Adenocarcinoma arising at the ileoileal anastomotic site of Scheele''s ring

Most tumors arising after augmentation ileocystoplasty have been reported to develop adjacent to the ileovesical anastomosis. Herein, we report a case of adenocarcinoma arising at the ileoileal anastomotic site 33 years after augmentation ileocystoplasty (Scheele's ring plasty) for tuberculous contracted bladder. The present case shows the possibility of late malignancy developing at the ileoileal junction after ileal neobladder.     

Clinical utility of ursodeoxycholic acid in preventing flutamide-induced hepatopathy in patients with prostate cancer: A preliminary study

BACKGROUND: The present study was designed to ascertain retrospectively the validity of ursodeoxycholic acid (UDCA) in the treatment of prostate cancer in terms of prophylactic effects on the occurrence of flutamide-induced hepatopathy in a large number of patients surveyed in a multi-center cooperative study. METHODS: One hundred and eighty-one patients (74.1 +/- 4.9 years) with prostate cancer treated with flutamide with (n = 70) or without (n = 111) UDCA were retrospectively evaluated and the occurrence of hepatopathy was compared between these two patient groups. RESULTS: Between patients treated with UDCA and those without it, no significant differences were noted in age, clinical stage, grade, duration of flutamide administration and serum prostate-specific antigen (PSA) levels before treatment. However, there were significant differences in the presence or absence of previous treatments and treatments used together with flutamide. The incidence of hepatopathy was 11.4% (8/70) in patients with UDCA and 32.4% (36/111) in those without it, showing a statistically significant difference (P < 0.05). The hepatopathy-free rate obtained by the Kaplan-Meier method was also significantly higher in patients with UDCA (88.4% 1 year following flutamide administration) than that in those without it (59.6%) (P < 0.005). CONCLUSION: These results suggest that UDCA has a prophylactic effect against flutamide-induced hepatopathy in patients with prostate cancer.     

Changes in extent and zonal distribution of prostatic adenocarcinoma in patients preoperatively treated with neoadjuvant endocrine therapy: Analysis on whole-mounted prostatectomy specimens

BACKGROUND: An increasing number of pharmacologic agents that induce reversible androgen deprivation are available for neoadjuvant endocrine therapy (NET) for prostatic adenocarcinoma (PCA). If information about the regression pattern of PCA after NET is recognized, more effective decision-making for subsequent therapies such as prostatectomy and radiotherapy, will be possible. METHODS: The extent and zonal distribution of PCA with or without NET were examined in totally embedded radical prostatectomy specimens obtained from 103 patients with PCA. Seventy-nine of the 103 patients received androgen deprivation therapy (castrated). The zonal location of PCA lesions (non-transition vs transition zone), was identified in three slices from the inferior, middle and superior parts of the prostate. The area of the PCA lesions in these zones was measured. RESULTS: Prostatic adenocarcinoma was identified in 94 of 103 cases: 24 of 24 cases (100%) and 70 of 79 cases (87%) in the non-castrated and castrated groups, respectively. The NET induced a mean of 21% reduction of the prostate volume and lowered the serum PSA level by one eighth. The frequency of capsular penetration in the castrated cases (57%) was lower than in the non-castrated cases (83%) and confinement of the PCA lesion was found in 32% of the castrated and 17% of the non-castrated cases. The reduction rate of the extent of the PCA lesions in the non-transition and transition zone was 33% and 28%, respectively. The extent of the PCA lesions were smaller in the anterior parts, especially at the superior portion of the prostate. CONCLUSION: Neoadjuvant endocrine therapy induced involutional changes of the PCA evenly across both the non-transition and transition zones. The density of the PCA lesions was low in the anterior part of the prostate. This information is useful for decision-making in post-NET.     

Characteristics of patients with staghorn calculi in our experience

PURPOSE: To elucidate the factors contributing to staghorn stone formation in patients. MATERIALS AND METHODS: The records of 82 patients (44 men and 38 women) with complete staghorn calculi were reviewed retrospectively for clinical presentation, metabolic disturbances and anatomical abnormalities. RESULTS: There were 79 unilateral and three bilateral cases. The patient performance of the activities of daily life was assessed with the modified Rankin scale (MRS) and it was found that 69 patients were functionally independent (84.1%, MRS 0-1) and 10 patients had a severe disability (12.2%, MRS 4-5). Seven patients had chronic indwelling catheters (8.5%). A positive urine culture was found in 24.4% of patients. Analysis of stone composition revealed magnesium ammonium phosphate and mixed calcium oxalate-phosphate were the most frequently identified types of stone (32.1% and 22.2%, respectively). Urinary pH was low in patients with uric acid stones (mean 5.4). Hyperuricemia, cystinuria and hypercalciuria were found in 14.6%, 2.4% and 37.8%, respectively. Hypercalciuria was found more frequently in calcium-stone cases. Eleven patients (13.4%) showed structural abnormalities of the kidney. CONCLUSIONS: Our data show that the patients with severe disability, urinary tract infection and hypercalciuria could be recognized more frequently in staghorn calculi compared with common urolithiasis. However, in Western countries, the frequency of both urinary tract infection and struvite stones is much higher than in our data. Other Japanese authors have also reported the low frequency of struvite stones in staghorn calculi, suggesting that various factors other than urinary tract infection possibly contribute to the formation of staghorn calculi in Japan.     

