Skokie Hospital

UNLABELLED: Postoperative pain can have a significant effect on patient recovery. An understanding of patient attitudes and concerns about postoperative pain is important for identifying ways health care professionals can improve postoperative care. To assess patients' postoperative pain experience and the status of acute pain management, we conducted a national study by using telephone questionnaires. A random sample of 250 adults who had undergone surgical procedures recently in the United States was obtained from National Family Opinion. Patients were asked about the severity of postsurgical pain, treatment, satisfaction with pain medication, patient education, and perceptions about postoperative pain and pain medications. Approximately 80% of patients experienced acute pain after surgery. Of these patients, 86% had moderate, severe, or extreme pain, with more patients experiencing pain after discharge than before discharge. Experiencing postoperative pain was the most common concern (59%) of patients. Almost 25% of patients who received pain medications experienced adverse effects; however, almost 90% of them were satisfied with their pain medications. Approximately two thirds of patients reported that a health care professional talked with them about their pain. Despite an increased focus on pain management programs and the development of new standards for pain management, many patients continue to experience intense pain after surgery. Additional efforts are required to improve patients' postoperative pain experience. IMPLICATIONS: A survey of 250 US adults who had undergone a recent surgical procedure asked about their postoperative pain experience. Approximately 80% of patients experienced pain after surgery. Of these patients, 86% had moderate, severe, or extreme pain. Additional efforts are required to improve patients' postoperative pain experience.

OBJECTIVE: The aim of this study was to assess the rate of upper gastrointestinal (UGI) ulcer complications (bleeding, perforation, or gastric outlet obstruction) associated with celecoxib, a specific COX-2 inhibitor, compared with the rate associated with nonspecific, nonsteroidal anti-inflammatory drugs (NSAIDs). METHODS: A pooled analysis was conducted of 14 multicenter, double-blind, randomized, controlled trials (RCTs) and a separate analysis of one long-term open label trial that assessed the efficacy and safety of celecoxib for symptomatic treatment of arthritis. The RCTs enrolled 11,008 patients with osteoarthritis or rheumatoid arthritis treated for 2-24 wk; the long-term open label trial enrolled 5,155 patients receiving celecoxib for a maximum of 2 yr. In the RCTs, patients were randomly assigned to receive placebo (n = 1,864; 208 patient-years), celecoxib 25-400 mg b.i.d. (n = 6,376; 1,020 patient-years), or a comparator NSAID (n = 2,768; 535 patient-years); NSAIDs were naproxen 500 mg b.i.d., diclofenac 50 or 75 mg b.i.d., or ibuprofen 800 mg t.i.d.). In the long-term, open-label trial, patients received celecoxib 100-400 mg b.i.d. for up to 2 yr (n = 5,155; 5,002 patient-years). The principal outcome measure of this analysis was development of a UGI ulcer complication, which was prospectively defined as bleeding, perforation, or gastric outlet obstruction. Ulcer complications were assessed and adjudicated by persons blinded to the patient's treatment assignment or the study in which the patient participated. RESULTS: In the RCTs, UGI ulcer complications occurred in no placebo patients (0 of 1,864 patients), in 2 of 6,376 celecoxib patients (0.03%), and in 9 of 2,768 patients receiving an NSAID (0.33%), corresponding to annual incidences of 0.20% for celecoxib (p > 0.05 vs placebo) and 1.68% for NSAIDs (p = 0.002 vs celecoxib and placebo). In the long-term open-label trial, nine UGI ulcer complications occurred, for an incidence of 0.17% and an annualized incidence of 0.18%. CONCLUSIONS: The incidence of UGI ulcer complications associated with celecoxib was 8-fold lower than with nonspecific NSAIDs. The incidence of ulcer complications observed in celecoxib-treated patients was similar to that in patients receiving placebo in the RCTs, and to that in non-NSAID users reported in the literature.

