Distant Peritoneal Metastasis to a Mesh-Plug Prosthesis in a Gastrointestinal Cancer Patient: Report of a Case

A case of distant metastasis to mesh-plug prosthesis in gastrointestinal cancer is presented herein. An 88-year-old man had received mesh-plug repair with high ligation for a recurrence of a right inguinal hernia. Six months later, advanced gastric cancer and advanced transverse colon cancer were detected, and therefore a distal gastrectomy and partial colectomy were performed. Two weeks after the operation, the patient complained of right groin tenderness, and the mesh-plug prosthesis was removed to control any infection. A histopathological investigation demonstrated adenocarcinoma in the plug prosthesis. The patient died of carcinomatosis peritonei 45 days after the last operation.     

Successful treatment of lymph node metastases recurring from gallbladder cancer

A 66-year-old woman who had undergone cholecystectomy for the treatment of gallbladder cancer 5 years and 10 months previously was referred to our center due to increased carbohydrate antigen (CA)19-9. Increased CA19-9 (136 U/ml) was the only abnormality detected on initial examination, and, despite various tests, clear signs of recurrence could not be detected. Subsequently, the patient was followed. Six months after the initial examination, dynamic computerized tomography confirmed lymphadenopathy. The results of fluoro-deoxy-glucose positron emission tomography suggested lymph node metastasis of the gallbladder cancer, and after consideration of the site of recurrence and the length of time between the primary surgery and detection of recurrence, the patient underwent extrahepatic bile duct resection and lymphadenectomy. Levels of CA19-9 normalized postoperatively, and, at the time of writing (26 months postoperatively), blood tests and diagnostic imaging revealed no signs of recurrence. Received: May 6, 2002 / Accepted: October 23, 2002 RID="*" ID="*" Offprint requests to: K. Tasaki     

The impact of repeated subclinical acute rejection on the progression of chronic allograft nephropathy

Chronic allograft nephropathy (CAN) is due to both immunologic and non-immunologic factors and results in the development of nonspecific pathologic features that may even be present in long-term well-functioning renal allografts. To investigate the natural history of CAN and potential risk factors associated with progression of these histologic lesions, this study evaluated the of histologic alterations of 124 sequential protocol biopsies performed at 2, 3, and 5 yr after transplantation in 46 patients who exhibited histologic evidence of CAN in the 1-yr biopsy. The occurrence of late acute rejection (AR) greater than 4 mo posttransplant was significantly associated with the development of histologic CAN. In contrast, early clinical AR occurring within 3 mo had no impact on the subsequent development of CAN at 1 yr. Subclinical AR was evident in association with CAN in 50%, 32%, 19%, and 16% of cases with CAN at 1, 2, 3, and 5 yr, respectively. These acute lesions correlated significantly with histologic progression defined as an increased CADI score of the follow-up biopsies. Furthermore, a group of patients who exhibited repeated subclinical AR in the sequential follow-up biopsies had a lower creatinine clearance at 5 yr after transplantation and worse long-term graft survival. In contrast, the absence of evidence of acute inflammation in association with CAN at any time point was associated with minimal deterioration in renal function or progression of renal lesions during the observation period. These results suggest that the persistence of chronic active inflammation may be responsible for the histologic progression of CAN.     

Effect of arch supports on ankle-subtalar complex instability: a biomechanical experimental study

BACKGROUND: Subtalar instability, which may cause persistent symptoms after severe inversion ankle sprains, often involves failure of the interosseous talocalcaneal ligament (ITCL). While several clinicians have reported surgical treatment for this pathology, nonsurgical management policy has not been well considered. Previously, it was proposed that ITCL failure possibly causes looseness of the tarsal arch construction resulting in abnormal ankle-subtalar kinematics occurring with axial forces. In the current study the author hypothesized that arch-support insole functions to improve abnormal joint kinematics in ankle-subtalar complex instability. METHODS: Five fresh-frozen cadaver lower extremities with simulated ankle-subtalar complex instability, which was created by combined sectioning of the anterior talofibular ligament (ATFL) and the ITCL, were subjected to a biomechanical experiment. Cyclic axial loading from 9.8 to 668 N was applied with a material testing machine, while three-dimensional angular displacements in both the ankle and subtalar joints were determined with electric goniometers. The specimens were tested before and after inserting an arch-support insole that supports the medial-longitudinal and transverse arches of the foot. RESULTS: Inserting the insole decreased the maximum ankle internal rotation, from 3.3 degrees +/- 0.9 degrees to 2.3 degrees +/- 0.4 degrees (p = .028), while subtalar rotation was not significantly changed. CONCLUSIONS: The medial longitudinal arch-support insole reduced abnormal ankle internal rotation created by combined sectioning of the ATFL and ITCL, likely due to improved arch configuration stability.     

