Mg Of Celecoxib Research Articles

Secondary Chemoprevention of Barrett's Esophagus With Celecoxib: Results of a Randomized Trial

Barrett's esophagus is a premalignant condition that is a risk factor for the development of esophageal adenocarcinoma, a disease whose incidence is rapidly increasing. Because aspirin and other nonsteroidal anti-inflammatory drugs, such as celecoxib, may decrease the risk of developing esophageal cancer, we investigated the effect of long-term administration of celecoxib in patients with Barrett's esophagus with dysplasia. Chemoprevention for Barrett's Esophagus Trial (CBET) is a phase IIb multicenter randomized placebo-controlled trial of celecoxib in patients with Barrett's esophagus and low- or high-grade dysplasia. Patients were randomly assigned to treatment with 200 mg of celecoxib or placebo, both administered orally twice daily, and then stratified by grade of dysplasia. The primary outcome was the change from baseline to 48 weeks of treatment in the proportion of biopsy samples with dysplasia between the celecoxib and placebo arms. Secondary and tertiary outcomes included evaluation of changes in histology and expression levels of relevant biomarkers. All statistical tests were two-sided. From April 1, 2000, through June 30, 2003, 222 patients were registered into CBET, and 100 of them with low- or high-grade Barrett's dysplasia were randomly assigned to treatment (49 to celecoxib and 51 to placebo). After 48 weeks of treatment, no difference was observed in the median change in the proportion of biopsy samples with dysplasia or cancer between treatment groups in either the low-grade (median change with celecoxib = -0.09, interquartile range [IQR] = -0.32 to 0.14 and with placebo = -0.07, IQR = -0.26 to 0.12; P = .64) or high-grade (median change with celecoxib = 0.12, IQR = -0.31 to 0.55, and with placebo = 0.02, IQR = -0.24 to 0.28; P = .88) stratum. No statistically significant differences in total surface area of the Barrett's esophagus; in prostaglandin levels; in cyclooxygenase-1/2 mRNA levels; or in methylation of tumor suppressor genes p16, adenomatous polyposis coli, and E-cadherin were found with celecoxib compared with placebo. Administration of 200 mg of celecoxib twice daily for 48 weeks of treatment does not appear to prevent progression of Barrett's dysplasia to cancer.

The cyclooxygenase 2 genetic variant −765G>C does not modulate the effects of celecoxib on prostaglandin E2 production

Our objective was to assess the role of the reportedly functional PTGS2 (prostaglandin-endoperoxide synthase 2/cyclooxygenase [COX] 2) promoter mutation -765G>C for the COX-2-inhibiting effects of celecoxib. Twenty healthy carriers of the -765GG genotype and -765CC genotype (n = 10 each) received 200 mg of celecoxib orally. Blood samples were drawn at baseline and at 1, 3, 6, 9, and 24 hours after administration. Plasma concentrations of celecoxib and concentrations of prostaglandin E(2) (PGE(2)) produced by peripheral blood monocytes stimulated ex vivo with bacterial lipopolysaccharide (LPS) were analyzed by liquid chromatography-tandem mass spectrometry. Expression of COX-2 messenger ribonucleic acid and protein expression with and without LPS stimulation were analyzed by real-time polymerase chain reaction and Western blotting, respectively. LPS induced PGE(2) production (P < .001), and celecoxib reduced PGE(2) production from 19.3 +/- 7.2 ng/mL at baseline to 7.4 +/- 4.8 ng/mL at 1 hour (P < .001). The effect of celecoxib lasted for 9 hours (repeated-measures ANOVA, P <or= .001). Celecoxib inhibited PGE(2) production at a potency (ie, 50% effective concentration [EC(50)]) of 155.1 ng/mL (95% confidence interval, 101.6-208.5 ng/mL) in the homozygous carriers of the PTGS2 wild-type -765G allele and at a potency (EC(50)) of 186.6 ng/mL (95% confidence interval, 142.6-230.5 ng/mL) in the homozygous carriers of the PTGS2 variant -765C allele, which was not statistically significantly different (P = .36). Baseline PGE(2) concentrations, minimum baseline PGE(2) concentrations, and areas under the PGE(2) concentration versus time curve also did not differ between PTGS2 genotypes (P > .28). LPS up-regulated COX-2 messenger ribonucleic acid expression (P = .016) but was independent of genotype (P = .36). COX-2 protein expression was similar for both -765G>C genotypes (P = .63). The PTGS2 -765G>C single-nucleotide polymorphism does not modulate COX-2 inhibitory effects of celecoxib as assessed by an ex vivo whole blood assay. Thus the results indicate the need for further investigation toward PTGS2 pharmacogenetics-based prescription of celecoxib.