OBJECTIVE: Nonsteroidal anti-inflammatory drugs (NSAIDs) block prostaglandin production by inhibiting cyclooxygenase (COX); they are believed to cause gastroduodenal damage by inhibiting the COX-1 isoform and to have analgesic and anti-inflammatory effects by inhibiting the COX-2 isoform. As compared to conventional NSAIDs, celecoxib, a COX-2 specific inhibitor, has been shown in previous single posttreatment endoscopy studies to be associated with lower gastroduodenal ulcer rates. In response to concerns that such studies may under-represent ulceration rates, the present serial endoscopy study was designed to compare cumulative gastroduodenal ulcer rates associated with the use of celecoxib to those of naproxen, a conventional NSAID. METHODS: In this double-blind, parallel-group, multicenter study, 537 patients with osteoarthritis (OA) or rheumatoid arthritis (RA) were randomized to treatment with celecoxib 200 mg b.i.d. (n = 270) or naproxen 500 mg b.i.d. (n = 267) for 12 wk. Gastroduodenal damage was determined from esophagogastroduodenoscopy after 4, 8, and 12 wk of therapy. Arthritis efficacy was evaluated with Patient's and Physician's Global Assessments. RESULTS: Gastroduodenal ulcer rates after celecoxib and naproxen treatment were 4% versus 19% in the 0-4 wk interval (p < 0.001), 2% versus 14% in the 4-8 wk interval (p < 0.001), and 2% versus 10% in the 8-12 wk interval (p < 0.001), respectively. After 12 wk of treatment, the cumulative incidence of gastroduodenal ulcers was 9% with celecoxib and 41% with naproxen. In the celecoxib group, gastroduodenal ulcers were significantly associated with Helicobacter pylori status (p < 0.05), concurrent aspirin usage (p = 0.001), and a history of ulcer (p = 0.010), but not with disease type (OA/RA), age, gender, other relevant medical histories, or concurrent corticosteroid or disease-modifying antirheumatic drugs usage (p > 0.05). Celecoxib produced a significantly lower incidence rate of both gastric (p < 0.001) and duodenal (p < 0.030) ulcers. The two agents produced similar improvements in Patient's and Physician's Global Assessments of arthritis efficacy. The incidence of adverse events and withdrawal rates did not differ significantly between treatments. CONCLUSIONS: As compared to naproxen (500 mg b.i.d.), use of celecoxib (200 mg b.i.d.), a COX-2 specific agent, at the recommended RA dose and twice the most frequently prescribed OA dose, was associated with lower rates of gastric, duodenal, and gastroduodenal ulcers but had comparable efficacy, in patients with OA and RA.

UNLABELLED: We sought to describe the economic and humanistic burden after total abdominal hysterectomy (TAH), total hip replacement (THR), or total knee replacement (TKR) surgery. Resource use and costs were estimated from the hospital perspective. The mean worst pain severity was 8.9, 8.1, and 7.6 on a 0- to 10-point scale after TAH, THR, and TKR, respectively. Postoperative pain was worst on postoperative day 1 after TAH or THR, and on postoperative day 2 after TKR. Analgesic medications relieved from 60% to nearly 78% of postoperative pain, but participants re- ported moderate-to-high levels of interference with general activity, walking ability, and sleep because of postoperative pain. Most costs were attributed to the hospital admission and operating room. The average length of hospitalization was 2.8 days after TAH, and 3.9 days after THR or TKR. This study provides insight into patients' experience with pain after common surgeries, perioperative costs, and medical resource use. IMPLICATIONS: Despite impressive relief with analgesics, postoperative pain interferes with patients' ability to sleep, walk, and participate in other activities. Medications used postoperatively account for a small portion of total costs. Satisfaction ratings alone are a poor indicator of pain control. These data can be used to help improve pain relief.

The novel cyclooxygenase- (COX)-2 inhibitor celecoxib is an effective treatment for the signs and symptoms of osteoarthritis and rheumatoid arthritis. Conventional treatment for these debilitating conditions routinely involves the use of conventional nonsteroidal anti-inflammatory drugs (NSAIDs), which are nonspecific inhibitors of COX-1 and COX-2. Numerous studies suggest that inhibition of renal prostaglandin synthesis by NSAIDs is deleterious to kidney function, particularly in high-risk patients. As celecoxib inhibits COX-2 and spares COX-1 at therapeutic doses, we hypothesized that it may offer an improved renal safety profile in patients at risk for NSAID-induced renal toxicity. This article represents a post hoc analysis of the renal safety of celecoxib, using the safety database generated during its clinical development program. This analysis includes data from more than 50 clinical studies involving more than 13,000 subjects. Most subjects were enrolled in randomized, controlled trials (of up to 12 weeks' duration); however, more than 5000 subjects received celecoxib for as long as 2 years in a long-term, open-label study at as much as twice the maximum recommended dosage. The overall incidence of renal adverse events after celecoxib was greater than that after placebo but similar to that after NSAIDs. The most common events reported after celecoxib, namely, peripheral edema (2.1%), hypertension (0.8%), and exacerbation of preexisting hypertension (0.6%), were not time- or dose-related. Peripheral edema was not associated with increased weight or blood pressure. Furthermore, there was no evidence of drug-drug interactions between celecoxib and concomitant angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, calcium channel blockers, or diuretics. We conclude that celecoxib is well tolerated by patients who may be at risk for NSAID-induced renal toxicity, such as the elderly and those with hypertension or preexisting chronic heart disease.

