Laparoscopic treatment of colonic stenosis due to perforation in crohn’s disease

A 23‐year‐old woman was admitted to the Teikyo University Hospital with symptoms of watery diarrhea and left lower abdominal pain. A painful mass was palpated in the left lower abdomen. Abdominal computed tomography demonstrated an inflammatory mass associated with gas accumulation. Abscess formation and perforation of the intestine was strongly suspected. Considering her general condition, antibiotic therapy was adopted first. The size of the mass decreased markedly with antibiotic administration. Upper gastrointestinal series showed no abnormalities in the small intestine. Barium enema showed complete obstruction of the descending colon. Colonoscopy revealed the granular change of the mucosa and stenosis at the descending colon. Non‐caseous granuloma was histopathologically noted. The condition of the patient was diagnosed as colonic stenosis due to the perforation at the descending colon as a complication of Crohn’s disease and laparoscopic resection of the colon was performed. Although marked adhesion was noted around the lesion, surgery was successfully completed. Crohn’s disease is a chronic, potentially panintestinal, incurable affliction. Colonic perforation in Crohn’s disease is a relatively rare complication. Surgical management should be as minimal as possible. Laparoscopic surgery for this particular patient was considered to be an adequate choice of treatment.     

Malignant transformation of renal angiomyolipoma

In the present paper, two cases of malignant transformation of renal angiomyolipoma without tuberous sclerosis are reported. Pathological examination revealed that, in both cases, in addition to the areas affected by typical angiomyolipoma, there were areas that contained elevated numbers of perivascular epithelioid cells with prominent nuclear pleomorphism. Immunohistochemical examination revealed that both cases were negative for keratin and epithelial membrane antigen, but were positive for the melanogenesis-related marker HMB-45. Metastatic diseases appeared 40 months after radical nephrectomy in the first case and 18 months in the second case.     

CASE REPORT: Steatonecrosis in the upper abdomen following transcatheter arterial embolization for hepatocellular carcinoma

A 66-year-old female with liver cirrhosis was treated by transcatheter arterial embolization (TAE) for a small hepatocellular carcinoma. She developed steatonecrosis with tenderness which occurred in the upper abdomen after TAE. The hepatic falciform artery from the middle hepatic artery was detected by arteriography. Necrosis in the upper abdomen was considered to be due to ischaemic changes caused by micromaterials for embolization of this artery, injuries of hepatic arterial endothelia slowly caused by carcinostatics, and chemotoxicity. It was considered that such complication as observed in this patient should be taken into consideration when performing TAE.     

Immunohistochemical analysis of development of desmin-positive hepatic stellate cells in mouse liver

Development of desmin-positive hepatic stellate cells was studied in mice using double immunofluorescent techniques and in vitro cultures with special attention given to their cell lineages. Several studies recently reported on the presence of cells that are immunologically reactive with both antidesmin and anticytokeratin antibodies in young fetal rat livers, and suggested the possibility that these cells give rise to hepatocytes and hepatic stellate cells. At early stages of mouse liver development, stellate cells with desmin-positive filaments were scattered in the liver parenchyma. However, the stellate cells definitely differed from hepatoblasts and hepatocytes in terms of their morphology and expression of desmin and hepatoblast and hepatocyte-specific E-cadherin in the liver. Fetal hepatoblasts and hepatocytes did not react with antidesmin antibodies, nor did desmin-positive stellate cells express E-cadherin in vivo and in vitro. Thus it is likely that desmin-positive stellate cells and hepatoblasts belong to different cell lineages. In the fetal liver, the desmin-positive stellate cells surrounded blood vessels, and extended their processes to haematopoietic cells and megakaryocytes. Many, but not all, hepatoblasts and hepatocytes were observed to be associated with the stellate cells. At fetal stages, cellular processes positive for desmin in the stellate cells were also thick compared with those in the adult liver, in which desmin-positive stellate cells lay in Disse's space and were closely associated with all hepatocytes. These developmental changes in the geography of desmin-positive cells in the liver parenchyma and their morphology may be associated with their maturation and interactions with other cell types.     

The determination of ofloxacin in human skin tissue by high-performance liquid chromatography and correlation between skin tissue concentration and serum level of ofloxacin

Abstract— A simple high-performance liquid chromatographic (HPLC) assay was developed for the measurement of ofloxacin in skin tissue, and the correlation between serum levels and skin tissue levels of ofloxacin was determined. The homogenized skin samples were directly introduced into an HPLC system after filtering through a Molcut II membrane filter to remove proteins. The filtrate was concentrated on a pre-column using a phenyl-stationary phase and was then introduced to an analytical column using an ODS-stationary phase by column-switching techniques. Ofloxacin and lomefloxacin as an internal standard were detected by UV absorbance at 300 nm. Determination was possible for ofloxacin over the concentration range 250–3000 ng (g skin tissue)^?1; the limit of detection was 100 ng g^?1. The absolute recovery of ofloxacin added to skin tissue homogenate was over 72% with a coefficient of variation of less than 4·1%. This method is applied to determination of skin tissue level of ofloxacin in patients after treatment with ofloxacin. The correlation between serum levels and skin tissue levels of ofloxacin was determined for 30 patients after oral administration of ofloxacin. Good correlation was obtained and the coefficient of correlation was 0·84.     

