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Looking at the field as a whole through metaanalysis, Shadish et al concluded (based on 162 studies) that marital and family therapies were significantly more effective than no treatment and at least as effective as other forms of psychotherapy. Although these reviews and others are positive, individual studies raise many questions. For instance, based on research findings, family treatments increasingly have become standard care for patients with schizophrenia. It remains unclear what degree and type of family involvement is needed for which patients at which stage of their disorder. In the area of anxiety and depression, there are too few studies to make any strong conclusion. Although investigators such as Barrett, Cobham, and Diamond have produced some positive results, the Lewinsohn and Clark studies fail to demonstrate the added benefit of family involvement. Although Brent's study showed CBT to reduce depression faster, family therapy and supportive therapy did just as well in the long run, and family conflict was a strong risk factor for relapse. In the area of anorexia, Russell and Robins produced strong results from family interventions, whereas Geist found no difference between different types of family interventions. Family treatments for obesity have been inconsistent. In a metaanalysis of 41 studies, parental involvement did not contribute significantly to outcomes. In the Epstein study, however, which included 5- and 10-year follow-up, the results of family intervention were impressive. Although many of these studies can be cited for various methodologic flaws, the most consistent problem is that sample sizes are too small to detect difference between two or more active treatments. The most consistent findings (and most well-done, large studies) that support the efficacy of family-based interventions are done with externalizing problems. Work groups led by Patterson, Eisenstadt, Webster-Stratton, Alexander, and Henggeler all have produced impressive reductions of oppositional and antisocial behavior. Clinical programs that treat these populations without using a family-based intervention as at least a component of a treatment package are seriously ignoring the findings of contemporary intervention science. Programs of research by Henggeler, Szapocznik, and Liddle demonstrate similarly impressive results for substance abusing adolescents. Although preliminary results from the Dennis et al study suggest that various treatment approaches may benefit this population. Family interventions have had less success in reducing ADHD symptoms, yet these psychosocial treatments have been essential in reducing much of the family and school behavior problems associated with this disorder. Many investigators would agree that a combined medication and family treatment approach may be the treatment of choice for children with ADHD. In fact, many studies across various disorders suggest that patients respond best to comprehensive treatment packages, of which a family treatment is at least one component. Although the data are promising, many challenges lie ahead. Although collectively many family intervention studies exist, many disorders lack enough rigorous and large-scale investigations to make any strong conclusions. Kazdin argues that sample sizes of 150 are essential to detect significant differences between active treatments, and few of the reviewed studies include these kinds of patient numbers. Furthermore, not enough committed and sophisticated family treatment researchers have carried out some of the major studies. For example, the Brent study on depression and the Barkley study of ADHD, although testing family approaches, lacked well-developed and published treatment manuals, a demonstration of the necessary expertise to supervise these treatments, and data about training and adherence to these models. Although the absence of expertise limits investigator allegiance biases, treatment development and modification are essential for tailoring family treatments to target family processes specific to each disorder. Investigators such as Patterson and Liddle have invested great effort in rigorously dismantling the treatment process, identifying and refining essential ingredients, and repackaging more potent treatment protocols. This process has paid off well. Programmatic treatment development is needed for many disorders to address myriad questions. What are the essential disorder-specific family processes that should be targeted by interventions? Hostility, criticism, communication, attachment and autonomy, attributional sets, and behavior management are important processes of family life, but each may have more relative importance for specific disorders. With a greater understanding of these processes, treatments could be tailored to target these mechanisms more efficiently and effectively. (ABSTRACT TRUNCATED)
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PMID:Current status of family intervention science. 1144 17

The incidence and mortality related to esophageal adenocarcinoma (EAC) have been increasing in the United States, several European countries, and Oceania for the past 2 to 3 decades. Survival remains dismal, with little improvement during the same time period. Variations in the coding, classification, and detection of gastroesophageal malignancy may have contributed partially to the observed trends. Remarkable differences related to gender, ethnicity, and geography characterize the epidemiology of EAC. Gastroesophageal reflux disease (GERD) is the main risk factor for Barrett's esophagus, which is the only known precursor lesion for EAC. Several risk factors that promote the development of GERD and/or Barrett's esophagus have been proposed to explain these rising trends; these factors include the declining rates of Helicobacter pylori infection, obesity, dietary factors, and certain drugs.
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PMID:The epidemic of esophageal adenocarcinoma. 1213 11

Barrett's metaplasia develops in 6-14% of individuals with gastroesophageal reflux. Barrett's adenocarcinomas are increasing in epidemic proportions for as yet unknown reasons, approximately 0.5-1% of patients with Barrett's will develop adenocarcinoma. Heartburn duration and frequency (but not severity), male gender, and Caucasian race are major risk factors for developing cancer. Obesity and smoking are weak risk factors. Survival is determined by depth of tumor invasion (stage). Once invasion of the muscularis propia occurs, the vast majority of patients will have developed widespread metastasis, even when clinical staging studies are negative. No currently available therapy results in prolonged survival once metastases develop. Thus, the more widespread use of effective surveillance strategies is the only currently available means for reducing the morbidity and mortality associated with Barrett's adenocarcinoma.
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PMID:Barrett's esophagus: clinical characteristics. 1213 12