The effect of deformation pattern on bond strength is studied using I in. (25 mm) diameter machined bars with deformation heights of0. 05, 0.075, and 0.10 in. ( 1.27, 1.91, and 2.54 mm) and deformation spacings ranging from 0.26 to 2.2 in. (6.7 to 56 mm). The combinations of rib height and spacing produce relative rib areas (ratio of projected rib area normal to bar axis to product of nominal bar perimeter and center-to-center rib spacing) of 0.20, 0.10, and 0.05 for each deformation height. Conventional reinforcing bars, with a relative rib area of0.07, are also studied. The effect of deformation pattern is evaluated using beam-end specimens with varying degrees of confinement provided to the test bars. Degrees of confinement are: 1) 2-in. ( (51-mm) cover with confining transverse stirrups, and 3) 3-in. (76-mm) cover without confining transverse stirrups. Bars with 2-in. (51-mm) cover have an initial unhanded length of 1 /z in. (13 mm) and a bonded length of 12 in. (305 mm). Bars with 3-in. (76-mm) cover have an initial unhanded length of 4 in. ( 102 mm) and a bonded length of 8 1 /z in. (216 mm).

We sought to describe the economic and humanistic burden after total abdominal hysterectomy (TAH), total hip replacement (THR), or total knee replacement (TKR) surgery. Resource use and costs were estimated from the hospital perspective. The mean worst pain severity was 8.9, 8.1, and 7.6 on a 0- to 10-point scale after TAH, THR, and TKR, respectively. Postoperative pain was worst on postoperative day 1 after TAH or THR, and on postoperative day 2 after TKR. Analgesic medications relieved from 60% to nearly 78% of postoperative pain, but participants re- ported moderate-to-high levels of interference with general activity, walking ability, and sleep because of postoperative pain. Most costs were attributed to the hospital admission and operating room. The average length of hospitalization was 2.8 days after TAH, and 3.9 days after THR or TKR. This study provides insight into patients’ experience with pain after common surgeries, perioperative costs, and medical resource use.

This is an article in the Core Entrustables in Clinical Pharmacology series that describes opioid therapy in acute and chronic pain. Opioid use during surgical procedures or anesthesia is not discussed. Basic pharmacokinetic and pharmacodynamic properties of opioids are reviewed. The safe and effective use of opioids, including clinical assessment and treatment plan, equianalgesic dosing, opioid rotation, opioid risks and side effects, and clinical adherence monitoring are discussed. Individualized opioid use can be a safe and effective component of a patient-specific multimodal treatment plan for acute or chronic pain. Adverse effects and risks can be prevented or effectively managed when anticipated and recognized. The article is followed by 4 clinical vignettes with discussions.

