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Biomedical subjects

M C Hou

Publications and source records attributed to M C Hou.

At least 73 records · Page 4Linked to original sources
PubMed1996

Hyperglucagonaemia in cirrhotic patients and its relationship to the severity of cirrhosis and haemodynamic values.

Plasma glucagon concentrations were measured in 160 cirrhotic patients (Pugh's grade A in 52 patients, Pugh's grade B in 64 patients and Pugh's grade C in 44 patients). These values were compared with plasma glucagon concentrations in 57 age and sex-matched healthy subjects. Systemic and portal haemodynamic measurements, effective renal plasma flow and creatinine clearance were recorded for each patient. Plasma glucagon levels were significantly increased in cirrhotic patients compared with healthy subjects. In addition, plasma glucagon levels were higher in cirrhotic patients with ascites than in those without ascites and were increased in relation to the severity of cirrhosis as assessed by Pugh's score. Multiple linear regression found that only Child-Pugh's score was estimated to be an independent predictor of hyperglucagonaemia in cirrhotic patients. However, in patients with different degrees of oesophageal varices and in patients without oesophageal varices, plasma glucagon concentrations were no different among the different groups of patients, but were still higher than plasma glucagon concentrations in healthy subjects. In contrast, plasma glucagon levels were negatively correlated with mean arterial pressure and systemic vascular resistance. The results of the present study suggest that impairment of liver function plays, in part, a role in increased plasma glucagon levels observed in patients with cirrhosis. In addition, these data support the hypothesis that hyperglucagonaemia may contribute, at least in part, to the pathogenesis of peripheral arterial vasodilatation in cirrhosis with portal hypertension.

Adult↗
PubMed1996

Plasma interleukin-8 levels in patients with post-hepatitic cirrhosis: relationship to severity of liver disease, portal hypertension and hyperdynamic circulation.

The present study investigated plasma levels of interleukin-8 (IL-8) in patients with post-hepatitic cirrhosis and correlated it with the severity of liver diseases and haemodynamic parameters. Plasma IL-8 levels were significantly higher in 57 post-hepatitic cirrhotic patients (7.5 +/- 1.8 pg/mL; P < 0.005) than those in 41 healthy subjects (2.0 +/- 0.2 pg/mL). Elevated (> 5 pg/mL) plasma IL-8 levels were found in up to 30% of cirrhotic patients. In cirrhotic patients, plasma IL-8 levels progressively increased in relation to the severity of liver dysfunction (4.5 +/- 1.0, 4.9 +/- 1.4 and 20.5 +/- 8.3 pg/mL for Pugh's class A, B and C, respectively; P < 0.005). A significant correlation was observed between plasma IL-8 levels and serum bilirubin levels (r = 0.72; P < 0.001). There were no differences in the hepatic venous pressure gradient (15.4 +/- 1.1 vs 15.1 +/- 0.9 mmHg; P > 0.05) and systemic vascular resistance (1119 +/- 118 vs 1199 +/- 54 dyn.s/cm5; P > 0.05) between cirrhotic patients with and without elevated plasma IL-8 levels. In addition, plasma IL-8 levels did not correlate with hepatic venous pressure gradient (r = 0.26; P > 0.05) and systemic vascular resistance (r = -0.24; P > 0.05). These results demonstrate that plasma IL-8 levels are increased in patients with post-hepatitic cirrhosis. The severity of liver cirrhosis is an important factor for the occurrence of enhanced IL-8 levels. IL-8 does not play a role in the hyperdynamic circulation observed in patients with post-hepatitic cirrhosis.

Bilirubin↗
PubMed1996

Portal hypertensive colopathy in patients with cirrhosis.

