bluuebunny/crossref_metadata_2025_split huggingface dataset:
Metabolic bone disease of liver cirrhosis: Is it parallel to the clinical severity of cirrhosis?
Authors: CHEN CHUN‐CHIA , WANG SUN‐SANG , JENG FONG‐SHYA , LEE SHOU‐DONG 
Published: March 2008

ABSTRACTMetabolic bone disease has long been recognized in chronic liver disease, especially cholestatic or alcoholic liver diseases. The aim of the present study was to investigate the prevalence and severity of osteodystrophy in cirrhotic men and the correlation of its incidence with the clinical severity of cirrhosis in an endemic area of post‐necrotic hepatitis. We measured serum levels of osteocalcin, 25‐hydroxyvitamin D, parathyroid hormone mid‐molecule, calcium and testosterone in 74 cirrhotic men (Child‐Pugh's classification grade A n= 30, B n= 21 and C n= 23) and 16 healthy controls. Standard X‐rays and bone mineral densities of lumbar spine were performed in 30 patients with post‐necrotic cirrhosis and 10 healthy controls. Serum levels of osteocalcin, parathyroid hormone and testosterone were significantly lower in patients with cirrhosis than in controls. Changes paralleling an increased severity of cirrhosis were found in the serum levels of 25–hydroxyvitamin D and testosterone, but not in the serum levels of osteocalcin and parathyroid hormone. The lumbar bone mineral density was significantly lower in patients with post‐necrotic cirrhosis than in controls (0.97 ± 0.13 vs 1.07±0.12 g/cm2, P<0.05) and was correlated with serum 25–hydroxyvitamin D levels (r = 0.467; P<0.005). There was no correlation between the bone mineral density and serum osteocalcin or the clinical severity of cirrhosis. The prevalence of spinal osteoporosis, as defined by a lumbar bone mineral density greater than two standard deviations below the mean value of the controls, was 20% in cirrhotic patients compared with 10% in controls. Two (6.7%) patients (both grade C) had spinal compression fractures compared with none in the control group. In conclusion, serum osteocalcin and lumbar bone mineral density were significantly lower in cirrhotic men than in controls. However, they were not correlated with each other or the clinical severity of cirrhosis.
Primary sclerosing cholangitis: An experience from India
Authors: KOCHHAR RAKESH , GOENKA MAHESH K , DAS KINSUK , NAGI BIRENDER , BHASIN DEEPAK K , CHAWLA YOGESH K , VAIPHEI KIM , SINGH KARTAR , DILAWARI JANG B 
Published: March 2008

ABSTRACTPrimary sclerosing cholangitis (PSC) is considered to be rare in India. The aim of the present study was to investigate the incidence, clinical profile and outcome of PSC seen in a tertiary care centre. Over a period of 10 years (July, 1984‐June, 1994) 18 patients of PSC were diagnosed at cholangiography (14 patients by endoscopic retrograde cholangiopancreatography, two patients by percutaneous transhepatic cholangiography and two patients by both methods). The presence of secondary causes, such as choledocholithiasis, biliary tract surgery, congenital biliary tract anomalies, cholangiocarcinoma and pancreatic diseases, were excluded. These patients were evaluated retrospectively with respect to their clinical presentation, radiological findings, presence of associated idiopathic ulcerative colitis (IUC), treatment instituted and outcome. The mean (±s.d.) age at diagnosis of PSC was 39.0 (±16.1) years with a male: female ratio of 1.57:1. Nine (50%) patients had associated IUC. The diagnosis of IUC preceded that of PSC in all but one case. Fifteen (83.3%) patients had cholestatic jaundice at presentation, while three (16.7%) patients had asymptomatic rise of alkaline phosphatase. Three (16.7%) patients had recurrent cholangitis and five (27.8%) patients developed portal hypertension during the course of the disease. At cholangiography, intrahepatic radicles were involved in all and extrahepatic radicles in 12 (66.6%) cases. Patients were managed with steroids (n= 7), colchicine (n= 3), ursodeoxycholic acid (UDCA; n= 2) and methotrexate (n= 1), along with symptomatic measures. Mean duration of follow up available in 11 (61%) patients was 20.1 months (range: 1 month‐8 years). Four (36.4%) patients died. Steroids and colchicine did not have any effect while the one patient on UDCA and one on methotrexate showed improvement. In conclusion, in India PSC does not seem to be a rare entity. Its clinical profile and outcome are somewhat similar to those seen in Western countries.
Clinical significance of serum hyaluronan in patients with chronic viral liver disease
Authors: MURAWAKI YOSHIKAZU , IKUTA YUJIRO , KODA MASAHIKO , NISHIMURA YUUKO , KAWASAKI HIRONAKA 
Published: March 2008