BACKGROUND: The trend toward day-case surgery, with discharge on oral medication, has highlighted the need for effective and safe analgesics that facilitate a rapid recovery and discharge time. This study evaluated the analgesic efficacy, dose dependency, duration of action, and safety of the cyclooxygenase-2 specific inhibitor, valdecoxib, administered before oral or orthopedic surgery. METHODS: Eligible healthy adult patients were scheduled to undergo either extraction of two impacted third molar teeth (n = 284) or bunionectomy surgery (n = 223) with local anesthesia in two randomized, double-blind, placebo-controlled studies conducted at three centers in the United States. Patients received a single, preoperatively administered oral dose of placebo or 10 (oral surgery only), 20, 40, or 80 mg valdecoxib. Analgesic efficacy was assessed postoperatively, over a 24-h treatment period, or until the patient required rescue medication. Efficacy measures included time to rescue medication, proportion of patients requiring such rescue, pain intensity, and the Patient's Global Evaluation of Study Medication. RESULTS: In both studies, all doses of valdecoxib produced analgesia with a duration (time to rescue analgesia) and magnitude (Pain Intensity, Patient's Global Evaluation) significantly greater than placebo. A dose-dependent effect was observed up to 40 mg valdecoxib, with an 80-mg dose providing no additional analgesic benefit. In both models, all doses of valdecoxib were well tolerated, with no clinically significant treatment-related gastrointestinal, renal, or platelet-derived adverse events, and no evidence of a dose-related increase in adverse events. CONCLUSIONS: Preoperative orally administered valdecoxib provides well-tolerated and effective analgesia for mild to moderate postoperative pain.

Abstract For the first 180 years following the founding of the US, physicians occasionally were sued for medical malpractice. Allegations of negligence were errors of commission – i.e. the physician made a mistake by doing something wrong, usually mistreatment of a fracture or dislocation, a complication or death following a surgical procedure, prescribing the wrong medication, and after the discovery of the X-ray by Roentgen in 1895, causing radiation burns. In the mid twentieth century malpractice allegations slowly changed from errors of commission to errors of omission – i.e. the physician failed to do something right: almost always, failed to make a diagnosis. The number of malpractice lawsuits increased at a geometric rate beginning in the 1960s, and in the 1970s physicians began practicing defensive medicine, which lead physicians to order unnecessary radiology exams and tests. In the past 20 years the number of malpractice lawsuits has been decreasing, but the practice of defensive medicine has continued. Unnecessary exams and tests increase the likelihood of overdiagnosis and overtreatment, i.e. a new kind of error of commission.

OBJECTIVE: To investigate the efficacy of venlafaxine for neuropathic pain and review literature to determine if the medication provides adequate neuropathic pain relief. METHODS: Literature was reviewed on MEDLINE using various key words. These key words include: "venlafaxine and pain," "venlafaxine ER and pain," "venlafaxine XR and pain," "venlafaxine and neuropathic pain," "venlafaxine and neuropathy," "SSRI and neuropathic pain," "SSRI and neuropathy," "SNRI and neuropathic pain," "SNRI and neuropathy," "serotonin reuptake inhibitor and neuropathic pain," "serotonin reuptake inhibitor and neuropathy," "serotonin norepinephrine reuptake inhibitor and neuropathic pain" and "serotonin norepinephrine reuptake inhibitor and neuropathy." Using this guideline, 13 articles were reviewed. RESULTS: A total of 13 studies reviewed, which are organized by date and diagnosis. It is evident that in the majority of studies, when compared with a placebo, there was a clinical significant reduction in neuropathic pain relief when using venlafaxine. Additionally, one study showed even more significant pain relief when using higher doses of venlafaxine (at least 150 mg). However, when compared with alternative neuropathic medications, venlafaxine for the most part did not perform any better in terms of efficacy. CONCLUSION: In conclusion, venlafaxine is a safe and well-tolerated analgesic drug for the symptomatic treatment of neuropathic pain, and there is limited evidence that high-dose venlafaxine (150 mg/day) can be even more beneficial. While the present evidence is quite encouraging regarding venlafaxine's use for neuropathic pain, further research is needed to continue to expand on these findings, particularly when in consideration with other possible pharmacological agents.

Metabolic syndrome (MSX) identifies clinical symptoms and lab results, including abdominal obesity, insulin resistance, hyperglycemia, hyperlipidemia, and hypertension, that lead to an increased risk of cardiovascular disease (CVD). Obesity typically results in insulin and leptin resistance and a shift from expansion of subcutaneous fat to deposition of abdominal and ectopic fat. These conditions cause metabolic dysregulation, elevated fatty acids (FFA), and increased secretion of pro-inflammatory "adipokines". Left untreated, these conditions cause lipotoxicity, chronic inflammation, hypertension, atherosclerosis, and CVD.

