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To determine whether infection with a Helicobacter pylori strain possessing cagA is associated with an increased risk of development of adenocarcinoma of the stomach, we used a nested case-control study based on a cohort of 5443 Japanese-American men in Oahu, Hawaii, who had a physical examination and a phlebotomy during 1967 to 1970. We matched 103 H. pylori-infected men who developed gastric cancer during a 21-year surveillence period with 103 H. pylori-infected men who did not develop gastric cancer and tested stored serum specimens from patients and controls for the presence of serum IgG to the cagA product of H. pylori using an ELISA. The serum IgG assay using a recombinant CagA fragment had a sensitivity of 94.4% and a specificity of 92.5% when used in a clinically defined population; serological results were stable for more than 7 years. For men with antibodies to CagA, the odds ratio of developing gastric cancer was 1.9 (95% confidence interval, 0.9-4.0); for intestinal type cancer of the distal stomach, the odds ratio was 2.3 (95% confidence interval, 1.0-5.2). Age < 72 years and advanced tumor stage at diagnosis were significantly associated with CagA seropositivity. We conclude that infection with a cagA-positive H. pylori strain in comparison with a cagA-negative strain somewhat increases the risk for development of gastric cancer, especially intestinal type affecting the distal stomach.
To determine whether cyclic antidepressants increase the risk of hip fracture, we conducted a population-based case-control study in the Canadian province of Saskatchewan. We identified 4501 persons 65 years of age or older with a first hospitalization for hip fracture between 1977 and 1985 and 24,041 comparable controls. Current antidepressant users had a relative risk of hip fracture of 1.6 (95% confidence interval, 1.3 to 1.9). Medical record review for a sample of 164 cases suggested this finding was not due to confounding by body mass, impaired ambulation, functional status, or dementia.
OBJECTIVE - To estimate the relative risk for peptic ulcer disease that is associated with the use of oral corticosteroids.
DESIGN - A nested case-control study.
SETTING - Tennessee Medicaid program.
PARTICIPANTS - The case patients (n = 1415) were hospitalized between 1984 and 1986 for gastric or duodenal ulcer or for upper gastrointestinal hemorrhage of unknown cause. The controls (n = 7063) were randomly selected from Medicaid enrollees not meeting the study criteria for inclusion as case patients.
MEASUREMENTS AND MAIN RESULTS - The estimated relative risk for the development of peptic ulcer disease among current users of oral corticosteroids was 2.0 (95% CI, 1.3 to 3.0). However, the risk was increased only in those who concurrently received nonsteroidal anti-inflammatory drugs (NSAIDs); these persons had an estimated relative risk associated with current corticosteroid use of 4.4 (CI, 2.0 to 9.7). In contrast, the estimated relative risk for those corticosteroid users not receiving NSAIDs was 1.1 (CI, 0.5 to 2.1). Persons concurrently receiving corticosteroids and NSAIDs had a risk for peptic ulcer disease that was 15 times greater than that of nonusers of either drug.
CONCLUSION - Discrepant findings among earlier studies regarding steroids and the risk for peptic ulcer disease could in part be due to differences in the use of NSAIDs among study participants. The high risk for peptic ulcer disease associated with combined use of NSAIDs and corticosteroids indicates the need to prescribe this drug combination cautiously.
OBJECTIVE - To evaluate the relative risk for peptic ulcer disease that is associated with the use of nonaspirin nonsteroidal anti-inflammatory drugs.
DESIGN - Nested case-control study.
SETTING - Tennessee Medicaid program.
PARTICIPANTS - Medicaid enrollees 65 years of age or older were included in the study. The 1415 case patients had been hospitalized for confirmed peptic ulcer disease at some point from 1984 through 1986. The 7063 control persons represented a stratified random sample of other Medicaid enrollees.
MEASUREMENTS AND MAIN RESULTS - The estimated relative risk for the development of peptic ulcer disease among current users of nonaspirin nonsteroidal anti-inflammatory drugs, compared with that among nonusers, was 4.1 (95% CI, 3.5 to 4.7). For current users, the risk increased with increasing dose, from a relative risk of 2.8 (CI, 1.8 to 4.3) for the lowest to a relative risk of 8.0 (CI, 4.4 to 14.8) for the highest dose category. The risk was greatest in the first month of use (relative risk, 7.2; CI, 4.9 to 10.5). If the association is fully causal, 29% of peptic ulcers in the study sample resulted from the use of these drugs, and the excess risk associated with such use was 17.4 hospitalizations for ulcer disease per 1000 person-years of exposure.
CONCLUSIONS - These data support other findings indicating that a clinically significant risk for serious ulcer disease is associated with the use of nonaspirin nonsteroidal anti-inflammatory drugs. The data show that this risk increases with dose and recency of use and that use of these drugs may be responsible for a large proportion of peptic ulcer disease among elderly persons.
We investigated the relationship of human papillomavirus (by cervicovaginal lavage and Southern blot), human immunodeficiency virus, and squamous intraepithelial lesions in 96 high-risk women in the Bronx, New York. Antibodies for human immunodeficiency virus were detected in 51 (53%) women. Of the 33 women with symptomatic human immunodeficiency virus infection, 23 (70%) had human papillomavirus infection compared with 4 of 18 (22%) asymptomatic women who were human immunodeficiency virus seropositive and 10 of 45 (22%) uninfected women (p less than 0.0001). The rate of squamous intraepithelial lesions was 52% (14 of 27) for women with both viruses detected, 18% (6 of 34) for women with either virus detected, and 9% (3 of 35) for uninfected women. Among symptomatic human immunodeficiency virus-infected women, a strong association between human papillomavirus infection and squamous intraepithelial lesions was demonstrated (odds ratio, 12; 95% confidence interval, 1.3 to 108). Risk was highest for younger women from ethnic or racial minority groups. Advanced human immunodeficiency virus-related disease, with its associated immunosuppression, seems to exacerbate human papillomavirus-mediated cervical cytologic abnormalities. Public health measures are needed to provide Papanicolaou smear screening and appropriate clinical follow-up and treatment for women at high risk for human immunodeficiency virus infection.
UNLABELLED - Cardioversion shocks given during ventricular tachycardia may cause ventricular fibrillation or acceleration of ventricular tachycardia, or arrest the tachycardia. A recently proposed theory may explain why the former two phenomena may occur. Briefly, this theory states that potential gradient shock fields of a critical strength delivered to tissue with a critical degree of refractoriness will cause circulating wave fronts of ventricular activation ("rotors") manifest as ventricular arrhythmia. We tested this theory by delivering nonsynchronized shocks 50% higher than defibrillation threshold or 50% lower than defibrillation threshold during 275 episodes of ventricular tachycardia in eight dogs with 5- to 7-day-old myocardial infarcts. Shocks stronger than the defibrillation threshold are likely to create shock fields in the ventricles everywhere stronger than this critical value, and therefore would not generate rotors. Shocks less strong than the defibrillation threshold may create shock fields within the ventricles that include the critical value, and therefore cause rotors if given when critically refractory tissue is present. Nonsynchronized shocks were used to increase the likelihood of encountering tissue with a critical degree of refractoriness. Ventricular fibrillation or acceleration of ventricular tachycardia occurred following 83 of 138 (60%) low strength shocks and following 20 of 137 (14.6%) high strength shocks. The pooled odds ratio for induction of ventricular fibrillation or accelerated ventricular tachycardia after low strength shocks as compared to high strength shocks was 8.9.
CONCLUSION - when given during ventricular tachycardia, low strength shocks are much more likely to cause ventricular fibrillation or accelerated ventricular tachycardia than are high strength shocks (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)