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Summary We have developed an ultrasound probe through the centre of which an epidural needle can pass, intended to reduce the rate of contact between bone and needle during epidural insertion. We tested the ability of this probe to identify the lumbar interspace, using A-mode ultrasound, in a submerged plastic model, a porcine phantom and five human volunteers. In the plastic model, the minimum echo representing the interspace was only 8.8% of the maximum echo from the ‘bone’. In the porcine model, the echo variations between the interspace and L3 were up to 48% and the needle was safely inserted into the interspace without bone contact under guidance. The human study also showed that the maximum bone echo was at least three times stronger than the interspace echo. Axial ultrasound guidance, with the needle passing through the probe, offers a method for reducing bone contact during epidural insertion.

This study investigated the effect of the anti-anginal drug, fendiline, on intracellular free Ca2+ levels ([Ca2+]i)inHA/ 22 human hepatoma cells by using fura-2 as a fluorescent Ca2+ dye. Fendiline (1-100 μM) increased [Ca2+]i with an EC50 of 25 μM. Removal of extracellular Ca2+ reduced the [Ca2+]i signals by 51-5%. Fendiline (10 μM)-induced Ca2+release was abolished by pretreatment with 1 μM thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor). Inhibition of phospholipase C with 2 μM 1-(6-((17β 3 methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H pyrrole-2,5-dione (U73122) did not alter 10 μM fendilineinducedCa2+ release.Severalothercalmodulinantagonists, such as phenoxybenzamine (100-200 μM), trifluoperazine (5-50 μM),andfluphenazine N-chloroethane(2-100 μM), hadno effect on[Ca2+]i. Together, it wasfound that fendiline increased [Ca2+]i in human hepatoma cells by discharging Ca2+ from the endoplasmic reticulum in an inositol 1,4,5 trisphosphate-independent manner and by inducing Ca2+entry. This effect of fendiline does not appear to be via antagonism of calmodulin.

Background—Endoscopic sphincterotomy (EST) is widely used for the removal of stones from the bile duct, but stones recur in about one fifth of patients.Aims—To investigate hepatic clearance by quantitative cholescintigraphy (QC) in patients after EST and to discern the relationship between biliary emptying and stone recurrence.Methods—One hundred and forty nine patients who had EST and clearance of the bile duct for choledocholithiasis were selected. All patients were confirmed to have complete EST by sphincter of Oddi manometry and underwent QC soon after normalisation of liver function. Regular clinical follow up was performed for each patient.Results—During a mean 36 month follow up, 22 (14.8%) patients developed recurrent stones in the bile duct. Irrespective of the status of the gall bladder, patients with recurrent stones had a slower hepatic clearance of radioisotope during QC compared with patients without stone recurrence, but only the differences in cholecystectomised patients had statistical significance. After carrying out multivariate analysis, one parameter of QC, percentage clearance of maximal count at 45 minutes, was found to be the only significant factor for stone recurrence. All recurrent stones in the common bile duct were successfully removed at endoscopy.Conclusion—Slower hepatic clearance as shown by QC is an important factor responsible for stone recurrence after sphincter ablation.

We report the long-term clinical outcome of spontaneous carotid cavernous sinus fistulae (CCF) originally supplied by branches arising from the internal carotid artery (Barrow's type B), or type-D lesion that became type B after particulate embolization. A total of 55 patients was included in this study. Their angiography revealed that cortical drainage was absent, and that the arteries supplying the fistulae originated in the dural branches of the internal carotid artery. Thirty-two patients had type-D lesions, which became type-B lesions after obliteration of the external carotid supply by endovascular treatment. The other 23 patients had type-B lesions documented by angiography, and had no embolization. The follow-up period ranged from 8 to 144.5 months. Clinical cure was achieved in 39 patients (70.9%), improvement in eight patients (14.5%), the lesion remained stable in four patients (7.3%), and was aggravated in four patients (7.3%). The number of drainage veins is the only radiographic factor that could predict the outcome. Those patients with single draining veins had a better chance of complete remission. The outcome between the group with original type D lesions after embolization and the group with original type B revealed no statistically significant difference. The time-course to complete cure was significantly shorter in the group with embolization of the external carotid supply. In the four patients whose symptoms were aggravated, embolization was performed, and the result was excellent. The clinical outcome of type-B CCF, or type D converted to type B, is good. Previous external carotid artery embolization can significantly shorten the time to complete cure. Aggressive treatment should be reserved for those who have aggravated symptoms.