ABSTRACTIn order to elucidate the clinical significance of serum hyaluronan in chronic viral hepatitis, serum hyaluronan concentrations were measured using a sandwich enzyme binding assay in 115 patients with chronic viral hepatitis. These findings were examined in relation to the results of laboratory liver tests, levels of serum markers for fibrosis and liver histological findings. Serum hyaluronan levels increased with the progress of liver disease, particularly in liver cirrhosis. There were no significant differences in serum hyaluronan levels among the cirrhotic patients according to Child's grade. Multivariate analysis showed that the significant independent predictors of serum hyaluronan were serum aspartate aminotransferase (P= 0.020), serum alanine aminotransferase (P= 0.008), serum cholinesterase (P< 0.001), particularly serum type IV collagen 7S domain (P< 0.0001), and the histological degree of liver fibrosis (P< 0.0001). These findings suggest that elevated serum hyaluronan levels are closely related to the severity of liver fibrosis. We assessed the predictive value of serum hyaluronan in differentiating cirrhosis from chronic hepatitis, constructing receiver operating curves; we found that serum hyaluronan was a better test for diagnosing cirrhosis than serum type IV collagen 7S domain and laboratory liver tests.
Distribution of peptide‐containing nerve fibres in achalasia of the oesophagus
Authors: WATTCHOW DAVID A , COSTA MARCELLO 
Published: March 2008

ABSTRACTIn this study the innervation of the normal human oesophagus was compared with samples taken from 12 patients undergoing Heller's cardiomyotomy for achalasia. The distribution of all nerve fibres in the oesophageal wall was revealed by immunoreactivity to neuron specific enolase and subpopulations of nerve fibres were revealed by immunoreactivity to vasoactive intestinal peptide, neuropeptide Y, enkephalin and substance P. In healthy oesophagus, many nerve fibres immunoreactive for vasoactive intestinal peptide and neuropeptide Y were present in the circular and longitudinal muscle layers of the oesophageal wall and in the cardia of the stomach, whereas fibres immunoreactive for enkephalin and substance P were uncommon. Neuropeptide Y‐reactive fibres were commonly seen around blood vessels. In the myenteric plexus cell bodies reactive for vasoactive intestinal peptide and neuropeptide Y were prevalent, as were varicose and non‐varicose fibres. In contrast, samples from patients with achalasia revealed few nerve fibres immunoreactive for vasoactive intestinal peptide or neuropeptide Y in either circular or longitudinal muscle, suggesting damage to the inhibitory motor neurons to the muscle layers. Very few fibres were found that were reactive for neuron‐specific enolase, indicating that other fibre populations (e.g. excitatory cholinergic motor neurons) are also damaged in achalasia. These abnormalities were observed in biopsies from both the constricted and dilated portions of the oesophagus, but the pattern of innervation in the gastric cardia was normal. Myenteric ganglion cells were seen in the oesophagus in only two patients and varicose nerve fibres in the myenteric plexus were uncommon. Neuropeptide Y‐reactive perivascular nerve fibres were still found in achalasia as well as non‐varicose nerve fibres in the myenteric plexus. These findings indicate damage to all intrinsic neurons in the oesophageal wall in achalasia; however, extrinsic nerve fibres appear to be intact.
Detection of duodenal fluid in the oesophagus with a sodium ion selective electrode*
Authors: WATSON DAVID I , SMYTHE ANNE , MANGNALL YVONNE F , JOHNSON ALAN G 
Published: March 2008

ABSTRACTThe assessment of duodeno‐oesophageal reflux is difficult as, until recently, no technique has been readily available for continuous ambulatory monitoring. A sodium ion selective electrode placed in the stomach has been previously shown to detect duodenogastric reflux by using sodium as a marker. This relies on the difference in sodium concentration between gastric (5–60 mmol/L) and duodenal, biliary and pancreatic (150 mmol/L) fluids. In this pilot study to assess the efficacy of the electrode in the distal oesophagus, eight subjects without symptomatic gastro‐oesophageal reflux and eight subjects with known duodenogastric reflux were studied. Thirty millilitre volumes of varying sodium solutions (40, 80, 100 and 140 mmol/L) were swallowed to assess the response of the electrode to sodium ions. In both groups, this revealed a constant and reproducible rise in response with increasing concentration (P< 0.0001). The stomachs of subjects with duodenogastric reflux were aspirated via a nasogastric tube to obtain 12 different samples of gastric fluid. This was assayed for sodium and bile acid concentration. The fluid was then reinfused as a 30 mL bolus into the oesophagus through a tube to simulate oesophageal reflux. A rise equivalent to 40–72 mmol/L Na+ was recorded by the electrode in response to samples that contained 58–81 mmol/L Na+ and 0.4–16 mmol/L bile acids, recorded by quantitative analysis, and a response of up to 20 mmol/L Na+ was recorded by the electrode to sodium concentrations < 49 mmol/L and bile acid concentrations of 0.005–0.6 mmol/L. The response was appropriate to the assayed bile acid concentration in all but one sample. The sodium ion selective electrode responds to bile containing fluids introduced into the oesophagus. Further investigation is warranted to determine its ability to measure duodeno‐oesophageal reflux continuously.
The Cathlocator: A novel non‐radiological method for the localization of enteral tubes
Authors: WILLIAMS AJK , FRASER R , CHORLEY DP , DENT J 
Published: March 2008