Celecoxib for the Prevention of Sporadic Colorectal Adenomas

Studies showing that drugs that inhibit cyclooxygenase-2 (COX-2) reduce the number of colorectal adenomas in animals and patients with familial adenomatous polyposis suggest that COX-2 inhibitors may also prevent sporadic colorectal neoplasia. We randomly assigned patients who had adenomas removed before study entry to receive placebo (679 patients) or 200 mg (685 patients) or 400 mg (671 patients) of celecoxib twice daily. Randomization was stratified for the use of low-dose aspirin. Follow-up colonoscopies were performed at one and three years after randomization. The occurrence of newly detected colorectal adenomas was compared among the groups with the life-table extension of the Mantel-Haenszel test. Follow-up colonoscopies were completed at year 1 in 89.5 percent of randomized patients, and at year 3 in 75.7 percent. The estimated cumulative incidence of the detection of one or more adenomas by year 3 was 60.7 percent for patients receiving placebo, as compared with 43.2 percent for those receiving 200 mg of celecoxib twice a day (risk ratio, 0.67; 95 percent confidence interval, 0.59 to 0.77; P<0.001) and 37.5 percent for those receiving 400 mg of celecoxib twice a day (risk ratio, 0.55; 95 percent confidence interval, 0.48 to 0.64; P<0.001). Serious adverse events occurred in 18.8 percent of patients in the placebo group, as compared with 20.4 percent of those in the low-dose celecoxib group (risk ratio, 1.1; 95 percent confidence interval, 0.9 to 1.3; P=0.5) and 23.0 percent of those in the high-dose group (risk ratio, 1.2; 95 percent confidence interval, 1.0 to 1.5; P=0.06). As compared with placebo, celecoxib was associated with an increased risk of cardiovascular events (risk ratio for the low dose, 2.6; 95 percent confidence interval, 1.1 to 6.1; and risk ratio for the high dose, 3.4; 95 percent confidence interval, 1.5 to 7.9). These findings indicate that celecoxib is an effective agent for the prevention of colorectal adenomas but, because of potential cardiovascular events, cannot be routinely recommended for this indication. (ClinicalTrials.gov number, NCT00005094 [ClinicalTrials.gov].).

Celecoxib for the Prevention of Colorectal Adenomatous Polyps

Overexpression of cyclooxygenase 2 (COX-2) has been associated with colorectal adenomatous polyps and cancer, prompting researchers to propose its inhibition as a chemopreventive intervention. The Prevention of Colorectal Sporadic Adenomatous Polyps trial was a randomized, placebo-controlled, double-blind study of the COX-2 inhibitor celecoxib given daily in a single 400-mg dose. At 107 centers in 32 countries, we randomly assigned 1561 subjects who had had adenomas removed before enrollment to receive celecoxib (933 subjects) or placebo (628 subjects) daily, after stratification according to the use or nonuse of low-dose aspirin. The primary outcome was detection of adenomas at either year 1 or year 3 by colonoscopy and was compared among the groups with the use of the Mantel-Cox test. Colonoscopies were performed at year 1 on 88.7 percent of the subjects who had undergone randomization and at year 3 on 79.2 percent. Of the 557 subjects in the placebo group and the 840 subjects in the celecoxib group who were included in the efficacy analysis, 264 and 270, respectively, were found to have at least one adenoma at year 1, at year 3, or both. The cumulative rate of adenomas detected through year 3 was 33.6 percent in the celecoxib group and 49.3 percent in the placebo group (relative risk, 0.64; 95 percent confidence interval, 0.56 to 0.75; P<0.001). The cumulative rate of advanced adenomas detected through year 3 was 5.3 percent in the celecoxib group and 10.4 percent in the placebo group (relative risk, 0.49; 95 percent confidence interval, 0.33 to 0.73; P<0.001). Adjudicated serious cardiovascular events occurred in 2.5 percent of subjects in the celecoxib group and 1.9 percent of those in the placebo group (relative risk, 1.30; 95 percent confidence interval, 0.65 to 2.62). The use of 400 mg of celecoxib once daily significantly reduced the occurrence of colorectal adenomas within three years after polypectomy. (ClinicalTrials.gov number, NCT00141193 [ClinicalTrials.gov].).