The effect of oleamide, a sleep-inducing endogenous lipid in animal models, on intracellular free levels of Ca(2+) ([Ca(2+)](i)) in non-excitable and excitable cells was examined by using fura-2 as a fluorescent dye. [Ca(2+)](i) in pheochromocytoma cells, renal tubular cells, osteoblast-like cells, and bladder cancer cells were increased on stimulation of 50 microM oleamide. The response in human bladder cancer cells (T24) was the greatest and was further explored. Oleamide (10-100 microM) increased [Ca(2+)](i) in a concentration-dependent fashion with an EC(50) of 50 microM. The [Ca(2+)](i) signal comprised an initial rise and a sustained plateau and was reduced by removing extracellular Ca(2+) by 85 +/- 5%. After pre-treatment with 10-100 microM oleamide in Ca(2+)-free medium, addition of 3 mM Ca(2+) increased [Ca(2+)](i) in a manner dependent on the concentration of oleamide. The [Ca(2+)](i) increase induced by 50 microM oleamide was reduced by 100 microM La(3+) by 40%, but was not altered by 10 microM nifedipine, 10 microM verapamil, and 50 microM Ni(2+). In Ca(2+)-free medium, pre-treatment with thapsigargin (1 microM), an endoplasmic reticulum Ca(2+) pump inhibitor, abolished 50 microM oleamide-induced [Ca(2+)](i) increases; conversely, pretreatment with 50 microM oleamide reduced 1 microM thapsigargin-induced [Ca(2+)](i) increases by 50 +/- 3%. Suppression of the activity of phospholipase C with 2 microM U73122 failed to alter 50 microM oleamide-induced Ca(2+) release. Linoleamide (10-100 microM), another sleep-inducing lipid with a structure similar to that of oleamide, also induced an increase in [Ca(2+)](i). Together, it was shown that oleamide induced significant [Ca(2+)](i) increases in cells by a phospholipase C-independent release of Ca(2+) from thapsigargin-sensitive stores and by inducing Ca(2+) entry.

The role of eradication therapy is still controversial in H. pylori-related nonulcer dyspepsia (NUD). The aim of this study was to follow up the H. pylori status after eradication therapy in patients with NUD by using l3C-urea breath test (UBT).Patients with a clinical and endoscopic diagnosis of NUD were included. H. pylori infection was established by endoscopic biopsies and 13C-UBT. Patients with H. pylori infection then received a quadruple therapy with colloidal bismuth subcitrate, metronidazole, tetracycline and lansoprazole. Two months after completion of therapy, endoscopic biopsies and 13C-UBT were performed again to confirm eradication. A follow-up 13C-UBT was carried out again in one year to detect recurrence of H. pylori infection.Eighty-eight of the 148 patients (59.5%) were found to have H. pylori infection by both endoscopic biopsies and 13C-UBT. Anti-H. pylori therapy was given for 55 patients and proved successful in 33 of them two months after the end of therapy. However, recurrence was found one year later in three of these 33 cases, making a recurrence rate of 9.1% (3/33). Three of the 22 cases with unsuccessful eradication were found to have H. pylori eradication at one year by follow-up 13C-UBT. One of the 33 H. pylori-positive patients without anti-H. pylori therapy, who had negative 13C-UBT in one year follow-up, was found taking a high dose and long period of antibiotics.The recurrence rate of H. pylori infection in our study was higher than that in the Western population. Delayed eradication of H. pylori may occur after anti-H. pylori therapy. Spontaneous eradication is rare in patients not receiving anti-H. pylori eradication.

Cathepsin E is found mainly over the gastric surface and foveolar epithelial cells, and it also is found in the metaplastic pyloric glands and cancer cells. The exact function of cathepsin E in gastric mucosa remains unclear. The colonic type (type III) of intestinal metaplasia (IM) is strongly associated with intestinal-type gastric carcinoma. IM is considered to be a precancerous lesion. The aim of this study was to find out the role of cathepsin E in IM, dysplasia and cancer of stomach.Sixty nine biopsy specimens with IM and dysplasia and 33 gastrectomy specimens with gastric carcinoma were fixed, sectioned and stained with PAS-alcian blue stain, high iron-diamine alcian blue stain to classify IM and immunohistochemical stain to localize cathepsin E. Those patients with dysplastic gastric lesions received regular endoscopic follow-up.Fifteen of 69 patients with gastric dysplasia developed cancer in a median 10.5 months follow-up. Severe dysplasia developed carcinoma significantly higher than mild dysplasia (12/20 vs. 1/25, p0.001), and type III intestinal metaplasia seemed to have significantly predilection for severe dysplasia and gastric cancer. Cathepsin E was stained in intestinal metaplasia with dysplastic change in 44/69 specimens (63.8%), and carcinoma in 28/48 (58.3%) specimens, there was no significant difference between intestinal type and diffuse type carcinoma in cathepsin E staining. The positive staining for cathepsin E decreased significantly in severe dysplastic gastric mucosa.Type III IM is commonly associated with severe dysplasia and cancer; it may be a precancerous lesion. The positive staining of cathepsin E decreased with the severity of gastric dysplasia, representing dedifferentiation of the cells.