Flow cytometric analysis of cell proliferation kinetics during duodenal ulcer healing

Cell proliferation in the gastroduodenal mucosa of patients with duodenal ulcers was evaluated using flow cytometry. Forty patients with duodenal ulcers and 12 normal subjects were investigated. Biopsy samples were obtained during endoscopic examination and subjected to DNA analysis by flow cytometry. Thirty patients with duodenal ulcers were healed within 3 months with H₂ blockers (tractable or responsive ulcers), whereas 10 patients did not respond to treatment (intractable ulcers). The percentage of cells at the DNA-synthetic phase, an index of cell proliferation, was constant in the adjacent duodenal mucosa 2cm from ulcer margin and antral mucosa during duodenal ulcer healing. The index at the margin of tractable ulcers was elevated during the active stage (12.9 ± 1.3), peaked during the healing stage (15.4 ± 2.8) and returned to the same level at the scarring stage (10.9 ± 2.0) as normal controls (10.3 ± 1.7). However, the index was not elevated in intractable ulcers (10.3 ± 1.7 in the healing stage) and was smaller than in tractable ulcers. These data indicate that augmented mucosal cell proliferation at the ulcer margin plays an important role in duodenal ulcer healing and intractable ulcers are characterized by an abnormal failure to accelerate DNA synthesis to achieve ulcer repair.     

Marked atrophy of the right lobe seen in idiopathic portal hypertension confirmed by laparoscopy

A 70‐year‐old‐male was hospitalized for the treatment of esophageal varices and close examination of the liver. Blood chemistry tests revealed mild liver dysfunction. Abdominal ultrasound and computed tomography scan revealed marked atrophy of the right and quadrate lobes of the liver without abnormalities of the biliary system. Abdominal angiography revealed marked atrophy of the right lobe of the liver, without obliteration in the portal venous system, but it could not be determined whether the atrophy was congenital or secondary. Subsequently performed laparoscopy revealed marked atrophy of the anterior segment of the right lobe and quadrate lobe with the whitish scarred edge demarcating the border between the edge and neighboring liver parenchyma. The liver surface appeared to be undulant, but non‐cirrhotic. These findings suggest secondary lobar atrophy of the liver, without cirrhosis. Liver biopsy of the left lobe showed the findings to be compatible with idiopathic portal hypertension (IPH), and we diagnosed IPH based on these findings and hepatic lobar atrophy was attributable to IPH. There have been few reports of cases with hepatic lobar atrophy associated with IPH, and the mechanism of atrophy is unclear. We report a case of IPH with marked liver atrophy in which laparoscopy is a decisive means whether liver atrophy is congenital or secondary.     

The mechanisms of hepatic sinusoidal endothelial cell regeneration: A possible communication system associated with vascular endothelial growth factor in liver cells

Vascular endothelial growth factor (VEGF) has been shown to induce proliferation of sinusoidal endothelial cells in primary culture. To elucidate the mechanisms of sinusoidal endothelial cell regeneration in vivo, mRNA expression of VEGF and its receptors, flt-1 and KDR/flk-1, were studied in rat livers. Northern blot analysis revealed that VEGF-mRNA was expressed in hepatocytes immediately after isolation from normal rats. In contrast, non-parenchymal cells, including sinusoidal endothelial cells, expressed VEGF receptor-mRNA. Vascular endothelial growth factor-mRNA expression in hepatocytes was decreased during primary culture, but increased following a peak of DNA synthesis, induced by addition of epidermal growth factor or hepatocyte growth factor to the culture medium at 24 h of plating. In a 70% resected rat liver, VEGF-mRNA expression increased with a peak at 72 h after the operation, and mRNA expression of VEGF receptors between 72 and 168 h. In such a liver, mitosis was maximal in hepatocytes at 36 h and in sinusoidal endothelial cells at 96 h. Also, mRNA expression of both VEGF and its receptors was significantly increased in carbon tetrachloride-intoxicated rat liver compared with normal rat liver. Vascular endothelial growth factor expression was minimal in Kupffer cells isolated from normal rats, but marked in activated Kupffer cells and hepatic macrophages from the intoxicated rats. Vascular endothelial growth factor-mRNA expression was also increased in activated stellate cells from these rats and in the cells activated during primary culture compared with quiescent cells. We conclude that increased levels of VEGF expression in regenerating hepatocytes may contribute to the proliferation of sinusoidal endothelial cells in partially resected rat liver, probably through VEGF receptors up-regulated on the cells. Also, VEGF derived from activated Kupffer cells, hepatic macrophages and stellate cells may be involved in this proliferation in injured rat liver.     

Intracavitary administration of OK-432 with subcutaneous priming for malignant ascites in a case of advanced renal cell carcinoma

The intracavitary injection of OK-432 (a streptococcal preparation) with subcutaneous priming has been shown to be an effective immunotherapy for patients with malignant effusion. We applied this treatment in a case of advanced renal cell carcinoma with massive ascites. The patient received 0.2 Klinishe Einheit (KE) OK-432 in the subcutaneous injection twice (day 1 and day 7) followed by 10KE OK-432 intra-abdominal administration (day 9). The treatment was performed safely without major side-effects except for transient pyrexia. A significant reduction of ascites was noted 1 month after the treatment without subsequent re-accumulation. Intracavitary injection of OK-432 with subcutaneous priming seems to be a simple, safe and effective treatment for ascites in advanced renal cell carcinoma.