Clinical pathway for bleeding peptic ulcers]

We devised and evaluated a clinical pathway (CP) protocol for patients with bleeding peptic ulcers (BPU). Patients without severe comorbidities, who had been diagnosed with BPU and who had undergone endoscopic treatment, were enrolled in our study. The CP adaptation rate for BPU patients was 78.8% (89/113). The variance rate was 13.5% (12/89). The median length of admission was 10.0 +/- 4.6 days (n = 78) before and 7.4 +/- 2.9 days (n = 77) after introducing CP. Our CP for BPU was safe and resulted in shorter hospital stays and, therefore, cost reductions. In elder patients, our CP was also successful, but the variance rate was higher than in younger patients.     

Experimental and clinical studies of urethral anesthesia on etiology and treatment of detrusor-sphincter dyssynergia

We studied whether detrusor-sphincter synergia during micturition was obtained by means of urethral anesthesia with lidocaine hydrochloride in five thoracic spinal cats and eight clinical cases with detrusor-sphincter dyssynergia. In thoracic spinal cats with detrusor-sphincter dyssynergia, urethral anesthesia produced detrusor-sphincter synergia, an increase in the maximum bladder pressure and a decrease in the residual volume. In clinical cases with detrusor-sphincter dyssynergia, urethral anesthesia produced detrusor-sphincter synergia or a decrease in the external urethral sphincter activities during micturition, and a decrease in the maximum urethral closure pressure and the residual volume. There were no remarkable changes of the external urethral sphincter activities during urine storage phase before and after urethral anesthesia in both spinal cats and clinical cases. These results suggest that urethral anesthesia blocks the urethro-urethral contraction reflex and secondarily activates vesico-urethral relaxation reflex. The block of urethral sensory nerves is thought to effectively treat detrusor-sphincter dyssynergia.     

Prediction of hematogenous recurrence in patients with esophageal carcinoma

Objectives: Despite recent advances in diagnosis and treatment of esophageal carcinoma, the future risk of hematogenous recurrence is still unpredictable. To identify risk factors of hematogenous recurrence in esophageal carcinoma, we used pathological and immunohistochemical analysis to examine relationships among clinical outcomes, clinicopathological features, and E-cadherin expression.Methods: Subjects were 102 patients with thoracic esophageal cancer who had undergone curative esophagectomy without preoperative treatment. We used univariate and multivariate logistic regression analyses to examine the relationship among clinical outcomes, clinicopathological features, and E-cadherin expression.Results: There was no significant relationship between E-cadherin expression and clinicopathological features at operation. However, the survival rates of patients with E-cadherin-negative tumors were significantly lower than those of patients with E-cadherin-weak and E-cadherin-positive tumors (P<0.01). Disease recurrence had occurred in 49 (48.0%), with hematogenous recurrence in 29 (28.4%), of the 102 patients at the time of analysis. Metastasis occurred in liver in 14 patients, lung in 13, bone in 6, and brain in 2. Comparisons of hematogenous recurrences and clinicopathological features by multivariate regression analyses revealed significant associations between hematogenous recurrences; particularly in liver and lung metastasis and negative E-cadherin expression. With regard to the associations between the organ with the recurrence and the number of positive nodes; hematogenous recurrence, equal to or higher than lymphatic recurrence, was more likely to have occurred in patients with high numbers of positive nodes. Interestingly, with regard to the sites of positive nodes, liver metastasis was closely correlated with lymph node metastasis in the mid-thoracic as opposed to the abdominal region. Further, lung metastasis was most likely to occur in patients with cervical lymph node metastasis.Conclusions: Esophageal carcinoma with negative E-cadherin expression tended to be associated with hematogenous recurrence, particularly with liver and lung metastasis. Hematogenous recurrences were significantly associated with high numbers and the site of positive nodes, as well as with lymphatic recurrence. Read at the Fifty-fifth Annual Meeting of The Japanese Association for Thoracic Surgery, Symposium, Fukuoka, October 9–11, 2002.     

DNA mutilation of the pepsin 1 gene during rat glandular stomach carcinogensis induced by N-methyl-N'-nitro-N-nitrosoguanidine or catechol