The effect of clomiphene, an ovulation-inducing agent, on cytosolic free Ca2+ levels ([Ca2+]i) in MG63 human osteosarcoma cells was explored by using fura-2 as a Ca2+ indicator. Clomiphene at concentrations between 5-75 microM increased [Ca2+]i in a concentration-dependent manner with an EC50 of 50 microM. The [Ca2+]i signal consisted of an initial rise and a sustained phase. Ca2+ removal reduced the Ca2+ signal by 40+/-10%. The [Ca2+]i increase induced by 50 microM clomiphene was inhibited by 80+/-5% by 10 microM nifedipine, but was insensitive to 50 microM La3+ or 10 microM verapamil. In Ca2+-free medium, pretreatment with 50 microM brefeldin A (to disrupt the Golgi complex Ca2+ store), 1 microM thapsigargin (to inhibit the endoplasmic reticulum Ca2+ pump), and carbonylcyanide m-chlorophenylhydrazone (CCCP; to uncouple mitochondria) inhibited 51+/-3% of 50 microM clomiphene-induced Ca2+ release; conversely, pretreatment with 50 microM clomiphene abolished the [Ca2+]i increase induced by thapsigargin, CCCP, and brefeldin A. The Ca2+ release-induced by 50 pM clomiphene was unchanged by inhibition of phospholipase C with 2 microM 1-(6-((17beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122). Collectively, the results suggest that clomiphene increased [Ca2+]i, in osteoblast-like cells, by releasing intracellular Ca2+ in a phospholipase C-independent manner and by causing nifedipine-sensitive Ca2+ influx.

The effect of histamine on intracellular free Ca2+ levels ([Ca2+](i)) in MG63 human osteosarcoma cells was explored using fura-2 as a Ca2+ dye. Histamine increased ([Ca2+](i)) in a concentration-dependent fashion with an EC(50) value of 0.5 microM. Extracellular Ca2+ removal inhibited the ([Ca2+](i)) signals. Histamine failed to increase ([Ca2+](i)) in Ca2+-free medium after cells were pretreated with thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor). Addition of Ca2+ induced concentration-dependent ([Ca2+](i)) increases after preincubation with histamine in Ca2+-free medium. Histamine-induced intracellular Ca2+ release was abolished by inhibiting phospholipase C with 1-(6-((17beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122). The ([Ca2+](i)) increase induced by histamine in Ca2+ medium was abolished by cimetidine, but was not altered by pyrilamine, nifedipine, verapamil, and La(3+). Together, this study shows that histamine increased in ([Ca2+](i)) in osteosarcoma cells by stimulating H2 histamine receptors. The Ca2+ signal was caused by Ca2+ release from the endoplasmic reticulum in a phospholipase C-dependent manner. The Ca2+ release was accompanied by Ca(2+) influx.

The effect of histamine on intracellular free Ca2+ levels ([Ca2+]i) in HA22/VGH human hepatoma cells were evaluated using fura-2 as a fluorescent Ca2+ dye. Histamine (0.2-5 microM) increased [Ca2+]i in a concentration-dependent manner with an EC50 value of about 1 microM. The [Ca2+]i response comprised an initial rise, a slow decay, and a sustained phase. Extracellular Ca2+ removal inhibited 50% of the [Ca2+]i signal. In Ca2+-free medium, after cells were treated with 1 microM thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor), 5 microM histamine failed to increase [Ca2+]i. After pretreatment with 5 microM histamine in Ca2+-free medium for 4 min, addition of 3 mM Ca2+ induced a [Ca2+]i increase of a magnitude 7-fold greater than control. Histamine (5 microM)-induced intracellular Ca2+ release was abolished by inhibiting phospholipase C with 2 microM 1-(6-((17beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122), and by 5 microM pyrilamine but was not altered by 50 microM cimetidine. Together, this study shows that histamine induced [Ca2+]i increases in human hepatoma cells by stimulating H1, but not H2, histamine receptors. The [Ca2+]i signal was caused by Ca2+ release from thapsigargin-sensitive endoplasmic reticulum in an inositol 1,4,5-trisphosphate-dependent manner, accompanied by Ca2+ entry.