BACKGROUND: Colonic vascular ectasias and colorectal varices have been observed in patients with cirrhosis. However, the pathogenesis of these vascular lesions has not been established. METHODS: We enrolled 35 cirrhotic patients and 20 normal controls in this study. All received colonoscopic examinations and measurements of plasma glucagon levels. Portal pressure measurements were performed in all the cirrhotic patients. RESULTS: Colonic vascular ectasias occurred more commonly in cirrhotic patients than in controls (17 of 35 versus 0 of 20; p = 0.009) and more commonly in cirrhotic patients with ascites than in those without (15 of 24 versus 2 of 11; p = 0.038). However, the presence of colonic vascular ectasias was not related to the hepatic venous pressure gradient or plasma glucagon levels. Colorectal varices also occurred more commonly in cirrhotic patients than in controls (16 of 35 versus of 1 of 20; p = 0.034), but the hepatic venous pressure gradient, plasma glucagon levels, and severity of cirrhosis were not related to the presence of colorectal varices. CONCLUSIONS: Portal hypertension per se and increased plasma glucagon levels may not play an important role in the pathogenesis of colonic vascular ectasias or colorectal varices in patients with cirrhosis.

Aged↗
PubMed1996

Plasma interleukin-6 levels in patients with cirrhosis. Relationship to endotoxemia, tumor necrosis factor-alpha, and hyperdynamic circulation.

BACKGROUND: Liver cirrhosis with portal hypertension is associated with hyperdynamic circulation characterized by generalized vasodilatation and increased cardiac output and regional blood flows. Patients with liver cirrhosis present with increased levels of interleukin-6 (IL-6), which may inhibit vascular smooth-muscle contraction. We investigated whether increased plasma IL-6 levels contribute to the pathogenesis of hyperdynamic circulation observed in cirrhotic patients and whether they are correlated with plasma tumor necrosis factor-alpha (TNF-alpha) and endotoxin concentrations. METHODS: In 58 consecutive cirrhotic patients and 34 healthy subjects the plasma concentrations of TNF-alpha and IL-6 were measured with enzyme-linked immunosorbent assay, and endotoxin determinations with a limulus assay. In addition, 52 cirrhotic patients underwent a hemodynamic study using Swan-Ganz catheterization. RESULTS: Plasma TNF-alpha, IL-6, and endotoxin levels were significantly higher in cirrhotic patients than in healthy subjects (7.3 +/- 0.2 versus 5.8 +/- 0.1 pg/ml, 6.4 +/ 0.8 versus 2.0 +/- 0.2 pg/ml, and 7.6 +/- 1.2 versus 2.8 +/- 0.3 pg/ml, respectively; p < 0.01). In cirrhotic patients the plasma levels of TNF-alpha IL-6, and endotoxin progressively increased in relation to the severity of liver dysfunction (graded by Pugh's classification). A significant correlation was observed between plasma TNF-alpha and IL-6 levels (r = 0.48, p < 0.001), whereas no correlation was observed between plasma endotoxin levels and plasma TNF-alpha and IL-6 levels. Plasma IL-6 levels correlated negatively with systemic vascular resistance in patients with cirrhosis (r = 0.5, p < 0.01). CONCLUSIONS: Plasma IL-6 levels are increased in patients with cirrhosis. The severity of liver cirrhosis is an important factor for the occurrence of increased IL-6 levels. IL-6 may play a role in the hyperdynamic circulation observed in patients with cirrhosis.

Blood Circulation↗
PubMed1996

Clinical implications of the white nipple sign and its role in the diagnosis of esophageal variceal hemorrhage.

OBJECTIVE: Differentiation of esophageal variceal hemorrhage from other sources of the GI tract is often difficult. This is a prospective investigation of the significance of the white nipple sign in patients with recent esophageal variceal hemorrhage. METHODS: One hundred sixty-six patients with recent variceal hemorrhage were prospectively studied with respect to presence or absence of the white nipple sign and other stigmata of hemorrhage and compared with 100 patients with known varices but without a clinical history of bleeding. RESULTS: The white nipple sign correlated positively with severity of bleeding (patients required more blood transfusion), hematemesis, and signs of shock. Patients with the white nipple sign also tended to undergo emergency endoscopy and have active bleeding at the time of endoscopy. There was no correlation between rebleeding rate after endoscopic therapy and presence of the white nipple sign. Appearance of the white nipple sign was closely related to the timing of endoscopy (p < 0.0001). The sensitivity and specificity of the white nipple sign in the diagnosis of esophageal variceal hemorrhage were 21 and 100%, respectively, compared with 100 and 54% for the red color sign. Furthermore, the sensitivity of the white nipple sign increased with shorter times between bleeding and endoscopy. CONCLUSIONS: In patients with upper GI bleeding, the white nipple sign suggests that the varices bled recently and that the bleeding was severe. However, it has no predictive value for rebleeding after endoscopic therapy. Earlier endoscopy (i.e., within 24 h of bleeding) is suggested to improve the diagnostic rate of esophageal variceal hemorrhage.