ABSTRACTSafe placement of nasogastric tubes requires reliable positioning of the tip of the tube within the stomach. Radiology and aspiration are currently used to confirm tube position, but suffer from significant problems of cost and efficacy, respectively. We have developed a novel method to locate the position of a catheter tip within the body, using the detection of a low energy electromagnetic field generated in a coil located in the catheter with an external hand‐held unit (Cathlocator). In vitro, the unit detected the distance of the coil from the detector with an accuracy of 0.1 cm over a range of 4–12 cm. In vivo studies were performed in 11 healthy volunteers using a purpose‐built manometric assembly that incorporated the signal generating coil in its tip. In all subjects the Cathlocator showed the position of the signal generating coil to be cranial to the xiphisternum when manometric and transmucosal potential difference criteria showed it to be located above the lower oesophageal sphincter. When the coil was within the stomach, the Cathlocator identified its position within the epigastric, umbilical and left hypochondrial regions of the abdomen. The distance of the coil from the surface was significantly greater when in the duodenum mean (±s.e.m. 7.6±0.3 cm; P<0.001) and oesophagus (8.6±0.2 cm; P<0.002) than the stomach (5.0±0.4 cm). In one subject studied twice there was a close correlation between the location and depth measured by the device on each occasion. The Cathlocator is a novel non‐radiological device that has the potential to be useful in the placement of gastrointestinal catheters.
An assembled electrogastrographic device to examine the meal effect on gastric slow wave
Authors: CHANG F‐Y , LEE C‐T , LEE S‐D , JANG H‐C , TSAI D‐S , FU S‐E 
Published: March 2008

ABSTRACTWe have assembled an electrogastrographic device based on the main components of amplifiers, a band‐pass filter, an analogue/digital converter, low band‐pass digital filters and a personal computer. The analysis software uses autoregressive moving average modelling to compute the frequency of slow waves and uses fast Fourier transformation for power spectral computation. Twenty healthy young male volunteers were enrolled in the study to test meal‐elicited responses of the slow wave. Subjects underwent a 15 min recording while fasting and then a standard breakfast, which included 250 mL milk and a cake with a total of 1.45 kj, was ingested within 5 min. The post‐prandial 15 min recording was immediately resumed after the meal. A slight but significant increase in the frequency of slow waves was seen in post‐prandial measurements (mean ± s.d., 0.0506±0.0005 vs 0.0497±0.0005 Hz; P<0.0001). Moreover, a significant enhancement of the power of slow waves was elicited following the meal (36.0±3.1 vs 27.6±3.1 dB; P<0.0001). We conclude that this assembled electrogastrographic device is a reliable means of monitoring gastric myoelectrical activity because the phenomenon of post‐prandial responses of slow waves in either frequency or power is well demonstrated.
Case report: Recurrent hyperammonaemic encephalopathy due to citrullinaemia in a 52 year old man
Authors: CHOW WC , NG HS , TAN† IK , THUM TY 
Published: March 2008

ABSTRACTThe present report describes a Chinese male who presented for the first time with recurrent encephalopathy and hyperammonaemia at the age of 52 years. He was found to have citrullinaemia. To our knowledge, this is the first Chinese with citrullinaemia and the first non‐Japanese who has the variant form of presentation. The patient also has the longest asymptomatic period for citruliinaemia so far described. The patient's biochemical derangement, clinical features and the postulation of his late presentation are discussed. It is noteworthy that simple therapeutic measures, such as lactulose and dietary protein restriction, controlled his symptoms well.
Serum hyaluronic acid reflects the effect of interferon treatment on hepatic fibrosis in patients with chronic hepatitis C
Authors: YAMADA MASAHIKO , FUKUDA YOSHIHIDE , KOYAMA YASUO , NAKANO ISAO , URANO FUMIHIRO , KATANO YOSHIAKI , HAYAKAWA TETSUO 
Published: March 2008

