Association of endoscopic appearances with dyspeptic symptoms

Background The relationship between endoscopic appearances such as endoscopic gastritis and duodenitis and dyspeptic symptoms has not been clearly demonstrated. We aimed to clarify the association of endoscopic appearances with Helicobacter pylori infection, histological severity of gastritis, and dyspeptic symptoms in a Japanese population. Methods We enrolled 87 dyspeptic and 93 nondyspeptic subjects in this study. All subjects underwent gastroscopy, and patients with active peptic ulcer disease, reflex esophagitis with erosion, polyps >1 cm, or cancer were excluded. Endoscopic appearances in patients with dyspeptic symptoms and in those without were assessed retrospectively on the basis of endoscopic images. The degree of atrophy by the Kimura-Takemoto classification system was also assessed. Helicobacter pylori infection status was examined by histology or antibody against H. pylori. Histological severity of inflammation and glandular atrophy in the antrum were assessed according to the updated Sydney System. The odds ratio (OR) and 95% confidence interval (CI) were calculated by logistic regression using the variables age, sex, H. pylori infection status, and all endoscopic appearances. Results The degree of atrophy tended to be lower among dyspeptic patients (P = 0.06). Among all endoscopic appearances, the liner redness (friability) in the antrum (OR = 3.90, 95% CI = 1.20−12.64) and duodenal ulcer (DU) scarring (OR = 3.41, 95% CI = 1.08−10.79) were independently associated with dyspepsia. Histological severity of inflammation and glandular atrophy were not associated with dyspeptic symptoms. Also, no correlation was found between endoscopic appearances and any of the different subgroups of dyspeptic symptoms. Patients with friability in the antrum and DU scar, which correlated with dyspeptic symptom showed some of communal symptoms such as epigastric pain, epigastric discomfort, hypochondriac pain, early satiation/postprandial fullness, and belching, but they differed considerably with respect to H. pylori positivity and the histological severity of gastritis. Conclusions Some endoscopic appearances such as friability in the antrum and DU scarring may be associated with dyspeptic symptoms, and endoscopic appearances may be useful markers to perform clinical implementation reflecting an individual’s pathophysiology of dyspeptic symptoms.     

Augmentation of tumor necrosis factor family-induced apoptosis by E3330 in human hepatocellular carcinoma cell lines via inhibition of NFκB

AIM: To investigate the reduction of cell viability in human hepatocellular carcinoma (HCC) cell lines induced by inhibition of nuclear factor κB (NFκB).METHODS: HLE, SKHep1, and HepG2 were incubated and E3330 was used to compare the stimulation of some chemotherapeutic drugs with that of TNF family, Fas ligand, TNFα and TNF-related apoptosis-inducing ligand (TRAIL) at the point of the reduction of cell viability by inhibiting NFκB.RESULTS: E3330 decreased NFκB levels in HLE cells stimulated by TNF and TRAIL. The cytotoxicity of the combination of TRAIL, TNFα, Fas ligand, and E3330increased synergistically in a dose-dependent manner compared to either E3330 alone in all HCC cell lines by MTT assay. However, the combination of some chemotherapeutic drugs and E3330 did not decrease the cell viability.CONCLUSION: Inhibition of NFκB sensitizes human HCC cell lines to TNF-mediated apoptosis including TRAIL, and TRAIL-based tumor therapy might be a powerful potential therapeutic tool in the treatment of human HCC.     

Acute pancreatitis associated with anomalous union of the pancreaticobiliary ductal system.

Between 1978 and 1989, 13 of 48 patients with anomalous union of the pancreaticobiliary ductal system (AUPBD) were diagnosed as having acute pancreatitis. We have studied the clinical, radiologic, and surgical features of these 13 patients. A transient rise in the intraductal pressure of the pancreatic duct during an episode of abdominal pain is responsible for pancreatitis in patients with AUPBD. This rise in the intraductal pressure must be due to bile reflux into the pancreatic duct when an abnormally long common channel is blocked by cholelithiasis, protein plug, or dysfunction of the sphincter of Oddi. The pancreatitis resolves when the common channel obstruction is removed, and bile and pancreatic juice flow easily into the duodenum. We believe that this phenomenon is responsible for acute relapsing pancreatitis. It is our belief that the pancreas appears almost normal during symptom-free intervals.     

