Biomedical subjects

Philip R Foulis

Publications and source records attributed to Philip R Foulis.

4 recordsLinked to original sources

PubMed2004

Does warfarin therapy influence the risk of bladder cancer?

There has been growing interest in studying the biological effects of certain drugs and their potential to reduce the risk of various cancers. One study reported a decrease in the incidence of urogenital cancers in a trial with patients who received warfarin for treatment of venous thromboembolism, but a limitation to this study of urogenital cancers was the very small number of bladder cancer cases that developed following warfarin therapy. The objective of the present study is to measure the association between warfarin use and bladder cancer. A total of 330 cases with bladder cancer were identified at the James A. Haley Veterans' Administration (VA) Hospital in Tampa, Florida, using a combination of computerized pathology records and inpatient and outpatient diagnoses. Controls were randomly selected from the VA computerized administrative database and 1293 controls were included for analysis. Unconditional logistic regression analysis was performed to assess the risk of bladder cancer after adjusting for age, gender, and cigarette smoking. Among warfarin users, although there was a 27% elevation in risk, it did not differ significantly from nonusers (OR = 1.27, 95% CI = 0.85, 1.89). No duration-response relationship was observed between anticoagulant use and risk of bladder cancer. The results suggest that warfarin does not protect against bladder cancer, at least in male smokers, the highest risk population for bladder cancer.

Age Factors↗

PubMed2003

Thromboembolism preceding cancer: a correlation study.

Thromboembolic (TE) events preceding cancer have been observed. Some studies failed to find this correlation. We retrospectively examined the cancer incidence following thromboembolic events in patients at our medical center. Medical records of 183 patients with established thromboembolic events documented in their records were selected and reviewed. Time interval between primary, secondary, and recurrent TE events preceding cancer diagnosis was analyzed. Two hundred age- and sex-matched controls seen during the same period and without any evidence of TE were randomly selected and charts reviewed for malignancy. Cancer occurred after TE in 48 of 183 patients (26.2%). In controls, cancer was diagnosed in 23 (11.5%). This was statistically significant with an odds ratio of 2.736 (1.586, 4.720). In the 64 primary TE patients, the cancer incidence was 37.5%. The 63 patients with recurrent TE had an incidence of 35.4%, and 56 secondary TE patients had an incidence of 27.1%. Time between initial TE and cancer diagnosis was <6 months in 27 (56.3%) patients, between 6 months and 1 year in 12 (25.0%), 1-5 years in 5 (10.4%), and >5 years in 4 (8.3%). Fourteen (31.1%) TE patients presented with metastatic cancer. This study indicates that thromboembolic events are important predictors of cancer. Cancer in this population occurs within a year in the majority of patients. Cancer screening in patients without identifiable risk factors for thrombosis could be helpful for early detection, diagnosis, and management of cancer.

Adult↗

PubMed2002

Pancreatitis-associated ascitic fluid induces hepatocyte death independent of local cytokines.

INTRODUCTION: Kupffer-cell-derived cytokines mediate liver injury, yet macrophage pacification does not abolish hepatocyte injury. We undertook this study to examine the role of pancreatitis-associated ascitic fluid (PAAF) in liver injury. METHODS: Pathogen-free PAAF was perfused into healthy rat livers in situ for 60 min (n = 5, sham = 5, LPS = 5). AST, ALT, LDH, and TNF were measured in the effluent. Primary cultures of rat Kupffer cells or hepatocytes were treated with PAAF; AST, ALT, LDH, and TNF were measured and cell proliferation was determined by MTT assay. A hepatocyte human cell line (CCL-13) was treated with PAAF and apoptosis was measured by flow cytometry. RESULTS: Liver perfusion with PAAF induced a >15-fold increase in AST/ALT/LDH (P < 0.001 PAAF vs sham), but not in TNF. In vitro, Kupffer cell viability was sharply reduced by PAAF in a dose-dependent manner; however, 5% PAAF (50% viability) did not induce TNF production from Kupffer cells. PAAF induced a multifold increase in AST/ALT/LDH from fresh hepatocytes (P < 0.001 vs control), which was not attenuated by a protease inhibitor. The CCL-13 cell population was reduced to 15 +/- 2% of baseline by PAAF (P < 0.001 vs control), whereas elastase, trypsin, or TNF had no effect. PAAF increased the percentage of nonviable CCL-13 cells (78 +/- 4% vs 28 +/- 1%, P < 0.001 vs control). Neither protease inhibitor nor heat inactivation of PAAF altered this pattern of hepatocyte death. CONCLUSION: PAAF induces direct hepatocyte injury and death by heat-stable factors other than pancreatic enzymes but not via local production of Kupffer-cell-derived cytokines.

Acute Disease↗

PubMedDate not supplied

Analgesic therapy and the prevention of bladder cancer.

The aim of this study was to measure the association between analgesic use and risk of bladder cancer among patients seen at the James A. Haley Veterans' Administration (VA) Hospital in Tampa, FL. A total of 330 cases were obtained using a combination of computerized pathology records, and inpatient and outpatient diagnoses. Controls were randomly selected from the VA computerized administrative database, and 1293 controls were included for analysis. Unconditional logistic regression analysis was performed to assess the risk of bladder cancer after adjusting for age, gender, and cigarette smoking. Among analgesic users, we were able to identify a nearly 20% reduction in risk potentially consistent with a protective role (OR = 0.81, 95% CI = 0.63, 1.05). Nonsmokers had a 43% decrease in risk (OR = 0.57, 95% CI = 0.33, 0.98). While smoking is a strong and recognized cause of bladder cancer, 50% of bladder cancer cases are not attributable to tobacco consumption. Given that nonsmokers prescribed nonsteroidal anti-inflammatory drugs (NSAIDs) were observed to have a 43% reduction in risk, it is important to study whether nonsmokers may benefit from therapy with NSAIDs.

Aged↗