ABSTRACTChanges in serum hyaluronic acid (HA) in 35 patients treated with interferon (IFN) were studied and the histological change in fibrosis was analysed. Serum HA levels and hepatitis C virus (HCV) RNA were followed from the start of therapy to 12 months after completion of treatment. Histological changes in pre‐ and post‐treatment liver biopsies were assessed using a modified Knodell's scoring system. The serum levels of HA (r = 0.79; P<0.0001) correlated with the degree of fibrosis more closely than with that of amino terminal peptides of type III procollagen (PIIIP; r = 0.45; P<0.05) or type IV collagen (IV‐C; r = 0.42; P<0.05). Only complete responders (CR) had a significant decrease in serum levels of HA and IV‐C (P<0.05), in parallel with histological improvement (P<0.01). Neither partial responders (PR) nor non‐responders (NR) had significant changes in histological scores and in serum levels of fibrotic markers. Significant differences were observed between CR and NR, both in HA levels (P<0.01) and PIIIP levels (P<0.05) 12 months after the cessation of treatment. These results suggest that serum HA is an indicator of the extent of fibrosis in chronic hepatitis C. Serial determinations of serum HA levels may be of use for monitoring the histological response of hepatic fibrosis to IFN treatment in chronic hepatitis C.
Premedication with cyclosporine and perindopril modifies the ischaemia‐reperfusion injury during liver resection in rats
Authors: HARDY KJ , TANCHEROEN S , SHULKES A 
Published: March 2008

ABSTRACTThe aim of the present study was to determine whether pretreatment with cyclosporine (CsA), or perindopril (an angiotensin converting enzyme inhibitor) would modify the ischaemia‐reperfusion injury of vascular occlusion during liver resection. Rats were allocated to four groups (n= 20 for each group): (i) sham operated; (ii) liver resection only; (iii) CsA (15 mg/kg); and (iv) perindopril (4 mg/kg during the three days before ischaemia‐reperfusion injury with liver resection). The ischaemia was produced by a 30 min continuous occlusion. The model was designed to study liver function tests as the principal parameter. Compared with liver resection only, bilirubin was significantly lower with perindopril on days 8 and 23, but significantly higher with CsA on days 1 and 2. The alanine aminotransferase peak (day 1) was significantly lower with both perindopril and CsA. The prothrombin time was significantly less on days 2 and 4 with perindopril and day 4 with CsA. Liver histological changes were minimal in all groups at 30 min ischaemia, but were significantly less severe in the perindopril group. There was a significant decrease in the weight of the regenerated liver at day 23 with perindopril and a significantly lower drop in weight on day 1 and the rate of gain was significantly greater. Perindopril (4 mg/kg) and CsA (15 mg/kg) significantly alter liver function tests, liver histology and bodyweight following an ischaemia‐reperfusion injury associated with liver resection. These findings could limit ischaemia‐reperfusion injury for major liver resections in the clinical setting.
Potentiation of carbon tetrachloride‐induced liver damage by dibutylyl‐3′,5′‐cyclic AMP in unstarved rats
Authors: IRITA KAZUO , OKABE HIRONAO , YAMAKAWA MASAE , YOSHITAKE JUN‐ICHI , TAKAHASHI SHOSUKE 
Published: March 2008

ABSTRACTIt has been reported that carbon tetrachloride‐induced liver damage is potentiated by starvation partly due to fat accumulation in the liver and a decrease in hepatic reduced glutathione concentration and that dibutylyl‐3′,5′‐cyclic AMP (DBcAMP) affects fuel metabolism and decreases hepatic reduced glutathione. We investigated the effects of DBcAMP on carbon tetrachloride‐induced liver damage both in unstarved and starved rats. In unstarved rats, intraperitoneal administration of DBcAMP potentiated an increase in serum alanine aminotransferase activity and fatty vacuolization in the liver, both of which were induced by carbon tetrachloride. Hepatic reduced glutathione concentration was also reduced by DBcAMP, although the change was not significant. In contrast, the administration of DBcAMP in starved rats did not affect carbon tetrachloride‐induced changes in serum alanine aminotransferase activity, histological alterations and hepatic reduced glutathione concentration. Administration of DBcAMP to control rats induced different responses in unstarved control rats compared with starved control rats: in unstarved rats, blood glucose concentration decreased but serum free fatty acid concentration increased, whereas in starved rats, blood glucose concentration increased and serum free fatty acid concentration decreased. It was suggested that DBcAMP potentiated carbon tetrachloride‐induced liver damage in unstarved rats, probably due to hepatic fat accumulation and a decreased hepatic reduced glutathione concentration. The former could increase the affinity of the liver for carbon tetrachloride and the latter could accelerate carbon tetrachloride‐induced lipid peroxidation. It was also suggested that DBcAMP failed to affect carbon tetrachloride‐induced liver damage in starved rats, probably because starvation had already decreased hepatic glutathione concentration and DBcAMP had different effects on fuel metabolism compared with effects observed in unstarved rats.
Microvascular disturbances in the colonic mucosa in antibiotic‐associated haemorrhagic colitis: Involvement of platelet aggregation
Authors: YONEI YOSHIKAZU , YOSHIZAKI YOSUKE , TSUKADA NOBUHIRO , INAGAKI YASUTAKA , MIYAMOTO KEI , SUZUKI OSAMU , KIRYU YASUYOSHI , HIBI TOSHIFUMI , ODA MASAYA , ISHII HIROMASA 
Published: March 2008

