1. Slater JE. Latex allergy--What do we know? J Allergy Clin Immunol 1992; 90: 279281 Latex allergy--an emerging healthcare problem. American College of Asthma Allergy and Immunology position statement. Ann Allergy Asthma Immunol 1995; 75: 1920 Blanco C, Carrillo T, Castillo R, Quiralte J, Cuevas M. Latex allergy: clinical features and crossreactivity with fruits. Ann Allergy 1994; 73: 309314 Rodriguez M, Vega F, Garcia MT, Panzo C, Laffond E, Montalvo A, Cuevas M. Hypersensitivity to latex, chestnut, and banana. Ann Allergy 1993; 70: 3133 Brehler R, Theissen U, Mohr C, Luger T. `Latex-fruit syndrome': frequency of crossreacting IgE antibodies. Allergy 1997; 52: 404410 Porri F, Lemiere C, Birnhaum J. Prevalence of latex allergy in atopic and non-atopic subjects from the general population. J Allergy Clin Immunol 1995; 95: 154 Hadjiliadis D, Khan K, Tarlo S. Skin test responses to latex in an allergy and asthma clinic. J Allergy Clin Immunol 1995; 96: 431432 Latex protein allergy: the latest position. International conference in Paris, 11 Jan 1995. European Rubber Journal 1995; 1927 9. Fuchs T. Latex allergy. J Allergy Clin Immunol 1994; 93: 951952.
Meet the Experts: Roadmap for Investigator-Initiated Clinical Research - A Route Less Traveled Multiple Roles for Clinical Pharmacologists in the Pharmaceutical Industry Pharmacodynamic and Pharmacogenomic Mechanisms and Models Regulation and Drug-Metabolizing Function of Intestinal CYP3A4 State of the Art Lecture: The Use of Pharmacogenomics to Improve Drug Therapy Opening Debate: Genetic Testing Oral Presentation Session I: Oral Session I-A Oral Session I-B Award Lecture: Mechanism-based PK PD: from Receptor Pharmacology to Clinical Trial and Beyond 4 Concurrent Scientific Section Workshops: Translating Scientific Advance in Pain Research into Improved Analgesic Drug Development Apoptosis and Drug Response Hormone Replacement Therapy: Cardioprotective or a Disaster? Drug Development of Monoclonal Antibodies as Anti-cancer Agents Poster Session I State of the Art Lecture: Drug Hepatotoxicity 2004 Award Lecture: Understanding Variable Beta-blocker Response: From Pharmacokinetics to Pharmacogenetics Special Workshop: Needs and Resources for Successful Training in Clinical Pharmacology Oral Presentation Session II: Oral Session II-A Oral Session II-B Award Lecture: Science vs. Empiricism in Clinical Drug Development Poster Discussion Session I: Session I-A Session I-B Featured Speaker: Individualization of Dosing Regimens in Special Populations-Still a Long Way to Go 2 Concurrent Symposia: Insights in Adverse Drug Reactions: An International Perspective Rational Drug Development for Dementia: Successes and Failures Poster Session II Public Policy Forum: Ephedra: Clinical Pharmacology At The Intersection Of Regulatory Policy And The Public Interest State of the Art Lecture: Benefit the Patient and Manage the Risk: A System Goal Featured Speaker: Genetic Polymorphisms in Treatment of Acute Leukemia 2 Concurrent Symposia: Drugs in Pregnancy - Treating the Mother, Protecting the Unborn Biomarkers in Drug Development and Registration 2 Concurrent Symposia: The CYP2C Gene Locus - A Hot Topic for Drug Treatment and Drug Development The Integration of Dose- and Exposure- Response Knowledge into Drug Development, Regulatory, and Clinical Decision-Making Meet the Experts: Pediatric Pharmacogenetics and Pharmacogenomics How Statistical Science Benefits Clinical Pharmacology Research: Statistical Issues in Clinical Pharmacology Scientific Papers - Getting Published and Reviewing the Work of Others Pharmacogenomics: Genotype-to-Phenotype and Back Poster Discussion Session II: Session II-A Session II-B 4 Concurrent Scientific Section Workshops: PGRN & PharmGKB: The Pharmacogenetics Research Network and Knowledge Base Prescription Drug Abuse: Quantifying the Risk of Diversion Method Effectiveness vs. Use Effectiveness: Maximizing the Clinical Explanatory Power of Drug Dosing History Data Microdialysis as an In Vivo Assessment of Dermal Drug Delivery and its Role in Drug Regulation, for example, nu terbinafine.