Although the eradication of Helicobacter pylori infection benefits patients with gastric or duodenal ulcers, the value of eradicating the infection in the patients with functional dyspepsia (FD) remains controversial.To determine whether eradicating H. pylori can prevent the subsequent development of ulcers or relieve the symptoms of functional dyspepsia patients.In a double-blind, placebo-controlled trial, 161 patients infected with H. pylori who had functional dyspepsia were randomly assigned to 7 days of treatment with a lansoprazole-based triple therapy or placebo and then followed for 1 year. The main outcome measures were the development of peptic ulcers and the resolution of symptoms.H. pylori was eradicated in 63 out of 81 patients (78%) in the treatment group and none of the 80 patients (0%) in the placebo group. During the follow-up period, two patients in the treatment group and six patients in the placebo group developed peptic ulcers at repeat endoscopy (2.5% vs. 7.5%; 95% CI: -12 to 2). The reduction in ulcer rates was statistically significant in the 'ulcer-like' sub-group (0% vs. 16.7%; 95% CI: -32 to -2), but not in the 'dysmotility-like' and 'unclassifiable' sub-groups. Regarding symptom response, the resolution rates of symptoms were similar between the treatment and placebo groups (58.0% vs. 55.0%, 95% CI: -12 to 18). Additionally, no significant differences existed in the symptom responses between the treatment and control arms in each of the dyspepsia sub-groups.Eradicating H. pylori can prevent the subsequent development of peptic ulcers in the patients with 'ulcer-like' functional dyspepsia. However, this approach does not significantly reduce the symptoms of functional dyspepsia patients.

Gallstones are a common problem in Taiwan and surgical removal remains the essential treatment. Successful dissolution of the stones with chemical solutions and then removal by endoscopic or percutaneous methods have previously been reported. We designed this study to find the ideal agent for dissolving gallstones.Twelve chemical solutions with dimethylsulfoxide (DMSO), methyl tert-butyl ether (MTBE) and ethylenediamine tetra-acetic acid (EDTA) in different mixtures were tested to investigate their ability to dissolve gallstones in vitro. The dissolution of stones was performed at 37 degrees C and each procedure was repeated five to seven times.The solvent containing DMSO/MTBE (1/1) had a higher dissolving capacity for cholesterol stones, with solubility reaching 96.8% after 6 hours. The solution containing DMSO/MTBE (7/3) had the maximal solubility for calcium bilirubinate stones, with solubility reaching 22.9% after 6 hours. Also, we found that the intact stones of calcium bilirubinate became fragmented after treatment with the DMSO/MTBE solution without stirring.The DMSO, MTBE and EDTA agents that we used effectively dissolved gallstones, especially cholesterol stones, in vitro. Further in vivo studies are necessary to confirm the efficacy and safety of these solvents before clinical application.

Hereditary hemorrhagic telangiectasia, commonly known as Osler-Weber-Rendu disease, is a systemic autosomal dominant inherited disorder, that occurs in Caucasian populations. We report the case of a 56-year-old housewife who was admitted to the gastrointestinal and cardiovascular ward because she had suffered from recurrent gastrointestinal bleeding and heart failure from 1994 to 1997. Panendoscopy showed vascular ectasia scattered over the tongue, larynx, esophagus, and posterior wall of the gastric body. Colonoscopy showed clusters of telangiectasia over the cecum and ascending colon. Arteriovenous malformations (AVMs) were found in the liver and lungs on computerized tomography. Recurrent gastrointestinal bleeding was controlled by estrogen treatment during the follow-up period. In July 1997, the patient was readmitted to our cardiovascular section due to aggravated dyspnea, orthopnea and bilateral lower leg edema. Cardiac catheterization showed a large fistula from the left pulmonary artery to the left atrium and left ventricle, pulmonary arterial pressure of 37/13 mmHg and cardiac output of 9.61/minute. Other studies excluded the possibility of sepsis, and high-output cardiac failure was suspected. The patient was discharged in a stable condition and scheduled for AVM embolization management. Unfortunately, she died of a suspected heart attack at home two weeks following discharge.