ABSTRACTAn ultrastructural study of the colonic mucosa was performed in four patients with antibiotic‐associated haemorrhagic colitis and new findings are reported. Colonoscopy was performed and biopsy specimens were obtained within 24 h of the onset of bloody diarrhoea. Colonoscopy demonstrated diffuse oedematous and haemorrhagic mucosa with erosions and white coat. Light microscopy revealed mucosal haemorrhage and inflammatory cell infiltration. Ultrastructurally, platelet aggregation was frequently present in the lumina of colonic mucosal capillaries, causing engorgement of red blood cells in adjacent microvessels. Mild to severe damage was observed in capillary endothelial cells, including discontinuity of basement membranes, gaps between endothelial cells and the destruction of capillaries. There was no evidence of microvascular spasm. In conclusion, our findings suggest that antibiotics directly or indirectly cause microcirculatory disturbances, which result in tissue damage and haemorrhage, in the colonic mucosa.
Case report: Hippocratic digital and Crohn's disease
Authors: MAKIYAMA KAZUYA , ISHIDA KAZUO , ZEA‐IRIARTE WALTER , ITSUNO MINORU , YAMAKAWA MASAKI , MORI NORIHIKO 
Published: March 2008

ABSTRACTA case of Hippocratic digital associated with secondary hypertrophic osteoarthropathy complicating Crohn's disease in a 29 year old Japanese male is reported. Hippocratic digital, or finger clubbing, complicating inflammatory bowel disease has been frequently reported in the Western hemisphere. However, its association with secondary hypertrophic osteoarthropathy has been very rarely found in that disease. In Japan, Hippocratic digital has not been described previously. With regard to the pathogenesis of Hippocratic digital and secondary hypertrophic osteoarthropathy, the theory that both entities belong to the same pathological spectrum and that megakaryocytes or platelet clumps may play the most important role, is discussed.
Inhibition of colon cancer precursors in the rat by sulindac sulphone is not dependent on inhibition of prostaglandin synthesis
Authors: CHARALAMBOUS DORA , O'BRIEN PAUL E 
Published: March 2008

AbstractThe non‐steroidal anti‐inflammatory drug, sulindac, inhibits the growth of colorectal tumours in animal models of colon cancer and causes regression of polyps in patients with familial adenomatous polyposis. The mechanism by which sulindac exerts this inhibitory effect is not known, but it has been postulated to be via the inhibition of prostaglandin synthesis. However, two recent studies have indicated that sulindac sulphone, the non‐prostaglandin inhibiting metabolite of sulindac, may be important in tumour inhibition. In the present study, we examined the effect of sulindac sulphone on the formation of aberrant crypt foci, the earliest identifiable lesions in the development of colorectal cancer, in the rat colon. We have previously shown that sulindac causes a dose dependent inhibition of aberrant crypt formation in this model. Aberrant crypt foci were induced with two oral doses of 1,2–dimethyl hydrazine at 25 mg/kg per dose. Treatment with sulindac sulphone at either 10 mg/kg b.d., or 20 mg/kg, b.d., was started on the day following administration of the first carcinogen dose and was continued for 3 weeks. Colons were then removed and examined for aberrant crypt foci. Colonic crypts were visualized by staining the unsectioned colon in 0.2% methylene blue solution. There was a significant reduction in the number of aberrant foci in rats treated with sulindac sulphone at 20 mg/kg, b.d. (ANOVA, P= 0.0054). The mechanism by which non‐steroidal anti‐inflammatory drugs inhibit formation of aberrant crypt foci is not clear; however, these data suggest that it is not due to the inhibition of prostaglandin synthesis.