The Use of Celecoxib for Reduction of Pain After Subpectoral Breast Augmentation

A study was conducted to determine whether a single 400-mg dose of oral celecoxib administered 30 min before surgery reduces the opioid requirement for patients undergoing aesthetic subpectoral breast augmentation. A total of 695 patients undergoing breast augmentation were randomly selected into either a placebo or a treatment group. The findings showed that patients who received 400 mg of celecoxib 30 min before surgery required significantly fewer opioid analgesics after the operation than those given a placebo (p < 0.001). It also was found that nonsmokers and multiparous women required significantly fewer opioids than smokers and nulliparous women (p < 0.001). On the basis of this prospective study, the authors recommend a single 400-mg dose of celecoxib administered 30 min before surgery to decrease opioid analgesic requirements after subpectoral breast augmentation.

Analysis of Recent Papers in Hypertension Jan Basile, MD, Senior Editor

Analysis of Recent Papers in Hypertension Jan Basile, MD, Senior Editor

Cardiovascular Risk Associated with Celecoxib in a Clinical Trial for Colorectal Adenoma Prevention

Selective cyclooxygenase-2 (COX-2) inhibitors have come under scrutiny because of reports suggesting an increased cardiovascular risk associated with their use. Experimental research suggesting that these drugs may contribute to a prothrombotic state provides support for this concern. We reviewed all potentially serious cardiovascular events among 2035 patients with a history of colorectal neoplasia who were enrolled in a trial comparing two doses of celecoxib (200 mg or 400 mg twice daily) with placebo for the prevention of colorectal adenomas. All deaths were categorized as cardiovascular or noncardiovascular, and nonfatal cardiovascular events were categorized in a blinded fashion according to a prespecified scheme. For all patients except those who died, 2.8 to 3.1 years of follow-up data were available. A composite cardiovascular end point of death from cardiovascular causes, myocardial infarction, stroke, or heart failure was reached in 7 of 679 patients in the placebo group (1.0 percent), as compared with 16 of 685 patients receiving 200 mg of celecoxib twice daily (2.3 percent; hazard ratio, 2.3; 95 percent confidence interval, 0.9 to 5.5) and with 23 of 671 patients receiving 400 mg of celecoxib twice daily (3.4 percent; hazard ratio, 3.4; 95 percent confidence interval, 1.4 to 7.8). Similar trends were observed for other composite end points. On the basis of these observations, the data and safety monitoring board recommended early discontinuation of the study drug. Celecoxib use was associated with a dose-related increase in the composite end point of death from cardiovascular causes, myocardial infarction, stroke, or heart failure. In light of recent reports of cardiovascular harm associated with treatment with other agents in this class, these data provide further evidence that the use of COX-2 inhibitors may increase the risk of serious cardiovascular events.

The Effects of Cyclooxygenase-2 Inhibitors and Nonsteroidal Anti-inflammatory Therapy on 24-Hour Blood Pressure in Patients With Hypertension, Osteoarthritis, and Type 2 Diabetes Mellitus

Nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 (COX-2) inhibitors may attenuate the efficacy of antihypertensive agents in high-risk patients. Therefore, we conducted a double-blind, randomized trial to evaluate the effects of celecoxib, rofecoxib, and naproxen on 24-hour blood pressure (BP) in patients with type 2 diabetes, hypertension, and osteoarthritis. Patients were randomly assigned to treatment with 200 mg of celecoxib once daily (n = 136), 25 mg of rofecoxib once daily (n = 138), or 500 mg of naproxen twice daily (n = 130) for 12 weeks. Twenty-four-hour ambulatory BP monitoring and validated arthritis efficacy assessments were conducted at randomization and at weeks 6 and 12 of treatment. The primary end point was the mean change from baseline in average 24-hour systolic BP at week 6. Reductions in osteoarthritis symptoms, including pain, mobility, and stiffness, were similar in all treatment groups. The mean +/- SE 24-hour systolic BP following 6 weeks of therapy was increased significantly by rofecoxib (from 130.3 +/- 1.2 to 134.5 +/- 1.4 mm Hg; P < .001) but not by celecoxib (132.0 +/- 1.3 to 131.9 +/- 1.3 mm Hg; P = .54) or naproxen (133.7 +/- 1.5 to 133.0 +/- 1.4 mm Hg; P = .74). The BP difference between rofecoxib and celecoxib was 3.78 mm Hg (95% confidence interval, 1.18-6.38; P = .005); between rofecoxib and naproxen, 3.85 mm Hg (95% confidence interval, 1.15-6.55; P = .005). The proportion of patients with controlled hypertension at baseline who developed ambulatory hypertension by week 6 (24-hour systolic BP>135 mm Hg) was significantly greater with rofecoxib (30%) than with celecoxib (16%) (P = .05) but not significantly greater than with naproxen (19%). At equally effective doses for osteoarthritis management, treatment with rofecoxib but not celecoxib or naproxen induced a significant increase in 24-hour systolic BP. However, destabilization of hypertension control occurred to some extent in all 3 treatment groups; this phenomenon was seen more often in patients treated with rofecoxib than with the other therapies.

