Repair using the pectoralis major musculocutaneous flap for refractory anastomotic leakage after total esophagectomy.

BACKGROUND: The pectoralis major musculocutaneous flap (PMMF) is a pedicled flap often used as a reconstruction option in head and neck surgery, especially in cases with poor wound healing. However, applying PMMF after esophageal surgery is uncommon. We report here, the case of a successfully repaired refractory anastomotic fistula (RF) after total esophagectomy, by PMMF. CASE PRESENTATION: A 73-year-old man had a history of hypopharyngolaryngectomy, cervical esophagectomy, and reconstruction using a free jejunal graft for hypopharyngeal carcinosarcoma at the age of 54. He also received conservative treatment for pharyngo-jejunal anastomotic leakage (AL), then postoperative radiation therapy. This time, he was diagnosed with carcinosarcoma in the upper thoracic esophagus; cT3rN0M0, cStageII, according to the Japanese Classification of Esophageal Cancer 12th Edition. As a salvage surgery, thoracoscopic total resection of the esophageal remnant and reconstruction using gastric tube via posterior mediastinal route was performed. The distal side of the jejunal graft was cut and re-anastomosed with the top of the gastric tube. An AL was observed on the 6th postoperative day (POD), and after 2 months of conservative treatment was then diagnosed as RF. The 3/4 circumference of the anterior wall of the gastric tube was ruptured for 6 cm in length, and surgical repair using PMMF was performed on POD71. The edge of the defect was exposed and the PMMF (10 × 5 cm) fed by thoracoacromial vessels was prepared. Then, the skin of the flap and the wedge of the leakage were hand sutured via double layers with the skin of the flap facing the intestinal lumen. Although a minor AL was observed on POD19, it healed with conservative treatment. No complications, such as stenosis, reflux, re-leakage, were observed over 3 years of postoperative follow-up. CONCLUSIONS: The PMMF is a useful option for repairing intractable AL after esophagectomy, especially in cases with large defect, as well as difficulties for microvascular anastomosis due to previous operation, radiation, or wound inflammation.

Postchallenge plasma glucose and glycemic spikes are associated with pulse pressure in patients with impaired glucose tolerance and essential hypertension.

Elevated pulse pressure (PP) is associated with an increased risk of cardiovascular events. We examined whether PP is associated with post-challenge hyperglycemia in Japanese patients with essential hypertension and impaired glucose tolerance (IGT). In a total of 70 untreated essential hypertensive patients (age: 57+/-4 years, mean+/-SD; males=35, females=35), 24-h ambulatory blood pressure (ABP) monitoring, 75 g oral glucose tolerance testing (OGTT), metabolic analysis and echocardiography were performed. Patients were categorized into a high PP group (PP>or=60 mmHg, n=33) or a normal PP group (PP<60 mmHg, n=37). In all patients, 24-h systolic ABP, daytime systolic ABP, nighttime systolic ABP, and nighttime heart rate were significantly higher in the high PP group. Additionally, fasting immunoreactive insulin (F-IRI), homeostasis model assessment (HOMA) index, left ventricular mass index (LVMI) were also elevated in the high PP group. Finally, the high PP group exhibited impaired insulin secretion, increased post-challenge glucose concentrations and greater glucose spikes (PGS) during 75 g OGTT. Of the parameters measured, 24-h PP correlated positively with age, triglyceride, uric acid, F-IRI, HOMA index, 1-h postload glucose and insulin, 2-h postload glucose and insulin, PGS60, PGS120, PGSmax, LVMI, and deceleration time but correlated negatively with HDL-cholesterol and E/A ratio. Multiple regression analysis revealed that PP level was independently predicted by age, LVMI, and PGS120. Our results show that age, LVMI, and PGS120 are significantly associated with high PP in Japanese patients with IGT and essential hypertension.

Lipoprotein (a) as a risk factor for silent cerebral infarction in hemodialysis patients.