Effects of H1-receptor stimulation on coronary arterial diameter and coronary hemodynamics in humans

Effects of H1-receptor stimulation on coronary arterial diameter and coronary hemodynamics were examined in 11 patients with angiographically normal coronary arteries and without variant angina or resting angina. Selective H1-receptor stimulation was achieved by infusing histamine into the left coronary artery at a rate of 2.0 micrograms/min for 5 minutes after pretreatment with cimetidine (25 mg/kg). Plasma histamine concentration in the coronary sinus, coronary sinus blood flow, heart rate, and aortic pressure were measured before, during, and after the histamine infusion. Coronary arterial diameter was measured by cinevideodensitometric analysis of coronary arteriograms performed before and immediately after the histamine infusion. During the histamine infusion, plasma histamine concentration in the coronary sinus increased from 0.33 +/- 0.06 to 5.86 +/- 0.71 ng/ml (p less than 0.01); coronary sinus blood flow increased from 98 +/- 12 to 124 +/- 13 ml/min (p less than 0.01), and coronary vascular resistance decreased from 1,113 +/- 117 to 851 +/- 91 mm Hg.min/l (p less than 0.01). Heart rate and aortic pressure remained unchanged. The mean luminal diameters of the proximal, middle, and distal left anterior descending artery increased by 9.4 +/- 3.6% (p less than 0.05), 19.2 +/- 3.8% (p less than 0.001), and 31.5 +/- 5.6% (p less than 0.001), respectively, after the histamine infusion. The mean luminal diameters of the proximal, middle, and distal left circumflex artery increased by 15.2 +/- 3.6% (p less than 0.01), 17.5 +/- 5.2% (p less than 0.01), and 20.6 +/- 4.3% (p less than 0.001), respectively, after the histamine infusion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Biochemical evidence for a deficiency of vitamin B6 in the carpal tunnel syndrome based on a crossover clinical study

In a patient with severe carpal tunnel syndrome and a significant deficiency of vitamin B(6), the evidence for the deficiency was an extraordinarily low basal specific activity of the glutamic-oxaloacetic transminase of the erythrocytes (EGOT). This enzyme was also deficient in pyridoxal phosphate. The patient was treated with the recommended dietary allowance of pyridoxine, 2 mg/day, for 11 weeks, then 100 mg/day for 12 weeks, a placebo for 9 weeks, and again pyridoxine at 100 mg/day for 11 weeks. Sixty-one monitorial assays of EGOT over 48 weeks supported the following interpretations. (i) His diet permitted the development of a debilitating carpal tunnel syndrome. (ii) Treatment with pyridoxine at 2 mg/day reduced the deficiency of EGOT activity from about 70% to 50%, maintained a deficiency of pyridoxal phosphate, and relieved but allowed a marginal syndrome. (iii) Treatment at 100 mg/day for 12 weeks nearly achieved a "ceiling" level of EGOT and eliminated the deficiency of pyridoxal phosphate. (iv) After placebo for 7 weeks, the deficiencies of EGOT activity and pyridoxal phosphate reappeared, and clinical symptoms become worse. (v) Retreatment at 100 mg/day reestablished a "ceiling" EGOT, with no deficiency of pyridoxal phosphate, and the patient was asymptomatic. These data also support the concept that a deficiency of vitamin B(6) is significant in the etiology of the carpal tunnel syndrome. Mechanistically, a state of deficiency of the coenzyme seems to lower the level of the apoenzyme; a state of no deficiency of the coenzyme regulates a ceiling level of the transaminase. The latter state is presumably desired for health.     

Contribution of long axis motion of left ventricular outflow to calculation of left ventricular stroke volume

Stroke volume can be calculated by using noninvasive Doppler techniques. The products of pulsed Doppler stroke distance of left ventricular outflow and left ventricular outflow area can often be used to calculate stroke volume. However, left ventricular outflow also moves longitudinally toward the apex of the ventricle during systole, so that zero velocity flow cannot be detected by the usual pulsed Doppler studies. We evaluated the contribution of these zero velocity flow to the noninvasive estimation of left ventricular stroke volume in 20 patients with left ventricular disease and in 20 age matched healthy controls. Left ventricular stroke distance was calculated by summing the Doppler stroke distance and the outflow long axis motion. The percentage of zero velocity flow for total stroke volume was calculated in each group. Cardiac output was also measured by thermo-dilution technique. The percentage of zero velocity flow for total noninvasive stroke volume in patients with left ventricular disease was 2.5±1.1 ml (4.0±1.5%), significantly lower than in normal subjects, 3.6±1.0 ml (5.5±1.5%) (p<0.05). These long axis motions are significantly reduced, especially in left ventricular disease. Amplitudes of the left ventricular outflow long axis motion were correlated with Doppler stroke distance in all (r=0.54, p<0.01). In patients with myocardial infarction, stroke volume by thermo-dilution methods and calculated stroke volume showed good correlation both only by Doppler stroke distance (y=1.044x+0.547, r=0.968) and by Doppler and long axis motion (y=0.989x+0.521, r=0.974). Compared with stroke volume measured by thermodilution method, stroke volume calculated only by Doppler stroke distance was underestimated. We thus demonstrated the influence of zero velocity flow on left ventricular outflow both in patients with left ventricular disease and in normal subjects.     