Chronic Helicobacter pylori infection leads to the development of mucosa-associated lymphoid tissue (MALT), gland atrophy, intestinal metaplasia, and in certain individuals, gastric lymphoma and adenocarcinoma. We conducted a prospective study to determine the effect of H pylori eradication on the development of MALT, gland atrophy and intestinal metaplasia.From July 1995 to October 1996, 63 consecutive patients with H pylori-associated peptic ulcer disease were enrolled in a bacterial eradication trial. The grade of MALT and the degree of gastritis of the antrum were assessed using Wotherspoon's scale and the Sydney system before treatment, and at eight weeks and one year after H pylori eradication therapy.During the study period, 43 patients received complete follow-up. In the patient group with eradication failure (n = 22), MALT score was significantly decreased at the end of the eighth week (p0.05) but returned to the initial level by one year of follow-up. There were no changes in the scores for inflammation, neutrophil activity, gland atrophy or intestinal metaplasia at the end of the eighth week and at one year following H pylori eradication therapy. In contrast, there was a marked reduction in the MALT, inflammation, and activity scores at eight weeks (p0.01,0.05 and0.05, respectively) and one year after treatment (p0.05,0.001 and0.001, respectively) in the patient group with successful eradication (n = 21). However, no significant changes in gland atrophy and intestinal metaplasia were observed during the follow-up period.Eradication of H pylori leads to regression of MALT in the stomach, but the degrees of gland atrophy and intestinal metaplasia remain unchanged, even after one-year of follow-up.

This study investigates the cell proliferation and the expression of p53 protein in Helicobacter pylori (H. pylori)-associated gastritis and assesses the effect of bacterial eradication on these epithelial factors.Seventy-nine patients with H. pylori-associated gastritis were randomized into the control group (n = 38) and anti-H. pylori group (n = 41). Each patient received endoscopic examinations with gastric biopsy before and 8 weeks after the treatment. The specimens from gastric antrum were immunostained for monoclonal antibodies against the proliferating cell nuclear antigen (PCNA) and p53 protein.In the control group, the total labeling index (L.I.) of PCNA and the positive index (P.I.) of p53 in the whole foveolar epithelium were unchanged after treatment. In the anti-H. pylori group, 35 of 41 cases (85.3%) achieved eradication of H. pylori. Amongst the H. pylori-eradicated cases, the total L.I. of PCNA in the whole foveolar epithelium did not meaningfully alter after H. pylori elimination (p0.05). However, a significant reduction of L.I. was observed in the middle compartments of the gastric pits (before vs. after treatment: 14.0 vs. 7.3, p0.05). With regard to the p53 expression, the P.I.s were significantly decreased in the whole foveolar epithelium (before vs. after treatment: 0.57 vs. 0.17, p0.05) and in each compartment of the gastric pits (before vs. after treatment: [upper compartment]: 0.34 vs. 0.15, p0.05; [middle compartment]: 0.67 vs. 0.23, p0.05; [lower compartment]: 0.71 vs. 0.20, p0.05) after eradication of H. pylori.Bacterial eradication reverses the hyperproliferating status of the foveolar epithelium in patients with H. pylori gastritis and leads to a decrease in p53 accumulation in the epithelial cells.

Endoscopic sphincterotomy and basket extraction are currently used to remove bile duct stones, with a duct clearance rate of 85% to 90%. A biliary endoprosthesis (stent) is an alternative method to treat difficult cases, especially high-risk surgical patients. The aim of this study was to investigate the long-term effect of biliary endoprostheses in patients with irretrievable common bile duct stones.From December, 1990, to November, 1998, 546 patients were referred to the Veterans General Hospital-Kaohsiung for endoscopic removal of common bile duct stones. Of them, 12 received long-term biliary endoprosthesis because endoscopic removal or surgery was not suitable. Large-caliber stents (10 French) were inserted into 12 patients (5 women and 7 men, mean age, 78.4 years) and they were followed up with regular clinical visits. Quantitative cholescintigraphy was performed in four patients to evaluate biliary emptying after liver function returned to normal.No early complications from stent insertion occurred and a satisfactory resolution of jaundice, pain and fever were noted in all patients. One patient had repeated cholangitis due to stent occlusion and five died from unrelated causes. The median effective period of stent placement was 11 months (range, 1-38 months). Quantitative cholescintigraphy revealed delayed biliary drainage in four patients despite an absence of symptoms after their liver function returned to normal.Large-caliber stents are a safe and effective treatment for long-term palliation in high-risk patients with retained common bile duct stones.

No stones are retrieved from the bile duct in 10-20% of patients with suspected common bile duct (CBD) stones after endoscopic sphincterotomy (EST). The clinical outcome in these patients remains unclear. This study followed patients from whom no stones were retrieved, to discover their clinical outcome.From October, 1990, to October, 1996, 401 patients with suspected CBD stones received EST for stone removal. Only patients from whom no stones were retrieved from the bile duct were included in this study. All enrolled patients were regularly interviewed and received liver function tests. Sonography, computerized tomography, endoscopic retrograde cholangiopancreatography (ERCP), and/or intrapapillary biopsy were performed as indicated.Forty-two patients were included in this study. The indications for EST included 34 cases with filling defects in the common bile duct on ERCP and eight cases with suspected impacted stones as seen by imaging studies. After a mean follow-up period of 28.6 months (range, 1-61 months), six patients developed biliary stones, four had carcinoma of the ampulla of Vater, one was found to have intrabiliary growth of hepatocellular carcinoma, and there was no pathologic change in 31 cases. Of the six patients with formation of biliary stones, two had an intact gallbladder and four had received previous cholecystectomy. Of the four patients with ampullary tumors, three were diagnosed by intrapapillary biopsy soon after EST, and one was diagnosed nine months later.Biliary problems were found in 26% of patients soon after EST, although no stones were retrieved from the bile duct. Regular follow-up is warranted.