Effects of Celecoxib on High‐Sensitivity C‐Reactive Protein in Chronic Peritoneal Dialysis Patients

To evaluate the effects of celecoxib, a cyclooxygenase‐2 inhibitor, on the level of high‐sensitivity C‐reactive protein (hs‐CRP), D‐dimer, von Willebrand factor (vWF) and troponin‐T, 46 chronic peritoneal dialysis (CPD) patients with hs‐CRP equal or greater than 0.25 mg/dL were randomized to the treatment group who took 200 mg of celecoxib daily for 4 weeks or to the control group who did not take the medication. The levels of hs‐CRP, albumin, D‐dimer, vWF and troponin‐T were measured at baseline and at 4 weeks of the study. Baseline values of all the parameters were not significantly different between the two groups. In the control group, the levels of hs‐CRP, albumin, D‐dimer, vWF and troponin‐T did not change. In the treatment group, administration of celecoxib for 4 weeks significantly reduced hs‐CRP from median 0.77 (range 0.25–7.08) to 0.39 mg/dL (range 0.11–5.22, p < 0.05). The levels of albumin, D‐dimer, vWF and troponin‐T levels were not affected by the administration of celecoxib. These results showed that celecoxib had an antiinflammatory effect in usual dosage in CPD patients.

Interaction of a selective cyclooxygenase-2 inhibitor with aspirin and NO-releasing aspirin in the human gastric mucosa

In addition to inhibiting cyclooxygenase (COX)-1-derived prostanoid biosynthesis, aspirin acetylates COX-2, enabling the conversion of arachidonic acid to 15(R)-epi lipoxin A4, or aspirin-triggered lipoxin (ATL). Selective COX-2 inhibitors block ATL formation and exacerbate mucosal injury in rats treated with aspirin. In the present study, we have examined whether inhibition of COX-2 activity in healthy volunteers taking aspirin exacerbates gastric mucosal injury and if such an effect would be prevented by NCX-4016, a NO-releasing derivative of aspirin. Thirty-two volunteers were randomized to receive 2 wk of treatment with NCX-4016 (800 mg twice a day) or aspirin (100 mg once a day) alone or in combination with 200 mg of celecoxib twice a day. Mucosal damage was assessed by endoscopy. The mean mucosal injury score was 5.8 +/- 1.8 in subjects treated with aspirin and 2.4 +/- 0.7 (P < 0.01 vs. aspirin) in subjects treated with NCX-4016. Administration of celecoxib increased the injury score in volunteers treated with aspirin (9.9 +/- 1.9) but not in subjects taking NCX-4016 (1.5 +/- 0.8). Aspirin and NCX-4016 caused a comparable suppression of serum thromboxane B2 levels and increased urinary excretion of ATL. Celecoxib inhibited endotoxin-induced prostaglandin E2 generation in whole blood by approximately 80% and abolished ATL formation. These findings suggests that (i) aspirin and NCX-4016 trigger ATL formation in humans, (ii) celecoxib inhibits ATL formation and exacerbates the mucosal injury caused by low doses of aspirin, and (iii) the NO-donating moiety of NCX-4016 protects the gastric mucosa even in the presence of suppression of COX-1 and COX-2.