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Particularly noteworthy is the low rate of relapse of infection after cure of chronic dermatophyte infections, since frequent relapse is a recognized problem with presently available antifungal drugs, terbinafine is ineffective when used systemically for pityriasis versicolor.
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DISCUSSION In treating onychomycosis, this study clearly confirms previous reports that demonstrate terbinafine to be economically superior to the oral and topical therapies evaluated in this analysis. There are studies that highlight the cost-effectiveness of itraconazole vs. "other" therapies. Nevertheless, the investigators know of no publications that claim that itra.
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Tion in dogs and healthy volunteers in investigational trials. The biochemical and or molecular mechanism of this cardiac effect is unknown.91, 92 Between September 1992 and April 2001, 58 cases of HF associated with itraconazole were filed with the Food and Drug Administration Adverse Drug Reaction Reporting System. It appears that this is not a class-related effect because of the lack of reports with similar antifungal agents eg, fluconazole, ketoconazole, miconazole, clotrimazole ; . Heart failure developed with itraconazole dosages ranging from 100 to 800 mg d, with both oral and intravenous routes of administration, and occurred with indications for onychomycosis, systemic fungal infections, and prophylactic treatment. Signs and symptoms among these patients included pulmonary and peripheral edema, dyspnea, and significant weight gain. Documented risk factors or diseases that might have confounded the association between itraconazole and HF were present in 74% of these patients.92 The product labeling and package insert for itraconazole carry a black boxed warning and contraindication for its use in onychomycosis in patients with evidence of LV dysfunction. Warnings for itraconazole use include patients at risk of HF, such as those with ischemic and valvular disease, chronic obstructive pulmonary disease, renal failure, and other edematous states.91 Other therapies for onychomycosis eg, ciclopirox or terbinafine ; should be considered first-line options in patients with existing HF. Patients with systemic fungal infections should be examined to determine whether alternative therapies might be appropriate; however, the severity of infection may outweigh the risk of HF exacerbation. If itraconazole therapy is considered essential in a patient with HF, increased monitoring and aggressive therapy for new or increased edema, weight gain, or dyspnea should be initiated immediately. CONCLUSIONS The information provided in this review must be used in conjunction!
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Accession number & update 16946693 Medline 20070106. Source CNS spectrums Sep 2006, vol. 11, no. 9, p. 680-9; quiz 719, ISSN: 1092-8529. Author s ; Black-Donald-W, Blum-Nancee, Letuchy-Elena, Carney-Doebbeling- Caroline, Forman-Hoffman-Valerie-L, Doebbeling-Bradley-N. Author affiliation Department of Psychiatry, University of Iowa Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA 52242, USA. donald-black uiowa . Abstract OBJECTIVE: To examine the presence of borderline personality disorder BPD ; traits in Gulf War veterans, and to assess psychiatric comorbidity, health status, healthcare utilization, and quality of life QOL ; along a continuum of BPD trait severity. METHOD: BPD and traits were evaluated using the Schedule for Non-Adaptive and Adaptive Personality in 576 veterans who were either deployed to the Persian Gulf 1990-1991 ; or were on active duty though not deployed to the Gulf. Demographic and military characteristics, personal and family history, psychiatric comorbidity, and QOL were also assessed. RESULTS: One or more BPD traits were present in 247 subjects 43% ; , and BPD 5 traits ; was identified in 15 subjects 3% ; . The number of traits was significantly associated with age and level of education. Lifetime psychiatric comorbidity was significantly associated with the number of BPD traits present, and level of functioning, health status, healthcare utilization, social functioning, self-injurious tendencies, and military behavioral problems. CONCLUSION: BPD and traits identified in Gulf War veterans were associated with significant psychiatric morbidity, poorer QOL, and increased utilization of healthcare resources. Early recognition and treatment of veterans with BPD symptoms may be warranted to minimize the burden on the healthcare system. Grant ID: MH-63746, Acronym: MH, Agency: NIMH. Language English. Publication year 2006 and