Angiogenesis occurs in response to tissue damage, and is of vital importance for tumor growth and metastasis. Basic fibroblast growth factor (bFGF), a well-known angiogenic factor, has been suggested to be a useful diagnostic marker in certain hypervascular tumors. However, the relevance of its detection has not been well evaluated in patients with hepatocellular carcinoma (HCC) and benign chronic liver diseases. In the current study, immunoassay of bFGF was performed on serum samples from 39 patients with HCC, 21 with liver cirrhosis, 22 with chronic hepatitis and 40 normal subjects. The serum bFGF level was significantly increased in patients with liver cirrhosis and HCC when compared with those with chronic hepatitis or normal subjects (all p-values0.001). However, no difference was observed between the groups with liver cirrhosis and HCC (p0.05). If we set 9.6 pg/ml (mean + 3 standard deviations of bFGF in the control group) as the upper limit of normal serum level of bFGF, elevated bFGF concentrations were noted in 9.1%, 42.9% and 51.3% of patients with chronic hepatitis, liver cirrhosis and HCC respectively. In non-cancer patients, the coexistence of acute illness (p = 0.000) was an independent factor related to the elevation of serum bFGF. On the other hand, a multivariate analysis demonstrated that both advanced stage of cancer (p = 0.026) and coexistence of acute illness (p = 0.000) influence the serum level of bFGF in patients with HCC. We conclude that serum bFGF levels are significantly higher in patients with HCC and are positively correlated with advanced tumor stage. Nevertheless, elevation of serum bFGF may also be observed in a significant number of patients with liver cirrhosis. Therefore, measurement of serum bFGF alone cannot be satisfactory as a tumor marker for diagnosis of HCC. In addition, it is important to point out that coexistence of acute illness may be a crucial confounding factor in the diagnosis or monitoring of any cancer by the estimation of serum bFGF.

Dysfunction of the sphincter of Oddi (SOD) is one of the causes of postcholecystectomy syndrome and biliary pain. Endoscopic sphincterotomy (EST) is recommended in some patients refractory to conservative treatment. This study was designed to evaluate the efficacy of, and complications from EST in patients with SOD.Between 1990 and 1993, 24 patients clinically diagnosed as having papillary stenosis were treated by endoscopic sphincterotomy. All patients had dilated common bile duct (CBD) in addition to 1) elevation of transaminases and alkaline phosphatase (n = 13); 2) elevation of transaminases and serum amylase (n = 4); 3) normal liver enzymes but delayed biliary emptying on quantitative hepatobiliary scintigraphy (QHS) (n = 7). No CBD stones, organic obstruction or other disorders were found in these patients.EST was successfully performed in 24 patients. One patient had minor hemorrhage and one patient developed pancreatitis after EST. Twenty-two of the 24 patients (91.7%) were symptomatically improved before discharge. Twenty-one patients were regularly followed over a median period of 18 months (range 5-36) after EST. Two patients with symptom had recurrence at five and eight month follow up because of restenosis of papilla; another two patients with recurrent biliary symptoms, but the sphincter of Oddi remained wide open. Seventeen of 21 regularly followed patients were symptom free after the median 18-month follow up.EST is an effective and safe modality for treatment of sphincter of Oddi dysfunction.

