Characteristics of Symptom Presentation and Risk Factors in Patients with Erosive Esophagitis and Nonerosive Reflux Disease

Objective

The aim of this study was to investigate the effect of gender on symptom presentation and quality of life of patients with erosive esophagitis (EE) and nonerosive reflux disorder (NERD).

Subjects and Methods

Medical records from patients with gastroesophageal reflux disease (GERD) between January and December 2009 were reviewed. The patients were assigned to either the EE or the NERD group. The general demographic data, the modified Chinese GERDQ scores and the Short Form (SF)-36 life quality questionnaire scores of the two groups of patients were compared.

Results

Of the 261 patients, 87 (33.3s%), 86 (33.0s%) and 88 (33.7s%) patients were classified into the EE, the NERD and the control groups, respectively. The patients in the EE group were significantly older (48.94 ± 17.38 vs. 43.34 ± 12.67 years), were predominately male (58.6 vs. 39.5s%), had more frequently hiatal hernia (34.5 vs 17.4s%), had a higher body weight (67.57 ± 15.13 vs. 61.06 ± 11.08 kg) and a higher body mass index (24.09 ± 4.61 vs. 22.68 ± 3.12) than those in the NERD group. The GERD-specific symptom scores and the general life quality scores of the EE and the NERD groups were similar, and both groups had lower life quality scores than the control group did. The female patients with NERD had a higher frequency of GERD symptoms and lower quality of life scores. Gender had no effect on symptom scores or life quality scores in the EE group.

Conclusion

The GERD-specific symptom severity and general quality of life scores of the EE and the NERD patients were similar. Gender had a great influence on symptom presentation and quality of life in patients with NERD, but not in those with EE.Key Words: Erosive esophagitis, Gastroesophageal reflux disease, Gender, Quality of life, Nonerosive reflux disease     

Sodium nitroprusside as a coronary vasodilator in man. I. Effect of intracoronary sodium nitroprusside on coronary arteries, angina pectoris, and coronary blood flow.

The effect of the intra-arterial injection of 5 to 10 microng of sodium nitroprusside on the caliber of normal and diseased coronary arteries was evaluated in 21 patients during diagnostic cardiac catheterization. In addition, the effect of intra-graft injection of 5 microng of the same agent on the blood flow in aorta-right coronary artery saphenous vein bypass grafts was also evaluated intra-operatively in two patients. The compound induced an increase in the caliber of both normal and stenosed coronary arteries as well as an increase of flow in the grafts. Consistent with measurements of coronary flow response to sodium nitroprusside, angina pectoris which developed in four patients during cardiac catheterization was immediately relieved and the ischemic ST-segment depression significantly reversed after injection of 5 to 10 microng of the drug into the left main coronary artery. Within the dose range used, the drug caused no significant effect on systemic blood pressure or apparently deleterious electrophysiologic changes. No side effects were observed. We conclude that the primary direct action of sodium nitroprusside in the human coronary artery is vasodilatory.     

Increased circulating calcitonin gene-related peptide in congestive heart failure caused by congenital heart disease

Calcitonin gene-related peptide has potent vasodilatory and inotropic actions. The aim of this study was to characterize the changes in this peptide in children with varying degrees of heart failure secondary to congenital heart disease with left to right shunt and to assess its relationship to systolic pulmonary arterial pressure. Plasma calcitonin gene-related peptide levels were measured in 131 children including 13 healthy ones, 43 with various degrees of heart failure secondary to congenital heart disease, and 75 with congenital heart disease without heart failure. In patients with heart failure, calcitonin gene-related peptide concentrations were markedly elevated (15.8 +/- 2.1 pg/mL) as compared with healthy control subjects (7.0 +/- 0.8 pg/mL, P < 0.05) or patients with congenital heart disease but without heart failure (18.6 +/- 1.2 pg/mL, P < 0.01). Compared with the controls, there were highly significant stepwise increases in the calcitonin gene-related peptide levels in the mild (n = 15), moderate (n = 12), and severe (n = 16) heart failure subgroups by 1.5, 1.7 and 3.4 fold, respectively. The plasma calcitonin gene-related peptide levels also correlated directly with the pulmonary arterial systolic pressure (r = 0.515, P < 0.0001). The results of this study indicate that congestive heart failure secondary to congenital heart disease with increased pulmonary flow is associated with elevated levels of calcitonin gene-related peptide that are related to disease severity. Pulmonary overcirculation may play a role in upregulation of calcitonin gene-related peptide in congestive heart failure.     