In patients with chronic renal failure undergoing hemodialysis (HD), silent cerebral infarctions (SCIs) are associated with high mortality. Levels of lipoprotein (a) (Lp[a]) increase with renal dysfunction and may be a novel predictor for cerebrovascular events. We tested the hypothesis that increased Lp(a) levels correlate with the occurrence of SCI in HD patients. Using cranial magnetic resonance imaging findings, we divided 62 Japanese patients undergoing HD into with-SCI group (61 +/- 7 years, mean +/- SD, n = 34) and without-SCI group (60 +/- 6 years, n = 28). We compared the sex, body mass index, metabolic profiles, Lp(a) levels, and smoking habits between the 2 groups. The following observations were noted: (1) The number of patients with diabetes or hypertension did not differ between the 2 groups. (2) The levels of Lp(a) were higher in the with-SCI group in comparison with the without-SCI group (P < .0001). (3) The proportion of smokers was higher in the with-SCI group than in the without-SCI group (P < .05). (4) Plasma levels of high-density lipoprotein cholesterol were lower, whereas uric acid was higher, in the with-SCI group than in the without-SCI group (P < .001 and P < .05, respectively). (5) Multiple logistic regression analysis identified Lp(a) levels as being significantly associated with the presence of SCI (odds ratio, 1.23; 95% confidence interval, 1.09-1.38; P < .0001). This study indicates that patients with chronic renal failure, who are maintained on HD, exhibit an increased prevalence of SCI and that Lp(a) is significantly associated with the presence of SCI in HD patients.

High-sensitivity C-reactive protein level is a significant risk factor for silent cerebral infarction in patients on hemodialysis.

In patients with chronic renal failure on hemodialysis (HD), silent cerebral infarctions (SCIs) are associated with high mortality. The levels of high-sensitivity C-reactive protein (HSCRP), a marker of inflammation and atherosclerosis, elevate with increasing renal dysfunction. We tested the hypothesis that increased HSCRP levels correlate with the occurrence of SCI in HD patients. By brain magnetic resonance imaging findings, we divided 54 patients undergoing HD into a with-SCI group (61 +/- 8 years, n = 30) and a without-SCI group (60 +/- 7 years, n = 24). We compared sex, body mass index, metabolic profiles, HSCRP levels, and smoking habits in Japanese patients on HD with and without SCI. We made the following observations: (1) The number of patients with diabetes or hypertension did not differ between the 2 groups. (2) The levels of HSCRP were higher in the with-SCI group in comparison with the without-SCI group (P < .0001). (3) The proportion of smokers was higher in the with-SCI group than in the without-SCI group (P < .05). (4) Plasma levels of high-density lipoprotein cholesterol were lower, whereas uric acid was higher, in the with-SCI group than in the without-SCI group (P < .05 and P < .0001, respectively). (5) Multivariate logistic analysis identified HSCRP levels as being significantly associated with the presence of SCI (odds ratio, 1.61; 95% confidence interval, 1.17-2.85; P < .001). This study indicates that patients in chronic renal failure who are maintained on HD exhibit an increased prevalence of SCI and that HSCRP is significantly associated with the presence of SCI in HD patients.

[Case of advanced gastric cancer successfully treated with chemotherapy of weekly paclitaxel].

We report a case of gastric cancer with ascites treated with chemotherapy. The patient is a 67-year-old male. Combination chemotherapy of S-1 and CDDP was given as the first-line treatment. However, the symptoms did not improve with that regimen, so we decided to change the chemotherapy to paclitaxel as second-line treatment. After 4 cycles, CT scan revealed decreasing ascites and endoscopy a reduction of the primary tumor. The patient has maintained a condition of decreasing ascites with improvement of QOL for 8 months. This regimen is considered effective treatment for unresectable gastric cancer.

High-density lipoprotein cholesterol and insulin resistance are independent and additive markers of left ventricular hypertrophy in essential hypertension.

We examined whether plasma high-density lipoprotein-cholesterol (HDL-C) levels and glucose metabolism parameters are independent or additive predictors of left ventricular hypertrophy (LVH) in patients with untreated essential hypertension. The study group consisted of 41 Japanese patients with untreated essential hypertension and LVH (left ventricular mass index [LVMI] >125 g/m2; age 58+/-6 years, mean+/-SD), and the control group consisted of 39 age-matched patients with untreated essential hypertension without LVH (LVMI

Correlations of urinary albumin excretion and atherosclerosis in Japanese type 2 diabetic patients.

