Clinical features of Japanese children and adolescents with systemic lupus erythematosus: Results of 1980–1994 survey

Marked advances have been made in the past decade in the management of adults with systemic lupus erythematosus (SLE). Therefore, a nationwide retrospective survey was conducted between 1980 and 1994 to investigate the clinical manifestations of SLE in Japanese children and adolescents. Questionnaires were sent to 340 hospitals. Of 405 patients reported by 176 hospitals, 373 patients, diagnosed by the criteria established by the Pediatric Study Group of the Japanese Ministry of Health and Welfare in 1985, were enrolled in the study. Forty-nine of the 354 patients (13.8%) had relatives with a connective tissue disease within the third degree of consanguinity. The frequent manifestations in 373 patients were the presence of antinuclear antibody (98.9%), immunologic disorders (93.0%), hypocomplementemia (87.1%), malar rash (79.6%) and fever (74.0%). Lupus nephritis was present in 148 of the 309 patients (47.9%) at their first visit to a clinic, and 261 of the 373 patients (70.0%) developed renal involvement during the observation period. Of 370 patients, 92 patients (24.9%) exhibited central nervous system lupus. Of 368 patients, 192 patients (52.2%) were treated by methylprednisolone pulse therapy and 148 patients (40.2%) received immunosuppressants in combination with steroid therapy at some stage during the observation period. Survival rate at 5 years from onset was 95.9%. Management of infection, coagulopathies, and central nervous system involvement is essential to improve the prognosis of SLE in Japanese children and adolescents.     

Hepatic stellate cell contraction is inhibited by lipo-prostaglandin E1 in vitro

Prostaglandin E₁ (PGE₁) has been reported to have, experimentally and clinically, a protective effect against liver damage. This effect may result from the relaxation of hepatic stellate cells, whose contraction induces vasoconstriction of hepatic sinusoids. However, prostaglandins are unstable and a new drug delivery system is necessary to administer a sufficient amount of prostaglandin to achieve a protective effect in the liver. The aim of the study is to investigate the effects of lipo-prostaglandin E₁ (lipo-PGE₁) which has a novel drug delivery system on the stellate cell contraction induced by endothelin-1 in vitro. Lipo-PGE₁ inhibited endothelin-1-induced stellate cell contraction in concentrations of 10, 30 and 50 ng/mL. Therefore, lipo-PGE₁ may show a cytoprotective effect in the liver through the relaxation of stellate cells and an increase in the hepatic sinusoidal blood flow.     

Effects of rebamipide on bile acid-induced inhibition of gastric epithelial repair in a rabbit cell culture model

Background : Anti-ulcer agents exert various functional effects on gastric epithelial cells.
Aim : The effects of a novel gastro-cytoprotective agent (rebamipide) on epithelial restoration following bile acid damage were assessed using primary cultured rabbit gastric epithelial cells.
Methods : Rebamipide was added to complete confluent cell sheets with deoxycholic acid just after creating a cell-free wound (2 mm²). The restoration was monitored and analysed by phase contrast microscopy and an image analyser for 48 h. The migration speed was measured during the initial 3 h after wounding. Cell proliferation was detected by staining for bromodeoxyuridine (BrdU) at 12-h intervals. The labelling index was calculated per unit area. The major cytoskeletal protein actin was detected by immunohistochemical staining.
Results : In the controls, restoration was completed 48 h following wounding. Deoxycholic acid retarded this process. The addition of rebamipide to deoxycholic acid abolished the bile acid-induced retardation. The migration speed was 26 μm/h in the controls, 15 μm/h in the deoxycholic acid group and 27 μm/h in the deoxycholic acid plus rebamipide group. In the controls, BrdU-positive cells, which were rarely detected in the initial 24 h, were maximal at 36 h (labelling index 1.7%). In the deoxycholic acid group, proliferation was inhibited (peak labeling index; 0.5% at 48 h). Actin-containing stress fibres were detected throughout the cells and the periphery of the lamellipodia in the controls, and were disrupted in the deoxycholic acid-treated group. Rebamipide prevented these effects.
Conclusions : Deoxycholic acid significantly retarded restoration by the inhibition of both cell migration and proliferation, potentially through an effect on the cytoskeleton. Rebamipide protected the mucosal cells from bile acid mediated injury.     

Marked retention of indocyanine green and sulfobromophthalein with chronic persistent hepatitis

A hepatitis B virus (HBV) carrier with marked retention of indocyanine green (ICG) and sulfobromophthalein (BSP) was admitted to our hospital for assessment of liver function. On admission, he was asymptomatic and blood chemistry tests showed normal values for transaminases and bilirubin. Serum hepatitis B surface antigen (HBsAg) and antibody to hepatitis B e antigen (anti-HBe) were positive. A history of drug abuse or alcoholism was denied. Dye excretion tests revealed marked retention of ICG (R₁₅= 70%) and BSP (R₄₅= 23%). Histopathological examination of a liver biopsy specimen obtained during laparoscopic observation showed chronic persistent hepatitis (CPH). Familial research of the patient failed to prove the existence of dye excretory defect in his siblings. Usual cases of CPH due to continuous HBV infection do not show such severe disturbance of organic anion transport. This pattern of the dye excretory defect with CPH has not been reported. Although the relationship between this dye excretory defect and HBV infection is unclear, the existence of the constitutional dye excretory defect due to abnormal organic anion transport in the liver might be considered.     

Basic fibroblast growth factor accelerates gastric mucosal restoration in vitro by promoting mesenchymal cell migration and proliferation

It has been generally accepted that basic fibroblast growth factor is a potent stimulator of duodenal ulcer healing. However, the detailed mechanism and mode of action of growth factor on gastric ulcer healing is still controversial. Therefore, in the present study, the effects of basic fibroblast growth factor on gastric mucosal repair were studied using an in vitro cultured cell system. Artificial wounds were made in confluent monolayer rabbit gastric fibroblast and epithelial cell sheets by mechanical denudation. Changes in the size of the cell-free area were analysed quantitatively. Cell proliferation was assessed by BrdU staining. For both cell types, mucosal restoration involved cell migration and proliferation. Although the speed of restoration of epithelial cells was not affected by the addition of basic fibroblast growth factor, it was much faster for epithelial cells than for fibroblasts. Basic fibroblast growth factor accelerated wound repair of fibroblasts but not epithelial cells. Basic fibroblast growth factor accelerated wound repair by stimulating both cell migration and proliferation. Therefore, the effects of basic fibroblast growth factor in peptic ulcer diseases may be mainly due to the stimulation of mesenchymal cells.