A Case of Small Cell Carcinoma of the Lung Producing ADH, ACTH, MSH and Calcitonin: Successful Treatment of Severe Hyponatremia with Furosemide and Hypertonic Saline

A 48-year-old man with a small cell carcinoma of the lung presentedhyponatremia and was diagnosed as having the syndrome of inappropriateADH secretion. A plasma ADH bioassay confirmed this syndrome.During the clinical course, the patient developed a hyponatremiccrisis with a serum sodium of 108mEq/l. His hyponatremia wasrapidly corrected by infusing furosemide in conjunction withhypertonic saline. The postmortem studies demonstrated ADH bioactivityin the tumor tissues, as well as immunoreactive ACTH, ß-MSHand calcitonin. Tumor hypersecretion of ACTH appeared to bethe cause of the patient's hyperresponsiveness to exogenousACTH and of the bilateral adrenocortical hyperplasia observedat the time of autopsy. Therefore, this was a case of a multiple hormone-producing smallcell carcinoma of the lung, in which the severe clinical manifestationsof SIADH were successfully treated with furosemide and hypertonicsaline.     

Primary adenocarcinoma of the rete testis with preceding diagnosis of pulmonary metastases

We report a case of primary adenocarcinoma of the rete testis in a 55-year-old man with pulmonary metastases that were detected 11 months prior to the diagnosis of the primary lesion. Primary adenocarcinoma of the rete testis is an extremely rare malignant tumor with a poor outcome. The most common primary symptom is a scrotal mass, often accompanied by hydrocele and chronic epididymitis. The diagnosis is often delayed because of non-specific clinical presentation and symptoms. We cannot forget that rete testis is a possible primary site for a primary, unknown metastatic adenocarcinoma.     

Intrahepatic expression of HBsAg and HBcAg in asymptomatic HBsAg carriers and its follow-up

Intrahepatic expression of hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (HBcAg) was investigated in 46 asymptomatic HBsAg carriers by a direct immuno-fluorescent method. In 21 HBeAg positive carriers, HBsAg was expressed diffusely on the membrane of hepatocytes, with associated cytoplasmic localization in a few scattered hepato-cytes. HBcAg was expressed in the nucleus of many hepatocytes and in the cytoplasm of a few scattered hepatocytes, but not on the cell membrane. In 25 anti-HBe positive carriers, HBsAg was expressed on the surface and in the cytoplasm of hepatocytes diffusely and/or focally, but neither intrahepatic HBcAg nor serum HBV-DNA was detected. Repeat liver biopsies were performed in 17 patients. In eight of 13 HBeAg-positive HBsAg carriers, who developed histologically proven chronic hepatitis and liver cirrhosis, the localization of HBsAg in liver had changed from a membranous to a mixed (membrane and cytoplasm) pattern, and localization of HBcAg in liver had changed from a predominantly nuclear to a predominantly membranous and cytoplasmic pattern. However, in two HBeAg and two anti-HBe positive cases who showed no biochemical and histologic change at follow-up, the intrahepatic expressions of HBsAg and HBcAg in the second biopsies remained unchanged. Thus, decrease in membranous expression of HBsAg and increase in membranous and cytoplasmic expression of HBcAg were associated with progression to chronic liver disease. This suggests that membranous HBcAg may represent the major target in the process of injury to hepatocytes.     

Clinical features of patients with chronic liver disease associated with hepatitis C virus genotype 1a/I in Okinawa, Japan

The clinical characteristics of chronic hepatitis C virus (HCV) carriers with HCV genotype 1a/I infection were investigated and compared with those of chronic HCV carriers infected with 1b/II, 2a/III, 2b/IV and the mixed type of infection. We found that 16 of 408 (3.9%) carriers had HCV genotype 1a infection, comprising four of 67 (6.0%) blood donors, 11 of 263 (4.2%) patients with chronic hepatitis and one of 39 (2.6%) patients with liver cirrhosis. Three of 408 subjects had a mixed infection of genotypes 1a/I and 1b/II. All carriers with genotype 1a (including those with the mixed infection) were of Japanese origin and all, except one who was born in Brazil, were born in Okinawa Prefecture. Nine of 14 patients infected with genotype 1a for whom medical records were obtained had a history suggestive of infection through blood exposure; six had had blood transfusions, one had tattoos, one is a nurse and one had a history of drug addiction. There were no haemophiliacs or other multitransfused patients in the genotype 1a group. Of 10 patients infected with genotype 1a who received interferon (IFN) therapy, four (40%) showed a complete response. Although the small number of patients infected with genotype 1a in the present study precluded statistical analysis of the response to IFN, the response in patients with genotype 1a was better than the response in those infected with genotype 1b and poorer than the response in those patients infected with genotype 2a/III or 2b/IV.