Case-Control Studies↗
PubMed1996

Effects of captopril on renal functions, renal and portal hemodynamics in patients with cirrhosis.

Renin-angiotensin system plays a prominent role in the sodium and water homeostasis. In addition, activation of renin-angiotensin system frequently occurs in patients with cirrhosis and ascites. Theoretically, administering of angiotensin converting enzyme inhibitors can enhance sodium and water retention in cirrhotic patients with ascites. In this study, we evaluate the role of low-dose captopril on renal function changes, renal plasma flow and hemodynamics in patients with cirrhosis and ascites. Fifty patients are randomly assigned to receive captopril or placebo for 14 days. Renal functions, renal plasma flow, plasma renin activity, plasma aldosterone concentration and systemic and hepatic hemodynamics are measured before and after treatment. Our results indicate that placebo administration did not affect any of the parameter measured in this study. The finding that low-dose captopril significantly increases plasma renin activity suggests that the dose used in this study effectively blocks the enzyme activity. However, low-dose captopril does not affect renal plasma flow, renal functions and systemic and hepatic hemodynamics. Results in this study demonstrate that inhibition of angiotensin converting enzyme alone may not improve sodium and water retention in cirrhotic patients with ascites.

Aldosterone↗
PubMed1995

Plasma endothelin levels in patients with cirrhosis and their relationships to the severity of cirrhosis and renal function.

BACKGROUND/AIMS: Increased plasma endothelin levels have been reported in patients with cirrhosis. However, the relationship between plasma endothelin concentrations and hyperdynamic circulation or renal functions has not been documented. METHODS: We measured the plasma endothelin-1 and endothelin-3 concentrations using radioimmunoassay in 96 patients with cirrhosis (Pugh's A in 26, Pugh's B in 45 and Pugh's C in 25) and compared these values to 56 age- and sex-matched healthy subjects. Systemic and portal hemodynamic measurements, effective renal plasma flow, creatinine clearance, plasma aldosterone concentration and plasma renin activity were recorded for each patient. RESULTS: Plasma endothelin-1 and endothelin-3 levels were significantly increased in patients with cirrhosis compared to healthy subjects. Additionally, plasma endothelin-1 and endothelin-3 values were higher in patients with cirrhosis and ascites than in those without ascites. Moreover, plasma endothelin-1 levels increased in relation to the severity of cirrhosis. On the other hand, modest negative correlations were found between endothelin-1 and creatinine clearance or effective renal plasma flow. CONCLUSIONS: Plasma endothelin-1 and endothelin-3 levels are increased in patients with cirrhosis compared to healthy subjects. The increase in plasma endothelin-1 levels is related at least in part to the severity of cirrhosis. Increased endothelin-1 levels may possibly contribute to renal dysfunction in patients with cirrhosis.

Adult↗
PubMed1995

Changes in portal hypertensive gastropathy after endoscopic variceal sclerotherapy or ligation: an endoscopic observation.

To determine the effect of endoscopic variceal sclerotherapy or ligation on portal hypertensive gastropathy, 90 cirrhotic patients with esophageal variceal bleeding were randomized to receive sclerotherapy (n = 44) or ligation (n = 46). Follow-up endoscopic observations of the gastric mucosa were recorded at 3-month intervals after variceal eradication. Clinical characteristics in both groups were similar. Probability for a change in the severity of portal hypertensive gastropathy was not related to method of eradication. Most cases of portal hypertensive gastropathy that changed in severity returned to baseline status with time, but the return was faster after ligation than after sclerotherapy. According to the results of multivariate analyses, sclerosant volume was the only factor associated with a significant difference between the group with static gastropathy (n = 15) and that with dynamic change in gastropathy (n = 23) after sclerotherapy. No relevant factors were found in the patients receiving ligation. We conclude that changes in the severity of portal hypertensive gastropathy after endoscopic variceal sclerotherapy or ligation are reversible. Most cases of gastropathy return to baseline status sooner or later.

Esophageal and Gastric Varices↗
PubMed1995

The effects of chronic administration of indomethacin and misoprostol on renal function in cirrhotic patients with and without ascites.

BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) often cause renal dysfunction in cirrhotic patients with ascites through inhibition of prostaglandin synthesis. However, their renal effects in cirrhotic patients without ascites are controversial. In addition, the role of prostaglandins in cirrhotic patients with ascites and in non-ascitic cirrhotic patients receiving NSAIDs also remains elusive. Thus we evaluated the chronic renal effects of indomethacin and misoprostol in 9 cirrhotic patients with ascites (protocol 1) and 21 cirrhotic patients without ascites (protocol 2). METHODS: The patients of protocol 1 received 200 micrograms of misoprostol every 6 h for 7 consecutive days. In protocol 2, 11 patients received 25 mg indomethacin three times a day for 7 consecutive days. The other 10 patients received 25 mg indomethacin three times a day plus 200 micrograms misoprostol every 6 h for 7 consecutive days. Renal function tests, plasma renin activity, and plasma aldosterone concentration were measured before and after treatment. RESULTS: In protocol 1, misoprostol tended to reduce the urinary sodium excretion (p = 0.08). In protocol 2, indomethacin alone greatly impaired renal plasma flow (p < 0.05), creatinine clearance (p < 0.05), blood urea nitrogen (p < 0.05), and serum creatinine (p = 0.06) in 11 patients. Similar magnitudes of renal dysfunction were observed in the other 10 patients despite the concomitant misoprostol treatment. CONCLUSION: Chronic administration of misoprostol may have caused a negative natriuretic effect in cirrhotic patients with ascites. In cirrhotic patients without ascites chronic administration of indomethacin may induce a renal dysfunction that cannot be reversed by misoprostol.

Aged↗
PubMed1995

Comparison of endoscopic variceal injection sclerotherapy and ligation for the treatment of esophageal variceal hemorrhage: a prospective randomized trial.

To determine the efficacy of endoscopic variceal sclerotherapy (EVS) and ligation (EVL) in the management of esophageal variceal bleeding, 134 cirrhotic patients were randomized to receive either treatment. The clinical and endoscopic characteristics were similar in both groups. Active bleeding was controlled with ligation (20 of 20) as efficiently as with sclerotherapy (14 of 16). Elective sclerotherapy consumed less time than ligation (7.9 +/- 1.8 minutes vs. 11.5 +/- 2.7 minutes, P < .001), but there was no difference between emergent sclerotherapy (14.5 +/- 5.8 minutes) and ligation (14.9 +/- 4.1 minutes). Ligation reduced one grade of variceal size more quickly than sclerotherapy (1.1 +/- 0.4 vs. 2.0 +/- 1.7 session, P < .001). The rebleeding rate was lower with ligation (13 of 67 vs. 28 of 67, P < .01). Esophageal ulcer was the most common source of rebleeding. Recurrence of varices appears more probable with ligation (P = .079). The complication rate was higher with sclerotherapy (15 of 67 vs. 3 of 67, P < .01), with esophageal stricture being the most common cause. Survival rate was the same in both groups even after stratifying patients into good and poor hepatic reserve groups. Hepatic failure was the major cause of death, followed by exsanguination. In summary, EVL was superior to EVS regarding rebleeding and complications but not in other aspects such as time consumption in elective treatment and recurrence of varices. Substantial results for long-term follow-up are required before conclusion of the treatment of choice.

Esophageal and Gastric Varices↗
PubMed1995

Prevalence of duodenal ulcer in cirrhotic patients and its relation to Helicobacter pylori and portal hypertension.