Poster 83: The role of backbuilders exercise program in low back pain

Objective: To evaluate the efficacy of the Back Builders exercise program on patients with diskogenic low back pain (LBP). Design: Prospective randomized trial. Setting: Outpatient clinical setting at a major university teaching hospital. Participants: Inclusion criteria were documented evidence of disk herniation (by magnetic resonance imaging) with at least 3 months symptoms of LBP and/or leg pain. The exclusion criterion was prior history of back surgery. Interventions: Patients were randomized into 2 groups. Group 1 (n=25) performed, for 15 minutes 3 times weekly, the Back Builders program designed by the principal author, who used the principles of medical yoga and Pilates to minimize disk pressures. In addition to the exercise program, patients took 200mg of celecoxib with hydrocodone and acetaminophen for breakthrough pain. Group 2 (n=25) underwent medication treatment with 200mg of celecoxib with hydrocodone and acetaminophen for breakthrough pain. Both groups were age and sex matched. Main Outcome Measures: Outcome measures included Roland-Morris Disability Questionnaire, numeric pain score, patient satisfaction, and distance from finger to floor (in centimeters). A successful outcome was defined as >50% pain reduction with good or better patient satisfaction. Results: At a minimum of 12 months of follow-up with an average follow-up of 12.3 months (range, 12–14mo), group 1 had 72% (18/25) successful outcomes and group 2 reported 36% (8/22, 3 lost to follow-up) successful outcomes ( P=.001). In group 1, 16% (y/25) reported recurrence of acute symptoms versus 50% (11/22) in group 2 ( P=.001). Conclusion: A well-designed program for patients with disk problems that minimizes disk pressures while restoring flexibility, strength, endurance, balance, and posture may yield superior results to oral medications with reduction in recurrence of back pain.

Poster 111: Treatment of chronic pain in a 17-year-old with Klippel-Trenaunay-Weber syndrome: a case report.

Setting: Outpatient pain management program. Patient: A 17-year-old girl with history of Klippel-Trenaunay-Weber syndrome (KTWS). Case Description: The patient was diagnosed at birth with KTWS, which affected her right leg and resulted in a propensity for bleeding due to cutaneous capillary malformations and severe edema due to deeper venous malformations. At age 3, she underwent amputation of 2 toes and a skin graft in an attempt to arrest bleeding. At presentation, she described constant burning pain of intensity 8 on a 0 to 10 pain scale and allodynia of the lateral ankle and medial thigh, which interfered with sleep, concentration, and gait. A 5% lidocaine transdermal patch to the ankle was added to her existing regimen of 300mg of gabapentin 3 times daily, 200mg of celecoxib every day, and weekly aquatic therapy. Because her pain remained unchanged at the 6-week follow-up, 2 lidocaine patches were placed on her ankle, gabapentin was increased to 300mg 4 times daily, and therapy was increased to twice a week. At 12 weeks, the pain intensity was still rated at 8, and the only change made to the regimen was the addition of a 50μg/h fentanyl transdermal patch. Fentanyl was not tolerated and was stopped by the patient at week 13. Assessment/Results: At 18-week follow-up, her pain had decreased to an intensity of 4 and her functional status and sleep were significantly improved. Discussion: A literature search has revealed no other examples of pain or treatment of pain caused by KTWS. From our experience with this case, gabapentin and lidocaine patch can decrease pain and, consequently, in conjunction with aquatic therapy, can increase the patient’s functional status. Conclusion: The sequence of medication choices and dosages in addition to the exercise modality provided effective treatment in this case of KTWS.

Biochemical and clinical evidence that aspirin-intolerant asthmatic subjects tolerate the cyclooxygenase 2-selective analgetic drug celecoxib