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Positive IWV ; in the right and left orbitofrontal cortex than healthy controls and significantly lower negative IWV F 3.2 4.3, p 0.017 0.011 ; in the right orbitofrontal cortex than psychiatric and healthy controls table 3, figure 4 ; . Compared to negative emotions, there is a reversal in the pattern of orbitofrontal activity. Whereas in negative emotions positive IWV were lower and negative IWV were higher in catatonia compared to both control groups, this pattern is reversed in positive emotions with higher positive IWV and lower negative IWV table 3, figure 4 ; . Second, we found significantly lower F 4.2-3.3, p 0.013-0.032 ; activity in catatonic and psychiatric control patients in the right and left lateral prefrontal cortex and
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The Medicare General Information, Eligibility, and Entitlement Manual, Pub. 100-1, Chapter 5 Definitions ; , Section 10.3 Under Arrangements ; can be found at the following CMS Online Manuals Website: : cms.hhs.gov manuals cmsindex Source Reference: CMS Manual System Pub. 100-04 Medicare Claims Processing Transmittal 183 CR #3248 May 21, 2004 and
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Generally, if you are taking a drug on our Formulary when you joined the plan, we will not discontinue or reduce coverage of the drug during the coverage year except when a new, less expensive generic drug becomes available or when new adverse information about the safety or effectiveness of a drug is released. Other types of Formulary changes, such as removing a drug from our Formulary, will not affect members who are currently taking the drug. It will remain available at the same cost-sharing for those members taking it for the remainder of the coverage year. We feel it is important that you have continued access for the remainder of the coverage year to the Formulary drugs that were available when you chose our plan, except for cases in which you can save additional money or improve the safety of your drugs. If we remove drugs from our Formulary, add prior authorization, quantity limits and or step therapy restrictions on a drug or move a drug to a higher costsharing tier, we must notify affected members of the change at least 60 days before the change becomes effective, or at the time the member requests a refill of the drug, at which time the member will receive a 60-day supply of the drug. If the Food and Drug Administration deems a drug on our Formulary to be unsafe or the drug's manufacturer removes the drug from the market, we will immediately remove the drug from our Formulary and provide notice to members who take the drug. The enclosed Formulary is current as of January 1, 2007. To get updated information about the drugs covered, please visit our Web site at bluecrosscamedicarerx or call Customer Service at: 2.
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After a full discussion of options, complications and the treatment regimen, he chose a combination of terbinafine and ciclopirox lacquer therapy and celecoxib.
Association between terbinafine and arthralgia, fever and urticaria methods, such as logistic regression analysis can be used to provide evidence for a possible underlying relationship between these different covariates. In the SRS databases the strength of the association between a drug and ADR can be studied by calculating Reporting Odds Ratios.21, 22 To study a possible relationship between fever, urticaria and arthralgia, the ADRs were considered being covariates and the presence of terbinafine as the suspected drug on the report form to be the dependent variable. The extent to which the covariates are interrelated can be examined by using statistical `interaction terms' in a logistic regression model. Since we were interested in expressing the presence of terbinafine as a function of arthralgia, fever and urticaria, cases were defined as reports on which terbinafine oral administration ; was mentioned as the suspected medication, non cases were defined as all other reports. Reporting Odds Ratios RORs ; were calculated, which were adjusted for age and gender of the patients, source of the reports and year of reporting. In the logistic regression analysis a forward stepwise approach was applied. SPSS 8.0 was used for all statistical assessments.