Role of nitric oxide and prostaglandin E2 in acute renal hypoperfusion

Although acute renal ischaemia alters the production of various paracrines, there has been little investigation examining the role of intrarenal vasoactive substances. In the present study, we investigated the role of intrarenal nitric oxide and prostaglandins in modulating the acute renal hypoperfusion-induced alterations in renal function. After a 90% clipping of the left renal artery for 60 min, the clip was released, and the renal haemodynamics and sodium excretion were evaluated in both clipped and non-clipped kidneys of anaesthetized dogs. Furthermore, the changes in renal contents of nitrate/nitrite (NOx) and prostaglandin E2 (PGE2) were assessed by using the renal microdialysis technique. The release of the clipping elicited a gradual recovery of renal plasma flow and glomerular filtration rate, and a sustained increase in fractional sodium excretion (FENa) in the clipped kidney. Renal interstitial NOx was reduced in both the cortex (from 8.2 +/- 1.1 to 2.5 +/- 0.3 micromol/L, P < 0.01) and medulla (from 10.1 +/- 0.9 to 3.1 +/- 0.2 micromol/L, P < 0.01), but the levels gradually elevated after declamping. The treatment with nitro-l-arginine methylester only modestly impaired the recovery of renal plasma flow (RPF; at hour 4) and glomerular filtration rate (GFR; at hours 3 and 4 after declamping), without affecting FENa. Conversely, the renal PGE2 levels increased prominently upon the onset of ischaemia (medulla, from 149 +/- 19 to 378 +/- 39 pg/mL, P < 0.01; cortex, from 107 +/- 13 to 302 +/- 34 pg/mL, P < 0.01). Furthermore, the pretreatment with a non-specific cyclo-oxygenase (COX) inhibitor, sulpyrine, and a COX-2-specific inhibitor, NS398, prominently inhibited the increases in FENa induced by the acute renal arterial clipping in a similar manner. In conclusion, in acute renal hypoperfusion, nitric oxide (NO) plays a permissive role in the recovery of the renal haemodynamics. In contrast, sustained increases in renal PGE2 in both clipped and non-clipped kidneys indicate that the COX-2-mediated PGE2 contributes importantly to the failure of the sodium reabsorption in response to acute renal hypoperfusion.     

Past medical history and risk of death due to hepatocellular carcinoma, univariate analysis of JACC study data

The relationship between the past history of selected diseases and the risk of dying from hepatocellular carcinoma (HCC) was analyzed using 110,792 cohort members (46,465 males and 64,327 females) recruited between 1988 and 1990 by the JACC Study (the Japan Collaborative Cohort Study for Evaluation of Cancer Risk). Significantly elevated hazard ratios (HRs) were observed in both genders for the past history of kidney diseases, liver diseases, gallstones or cholecystitis, diabetes mellitus, and blood transfusion. Further, when analyzed by age group (those 40-59 years of age were "younger" and those 60-79 years of age were "older"), although the significant associations were generally maintained, the magnitude of the HRs for liver diseases and diabetes mellitus seemed to be considerably different between the younger and older age groups for male cohort members. When the analyses were limited to cohort members without the past history of liver diseases, the past histories which had significantly elevated HRs were hypertension (HR = 3.14, 95% confidence interval (CI): 1.25-7.89), diabetes mellitus (HR = 4.17, 95% CI: 1.22-14.25), and blood transfusion (HR = 7.69, 95% CI: 3.09-19.15) in the younger male age group and gallstone or cholecystitis (HR = 2.58, 95% CI: 1.11-5.98) in the older male age group. On the other hand, for females, the significantly elevated HRs were gastric or duodenal ulcer (HR = 4.33, 95% CI: 1.09-17.25) in the younger age group and diabetes mellitus (HR = 6.16, 95%CI: 2.25-16.90) and blood transfusion (HR = 3.86, 95%CI: 1.58-9.41) in the older age group. However, since the evidence from our univariate analyses might not be decisive, multivariate Cox proportional hazards models controlling for potential confounders and effect modifiers will be required to obtain more valid or unbiased hazard ratios.     

Nitric oxide synthase expressions in rat dorsal root ganglion after a hind limb tourniquet

We investigated the mRNA levels of neuronal, inducible, endothelial nitric oxide synthases (nNOS, iNOS, eNOS) and tumor necrosis factor-alpha (TNF-alpha) in a rat dorsal root ganglion (DRG) after tourniquet application to a hind limb to identify molecules that trigger secondary events after peripheral nerve injury. Significantly high nNOS, iNOS mRNA and protein levels were observed in the ipsilateral DRGs 4 h after tourniquet application but not in the contralateral or control DRGs. The levels of TNF-alpha, an inducer of iNOS, were significantly increased in the ipsilateral DRGs 1 h after tourniquet application. Large amounts of NO might result in damage to the host cells and induce apotosis to eliminate damaged cells during the early stage of nerve injury.