BACKGROUND: The prevalence of duodenal ulcer increases in cirrhotic patients. However, the pathogenesis remains unclear. METHODS: The prevalence of duodenal ulcer and their relationship to cirrhosis and portal hypertension were evaluated in 325 cirrhotic patients, and compared with 325 age- and sex-matched healthy subjects. Portal and systemic hemodynamic studies were performed in all cirrhotic patients. Histological examination of gastric antral mucosa for Helicobacter pylori (H. pylori) was performed in 16 cirrhotic patients with duodenal ulcer and in 34 cirrhotic patients without duodenal lesions. RESULTS: The prevalence of duodenal ulcer in cirrhotic patients was 9.5% (31 out of 325), significantly higher than 4.0% (13 out of 325) in the healthy controls (p = 0.007), but was not related to the severity of liver cirrhosis. The positive rate of H. pylori was not different between cirrhotic patients with duodenal ulcer and those without duodenal lesions (9/16 vs. 18/34, p > 0.05). The hepatic venous pressure gradient was also not different between these groups (17.2 +/- 5.1 vs. 16.1 +/- 4.9 mmHg, p > 0.05). Other variables including sex, smoking, and etiology of cirrhosis did not show significant differences. CONCLUSIONS: The prevalence of duodenal ulcer is significantly higher in cirrhotic patients than in the age- and sex-matched healthy subjects. The severity of cirrhosis, the presence of H. pylori or portal hypertension per se does not play an important role in the increased prevalence of duodenal ulcer in cirrhotic patients.

Duodenal Ulcer↗
PubMed1994

Multiple viral infection as the most common cause of fulminant and subfulminant viral hepatitis in an area endemic for hepatitis B: application and limitations of the polymerase chain reaction.

We tested serum samples from 25 fulminant hepatitis and 7 subfulminant hepatitis patients for hepatitis A, B, C, D and E viral markers and nucleic acids by means of polymerase chain reaction to determine the role of each virus on such catastrophic events in an area endemic for hepatitis B. Of these 32 patients, 14 (44%) were hepatitis B virus carriers with hepatitis D virus superinfection (1 with hepatitis C virus infection), 3 others had coexisting hepatitis B virus and hepatitis C virus infections, 6 had reactivation of underlying chronic hepatitis B, 4 had acute hepatitis B, 2 had acute hepatitis C and 1 had acute hepatitis E. Pathogenesis in the remaining two cases was unclear. Serum hepatitis B virus DNA was detectable in most carriers without superinfection and in one third of those with superinfection detected on polymerase chain reaction (6 of 7 vs. 6 of 16, p < 0.05). Of the polymerase chain reaction-positive samples, only 17% yielded positive results on spot hybridization. Hepatitis B virus DNA was the only marker to indicate coexisting hepatitis B virus infection in one patient positive for hepatitis C virus antibody. Only three of the six hepatitis C virus-infected cases were positive for hepatitis C virus antibody; diagnoses in the remaining three were established by means of detection of hepatitis C virus RNA. Of the hepatitis D virus-infected patients, infection in only half was diagnosed by means of total hepatitis D virus antibody assay. Twelve (86%) were positive for anti-hepatitis D virus IgM and nine (64%) had detectable hepatitis D virus RNA on reverse transcription-polymerase chain reaction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Okadaic acid as an inducer of the 78-kDa glucose-regulated protein in 9L rat brain tumor cells.

Okadaic acid (OA), a potent inhibitor of protein phosphatases 1 and 2A, has been widely used as a tool for unravelling the regulation of cellular metabolic processes involving protein phosphorylation/dephosphorylation. It has recently been found that OA can induce reversible hyperphosphorylation of vimentin and reorganization of intermediate filaments [Lee et al., J. Cell. Biochem. 49: 378-393, 1992]. We report here that OA specifically induced the synthesis of a 78-kDa protein, which was identified as the 78-kDa glucose-regulated protein (GRP78) by two-dimensional sodium dodecylsulfate-polyacrylamide gel electrophoresis and peptide mapping. The induction of GRP78 by OA was dose-dependent and reversible. For 7 h treatments, GRP78 synthesis was initially enhanced under 50 nM OA and became the highest (about 6-fold) under 200 nM OA. Meanwhile, under 200 nM OA, GRP78 synthesis was initially enhanced after 4 h and reached its maximal level (about 8-fold) after 15 h of treatment. Subsequently, upon removal of OA, the level of OA-induced GRP78 was reduced to basal level after 12 h of recovery. Induction of GRP78 synthesis by OA was abolished in cells pretreated with actinomycin D and cycloheximide, indicating that it was regulated at the transcriptional level and its induction required de novo protein synthesis. Furthermore, OA suppressed protein glycosylation, and the result lent support to the hypothesis that suppression of protein glycosylation may correlate with induction of GRP78 synthesis.

Animals↗
PubMed1993

Enhanced phosphorylation of a 65 kDa protein is associated with rapid induction of stress proteins in 9L rat brain tumor cells.