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Current therapy. The W. B. Saunders Co., Philadelphia, Pa. 55. Scher, R. K. 1996. Onychomycosis: a significant medical disorder. J. Am. Acad. Dermatol. 35 Part 2 ; : S2S5. 56. Scher, R. K., D. Breneman, P. Rich, R. C. Savin, D. S. Feingold, N. Konnikov, J. L. Shupack, S. Pinnell, N Levine, N. J. Lowe, R. Aly, R. B. Odom, D. L. Greer, M. R. Morman, A. D. Monroe, E. H. Tschen, B. E. Elewski, and E. B. Smith. A placebo-controlled, randomized, double-blind trial of onceweekly fluconazole 150 mg, 300 mg, or 450 mg ; in the treatment of distal subungual onychomycosis of the toenail. J. Am. Acad. Dermatol., in press. 57. Sigler, L., and H. Congly. 1990. Toenail infection caused by Onychocola canadensis gen. et sp. nov. J. Med Vet. Mycol. 28: 40517. 58. Summerbell, R. C. 1997. Epidemiology and ecology of onychomycosis. Dermatology 194 Suppl. 1 ; : 3236. 59. Summerbell, R. C., J. Kane, and S. Krajden. 1989. Onychomycosis, tinea pedis, and tinea manuum caused by non-dermatophytic filamentous fungi. Mycoses 32: 609619. 60. Tausch, I., M. Brautigam, G. Weidinger, T. C. Jones, and the Lagos V Study Group. 1997. Evaluation of 6 weeks treatment of terbinafine in tinea unguium in a double-blind trial comparing 6 and 12 weeks therapy. Br. J. Dermatol. 136: 737742. 61. Tosti, A., B. M. Piraccini, C. Stinchi, N. Venturo, F. Bardazzi, and M. D. Colombo. 1996. Treatment of dermatophyte nail infections: an open randomized study comparing intermittent terbinafine therapy with continuous terbinafine treatment and intermittent itraconazole therapy. J. Am. Acad. Dermatol. 34: 595600. 62. Van der Schroeff, J. G., P. K. S. Cirkel, M. B. Crijns, T. J. A. Van Kijk, F. J. Govaert, D. A. Groeneweg, D. J. Tazelaar, R. F. E. DeWitt, and J. Wuite. 1992. A randomized treatment duration-finding study of terbinafine in onychomycosis. Br. J. Dermatol. 126 Suppl. 39 ; : 3639. 63. Weitzman, I., and R. C. Summerbell. 1995. The dermatophytes. Clin. Microbiol. Rev. 8: 240259. 64. Winn, W. C., Jr. 1996. Mycotic diseases, p. 12101251. In J. B. Henry ed. ; , Clinical diagnosis and management. The W. B. Saunders Co., Philadelphia, Pa. 65. Zaias, N. 1972. Onychomycosis. Arch. Dermatol. 105: 263274. 66. Zaias, N., B. Glick, and G. Rebell. 1996. Diagnosing and treating onychomycosis. J. Fam. Pract. 42: 513518. 67. Zaias, N., A. Tosti, G. Rebell, R. Morelli, F. Bardazzi, H. Bieley, N. Zaiac, B. Glick, B. Paley, M. Allevato, and R. Baran. 1996. Autosomal dominant pattern of distal subungual onychomycosis caused by Trichophyton rubrum. J. Am. Acad. Dermatol. 34 2 Pt 302304.
NRL of Pharmaceutical Technology, College of Pharmacy, Chungnam National University, 220 Gung-dong, Yuseong-gu, Daejeon 305-764, Korea, 1Lab Frontier, Co., ltd., KSBC Bldg, #Mt, 11 1-8, Lui-dong, Paldal-ku, Suwon, Kyonggi-do, 442-270, Korea, and 2Green Cross Reference Laboratory, 164-10 Poyi-dong, Kangnam-ku, Seoul, 135-260, Korea, because terbinafine pregnancy.
Humoral immune responses and atopy by genome-wide mouse mutagenesis. Immunity 18, 751 -762 2003 ; . McAllister-Lucas, L. M. et al. Bimp1, a MAGUK family member linking protein kinase C activation to Bcl10-mediated NF-kB induction. J. Biol. Chem. 276, 30589 -30597 2001 ; . Gaide, O. et al. Carma1, a CARD-containing binding partner of Bcl10, induces Bcl10 phosphorylation and NF-kB activation. FEBS Lett. 496, 121 -127 2001 ; . Bertin, J. et al. CARD11 and CARD14 are novel caspase recruitment domain CARD ; membrane-associated guanylate kinase MAGUK ; family members -11882 that interact with BCL10 and activate NF-kB. J. Biol. Chem. 276, 11877 2001 ; . Zhou, H. et al. Bcl10 activates the NF-kB pathway through ubiquitination of NEMO. Nature 427, 167 -171 2004 ; . Sun, L., Deng, L., Ea, C. K., Xia, Z. P. & Chen, Z. J. The TRAF6 ubiquitin ligase and TAK1 kinase mediate IKK activation by BCL10 and MALT1 in T lymphocytes. Mol. Cell 14, 289 -301 2004 ; . Kolfschoten, I. G. et al. A genetic screen identifies PITX1 as a suppressor of RAS activity and tumorigenicity. Cell 121, 849 -858 2005 ; . Westbrook, T. F. et al. A genetic screen for candidate tumor suppressors identifies REST. Cell 121, 837 -848 2005 ; . Brummelkamp, T. R., Bernards, R. & Agami, R. Stable suppression of tumorigenicity by virus-mediated RNA interference. Cancer Cell 2, 243 -247 2002 ; . van de Wetering, M. et al. Specific inhibition of gene expression using a stably integrated, inducible small-interfering-RNA vector. EMBO Rep. 4, 609 -615 2003 ; . Reynolds, A. et al. Rational siRNA design for RNA interference. Nature Biotechnol. 22, 326 -330 2004 and tetracycline.