Variceal bleeding is a major life-threatening complication of cirrhosis of the liver. Transjugular intrahepatic portosystemic shunts (TIPS) have been accepted as an effective method for portal decompression. Experiences here with the use of TIPS for control of gastroesophageal variceal bleeding is presented.Sixteen TIPS procedures were performed for 15 patients who suffered from intractable gastroesophageal variceal bleeding. Nine cases (60%) were hepatitis-related cirrhosis of liver, four (27%) were alcoholic liver cirrhosis and two were cryptogenic in origin. Liver function tests revealed four patients were Child-Pugh's classification A, five were B and six, C. Twelve cases had received failed endoscopic management of varices; and one patient had recurrent variceal bleeding after devascularization. TIPS procedure was performed electively in nine cases and, as an emergency in six cases.Fifteen of the 16 TIPS procedures attempted were successfully performed. The technically successful rate was 94% (15/16), but two cases with successful TIPS procedure expired at the end of the procedure from hypovolemic shock and acute respiratory distress, respectively; thus the completely successful rate was 81% (13/16), The initial bleeding control rate was 83% (5/6) for the six patients with active bleeding. Portal venous pressure was significantly decreased from 30.8 +/- 5.8 mmHg before TIPS to 21.7 +/- 6.0 mmHg after the procedure (P0.01) and the porto-systemic pressure gradient also significantly decreased from 23.0 +/- 3.6 mmHg to 11.9 +/- 2.7 mmHg after TIPS (P0.01). Recurrent variceal bleeding was noted in four patients (33%) and that was managed by percutaneous transluminal angioplasty (PTA) of shunt, placement of additional stent, second TIPS procedure and a devascularization operation. Hepatic encephalopathy was noted in three patients (25%) after TIPS.TIPS is an effective method to control variceal bleeding caused by portal hypertension, especially when endoscopic or surgical management has failed or is contraindicated.

We report a previously undescribed ultrastructural calcification of glomerular immune complex depositions in a patient with lupus nephritis. Such processes give rise to a distinctive ultrastructural calcified microspheriol in electron-dense immune deposits, and were associated with hypercalcemia and nephrocalcinosis. The cause of hypercalcemia in this patient was uncertain, but related to a granulomatous inflammation and abscess of the breast. Whereas ultrastructural microcalcification was associated with hypercalcemia, its distribution in the segmental glomerular lesions suggests that an inflammatory process was contributory. The clinical follow-up indicates that the microcalcifications of immune complexes have not affected the outcome of nephritis and renal function.

Recurrent common bile duct (CBD) stones after cholecystectomy are a common biliary tract disease. The role of biliary emptying in the formation of these stones is not yet well defined.Cholescintigraphy was used to evaluate the biliary motility in 50 cholecystectomized patients with recurrent CBD stones after endoscopic sphincterotomy (EST) with stone extraction. Complete clearance of the CBD stones was confirmed in all patients by endoscopic retrograde cholangiopancreatography. Absence of sphincter of Oddi (SO) pressure after EST was determined by means of biliary manometry, and 99mTc-diisopropyl iminodiacetic acid (DISIDA) cholescintigraphy was performed four to six weeks after recovery from sphincterotomy.Complete clearance of the radioisotopes from the bile duct within 1, and more than 1 hour, was observed in 3 (6%) and 47 (94%) of the patients, respectively. When a cutoff value of 2 hours indicating abnormal biliary motility was employed, 31 out of the 50 patients (62%) had delayed biliary emptying. In comparing the clinical parameters between the two groups, patients with delayed biliary emptying time demonstrated an increase in CBD size greater than those of the normals (11.7 +/- 0.5 vs 9.2 +/- 0.4 mm, p0.05), while the presence of juxtapapillary diverticula and length of time for recurrence of CBD stones after cholecystectomy were not significant. Follow-up study showed that repeated recurrence rate of CBD stones appeared to be higher in the patients associated with delayed (12.9%) rather than normal (5.3%) biliary emptying.These results suggested that, in the absence of a functioning SO, abnormal biliary motility in cholecystectomized patients is one of the clinical factors involved in the pathogenesis of recurrent CBD stones.

Endoscopic nasobiliary drainage (ENBD) is a safe and effective modality which has been well documented for obstructive jaundice. However, factors predicting success rate of ENBD remain inconclusively. This study analyses those factors and discusses the outcome of patients with obstructive jaundice.One hundred and sixteen patients (male 99, female 17; mean age 68.2 years) with obstructive jaundice received ENBD after endoscopic retrograde cholangiogram (ERC) by Olympus JF-lT20 endoscope and 7F Wilson-Cook nasobiliary catheter from Sep. 1990 to Oct. 1993. Bile output (QD), serum bilirubin (BIW), liver biochemistry (QW), bile culture (next day), blood culture (if BT38.5 degrees C) were checked until definite treatment or death. Adequate drainage was defined as a daily output of bile more than 200cc, a gradual drop in serum bilirubin and no signs of cholangitis. Factors such as causes of jaundice, obstruction level, serum bilirubin, albumin, juxtapapillary diverticulum (JPD), bacteremia, fever before ERCP and ascites were analyzed.The success rate was 86.2% (100/116) in ERC and 78% (78/100) in ENBD. Adequate biliary drainage was 82.1% (64/78), and serum bilirubin was reduced from 14.3 +/- 8.5 mg% to 7.5 +/- 5.6 mg% within one week. In patients with non-cancerous causes, higher success rate and adequate drainage rate were obtained compared with those with cancerous causes (94.3% vs. 69.2%, p0.01 and 88.6% vs. 50.8%, p0.01, respectively). In all patients, a higher success rate was achieved at the obstruction level at the common bile duct (CBD) compared with periampullary and hilar levels (90.7% vs 69.2%, p0.05 and 90.7% vs 28.6%, p0.001, respectively). In patients with cancer as a cause, higher success rate was achieved at CBD level than at hilar level (85% vs 28.6%, p0.05). Those patients with cancer and serum bilirubin above 15 mg/dl had a higher failure rate in ENBD. Success rate of ENBD was not related to the presence of JPD, bacteremia or fever before ERCP and serum albumin level.Factors decreasing the success rates of ENBD were underlying cancerous causes, obstruction level at hilum or periampullary region and serum bilirubin level more than 15 mg%.