Background: Subjects with aspirin-intolerant asthma (AIA) respond with bronchoconstriction and extrapulmonary adverse reactions to conventional nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit the cyclooxygenase (COX) step in the biosynthesis of prostaglandins. Recently, 2 isotypes of COX have been identified, and COX-2-selective NSAIDs have been developed for treatment of inflammatory disorders. Objective: We investigated whether 33 subjects with a typical history of AIA tolerated the new COX-2-selective NSAID celecoxib. Methods: All subjects displayed current aspirin sensitivity in oral or inhalation challenge tests. The subjects first underwent a double-blind, randomized, cross-over, increasing-dose challenge with placebo or celecoxib (10, 30, or 100 mg in suspension) on 2 occasions 7 days apart. Thereafter, all subjects were exposed to 400 mg of celecoxib administered during an open challenge session as two 200-mg doses 2 hours apart. Lung function, clinical symptoms, and urinary excretion of leukotriene E4 (LTE4) were monitored, with the latter being a sensitive biochemical marker of aspirin intolerance. Results: There were no changes in lung function or extrapulmonary symptoms during the double-blind sessions or in urinary excretion of LTE4. Also, the highest recommended daily dose of celecoxib was well tolerated, with no symptoms, lung function changes, or alterations in urinary LTE4 levels. Conclusions: A group of subjects with clinically well-documented AIA tolerated acute challenge with the selective COX-2 inhibitor celecoxib. The findings indicate that the intolerance reaction in AIA is due to inhibition of COX-1. Large long-term studies of COX-2 inhibitors in AIA should be undertaken. (J Allergy Clin Immunol 2003;111:1116-21.)

Systemic biosynthesis of prostacyclin by cyclooxygenase (COX)-2: the human pharmacology of a selective inhibitor of COX-2.

Prostaglandins (PG) are synthesized by two isoforms of the enzyme PG G/H synthase [cyclooxygenase (COX)]. To examine selectivity of tolerated doses of an inhibitor of the inducible COX-2 in humans, we examined the effects of celecoxib on indices of COX-1-dependent platelet thromboxane (Tx) A2 and on systemic biosynthesis of prostacyclin in vivo. Volunteers received doses of 100, 400, or 800 mg of celecoxib or 800 mg of a nonselective inhibitor, ibuprofen. Ibuprofen, but not celecoxib, significantly inhibited TxA2-dependent aggregation, induced ex vivo by arachidonic acid (83 +/- 11% vs. 11. 9 +/- 2.2%; P < 0.005) and by collagen. Neither agent altered aggregation induced by thromboxane mimetic, U46619. Ibuprofen reduced serum TxB2 (-95 +/- 2% vs. -6.9 +/- 4.2%; P < 0.001) and urinary excretion of the major Tx metabolite, 11-dehydro TxB2 (-70 +/- 9.9% vs. -20.3 +/- 5.3%; P < 0.05) when compared with placebo. Despite a failure to suppress TxA2-dependant platelet aggregation, celecoxib had a modest but significant inhibitory effect on serum TxB2 4 hr after dosing. By contrast, both ibuprofen and celecoxib suppressed a biochemical index of COX-2 activity (endotoxin induced PGE2 in whole blood ex vivo) to a comparable degree (-93.3 +/- 2% vs. -83 +/- 6.1%). There was no significant difference between the doses of celecoxib on COX-2 inhibition. Celecoxib and ibuprofen suppressed urinary excretion of the prostacyclin metabolite 2,3 dinor 6-keto PGF1alpha. These data suggest that (i) platelet COX-1-dependent aggregation is not inhibited by up to 800 mg of celecoxib; (ii) comparable COX-2 inhibition is attained by celecoxib (100-800 mg) and ibuprofen (800 mg) after acute dosing; and (iii) COX-2 is a major source of systemic prostacyclin biosynthesis in healthy humans.

Factors associated with pediculosis pubis and scabies.

To ascertain factors associated with genital pediculosis and scabies infestations among attenders at an STD clinic. Cross sectional assessment of potential risk factors by multiple logistic regression. A central city sexually transmitted diseases (STD) clinic in Adelaide, South Australia. All men and women patients attending from 1988 to 1991. Pediculosis pubis was diagnosed in 205 of 12,170 (1.7%) men and 65 (1.1%) of 6125 women, and scabies in 56 (0.5%) men and 6 (0.1%) women attending an STD clinic from 1988-1991. Independent risk factors by multivariate analysis for pediculosis pubis in women were pregnancy (odds ratio (OR) = 2.3), sex outside the state (OR = 2.2) and age under 25 (OR = 2.0). Many factors were associated with pediculosis pubis in men, including no steady partner (OR = 1.4), multiple partners (OR = 1.6), being unmarried (OR = 2.0) and homosexual behaviour (OR = 1.6). None of these factors was associated with scabies infestation which was strongly associated with being Aboriginal (OR = 6.8) and being unemployed (OR = 2.5). In this setting scabies appears to be determined by socioeconomic factors and pediculosis pubis predominantly by sexual activity factors.