Induction of heat-shock proteins and glucose-regulated proteins in 9L rat brain tumor cells can be differentially elicited by sodium arsenite, cadmium chloride, zinc chloride, copper sulfate, sodium fluoride, and L-azetidine-2-carboxylic acid. The kinds of stress protein induced by the above chemicals varied considerably, mainly determined by the nature and the concentration of the chemicals, as well as the treatment protocols. In addition, at the concentrations where stress proteins can be induced, the above chemicals were able to suppress general protein synthesis and were cytotoxic. Enhanced phosphorylation of a protein with an apparent molecular weight of 65 kDa was detected during the induction of stress proteins except in azetidine treatments during which uptake of phosphate by the cells was impaired after prolonged incubation. The phosphate moiety on the 65 kDa phosphoprotein appeared to be alkaline-stable and two-dimensional gel electrophoresis revealed that the phosphoprotein resolved into four isoforms with isoelectric points ranging from 5.1 to 5.6. Enhanced phosphorylation of the same protein was also detected in heat-shocked and withangulatin A-treated 9L cells in which stress proteins were induced. It is suggested that this phosphoprotein may be a common target for heat stress response-stimulated phosphorylation and important in the further metabolic responses of the cell to stress.

Animals↗
PubMed1993

Heterosexual transmission as the most common route of acute hepatitis B virus infection among adults in Taiwan--the importance of extending vaccination to susceptible adults.

Sixty adult patients with acute viral hepatitis B (AVHB) and 93 controls were interviewed to assess potential risk factors of hepatitis B. Heterosexual contact was the only significant factor, and it was associated with 83% of cases. A history of having new sex partners or multiple sex partners within 6 months before the onset of AVHB or first sexual contact before 20 years of age were significantly associated with HBV infection (P < .005, respectively). There was a dose-response relationship between the number of sex partners and the risk of HBV infection. In multivariate analyses, a history of having new sex partners was the most important factor. Moreover, 18 of 24 sex partners of the patients were serum hepatitis B surface antigen- and HBV DNA-positive. Heterosexual contact is, therefore, the predominant route of HBV transmission among adults in Taiwan. Susceptible adults should receive vaccination.

Acute Disease↗
PubMedDate not supplied

Oesophageal perforation following endoscopic variceal ligation and balloon tamponade.

Endoscopic variceal ligation (EVL) related complication is rarely reported. A case is presented of a 74 year old man with oesophageal variceal bleeding who developed oesophageal perforation following EVL and balloon tamponade. An oesophageal wall defect was induced by EVL and tissue repair was hindered by decompensated liver reserve and shock status; concomitant balloon tamponade precipitated oesophageal perforation. The case is reported to draw attention to oesophageal perforation after concurrent use of balloon tamponade and EVL.

Aged↗
PubMedDate not supplied

Haemodynamic effects of a combination of propranolol and clonidine in patients with post-hepatitic cirrhosis.

The haemodynamic effects of a combination of propranolol and clonidine were evaluated in 20 patients with post-hepatitic cirrhosis. Haemodynamic measurements were taken before and 30 min after an intravenous injection of 0.1 mg/kg of propranolol. Thereafter, each patient was given an oral dose of 150 micrograms of clonidine and re-measured 60 min later. In this series, eight patients were defined as 'non-responders' (a decrease in hepatic venous pressure gradient of < 10%) after propranolol treatment. Of both the responders and non-responders, propranolol caused expected decreases in the cardiac index and heart rate while mean arterial pressure remained unchanged. Of the propranolol responders, a significant decrease in hepatic venous pressure gradient was observed. After the addition of clonidine, in both the responders and non-responders there was a further decrease in hepatic venous pressure gradient with a concurrent drop in mean arterial pressure, but cardiac index and heart rate remained unaltered. In conclusion, the combination of propranolol and clonidine in post-hepatitic cirrhotic patients enhanced the reduction of portal pressure achieved by propranolol alone. The beneficial effects of the combination of the two in the reduction of portal pressure appeared to be similar in both the propranolol responders and non-responders. However, the drop in mean arterial pressure following the addition of clonidine may be hazardous to cirrhotic patients.

Adrenergic alpha-Agonists↗