Liver diseases.

Liver diseases in the elderly often reflect an age-associated decrease in the capacity to respond to metabolic and infectious insults. Because the geriatric population is growing rapidly, physicians can expect to encounter an increasing number of older patients with liver disease. In this article, the authors discuss the clinical manifestations of the most common liver diseases seen in the geriatric population.

Decreased prevalence of Helicobacter pylori infection in gastroesophageal reflux disease.

BACKGROUND: An increased incidence of reflux esophagitis has been reported after eradication of H. pylori in patients with duodenal ulcer. To determine if H. pylori is associated with lower rates of esophagitis, we studied the prevalence of H. pylori infection in patients with and without reflux esophagitis and a subgroup of patients with concomitant peptic ulcer disease. METHODS: Patients who underwent esophagogastroduodenoscopy and had diagnostic testing for H. pylori over a 30-month period were studied. H. pylori infection was determined by rapid urease testing, gastric histopathology, or serology. Reflux esophagitis was determined by endoscopic and/or histologic criteria. RESULTS: Of 514 patients, 39.5% had H. pylori infection and 22.2% had reflux esophagitis. The prevalence of H. pylori infection in patients with reflux esophagitis was 30.7%, compared with 42.0% in patients without esophagitis (p = 0.039). The odds ratio for esophagitis risk with H. pylori infection was 0.61 (95% CI, 0.39-0.95). Neither patient age nor gender affected H. pylori prevalence. In patients with duodenal ulcer, H. pylori was present in 36.4% of patients with esophagitis and in 69.2% of patients without esophagitis (p = 0.018). The odds ratio for esophagitis with H. pylori infection in these patients was 0.25 (95% CI, 0.09-0.73). CONCLUSIONS: Our study demonstrates that H. pylori infection is significantly less prevalent in patients with reflux esophagitis and may protect against its development. In duodenal ulcer patients, this effect was more dramatic. Further study is required to confirm these findings and elucidate mechanisms underlying possible beneficial effects of H. pylori.

Breast carcinoma metastatic to the esophagus: clinicopathological and management features of four cases, and literature review.

Dysphagia due to esophageal metastases from primary breast carcinoma is an unusual entity. In this series of cases, we describe the clinical features of dysphagia due to metastatic esophageal lesions in four patients (with a primary diagnosis of breast cancer made 8-22 yr previously). We provide the first endoscopic ultrasound characterization of metastatic lesions to the esophagus from breast carcinoma. Endoscopic management of these strictures with both bougienage and balloon dilation techniques resulted in esophageal perforation in three of our four patients. We believe that endoscopic ultrasound is helpful in the diagnosis of metastatic breast cancer to the esophagus. However, endoscopic dilation of these strictures should be done gently and only after other treatment options have been carefully considered.

Ornithine oxoglutarate therapy improves nutrition status.

Ornithine oxoglutarate (OGO) has been previously demonstrated to improve nutrition status in burn and trauma patients. Recently, OGO supplementation was shown to improve nutrition status, ameliorate quality of life, and reduce health care costs when given to elderly patients soon after discharge from the hospital.

Fine structure analysis of the WT1 gene in sporadic Wilms tumors.

Molecular genetic studies indicate that the etiology of Wilms tumor (WT) is complex, involving at least three loci. Germ-line mutations in the tumor suppressor gene, WT1, have been documented in children with WTs and urogenital developmental anomalies. Sporadic tumors constitute the majority (> 90%) of WT cases and previous molecular analyses of the WT1 gene have focused only on the DNA-binding domain. Using the single-strand conformational polymorphism (SSCP) assay, we analyzed the structural integrity of the entire WT1 gene in 98 sporadic WTs. By PCR-SSCP we find that mutations in the WT1 gene are rare, occurring in only six tumors analyzed. In one sample, two independent intragenic mutations inactivated both WT1 alleles, providing a singular example of two different somatic alterations restricted to the WT1 gene. This case is consistent with the existence of only one tumor suppressor gene at 11p13 involved in the pathogenesis of WTs. Our data, together with the previously ascertained occurrence of large deletions/insertions in WT1, define the frequency at which the WT1 gene is altered in sporadic tumors.