During the 10-year period beginning in 1949 with publication of five articles in two radiology journals and UKs The Lancet, a California radiologist named L.H. Garland almost single-handedly shocked the entire medical and especially the radiologic community. He focused their attention on the fact now known and accepted by all, but at that time not previously recognized and acknowledged only with great reluctance, that a substantial degree of observer error was prevalent in radiologic interpretation. In the more than half-century that followed, Garland's pioneering work has been affirmed and reaffirmed by numerous researchers. Retrospective studies disclosed then and still disclose today that diagnostic errors in radiologic interpretations of plain radiographic (as well as CT, MR, ultrasound, and radionuclide) images hover in the 30% range, not too dissimilar to the error rates in clinical medicine. Seventy percent of these errors are perceptual in nature, i.e., the radiologist does not "see" the abnormality on the imaging exam, perhaps due to poor conspicuity, satisfaction of search, or simply the "inexplicable psycho-visual phenomena of human perception." The remainder are cognitive errors: the radiologist sees an abnormality but fails to render a correct diagnoses by attaching the wrong significance to what is seen, perhaps due to inadequate knowledge, or an alliterative or judgmental error. Computer-assisted detection (CAD), a technology that for the past two decades has been utilized primarily in mammographic interpretation, increases sensitivity but at the same time decreases specificity; whether it reduces errors is debatable. Efforts to reduce diagnostic radiological errors continue, but the degree to which they will be successful remains to be determined.

BACKGROUND: The inducible cyclooxygenase-2 (COX-2) enzyme is upregulated in inflammatory diseases, as well as in epithelial cancers, and has an established role in angiogenesis and tissue repair. OBJECTIVE: Because of these physiological effects and the widespread use of the selective COX-2 inhibitor, celecoxib, we wanted to determine if inhibition of COX-2 would affect incisional skin wound healing. METHODS: Using a cutaneous full-thickness, sutured, incisional wound model in hairless SKH-1 mice, we evaluated the role of COX-2 in the wound healing process by comparing the effects of a nonselective COX inhibitor, diclofenac, with a selective COX-2 inhibitor, SC-791. Healing was monitored for up to 28 days postincision histologically and for recovery of wound strength. RESULTS: COX-2 expression was observed over the first week of healing, peaking at day 3 and was not affected by treatment with the selective COX-2 or nonselective COX inhibitors. Infiltrating macrophages, as well as keratinocytes and dermal fibroblasts at the wound site, expressed COX-2. Neither selective COX-2, nor nonselective COX inhibition had a significant effect on the macroscopic or microscopic morphology of the wounds, whereas dexamethasone treatment resulted in epidermal and granulation tissue atrophy. In addition, neither selective COX-2, nor nonselective COX inhibition altered keratinocyte proliferation and differentiation, dermal angiogenesis or the recovery of wound tensile strength, whereas dexamethasone reduced the tensile strength of the wounds by 30-38% throughout the healing period. CONCLUSIONS: These data indicate that selective COX-2 inhibition does not affect the healing of surgical skin wounds.

Serotonin acts as a neurotransmitter, neuromodulator, and hormone in mammals, and it is known to exhibit profound pharmacological activities in the central nervous system, autonomic nervous system, enteric nervous system, and cardiovascular system. Among monoamine neuro-transmitters, serotonin is unsurpassed in the number of receptor subtypes identified. Until recently, serotonin was thought to act through receptors subtyped as 5-HT1, 5-HT2, and 5-HT3. Furthermore, even these subtypes have been subclassed to now include 5-HT1A, 5-HT1B, 5-HTlc, 5-HT1D, 5-HT2A, 5-HT2B, and 5-HT3A ,5-HT3B ,and 5-HT33C.2

Inhibition of the cyclooxygenase (COX)-2 enzyme has been shown previously to reduce pain and inflammation. Valdecoxib is a new highly selective COX-2 inhibitor with a rapid onset of action and significant analgesic properties. This study compared the analgesic efficacy of valdecoxib and rofecoxib in treating postoperative pain in patients undergoing oral surgery. This randomized, double-blind, placebo-controlled study compared the efficacy of 40 mg valdecoxib with that of 50 mg rofecoxib and placebo. Efficacy was assessed by the onset of analgesia, pain intensity levels, and pain relief over 24 hours, time-weighted sum of total pain, sum of pain intensity difference, the percentage of patients requiring rescue medication and experiencing regimen failure, and patients' global evaluation. Patients receiving valdecoxib experienced a significantly quicker onset of analgesia, significantly improved pain relief, and lower pain intensity compared with patients receiving rofecoxib and greater satisfaction with their study medication after a single dose. Valdecoxib also demonstrated efficacy that was superior to that of rofecoxib with respect to the percentage of patients requiring rescue medication or experiencing regimen failure (p < or =.05). Valdecoxib, rofecoxib, and placebo were equally well tolerated. This study demonstrates that valdecoxib provides significantly greater analgesic efficacy than rofecoxib in the management of pain after oral surgery.

