not increase the basal GH secretion but enhanced TRH-induced GH release. These findings suggest that endogenous NO plays an inhibitory role on basal GH release and TRH-stimulated hormone release from GH3 cells in an autocrine or paracrine fashion, at least partly, through a cGMP-dependent pathway. It is also suggested that endogenous THB plays a role in NO production and subsequent inhibition of hormone secretion in GH3 cells.     

Hemodynamic effects of inhaled nitric oxide using pulse delivery and continuous delivery systems in pulmonary hypertension

OBJECTIVE: Inhaled nitric oxide (NO) has been used for pulmonary vasodilation therapy in patients with pulmonary hypertension. Inhaled NO for awake and ambulatory patients, however, is unusual because it requires intubation or a tightly fitting facemask, and a large-scale delivery system for the safe management of toxic nitrogen oxides. We undertook this study to investigate the possibility of using inhaled NO therapy for awake and ambulatory patients with pulmonary hypertension. METHODS: Patients with pulmonary hypertension underwent cardiac catheterization and hemodynamic variables were measured at the baseline, after inhaled NO using our pulse delivery system, which involved a nasal cannula and a pulse device, and after inhaled NO using a continuous delivery system. PATIENTS OR MATERIALS: We studied seventeen patients with precapillary pulmonary hypertension (4 men and 13 women; age, 41+/-3, ranging from 19 to 61). RESULTS: Cardiac output was increased significantly by each system. Pulmonary vascular resistance was decreased significantly by each system. There was no significant change in mean pulmonary artery pressure, mean systemic artery pressure, or systemic vascular resistance. The concentrations of NO and nitrogen dioxide (NO2) in the expiratory gas using the pulse delivery system were 0.0 ppm as long as the pulse device was synchronized with the patient's respiratory cycle. CONCLUSION: Inhaled NO using our pulse delivery system changed the hemodynamic variables similarly to those when using the continuous delivery system. The concentrations of NO and NO2 in the expiratory gas using the pulse delivery system were within safe limits.     

Primary liver cancer

Liver cancer, whether primary or secondary, is one of the most difficult to treat among malignant solid tumors, with a miserable prognosis. In view of the relative lack of exciting progress in the management of metastatic liver cancer in recent years this lecture necessarily concerns primary liver cancer, particularly hepatocellular carcinoma (HCC). Time permits coverage of only several important aspects of general interest and recent advances in the study of HCC.     

Rationale and design of a randomized trial to assess the effects of beta-blocker in diastolic heart failure; Japanese Diastolic Heart Failure Study (J-DHF)

BACKGROUND: Heart failure consists of two phenotypes: systolic heart failure and diastolic heart failure (DHF). A growing body of evidence demonstrated benefits of beta-blocker, angiotensin-converting enzyme inhibitor, and angiotensin II receptor blocker in systolic heart failure; however, evidence leading to therapeutic strategy of DHF is lacking. METHODS AND RESULTS: The Japanese Diastolic Heart Failure Study (J-DHF) is a multicenter, prospective, randomized trial designed to assess effects of beta-blocker in patients with DHF. A total of 800 patients (400 patients in each group) will be enrolled. The primary outcome is a composite of cardiovascular death and unplanned admission to hospital for congestive heart failure. Other outcomes include all-cause mortality, worsening of the symptoms of heart failure, or a need for modification of the treatment for heart failure. Serial assessment of echocardiographic and neurohumoral parameters and cost analysis of the treatment regimen will be conducted. The follow-up period is a minimum of 2 years. CONCLUSION: This study will provide important evidences for the treatment of DHF.     

Improvement of endothelial dysfunction by angiotensin II blockade accompanied by induction of vascular hepatocyte growth factor system in diabetic spontaneously hypertensive rats

 Hepatocyte growth factor (HGF) is a unique growth factor with many protective functions. Previously, we demonstrated that HGF stimulated growth of endothelial cells without replication of vascular smooth muscle cells (VSMC) and that angiotensin (Ang) II significantly decreased local HGF production in VSMC. Moreover, we also reported that high glucose significantly decreased local vascular HGF production. Therefore, we examined effects of Ang II blockade on vascular HGF expression and endothelial injury in diabetic hypertensive rats. An angiotensin-converting enzyme inhibitor (quinapril) and an Ang II type 1 receptor antagonist (GA-0113) or vehicle was administrated to diabetic spontaneously hypertensive rats (SHR-DM), in whom diabetes was induced by streptozotocin. Endothelial function was evaluated by the vasodilator response to acetylcholine, and the expression of vascular HGF and its receptor, c-met, was examined by immunohistochemistry. Both quinapril and GA-0113 significantly improved the vasodilator response to acetylcholine (P < 0.01), while vehicle did not as compared to untreated normotensive Wistar-Kyoto rats (WKY). We next examined the effects of Ang II blockade on vascular HGF expression in SHR-DM. Importantly, the vascular HGF level was markedly decreased in SHR-DM as compared to WKY, while Ang II blockade by quinapril or GA-0113 significantly increased positive staining for HGF in SHR-DM. Similarly, staining of its specific receptor, c-met, was less in the blood vessels of SHR-DM as compared to WKY. In contrast, Ang II blockade also significantly increased c-met production in SHR-DM. The present data demonstrated the improvement of endothelial dysfunction by Ang II blockade in SHR-SM, accompanied by an increase in vascular HGF and c-met. Received: June 7, 2002 / Accepted: September 21, 2002 Acknowledgments We wish to thank Rie Kosai and Keiko Yamaguchi for their excellent technical assistance. This work was partially supported by grants from the Japan Health Sciences Foundation, a Grant-in-Aid from The Ministry of Public Health and Welfare, a Grant-in-Aid for the Development of Innovative Technology, a Grant-in-Aid from Japan Promotion of Science, and through Special Coordination Funds of the Ministry of Education, Culture, Sports, Science and Technology, the Japanese Government. Correspondence to N. Tomita     

Failure to find an association between CD14-159C/T polymorphism and asthma: a family-based association test and meta-analysis.

BACKGROUND: CD14 is an essential component of the receptor for lipopolysaccharide (LPS). LPS stimulates T-helper type 1 (Th1) cytokine expression, potentially suppressing Th2 immune responses involved in IgE-mediated allergic diseases. Previous studies have reported that -159C/T, a promoter polymorphism of CD14, is associated with total serum IgE levels and atopy, but other studies have shown conflicting results. METHODS: To examine possible associations of CD14 polymorphisms with asthma susceptibility, we performed transmission disequilibrium tests (TDTs) of 137 Japanese families identified through children with atopic asthma. RESULTS: We found no association between -159C/T polymorphism and asthma (p= 0.37). Quantitative TDT and ANOVA showed no association between the -159C/T genotype and total serum IgE levels. We also performed a meta-analysis of data from all available studies. Neither a fixed-effects model nor a random-effect model showed a significant odds ratio for the -159C/T polymorphism (p > 0.1). CONCLUSIONS: Our data indicate that CD14 does not contribute substantially to susceptibility to asthma. Further studies examining both genotypes and environmental factors will be necessary to elucidate the role of CD14 in the development of allergic diseases.