A survey of female nursing students' knowledge, health beliefs, perceptions of risk, and risk behaviors regarding human papillomavirus and cervical cancer.

PURPOSE: The purpose of the study was to assess knowledge of, perceived susceptibility to, perceived seriousness of, and risk behaviors regarding human papillomavirus (HPV) and cervical cancer among female nursing students. DATA SOURCES: A 40-item survey of HPV and cervical cancer was distributed to a convenience sample of 240 female nursing students enrolled in a baccalaureate nursing program. CONCLUSIONS: Female nursing students participate in high-risk sexual behaviors and have a fairly low knowledge level, low perceived susceptibility, and low perceived seriousness regarding HPV and cervical cancer. Knowledge and perceived susceptibility were positively related to number of sexual partners. This may indicate that the women who engage in riskier behavior are more knowledgeable about HPV and their risk of contracting the disease. IMPLICATIONS FOR PRACTICE: Results indicate that all practitioners involved in the care of women should educate them about HPV and its relationship to cervical cancer. Education should include the need to use condoms to prevent HPV and other sexually transmitted diseases.

Interactions between non-steroidal anti-inflammatory drugs and H2-receptor antagonists or prostaglandin analogues.

Published pharmacokinetic studies investigating possible interaction between H2-receptor antagonists (n = 22) or prostaglandin analogues (n = 6) and nonsteroidal anti-inflammatory drugs (NSAIDs) have been reviewed. With two exceptions the studies were carried out in young, healthy male volunteers rather than in arthritis patients. In addition some of the studies were poorly designed and inadequately described. Cimetidine appeared to increase the area under the plasma concentration-time curve, and hence to decrease the apparent oral clearance, of several NSAIDs including piroxicam, indomethacin, flurbiprofen, sulindac, oxaprozin and aspirin, while ranitidine co-administration resulted in similar changes for oxyprozin alone. The data currently available for prostaglandin analogues are insufficient to draw firm conclusions. It therefore remains a possibility that clinically relevant pharmacokinetic interactions may occur in elderly arthritic patients, and this issue needs to be addressed.

A lack of pharmacokinetic interaction between ranitidine and piroxicam.

The effects of piroxicam (40 mg) on the pharmacokinetics of ranitidine (150 mg) and of ranitidine (150 mg bid) on the pharmacokinetics of piroxicam (20 mg) were assessed in two 2-way crossover studies in two groups of 18 healthy male subjects. In the first study there were no statistically significant differences between the pharmacokinetic variables for ranitidine in the presence or absence of piroxicam. The mean maximum plasma concentration (Cmax) was 467 ng.ml-1 for ranitidine alone and 466 ng.ml-1 in the presence of piroxicam: mean area under the plasma concentration vs time curve (AUC) was 2460 h.ng ml-1 and 2551 h.ng ml-1 respectively; and the mean terminal half-life (t 1/2) was 3.6 h and 3.8 h respectively. In the second study there were no statistically significant differences between the pharmacokinetic variables for piroxicam in the presence or absence of ranitidine. The mean Cmax was 2.1 micrograms.ml-1 in the presence of placebo and 2.0 micrograms.ml-1 in the presence of ranitidine respectively; mean AUC was 133 h.microgram ml-1 and 137 h.microgram ml-1 respectively, and the mean t 1/2 was 53.6 h and 54.5 h respectively.

Can higher doses of an H2-receptor antagonist accelerate duodenal ulcer healing?

Drugs that inhibit gastric acid secretion heal duodenal ulcers at a rate that correlates with the ability of individual treatment regimens to decrease 24-h intragastric acidity. As current therapeutic regimens of ranitidine decrease 24-h intragastric acidity submaximally, higher dosages may expedite duodenal ulcer healing. To test this hypothesis a randomized, double-blind clinical trial was conducted in 245 patients with duodenal ulcer to compare the effects of standard dose (300 mg nocte) and high-dose (300 mg q.d.s.) ranitidine. Patients were assessed after 2 weeks of treatment and, if unhealed, after a further 2 weeks of therapy. The therapeutic gain in ulcer healing at the 2-week endoscopy of the higher dose over the lower dose of ranitidine was 22% (68% vs 46%, P less than 0.001). The cumulative ulcer healing rates at the 4-week endoscopy were 88% and 92% for the standard and high-dose ranitidine groups, respectively (N.S.). By 2 weeks, 61% of patients treated with standard ranitidine therapy and 79% of those receiving 300 mg ranitidine q.d.s. were pain-free (P less than 0.01). A further 2 weeks of therapy enabled 88% and 97% of patients (N.S.) to become pain-free on these two regimens, respectively. The drug regimens were equally well tolerated. Thus higher-dose ranitidine can significantly accelerate the healing of duodenal ulcer with improvement in pain relief.