Pain management of patients continues to pose challenges to clinicians. Given the multiple dimensions of pain--whether acute or chronic, mild, moderate, or severe, nociceptive or neuropathic--a multimodal approach may be needed. Fortunately, clinicians have an array of nonpharmacologic and pharmacologic treatment choices; however, each modality must be chosen carefully, because some often used oral agents are associated with safety and tolerability issues that restrict their use in certain patients. In particular, orally administered nonsteroidal antiinflammatory drugs, opioids, antidepressants, and anticonvulsants are known to cause systemic adverse effects in some patients. To address this problem, a number of topical therapies in various therapeutic classes have been developed to reduce systemic exposure and minimize the risks of patients developing adverse events. For example, topical nonsteroidal anti-inflammatory drug formulations produce a site-specific effect (ie, cyclo-oxygenase inhibition) while decreasing the systemic exposure that may lead to undesired effects in patients. Similarly, derivatives of acetylsalicylic acid (ie, salicylates) are used in topical analgesic formulations that do not significantly enter the patient's systemic circulation. Salicylates, along with capsaicin, menthol, and camphor, compose the counterirritant class of topical analgesics, which produce analgesia by activating and then desensitizing epidermal nociceptors. Additionally, patches and creams that contain the local anesthetic lidocaine, alone or co-formulated with other local anesthetics, are also used to manage patients with select acute and chronic pain states. Perhaps the most common topical analgesic modality is the cautious application of cutaneous cold and heat. Such treatments may decrease pain not by reaching the target tissue through systemic distribution, but by acting more directly on the affected tissue. Despite the tolerability benefits associated with avoiding systemic circulation, topically applied analgesics are associated with application-site reactions in patients, such as dryness, erythema, burning, and discoloration. Furthermore, some adverse events that have been observed in patients may be suggestive of some degree of systemic exposure. This article reviews the mechanisms of action, pharmacokinetics, and tolerability of topical treatments for the management of patient pain.

OBJECTIVES: It is known that psychotropic medications have an impact on the readings found in Electroencephalogram (EEG). In the field of psychiatry, there are several psychotropics utilized by clinicians. This review seeks to investigate all the available data for psychotropic drugs and their impact on EEG changes. METHODS: A systematic review of all the published and ongoing literature was conducted via PubMed. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) method was used for each search. Key words for searches include 'EEG and Psychotropics', 'EEG and Mood Stabilizers', 'EEG and Clozapine', 'EEG and Bupropion', 'EEG and SSRI', 'EEG and Lamotrigine', 'EEG and Carbamazepine', 'EEG and Lithium' and 'EEG and Valproate', 'EEG and Haloperidol', 'EEG and Aripiprazole', 'EEG and Methylphenidate', 'EEG and Topiramate', 'EEG and Gabapentin' and 'EEG and Oxcarbamazepine'. After applying the inclusion criteria, 201 articles were eligible and reviewed. RESULTS: Following an extensive review of selected studies from the 201 articles, the studies indicate that each of the psychotropic medications reviewed impact alpha, beta, delta and theta waves independently and differently from each other. Additionally, certain medications, particularly haloperidol and valproic acid, have dissimilar results exemplified in all waveforms. CONCLUSIONS: This PRISMA systematic review illustrates that while there is available data on psychotropic medications and their proposed effect on EEG activity, further research is needed to confirm these findings to help allow clinical correlations to be made between the patient's response and the psychotropic agent.

