Prostaglandin E1‐effective,transient‐type ischemic colitis developed after surgical resection of sigmoid colon cancer. A case report

A 55‐year‐old‐man had a laparoscopic resection of the sigmoid colon due to colon cancer with submucosal invasion. After the surgery he suffered ileus and had a laparotomy. Six months later he complained of frequent defecation. Colonoscopy confirmed a circular ulcer extending from the anal side of the anastomosis in the sigmoid colon to the mid rectum. Endoscopic ultrasound demonstrated thickening of all layers of the diseased colon and rectum. We diagnosed ischemic colitis. After intravenous drip infusion of prostaglandin, symptoms and colonic stricture gradually improved. Although abdominal angiography revealed a narrowing of the peripheral sigmoid branch of the inferior mesenteric artery, blood flow was unrestricted. Colonoscopy performed 84 days after discharge revealed an ulcer scar.     

Cyclosporine therapy affects aminotransferase activity but not hepatitis C virus RNA levels in chronic hepatitis C

Interferon (IFN) therapy is of proven efficacy in chronic hepatitis C, but it is not universally effective and is often limited by side effects. Cyclosporine A (CsA) is a potent immunosuppressant widely used in organ transplantation. We conducted a pilot study to determine whether CsA therapy could affect aminotransferase activity and hepatitis C virus RNA levels in patients with chronic hepatitis C. Cyclosporine A was administered to 10 patients (mean age of 59 years; male: female = 9:1) who did not respond to IFN therapy previously and who had elevated serum alanine aminotransferase (ALT) values for at least 6 months. All patients were positive for HCV-RNA by RT-PCR with genotype 1b. Their mean duration of hepatitis was 15 years. Oral CsA was given for 3 months in a dose that was increased at 1 month intervals from 1.5–2.0 to 2.0–3.0 and 3.0–4.0 mg/kg per day. All patients completed the treatment schedule, although two patients developed mild non-symptomatic hypertension. Serum ALT levels gradually decreased in all but one patient. The mean percentage decrease was 59.5% at the end of therapy (from 153 ± 82 to 62 ± 48 IU/L; P < 0.02). The ALT levels fell to the normal range in five patients, although once therapy was discontinued the enzyme levels tended to return to pretreatment levels. Serum aspartate aminotransferase and g-glutamyl transpeptidase levels similarly decreased. The serum HCV-RNA titre, determined by competitive RT-PCR, did not change in any patient throughout the study period. There were no appreciable alterations in other laboratory tests, such as serum creatinine levels and lymphocyte subsets, except for an increase in serum alkaline phosphatase levels. These findings suggest that CsA, even in a relatively low dose, reduces serum aminotransferase levels without serious side effects in patients with chronic-hepatitis C, although an antiviral effect was not noted.     

HYPOURICAEMIA WITH ACUTE VIRAL HEPATITIS

We report five female cases of hypouricaemia accompanied byacute viral hepatitis (serum urate 101 ± 12 µmol/1,mean ± SD). Their urate clearance was increased to 14.2±3.4 ml/min during hyperbilirubinaemia but 24-h urateexcretion was not elevated (2.09 ± 0.64 mmol/24 h). Noother renal tubular abnormalities were detected. Comparing uratemetabolism with that of four cases of inborn renal hypouricaemia,the degree of uricosuria was lower. One patient showed elevationof serum and urinary oxypurine, which normalized with returnof a normal blood uric acid level. In all cases, the serum uratereturned to normal after improvement of liver function. We suggestthat renal uricosuria due to an isolated renal defect of uratetransport might contribute to hypouricaemia in these cases butthat inhibition of xanthine oxidase activity might also contributeto this phenomenon. KEY WORDS: Liver disease, Purine synthesisPurine synthesis, Purine synthesis, Kidney, Tubular function, Xanthine oxidase     

Serum levels of IL-10, IL-15 and soluble tumour necrosis factor-alpha (TNF-α) receptors in type C chronic liver disease

We previously reported that the number of TNF-α-producing cells was increased in the liver of patients with type C chronic liver disease. To understand further the pathophysiology of this change, we examined serum levels of two soluble TNF receptors, TNF-αRI (p55) and -αRII (p75), and IL-10, all of which act as TNF-α buffer, and IL-15, a novel cytokine sharing many immunological activities with IL-2, using ELISA methods. We studied control individuals and patients with type C chronic liver disease, including asymptomatic hepatitis C virus (HCV) carriers with persistently normal serum ALT values, and those with chronic hepatitis (CH), liver cirrhosis (LC) and hepatocellular carcinoma (HCC). Both types of sTNF-αR closely correlated with disease progression. Patients with LC and HCC had significantly elevated levels for sTNF-αRII compared with the other patient groups and controls. Serum IL-10 levels were significantly greater in all chronic liver disease groups than in controls. With respect to IL-15, the values were high in CH, LC and HCC compared with those of controls. Notably, HCC patients showed highest values for both IL-10 and IL-15, with significant differences from the other patient groups. Serial determinations revealed that interferon (IFN) treatment for CH patients resulted in the suppression of circulating IL-10 and IL-15 levels along with decrease in serum aminotransferase values. Both cytokines remained at decreased levels after cessation of therapy in patients who went into clinical and virological remission. On the other hand, treatment did not affect serum levels of sTNF-αRs. These findings indicate that serum levels of these molecules correlated with disease progress in chronic HCV infection, and that IL-10 and IL-15 may reflect the degree of inflammation in the liver. It is also suggested that both cytokines may be related to the development of HCC.     