The methylation patterns of the rat pepsinogen 1 (Pg1) genein preneoplastic and neoplastic stomach lesions induced by genotoxicN-methyl-N'-nitro-N-nitrosoguanidine (MNNG) or the non-genotoxiccarcinogen catechol were investigated. Male WKY/Ncrj rats weregiven MNNG in their drinking water (50 mg/l) for 30 weeks or0.8% catechol throughout the experiment (60 weeks). MNNG inducedPg1 altered pyloric glands (PAPG), adenomatous hyperplasiasand well-differentiated adenocarcinomas. Catechol also inducedPAPG and adenomatous hyperplasias although cancers did not develop.Adenomatous hyperplasias and adenocarcinomas all consideredof gastric type cells resembling surface mucous cells or pyloricgland cells with little or no Pg1 expression. In MNNG-inducedstomach cancers generally lacking Pg1, altered Pg1 gene methylationwas observed with both CCGG and GCGC sites being methylatedmore than normal pyloric mucosa. MNNG or catechol-induced adenomatoushyperplasias also demonstrated essentially the same methylationchanges in the CCGG, but not in the GCGC sites. In the mucosacontaining PAPG in groups treated with MNNG or catechol themethylation patterns of the Pg1 gene were quite similar to thoseof normal pyloric mucosa, although the CCGG sites tended todemonstrate slightly increased methylation. The results suggestthat the altered methylation of the Pg1 gene observed in stomachcancers is acquired early in the carcinogenic process and progressivemethylation changes occur with tumor development.     

Increases levels of circulating intercellular adhesion molecule-1 in multiple sclerosis and human T-lymphotropic virus type I-associated myelopathy

We evaluated the presence of soluble intercellular adhesion molecule-1(slCAM-1)antigen in the sera of patients with multiple sclerosis and human T-lymphotropic virus type I(HTLV-I)-associated myelopathy (HAM) using an enzyme-linked immunosorbent assay. Patients with multiple sclerosis in the active phase had higher sICAM serum levels than did control subject (p < 0.01). In addition, a significantly increased serum level of sICAM-1 was found in patients with HAM ( p < 0.001). Furthermore, we found a positive correlation with HAM sICAM-1 and tumor necrosis factor-α levels in the sera of patients with multiple sclerosis in the active phase (=0.88, p < 0.01) and in those with HAM (r=0.86, p < 0.01). These results suggest that serum sICAM-1 may be related to clinical activity in patients with multiple sclerosis and the detection of sICAM-1 could be useful as a marker of inflammatory disease.     

Successful treatment with a small dose of N4-behenoyl-1-beta-D-arabinofuranosylcytosine in a case of chronic myelomonocytic leukemia in blastic crisis

A 56-year-old female was admitted for the examination of leukocytosis in May, 1982. The hematological examination showed hemoglobin 12.0g/dl, platelets 14.5 X 10(4)/microliters and leukocytes 18,000/microliters with 28% of monocytes. A bone marrow aspiration revealed granulocytic hyperplasia. Granulocytes showed nuclear abnormalities, such as folding or lobulation. From these data, a diagnosis of chronic myelomonocytic leukemia (CMMoL) was made and followed with no treatment for 2 years. However, fever, bone pain, anemia, thrombocytopenia and the increase of monoblasts in the peripheral blood and bone marrow were observed in May, 1984. These findings indicated that she was in the blastic phase. She was treated by intensive combination chemotherapy (BHAC-AMP), but did not attain any remission. Therefore, a small dose of N4-behenoyl-1-beta-D-arabinofuranosylcytosine (BH-AC; 1 mg/kg/day) was administered for 70 days. As a result, complete remission was obtained and continued for 37 months with the same therapy. The experience of this case suggests that small dose of BH-AC could be applied to a case of CMMoL in blastic crisis.     

Anomalous arrangement of pancreaticobiliary ductal system associated with cholangiocellular carcinoma

A 66-year-old man with congenital cystic dilatation of the common bile duct (CDB; Alonso-Lej Type I) and anomalous arrangement of the pancreaticobiliary ductal system (AAPB) associated with intrahepatic bile duct cancer (cholangiocellular carcinoma; CCC) underwent an extended right hepatic lobectomy. In the resected specimen, the CCC was located in Couinaud’s segment V, with invasion to segment IV and the right hepatic duct and right portal vein. However, there was no cancer involvement of the dilated extrahepatic bile ducts, except for histologic findings of chronic inflammatory cellular infiltration and intestinal metaplasia. It is presumed that the probable mechanisms underlying carcinogenesis in CCC developing from the epithelium of intrahepatic bile ducts are the same mechanisms as those operating in carcinoma of the extrahepatic bile duct in patients with AAPB, although AAPB associated with CCC is uncommon. AAPB appeared to be related to the development of the CCC.     

Nasal lymphoma of natural killer cell origin

We report a case of nasal lymphoma with characteristics of natural killer (NH) cells. A 44-year-old man was admitted to our hospital because of right nasal obstruction. Physical examination revealed a tumor in the right nasal cavity and swelling of the right cervical lymph nodes. Histopathological examination showed diffuse medium sized cell lymphoma. The neoplastic cells expressed CD2, NKH-1, HLA-DR and leukocyte common antigen, but lacked other T-cell, B-cell and myeloid markers. They were in germline configuration for immunoglobulin heavy chain and T-cell receptor genes by southern blot analysis. These findings suggest that they are derived from NK cell.