Microalbuminuria and aortic stiffness are associated with high mortality in type 2 diabetic patients. We tested the hypothesis that the presence of microalbuminuria correlates with aortic stiffness and insulin resistance in type 2 diabetic patients. The study consisted of 36 Japanese patients with type 2 diabetes and microalbuminuria (age: 56+/-9 years, mean+/-S.D.) and a control group of 44 age-matched patients with normoalbuminuria (56+/-7 years). Brachial-ankle pulse wave velocity (BaPWV) was measured by automatic oscillometric method. BaPWV was used as an index of atherosclerosis. The BaPWV was higher in the microalbuminuria group than in the normoalbuminuria group (p<0.005). Fasting plasma glucose (p<0.05) and insulin concentrations (p<0.005), and the homeostasis model assessment (HOMA) index (p<0.0005), were higher in the microalbuminuria group than in the normoalbuminuria group. Multiple regression analysis showed that urinary albumin excretion was independently predicted by BaPWV and HOMA index. Our results indicate that the presence of microalbuminuria in Japanese patients with type 2 diabetes is characterized by increased aortic stiffness and insulin resistance, and that the BaPWV, HOMA index are independent predictors of urine albumin excretion.

Role of protein kinase C in geranylgeranylacetone-induced expression of heat-shock protein 72 and cardioprotection in the rat heart.

We recently demonstrated that oral administration of geranylgeranylacetone (GGA), an antiulcer agent, induces heat-shock protein 72 (HSP72) in the rat heart and renders cardioprotection against ischemia/reperfusion injury. However, the signaling pathways remain to be elucidated. The present study tested the hypothesis that oral GGA would activate protein kinase C (PKC), leading to the phosphorylation and translocation of heat-shock factor 1 (HSF1), and thus, promote the expression of HSP72 protein. Rats were classified into four groups: a control (CNT) group (vehicle administration), a GGA group (GGA 200 mg/kg administration), a chelerythrine (CHE)-CNT group (pretreated with intravenous (i.v.) injection of 5 mg/kg CHE before vehicle administration), and a CHE-GGA group (pretreated with CHE before GGA administration). After 24 h administration, oral GGA-induced overexpression of HSP72, increased amount of the phosphorylated form of HSF1 in the nucleus, produced heat-shock element-specific DNA-HSF1 complex, and caused translocation of protein kinase C (PKC)delta, all of which were prevented by pretreatment with CHE. GGA also increased the PKC activity in a particulate fraction, which was prevented by pretreatment with rottlerin, a specific inhibitor of PKCdelta. Isolated-perfused heart experiments revealed that the better functional recovery observed in the GGA group during the reperfusion period following the 20 min of no-flow global ischemia, compared with the CNT group, was abolished by pretreatment with CHE. These results suggest that activation of PKC (translocation of PKCdelta), which primes the phosphorylation of HSF1, plays an essential role in the cardiac overexpression of HSP72 by GGA that leads to cardioprotection.

Cardioprotection by streptozotocin-induced diabetes and insulin against ischemia/reperfusion injury in rats.

The effects of streptozotocin (STZ)-induced diabetes (DM) and insulin on cardiac performance were investigated during reperfusion after low-flow ischemia in rats. Hearts were isolated 4 weeks after intravenous injection of STZ (65 mg/kg) or vehicle and retrogradely perfused in the presence (throughout the perfusion period) or absence of 1 U/L insulin using a Langendorff apparatus. Normothermic low-flow global ischemia was instituted by reducing the flow rate to 5% of baseline for 30 min, followed by reperfusion for 30 min. Rate pressure product (left ventricular developed pressure x heart rate) was calculated as an index of cardiac performance. Myocardial concentrations of adenine nucleotides, creatine phosphate (CP) and glycogen were measured. Insulin perfusion increased preischemic myocardial glycogen content in both DM and control hearts. Recovery of cardiac performance and myocardial CP concentrations in the absence of insulin was greater in the DM hearts than in controls during reperfusion. Insulin perfusion improved recovery of cardiac performance and elevated CP concentrations in both DM and control hearts. These results demonstrate greater cardioprotection against ischemia/reperfusion injury in the STZ-DM state and with insulin perfusion. These protective effects may be associated with augmented resynthesis of high-energy phosphates during reperfusion.