Plaque 210 cm in diameter, the `herald patch', may develop on the trunk 12 weeks before the other lesions. Pityriasis rosea has been reported at all ages, 509 but the majority of patients are between 10 and 35 years.510 Clinical variants include those with acral or facial involvement, 509 oral lesions, 511 a unilateral or local distribution, 512, 513 or the presence of pustular, purpuric or vesicular lesions.508, 514, 515 The etiology is unknown, but an infectious etiology, particularly a virus, has long been suspected. This is supported by a history of a preceding upper respiratory tract infection in some patients, 516 occasional involvement of close-contact pairs, 510 case clustering, 517 modification of the disease by the use of convalescent serum or erythromycin, 518 and the development of a pityriasis rosea-like eruption in some cases of infection by ECHO 6 virus and by Mycoplasma.508 There has been recent interest in the role of human herpesvirus-6 HHV-6 ; and -7 HHV-7 ; in the etiology of pityriasis rosea. While HHV-6 and HHV-7 may play a role in some patients, 519521 the low detection rate of HHV-7 DNA sequences argues against a causative role for this virus.522 In the case of HHV-6, reactivation of the virus during the early stages of the disease might explain its detection in some cases.523 Particles resembling togavirus or arenavirus have been found on electron microscopy of a herald patch, 524 suggesting that this might be the inoculation site. No virus has ever been cultured.525 Immunological reactions, 526 particularly cellmediated, have also been regarded as important.527 A pityriasis rosea-like eruption has been reported in association with the administration of many drugs, 508 including gold, bismuth, arsenicals, ketotifen, clonidine, barbiturates, methoxypromazine, omeprazole, 528 terbinafine, benfluorex, 529 pyribenzamine, penicillamine, isotretinoin, metronidazole530 and captopril.531 A pityriasis rosea-like eruption has also been recorded as a complication of graft-versus-host reaction, following bone marrow transplantation.532.
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5. Rapoport AM. Recurrent migraine: cost-effective care. Neurology 1994; 44 Suppl 3 ; : S25-8. 6. Goadsby PJ. Diagnosis and optimal treatment of migraine. CNS Drugs 1994; 1: 245-53. Welch KMA. Drug therapy of migraine. N Engl J Med 1993; 329: 1476-83. Stewart WF, Lipton RB, Celentano DD, Reed ML. Prevalence of migraine headache in the United States. JAMA 1992; 267: 64-9. Staffa JA, Lipton RB, Stewart WF. The epidemiology of migraine headache. Rev Contemp Pharmacother 1994; 5: 241-52. Fullerton T. Recent advances in the understanding and treatment of migraine. J Pharmacy Practice 1993; VI: 253-70. 11. Kubacka RT. Practical approaches to the management of migraine. Pharm 1994; NS34: 34-44. 12. Saxena PR. The pathogenesis and pharmacology of migraine. Rev Contemp Pharmacother 1994; 5: 259-69. Solomon GD. Therapeutic advances in migraine. J Clin Pharmacol 1993; 33: 200-9. Lance JW. Current concepts of migraine pathogenesis. Neurology 1993; 43 Suppl 3 ; : S11-5. 15. Silberstein SD. Serotonin 5-HT ; and migraine. Headache 1994; 34: 408-17. Olesen J, Lipton RB. Migraine classification and diagnosis. Neurology 1994; 44 Suppl 4 ; : S6-10. 17. Edmeads J. The diagnosis and treatment of migraine: a clinician's view. Eur Neurol 1994; 34 Suppl 2 ; : 2-5. 18. Baker C. Headache: keys to the differential diagnosis. Modern Medicine 1993; 61: 40-51.
SCPT is pleased to offer the latest installment of its annual Trainee Luncheon. The program features numerous clinical pharmacologists discussing career opportunities in industry, government, academia, and the military. Those in attendance will have an opportunity to engage in a two-way discussion with experts in the field on a variety of issues such as: Transition from a training program what to expect in the first 6 months on the job ; Long-term growth opportunities Advantages and disadvantages, likes and dislikes of the various types of positions available Salary expectations and other benefits THIS YEAR'S LIST OF FACULTY PARTICIPANTS INCLUDES.
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Reports of sudden deaths of children and adolescents treated with psychotropic medications have raised concerns regarding the appropriateness of this therapy, as well as the advisability of baseline and periodic electrocardiographic ECG ; monitoring of such patients.1 4 What follows is a review of the drug effects on the ECG, cardiovascular effects of the commonly used psychotropic medications in children and adolescents, a summary of potentially dangerous drug interactions, and recommendations for cardiovascular monitoring. tricular tachycardia, seem unlikely causes of sudden death in patients receiving psychotropic medications. Additionally, the rSR pattern in lead V1, sometimes referred to as incomplete right bundle-branch block or right ventricular conduction delay, is a normal childhood variant and is not a risk factor for sudden death.