OctreoTher: ongoing early clinical development of a somatostatin-receptor-targeted radionuclide antineoplastic therapy

OctreoTher ((90)Y-DOTA-D-Phe(1)-Tyr(3)-octreotide, a.k.a. (90)Y-SMT 487) consists of a somatostatin peptide analogue (Tyr(3)-octreotide), coupled with a complexing moiety (DOTA), and labeled with a tightly bound beta-emitter (yttrium-90). By targeting somatostatin receptor-positive tumors (as imaged by OctreaScan it may deliver a tumoricidal dose of radiation. Phase I clinical trials, conducted in patients with neuroendocrine tumors, established the safety and tolerability of the dose selected for further study and demonstrated the capacity of OctreoTher to deliver radiation doses to tumors that resulted in significant neuroendocrine tumor shrinkage. Novartis-sponsored phase II studies will soon begin to test the efficacy of OctreoTher in breast and small cell lung cancer. A fixed-dose regimen of 120 mCi/cycle x 3 cycles administered with concomitant amino acid infusion has been chosen for the study. Phase I data and published literature support that this fixed dose regimen will be safely tolerated.     

The accuracy of endoscopic ultrasound, endoscopic retrograde cholangiopancreatography, computed tomography, and transabdominal ultrasound in the detection and staging of primary ampullary tumors

BACKGROUND/AIMS: To compare the accuracy between EUS (endoscopic ultrasound), ERCP (endoscopic retrograde cholangiopancreatography), CT (computed tomography), and transabdominal US (ultrasound) in the detection and staging of primary ampullary tumors. We will also try to discuss the influence of endobiliary stent on EUS in staging ampullary tumors. METHODOLOGY: Twenty-one patients with ampullary tumors were evaluated by EUS, ERCP, CT, and US before operation. The accuracy was assessed with TNM staging and compared with the surgical-pathological findings. RESULTS: EUS was superior to CT and US in detecting ampullary tumors, but EUS and ERCP are of similar sensitivity (EUS 95%, ERCP 95%, CT 19%, US 5%). EUS was superior to CT and US in T staging (EUS 75%, CT 5%, US 0%) and detecting lymph node metastasis (EUS 50%, CT 33%, US 0%) of ampullary tumors. The accuracy of EUS in T and N staging of ampullary tumors tended to be decreased in the presence of endobiliary stent (stenting: T 71%, N 75%; nonstenting T 83%, N 100%), but there was no statistical significance. CONCLUSIONS: EUS was superior to CT and US in assessing primary ampullary tumors, but it was not significantly superior to ERCP in detecting ampullary tumors. The presence of endobiliary stent may decrease the accuracy of EUS in staging ampullary tumors.     

Viral hepatocarcinogenesis: from infection to cancer

Hepatocellular carcinoma (HCC) is a worldwide health issue that has started receiving attention but is still poorly understood. However, the hepatitis B virus (HBV) and the hepatitis C virus (HCV) are known to be two major causative agents of HCC. They differ in their modes of infection, their treatment options, their genomes and their carcinogenic abilities. However, both share a link with HCC through alterations of the host genome. In order to continue in our search for the mechanisms behind viral hepatocarcinogenesis, the individual entities (HBV, HCV, HCC and host), their natural history, treatment options and genomic properties must be further understood. Additionally, an understanding of the genomics, the link between the entities, is crucial for the success of the ongoing search for therapeutic options for HCC. Similar to most types of cancer, hepatocarcinogenesis is a multistep process involving different genetic alterations that ultimately lead to malignant transformation of the hepatocyte. As technology advances and research continues, the genetic changes and influences among these entities will prove essential to improved diagnostic and therapeutic options. It remains a challenge to provide a clear picture of the connection between virus and cancer. We review (i) the epidemiological link between HBV/HCV infection to HCC; (ii) prevention and control of chronic hepatitis B or C in reducing HCC risk; and (iii) genetic characters of viruses and hosts and the mechanisms associated with HCC susceptibilities, with the intention of providing a direction for future research and treatment.     