A dramatic increase in the incidence of esophageal adenocarcinoma has occurred among men in the United States over the last two decades. The underlying reasons remain largely unknown, although the increasing prevalence of obesity likely plays a role. Most adenocarcinomas arise in a metaplastic epithelium termed Barrett's esophagus (BE) that develops in approximately 10% of persons who have chronic gastroesophageal reflux. Persons with BE are at high risk (0.5-1.0%/year) of progressing to cancer. In a cross-sectional study of 429 persons with BE, we evaluated the associations between increased body mass index, anthropometric measures, cigarette smoking, use of nonsteroidal anti-inflammatory drugs (NSAIDs) and markers of increased risk, including aneuploidy, increased 4N fraction, loss of heterozygosity (LOH) of 17p and 9p alleles, and high-grade dysplasia (HGD). In logistic regression models adjusting for age, gender, NSAID use, and cigarette smoking, increasing waist:hip ratio was related to increasing risk of aneuploidy (trend P = 0.01), 17p LOH (trend P = 0.005), and 9p LOH (trend P = 0.007). The odds ratios comparing highest to lowest quartiles were 4.3 [95% confidence interval (CI), 1.2-15.6] for aneuploidy, 3.9 (95% CI, 1.3-11.4) for 17p LOH, and 2.7 (95% CI, 1.2-6.3) for 9p LOH. A nonsignificant trend was also observed for increased 4N fraction, whereas little association was found for HGD. Similar patterns of risk were noted for other anthropometric measures such as waist:thigh and abdomen:thigh ratios. There was no evidence that elevated body mass index increased risk of any of the biomarkers. Suggestive evidence also was found for a protective effect of NSAID use. The odds ratios for current users, compared with those who never used NSAIDs regularly, were 0.6 (95% CI, 0.3-1.4) for increased 4N, 0.6 (95% CI, 0.3-1.3) for aneuploidy, 0.3 (95% CI, 0.1-0.7) for 17p LOH, and 0.7 (95% CI, 0.4-1.2) for HGD. There was no association between NSAID use and risk of 9p LOH. We conclude that an abdominal distribution of body fat, which is more common in men and is termed male-pattern obesity, may be a strong predictor of risk of neoplastic progression among persons with BE and may account in part for the male predominance of BE and esophageal adenocarcinoma. We also conclude that NSAID use may reduce the risk of progression to cancer in this population. Prospective studies are needed to confirm these results.
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PMID:Nonsteroidal anti-inflammatory drug use, body mass index, and anthropometry in relation to genetic and flow cytometric abnormalities in Barrett's esophagus. 1216 28

Adenocarcinoma of the esophagus and the gastroesophageal junction is the twentieth most common malignancy in the United States. In developed countries, the incidence of esophageal adenocarcinoma is increasing 5% to 10% per year. Despite the use of endoscopy for earlier detection, mortality from esophageal adenocarcinoma has not declined. Using an evidence-based approach, we review screening methods for esophageal adenocarcinoma, including the use of a symptom questionnaire, identification of patients with a family history of Barrett's esophagus, peroral or transnasal endoscopy, barium swallow, fecal occult blood testing, and brush and balloon cytology. Screening has not been shown to reduce rate of progression of Barrett's esophagus to esophageal cancer. Many treatment options for dysplastic Barrett's esophagus or early carcinoma appear effective, but long-term follow-up data are not available. There is currently insufficient evidence supporting population-based screening for Barrett's esophagus. Several risk factors, including severe reflux symptoms, male sex, and obesity, may identify patients with gastroesophageal reflux disease who are at the greatest risk of the development of cancer.
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PMID:Screening for esophageal adenocarcinoma: an evidence-based approach. 1242

Concern has been expressed about the rapid increase in the incidence of esophageal carcinoma in the United States. This rise is due to an increase in the number of cases of adenocarcinoma of the esophagus. Because of the relatively small number of cases of esophageal carcinoma, the absolute risk of developing this cancer in the United States remains small. Potential origins for this increase in esophageal adenocarcinoma are examined in this review, including the risk induced by obesity, low dietary antioxidants, high dietary fat, family history of breast cancer, smoking, gastroesophageal reflux, and Barrett's esophagus. The risk of esophageal adenocarcinoma is inversely associated with infection by Helicobacter pylori organisms. A better understanding of risk factors involved in the increased incidence of esophageal adenocarcinoma is important for development of new preventive strategies for this serious disorder.
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PMID:The changing face of esophageal malignancy. 1273 39