No AccessJournal of Urology1 Oct 1974Squamous Metaplasia of the Bladder: A Study of 450 Patients Jerrold Widran, Ramon Sanchez, and John Gruhn Jerrold WidranJerrold Widran , Ramon SanchezRamon Sanchez , and John GruhnJohn Gruhn View All Author Informationhttps://doi.org/10.1016/S0022-5347(17)59765-7AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail © 1974 by The American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetailsCited BySideri M, De Virgiliis G, Rainoldi R, Ferrari A and Remotti G (2018) Junctional Pattern in the Squamous Metaplasia of the Female Trigone. A Freeze-Fracture StudyJournal of Urology, VOL. 129, NO. 2, (280-283), Online publication date: 1-Feb-1983.Broecker B, Klein F and Hackler R (2018) Cancer of the Bladder in Spinal Cord Injury PatientsJournal of Urology, VOL. 125, NO. 2, (196-197), Online publication date: 1-Feb-1981.Droller M (2018) Editorial CommentJournal of Urology, VOL. 125, NO. 2, (197-197), Online publication date: 1-Feb-1981.Wiener D, Koss L, Sablay B and Freed S (2018) The Prevalence and Significance of Brunn's Nests, Cystitis Cystica and Squamous Metaplasia in Normal BladdersJournal of Urology, VOL. 122, NO. 3, (317-321), Online publication date: 1-Sep-1979.Eggleston J (2018) Editorial CommentJournal of Urology, VOL. 122, NO. 3, (321-321), Online publication date: 1-Sep-1979. (2018) Reply by AuthorsJournal of Urology, VOL. 122, NO. 3, (321-321), Online publication date: 1-Sep-1979.Colapinto V and Evans D (2018) Primary Carcinoma of the Male Urethra Developing after Urethroplasty for StrictureJournal of Urology, VOL. 118, NO. 4, (581-584), Online publication date: 1-Oct-1977.Murphy W (2018) Falsely Positive Urinary Cytology: Pathologist's Error or Preclinical Cancer?Journal of Urology, VOL. 118, NO. 5, (811-813), Online publication date: 1-Nov-1977.Kaufman J, Fam B, Jacobs S, Gabilondo F, Yalla S, Kane J and Rossier A (2018) Bladder Cancer and Squamous Metaplasia in Spinal Cord Injury PatientsJournal of Urology, VOL. 118, NO. 6, (967-971), Online publication date: 1-Dec-1977.Reece R and Koontz W (2018) Leukoplakia of the Urinary Tract: A ReviewJournal of Urology, VOL. 114, NO. 2, (165-171), Online publication date: 1-Aug-1975.Duncan R, Keys R, Bennett D, Evans A, Fidler J and Alexander J (2018) Squamous Cell Carcinoma of the Ureterovesical Junction after Renal TransplantationJournal of Urology, VOL. 114, NO. 4, (628-630), Online publication date: 1-Oct-1975. Volume 112Issue 4October 1974Page: 479-482 Advertisement Copyright & Permissions© 1974 by The American Urological Association Education and Research, Inc.MetricsAuthor Information Jerrold Widran More articles by this author Ramon Sanchez More articles by this author John Gruhn More articles by this author Expand All Advertisement Loading ...

Nonsteroidal anti-inflammatory drugs have been a mainstay in the treatment of inflammatory diseases such as rheumatoid arthritis. However, these agents can result in severe and occasionally life-threatening adverse effects that can limit therapeutic benefit. Progress toward safer anti-inflammatory therapy was aided by the discovery that cyclooxygenase (COX) exists as two isozymes, COX-1 and COX-2. Both isozymes form prostaglandins that support physiologic functions; however, the formation of proinflammatory prostaglandins is catalyzed by COX-2. Inhibition of COX-2 accounts for the anti-inflammatory and analgesic action of NSAIDs; however, concurrent inhibition of COX-1 inhibits prostaglandin-dependent mechanisms such as gastroduodenal mucosal defense and platelet aggregation. This inhibition is the basis of the gastrointestinal toxicity and bleeding characteristic of these drugs. These findings led to the hypothesis that agents that selectively inhibit COX-2 would possess anti-inflammatory and analgesic action but would spare COX-1, thereby avoiding adverse effects in the gastrointestinal tract and platelets. Selective COX-2 inhibitors are now available. The novelty of these agents has raised questions in the medical community as to what constitutes selectivity for COX-2. This review outlines the criteria that must be met to characterize a compound as COX-2-specific. Clinical evidence of clear improvement in gastrointestinal tolerability and safety must be demonstrated in addition to complementary evidence of COX-2 selectivity obtained from enzyme, biochemical, and clinical pharmacology evaluations.