Use of prostaglandin I2 analog in treatment of massive hepatic necrosis associated with endothelial cell injury and diffuse sinusoidal fibrin deposition

Endothelial cell damage causes massive hepatic necrosis as a result of fibrin deposition in the hepatic sinusoids. When a stable analog of prostaglandin I₂, beraprost sodium, was administered to rats given either dimethylnitrosamine, carbon tetrachloride, or endotoxin followingCorynebacterium parvum administration, the hepatic necrosis produced in each was attenuated, but to a greater extent in the dimethylnitrosamine and endotoxin/Corynebacterium parvum models, where fibrin deposition in the hepatic sinusoids occurs, as compared to the carbon tetrachloride model, where such fibrin deposition does not occur. Beraprost sodium reduced the expected increase of portal venous pressure in the endotoxin/Corynebacterium parvum model without affecting plasma thrombin-antithrombin III complex levels. Beraprost sodium also significantly reduced cell killing of both isolated rat hepatocytes and hepatic sinusoidal endothelial cells exposed totert-butyl hydroperoxide when compared to controls. Beraprost sodium could prove to be a therapeutic candidate for the treatment of hepatic necrosis, particularly in cases associated with fibrin deposition in the hepatic sinusoids because of its fibrin clot-clearning action.     

Comparative therapeutic effects of vitamin D3 and its derivatives on experimental renal osteodystrophy

The comparative effectiveness of vitamin D3 and its derivatives in curing hyperparathyroidism and osteodystrophic bone lesions was examined in a laboratory model of renal osteodystrophy associated with marked secondary hyperparathyroidism in rats. The experimental model was prepared by a single injection of homologous glycopeptide. Plasma levels of 1 alpha,25-dihydroxyvitamin D3 [1 alpha,25(OH)2D3] appeared to decrease in the rats receiving glycopeptide. Various doses of vitamin D3 derivatives [2 or 10 microgram/kg D3, 2 microgram/kg 25-hydroxyvitamin D3 (25OHD3), 0.1 microgram/kg 1 alpha,25(OH)2D3, and 0.1 or 0.2 microgram/kg 1 alpha-hydroxyvitamin D3 (1 alpha OHD3)] were daily administered orally to the nephritic rats for 23 days before sacrifice. 1 alpha,25(OH)2D3 and 1 alpha OHD3 were much more potent than 25OHD3 and D3 in reducing the hyperplasia of parathyroir glands. The potency of 1 alpha OHD3 in curing the histological changes of osteodystrophy appeared to be greater than that of 1 alpha,25(OH)2D3. The same dose level of 1 alpha OHD3 was more effective than 1 alpha,25(OH)2D3 in enhancing plasma 1 alpha,25(OH)2D3 levels.     

Initial depolarizing potentials in wolff-parkinson-white syndrome using signal-averaged electrocardiograms: Correlation with reciprocating tachycardia

Initial depolarizing potentials were examined in patients with Wolff-Parkinson-White (WPW) syndrome using signal-averaging techniques. In all, 25 WPW patients and 21 agematched healthy children were studied. Ten of the patients were symptomatic and 15 were asymptomatic. Symptomatic patients with supraventricular tachycardias had longer durations of lowamplitude signals (LAS) < 40 μ V in the initial portion of the QRS complex (initial LAS, 49 ± 7 ms vs. 37 ± 9 ms, p < 0.01) and lower root-mean-square (RMS) voltage in the initial 40 ms of the QRS complex (initial RMS, 12 ± 4 μ V vs. 23 ± 8 μ V, p < 0.01) compared with asymptomatic patients. When a symptomatic patient was defined as having an initial LAS of > 46 ms or an initial RMS of < 15 μ V, the sensitivity and specificity for predicting documented supraventricular tachycardia were 100 and 67%, respectively. These SA-ECG findings may reflect instability of conduction in symptomatic patients through an accessory pathway and may identify those at high risk for supraventricular tachycardia.