Serial electrophysiologic studies of the effects of oral diltiazem on paroxysmal supraventricular tachycardia

In 16 patients with paroxysmal supraventricular tachycardia, electrophysiologic studies were done before and serially at hourly intervals for eight hours after the third oral dose of 90 mg diltiazem given every eight hours. Diltiazem increased both the longest atrial paced cycle length producing type 1 atrioventricular block and the effective refractory period of the atrioventricular conducting system at all measurements. Before diltiazem, all 16 patients had induction of sustained tachycardia. After diltiazem, sustained tachycardia could not be induced in ten patients at any measurements; in these patients, either echo or nonsustained tachycardia was induced. In the remaining six patients, sustained tachycardia was induced, particularly after six hours. Follow-up observations in 12 patients receiving the same dosage of oral diltiazem for 6 +/- 2 months (mean +/- SD), showed that of the eight patients in whom electrophysiologic testing induced either echo or nonsustained tachycardia, six were asymptomatic and two experienced transient palpitation. Of the other four patients with induction of sustained tachycardia, three had transient palpitation and one had occasional attacks of sustained tachycardia requiring modification of therapy. Thus, oral diltiazem increases atrioventricular nodal refractoriness, with an effect lasting up to eight hours. It is an effective agent for the prophylaxis of paroxysmal supraventricular tachycardia.     

Signal transduction and the regulation of actin conformation during myeloid maturation: studies in HL60 cells

Maturation of human myeloid cells is associated with quantitative and qualitative changes in protein kinase C (PKC) and increases in N-formyl- L-methionyl-L-leucyl-L-phenylalanine (FMLP) receptors, actin, and actin regulatory proteins. We have studied the actin responses and cell shape changes caused by FMLP and its second messenger pathways in HL60 cells undergoing neutrophilic maturation. In uninduced cells, the PKC activators 12-O-tetradecanoyl phorbol-13-acetate (TPA), bryostatin, and 1-oleyl-2-acetylglycerol (OAG) resulted in 15% to 30% decreases in F- actin, whereas FMLP had no effect. Ionomycin had no effect on actin but did cause a 10-fold increase in intracellular calcium. Cells grown for 24 hours in 1% dimethyl sulfoxide (DMSO) acquired the ability to polymerize actin in response to FMLP and ionomycin. TPA continued to cause a decrease in F-actin at 24 hours, but caused an increase in F- actin at 48 to 72 hours of maturation. The PKC inhibitor 1-5- isoquinolinesulfonyl 2-methylpiperazine (H7) partially blocked the F- actin increase caused by TPA in induced cells, but had no effect on the decrease in F-actin caused by TPA in uninduced cells or the increase in F-actin seen in FMLP-treated neutrophils. F-actin rich pseudopods developed following TPA or FMLP stimulation of induced HL60 cells; in uninduced cells neither agent caused pseudopod formation but TPA caused a dramatic loss of surface ruffles. The ability of FMLP and ionomycin to elicit a neutrophil-like actin response in HL60 cells within 24 hours after DMSO treatment shows that the actin regulatory mechanism is mature by that time. The inability of ionomycin to increase F-actin in uninduced cells supports the view that calcium increases alone are insufficient for actin polymerization. The longer maturation time required for HL60 cells to develop an actin polymerization response to TPA compared with FMLP, coupled with the inability of H7 to block the FMLP-mediated F-actin increase in neutrophils, suggests that the F- actin increase caused by FMLP is not mediated solely by PKC. Lastly, the TPA-induced F-actin decrease and shape changes in uninduced HL60 cells, and the longer time required for a "mature" response to TPA, may reflect immaturity in the PKC isoenzyme pattern rather than immaturity of the actin regulatory mechanism.     

A second BamHI DNA polymorphism and haplotype association in the factor IX gene

A second BamHI DNA polymorphism has been identified in the factor IX gene in an American black population at an allelic frequency of 0.13. This site has been localized within 500 basepairs (bp) 5' to the XmnI intron 3 polymorphic site and increases the heterozygosity of black females at the factor IX gene locus. In addition, haplotype analysis of factor IX genes at five polymorphic loci indicates that although there is conservation of sequences between the races, factor IX genes show more heterogeneity in an American black population and thus more heterozygosity is observed in black females compared with whites. This increased heterogeneity is due to DNA polymorphisms unique to black populations and to linkage equilibrium between the most 5' and 3' polymorphic sites in factor IX genes in blacks.