We conducted a prospective, randomized trial comparing sclerotherapy and ligation in 120 patients with acute bleeding of esophageal varices. All the patients were cirrhotic, 59 received sclerotherapy, and 61 received ligation. Treatment was repeated regularly until the varices were obliterated. The mean follow-up period was 295 +/- 120 days and 310 +/- 105 days for the sclerotherapy and ligation groups, respectively. The control of active bleeding was 12/15 (80%) in the sclerotherapy group and 18/19 (94%) in the ligation group (P = .23). The numbers of treatment sessions required to achieve variceal obliteration were 6.5 +/- 1.2 in the sclerotherapy group and 3.8 +/- 0.4 in the ligation group (P.001). Recurrent bleeding from the gastrointestinal tract was 51% in the sclerotherapy group compared with 33% in the ligation group (P.05). Recurrent bleeding from esophageal varices was 36% in the sclerotherapy group and 11% in the ligation group (P.01). However, bleeding from ectopic varices and congestive gastropathy was less common in the sclerotherapy group (7%) than in the ligation group (18%) (P = .05). Significant complications were encountered in 19% of the sclerotherapy group and in 3.3% of the ligation group (P.01). Comparison of Kaplan-Meier estimates of time to death of both groups showed a significantly lower mortality in the ligation group (P = .011). Both sclerotherapy and ligation can effectively arrest active bleeding from esophageal varices. However, ligation is more effective than sclerotherapy in decreasing the risk of rebleeding from esophageal varices with fewer complications. Ligation can also achieve obliteration of esophageal varices more rapidly than sclerotherapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Fifty-two patients with Forrest Ia or Ib bleeding ulcers were randomized to receive endoscopic injection therapy with either 1:10,000 epinephrine in water (Group I) or distilled water (Group II). Twenty-five out of 27 patients in group I, versus 22 out of 25 patients in group II, achieved initial hemostasis after endoscopic injection therapy (p > 0.05). Five patients who did not respond to local injection had bleeding controlled by heater probe thermocoagulation or surgical intervention. Three patients in each group developed rebleeding after initial hemostasis. Four of these patients had bleeding controlled by surgical intervention, while the other two died of underlying diseases. No change in systemic blood pressure, but a significant drop in the pulse rate were noted in both groups after injection therapy. Patients with shock at admission or ulcer size greater than 2 cm had a significantly higher rebleeding rate after initial hemostasis than patients with normal blood pressure and ulcers under 2 cm (p < 0.05). No serious complications were observed after injection therapy, and no significant difference in the amounts of solution required for successful hemostasis was noted between the two groups. We conclude that a local tamponade with distilled water is as effective and safe as diluted epinephrine solution for endoscopic injection therapy.

The mechanisms of hypoglycemia and hypolipacidemia due to insulin and growth hormone were investigated in human volunteers. 6-14C-glucose and 1-14C-palmitic acid were infused simultaneously at a constant rate into healthy adults. Plasma glucose and free fatty acid concentrations and specific activities were measured. The data so obtained were used to compute the inflow and outflow rates of plasma glucose and plasma FFA, with equations derived from a model of a single open pool system. Insulin at a dose below 0.05 U/kg body weight caused hypoglycemia by decreasing the inflow of glucose; at higher doses it caused hypoglycemia by both decreasing the rate of inflow and increasing the rate of outflow. When the subjects were pretreated with 5 mg of growth hormone, insulin action on flux rates was diminished, probably by both inflow and outflow mechanisms. Insulin caused hypolipacidemia by decreasing inflow; the dose for maximal effect was much less than that for maximal hypoglycemic effect, and growth ...