Transient Depletion of T Cells with Bright CD11a/CD18 Expression from Peripheral Circulation during Acute Kawasaki Disease

To clarify the activation of peripheral blood T cells in Kawasaki disease (KD) patients, we investigated whether expression of lymphocyte function-associated antigen-1 (LFA-1, CD11a/CD18) and/or intercellular adhesion molecule-1 (ICAM-1, CDS4) on peripheral blood T cells increases during the acute stage. Expression of cellular adhesion molecules was measured using flow cytometry. There was a decrease in the percentage of CD3⁺ T cells in the bright LFA-1α and LFA-1β population and a concomitant increase in the dim population of LFA-1α and LFA-1β during the acute stage, in comparison with those of the convalescent stage. In addition, we observed no significant differences in ICAM-1 expression during the acute stage compared with that of the convalescent stage. In our view the present data, in conjunction with previous reports on T-cell function during acute KD, suggest that activated T cells are temporarily withdrawn from peripheral circulation during acute KD.     

Functional CD86 (B7-2/B70) is predominantly expressed on Langerhans cells in atopic dermatitis

Recently, we reported the functional expression of CD86 on cultured human Langerhans cells derived from normal epidermis. In the present study, we investigated the expression and function of co-stimulatory molecules in the pathogenesis of atopic dermatitis. In immunohistochemical analysis, CD80 and/or CD86 were detected on dendritic-shaped cells not only in the epidermis but also in the dermis in the inflammatory lesions of atopic dermatitis (n = 12). CD80 was expressed in only five cases (42%), while CD86 was expressed in all cases (100%). These molecules were not detected in normal control subjects (n = 8). In non-lesional skin of atopic dermatitis (n = 4). CD86 but not CD80 was detected in one case. CD86 was preferentially induced on dendritic-shaped cells in positive patch test sites to Dermatophagoides pteronyssinus or house dust allergen in atopic dermatitis (n = 4). The CD80- or CD86-positive cells were confirmed as Langerhans cells by double immunostaining using anti-CD1a monoclonal antibody. Neither CD86 over that CD80 was detected n keratinocytes. Similar results of the stronger expression of CD86 over that of CD80 were obtained from psoriasis vulgaris (n = 11) and from contact dermatitis (n=7), although CD86 was expressed only in 57% of the contact dermatitis cases. The percentage of Langerhans cells positive for CD86 was higher than for CD80, i.e. 48% compared with 9%, respectively, in the epidermis of lesional skin of atopic dermatitis (n=8). The expression rate of these molecules on Langerhans cells increased in the dermis. To investigate the function of co-stimulatory molecules on Langerhans cells in atopic dermatitis, we conducted an inhibition test with antibodies. Anti-CD86 monoclonal antibody almost completely nhibited T-cell proliferation stimulated with crude extract of D. pteronyssinus in the presence of epidermal cells as antigen-presenting cells, whereas anti-CD80 monoclonal antibody produced less of an inhibitory effect. These data indicate that CD86 expressed on Langerhans cells may play an important part in the pathogenesis of atopic dermatitis.for Investigative Dermatology. Washington, DC (1–5 May 1996).     

TEMPERATURE MONITORING DURING GENERAL ANAESTHESIA

A study of core temperature monitoring during general anaesthesiaindicates that this can be introduced as a routine procedurein order to reduce mortality from malignant hyperpyrexia. Thetemperature profiles of 2410 patients are presented. Both meanrectal and mean oesophageal temperatures decreased during generalanaesthesia. The mean oesophageal temperatures were on average0.6°C less than the mean rectal temperatures during thefirst hour of anaesthesia. An increase in core temperature occurredin nearly 20% of patients. This appeared to be related to aninitially low body temperature. Core temperatures during generalanaesthesia were significantly greater in patients who receivedthe combination of suxamethonium and halothane than in patientsreceiving other drugs. This observation is of theoretical interestand suggests that the increase of temperature in malignant hyperpyrexiamay be an exaggeration of a normal response to these agents. ^* Present address: Department of Anaesthesia, National CardiovascularCentre, Osaka, Japan.     

Effects of Cyanoacrylate on the Gastric Mucosa of Dogs –Endoscopic and Histopathological Studies for Sclerotherapy of Gastric Varices–

Abstract: The effect of cyanoacrylate tissue adhesive (C. A.) on the gastric mucosa of dogs was investigated endoscopically and histopathologically. When C. A. was applied to the surface of the gastric mucosa, the endoscopic findings the next day showed local redness at the applied site (Fig. 1-a) and histopathology revealed degenerative changes in the gastric mucosa (Fig. 1-b). When C. A. was endoscopically injected into the gastric mucosa, the endoscopic findings revealed a submucosal tumor-like lesion (Fig. 2-a). One day after treatment, the endoscopic findings showed a hemorrhagic erosion on the surface of the lesion (Fig. 2-b). An histopathological examination of the resected stomach revealed C. A. in the submucosal layer (Fig. 3-a, 3-b) and the lymph duct around the muscularis mucosa with severe acute inflammation (Fig. 4-a, 4-b). One week after treatment, a deep ulcer (Ul-IV) was observed (Fig. 5, 6) and a histopathological examination of the resected specimen revealed C. A. at the site of the ulcer and inflammatory cell infiltration by fibroblasts and giant cells (Fig. 7-a, 7-b). One month after treatment, the ulcer had healed and was replaced by a scar (Fig. 8). Histopathological examination of the resected stomach revealed C. A. in both the muscularis mucosa and the submucosa and also inflammatory cell infiltration by giant cells in addition to the fibrosis (Fig. 9). When using endoscopic sclerotherapy with C. A., it should be kept in mind that there is the possibility of such a lesion occurring as demonstrated by our study.