Prevention of gastroduodenal damage induced by non-steroidal anti-inflammatory drugs: controlled trial of ranitidine.

OBJECTIVE: To evaluate the prophylactic effect of ranitidine 150 mg twice daily in patients requiring one of the following non-steroidal anti-inflammatory drugs: naproxen, piroxicam, diclofenac, and indomethacin. In addition, risk factors were studied in order to help in targeting of such treatment to specific groups of patients. DESIGN: Double blind, placebo controlled, randomised, parallel group with endoscopic assessments at 0, 4, and 8 weeks. SETTING: Multicentre outpatient study at secondary referral centres in five European countries. PATIENTS--297 patients with rheumatoid arthritis or osteoarthritis over the age of 18 without lesions in the stomach and duodenum at baseline endoscopy (after one week without taking non-steroidal anti-inflammatory drugs). Those taking other antirheumatic agents, concomitant ulcerogenic drugs, or treatment for peptic ulcers within the previous 30 days were excluded. Age, sex, arthritic disease, and type of non-steroidal anti-inflammatory drug used were comparable in the two treatment groups. In all, 263 patients completed the trial. INTERVENTIONS: Ranitidine 150 mg twice daily or placebo (plus the selected non-steroidal anti-inflammatory drug) was prescribed within five days after the baseline endoscopy for two consecutive periods of four weeks. Paracetamol was permitted during the study, but not antacids. Patients were withdrawn if the most severe grade of damage (including ulceration) was found at the four week endoscopy or when indicated, or with lesser damage at the investigator's discretion. END POINT: Frequency of gastric and duodenal ulceration or lesions, or both. MEASUREMENTS AND MAIN RESULTS: The cumulative incidence of peptic ulceration by eight weeks was 10.3% (27/263); 2 out of 135 (1.5%) developed duodenal ulceration in the ranitidine group, compared with 10 out of 126 (8%) taking placebo. The frequency of gastric ulceration was the same (6%) for the two groups at eight weeks. Though significantly fewer gastric lesions developed in the ranitidine group by eight weeks. The frequency of non-ulcerative lesions in the duodenum did not differ greatly for the two groups at either time point. Twelve out of 75 (16%) patients taking piroxicam developed peptic ulceration, of whom two thirds had duodenal ulceration. Patients with a history of peptic ulcer were particularly susceptible to recurrent ulceration, against which ranitidine offered some protection. CONCLUSIONS: Ranitidine 150 mg twice daily significantly reduced the incidence of duodenal ulceration but not gastric ulceration when prescribed concomitantly with one of four commonly used non-steroidal anti-inflammatory drugs.

Alteration of normal gastric flora in critical care patients receiving antacid and cimetidine therapy.

One hundred fifty-three critical care patients with documented cimetidine and antacid use were prospectively studied with serial gastric pH determinations and semiquantitative gastric fluid cultures. This study documents the abnormal gastric colonization of patients with therapeutically altered gastric acidity by hospital acquired gram negative rods (GNR). Three hundred twenty-four gastric fluid cultures from 153 patients revealed 152 (47%) positive cultures for GNR, 78 (24%) sterile specimens, and 94 (29%) positive for mixed oropharyngeal flora. One hundred forty (59%) of the 236 cultures at a pH of 4 or greater were positive for GNR. In contrast, only 12 (14%) of the 88 cultures at a pH of less than 4 were positive for GNR (p less than .001). Forty-six (52%) of 88 cultures at a pH of less than 4 were sterile as compared to only 32 (14%) of 236 sterile cultures at a pH of 4 or greater (p less than .001). At low pH, cultures are predominantly sterile and at a pH of 4 or greater the flora dramatically changes to hospital acquired GNR. This artificially maintained reservoir of gram negative rods in the critically ill patient is a potential reservoir of organisms causing nosocomial bacteremia or pneumonia in this high risk population.

The effects of hygiene interventions on the cerebrovascular status of severe closed head injured persons.

The cerebrovascular status of 19 severe closed head injured patients was assessed during oral, body, and indwelling catheter care. Heart rates, mean arterial blood pressures, mean intracranial pressures, and cerebral perfusion pressures were recorded at baseline, peak nursing intervention, and 1-minute recovery times. Significant increases (p less than or equal to .05) in the dependent variables were noted at peak intervention; by recovery time these elevated values had returned to baseline levels. Physiologic responses that did not prove clinically significant are discussed to account for the observed changes. Since cerebral perfusion pressures never fell below 50 mm Hg, the three hygiene interventions are procedures considered safe and beneficial to the patient with closed head injury.