Most available information on the epidemiology of Barrettacute;s esophagus (BE) relates to patients with long segments (> 3 cm) of specialized intestinal metaplasia (SIM). Its prevalence is 3% in patients undergoing endoscopy for reflux symptoms and 1% in those undergoing endoscopy for any clinical indication. The latter prevalence is similar to the 1% found in autopsy series. A "silent majority" with BE remain unrecognized in the general population. BE is more common in men, and the prevalence rises with age. Recent endoscopic series document a rise in the diagnosis of endoscopically apparent short segments (< 3 cm) of BE (SSBE). The prevalence of SSBE in both unselected and reflux patients is 8% to 12%. Specialized intestinal metaplasia at the cardia, below a normal-appearing squamocolumnar junction, has been reported to vary from 6% to 25% in patients presenting for upper endoscopy. Unlike patients with long segment Barrett's esophagus (LSBE), the role of gastroesophageal reflux disease in the pathogenesis of SSBE and SIM of the cardia is controversial. Recent data suggest that the etiology of SIM of the cardia might be secondary to Helicobacter pylori infection, although the role of other environmental factors cannot be ruled out. The incidence of adenocarcinoma of the esophagus and esophagogastric juction (EGJ) has been increasing over the past 15 years in Western countries. Surgical series and population-based studies show that by 1994 adenocarcinomas of the esophagus accounted for half of all esophageal cancer among white men. LSBE and SSBE predispose to the development of adenocarcinoma of the esophagus and EGJ. The role of SIM of the cardia as a precursor lesion for EGJ adenocarcinoma is still unclear. The prevalences of dysplasia in LSBE and SSBE are around 6% and 8%, respectively. The incidence of adenocarcinoma in patients with LSBE is about 1 in 100 patient-years. Cancer risk for SSBE and SIM at the cardia is unknown. Smoking and obesity increase the risk for esophageal and EGJ adenocarcinomas.
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PMID:Trends in incidence and prevalence of specialized intestinal metaplasia, barrett's esophagus, and adenocarcinoma of the gastroesophageal junction. 1291 64

Gastroesophageal reflux disease (GERD) is a condition commonly managed in the primary care setting. Patients with GERD may develop reflux esophagitis as the esophagus repeatedly is exposed to acidic gastric contents. Over time, untreated reflux esophagitis may lead to chronic complications such as esophageal stricture or the development of Barrett's esophagus. Barrett's esophagus is a premalignant metaplastic process that typically involves the distal esophagus. Its presence is suspected by endoscopic evaluation of the esophagus, but the diagnosis is confirmed by histologic analysis of endoscopically biopsied tissue. Risk factors for Barrett's esophagus include GERD, white or Hispanic race, male sex, advancing age, smoking, and obesity. Although Barrett's esophagus rarely progresses to adenocarcinoma, optimal management is a matter of debate. Current treatment guidelines include relieving GERD symptoms with medical or surgical measures (similar to the treatment of GERD that is not associated with Barrett's esophagus) and surveillance endoscopy. Guidelines for surveillance endoscopy have been published; however, no studies have verified that any specific treatment or management strategy has decreased the rate of mortality from adenocarcinoma.
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PMID:Barrett's esophagus. 1515 58

Symptoms of gastro-oesophageal reflux disease are highly prevalent in Western countries; however, it is less certain how many individuals with heartburn have clinically relevant disease. Although the prevalence of gastro-oesophageal reflux disease in Asia is substantially lower, the incidence may be increasing. How much of this increase is explained by the increasing recognition of heartburn in clinical practice, dietary changes and increasing obesity, or the eradication of Helicobacter pylori, remains unclear. There has been speculation that endoscopy-negative reflux disease represents a separate entity from reflux oesophagitis (as defined by the Los Angeles classification), but the evidence that might support this proposal is unconvincing. Patients with chronic reflux symptoms have a higher risk of Barrett's oesophagus, and the increased risk of developing oesophageal adenocarcinoma in individuals with a long history of heartburn is also well documented, but whether this always occurs via Barrett's oesophagus is debatable. Moreover, treatment with standard-dose antisecretory therapies and anti-reflux surgery seems unlikely, based on current evidence, to reduce the cancer risk in patients with Barrett's oesophagus. Gastro-oesophageal reflux disease has also been implicated in an increasing array of other conditions, but arguably in these settings it is often over-diagnosed.
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PMID:Review article: gastro-oesophageal reflux disease -- how wide is its span? 1545 61

This article reviews the epidemiology of cancers arising in the distal oesophagus and proximal stomach, sometimes collectively termed oesophago-gastric junctional adenocarcinomas. The several complexities involved in defining this group of cancers are considered and the reported increasing trends in incidence are reviewed, together with the descriptive epidemiology. The rates of these cancers are increasing, but not as dramatically as sometimes reported. They are also more common in white males than in other ethnic groups or in females. Although several aetiological risk factors have been reported, the two most consistent are an elevated body mass index (obesity) and a history of gastro-oesophageal reflux disease. Reflux is also associated with Barrett's oesophagus, an important and increasingly diagnosed premalignant lesion. The rate of progression from Barrett's oesophagus to cancer is controversial, as is the cost-benefit balance of routine endoscopic surveillance of such patients. The development of molecular biomarkers to identify Barrett's oesophagus patients with high rates of malignant transformation would represent a significant advance.
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PMID:Review article: oesophago-gastric adenocarcinoma -- an epidemiological perspective. 1545 65


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