TABLE 1. Effect of betamethasone administration on maternal and fetal serum estradiol, DHAS, and cortisol concentrations in baboons at midgestation.
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SUMMARY The effect of vitamin E, betamethasone and mannitol upon a series of pathological free radical reactions within hypoxic brain tissue was evaluated by the chemiluminescence method. Hypoxia was induced by arterial hypoxemia PaC 217-22 mmHg ; with normocapnia PaCO2 28-38 mmHg ; and normotension MABP 100-140 mmHg ; . 4%C 2-96%N2 mixed gas was used to obtain the lowered PaO2. In the untreated group, increased chemiluminescence was measured in the hypoxic state and the early stage of the initial post-hypoxic state. In the groups administered vitamin E, betamethasone, mannitol and a combination of them reduced chemiluminescence was detected. To explore the reaction stage at which the drugs act in lipid peroxidation, chemiluminescence spectra was analyzed using the brain homogenate with the drugs added. Intensity peaks of the spectra were around at 480, 520-530, 570, nm before addition of the drugs. All the intensity peaks diminished after addition of vitamin E and betamethasone, but very little decrease occurred after mannitol. The lowered chemiluminescence value may indicate the free radical scavenging action of vitamin E, betamethasone and mannitol in vivo. Chemiluminescence spectroanalysis shows that vitamin E arid betamethasone act on the late chain reaction following hydroperoxide and mannitol acts on the early reaction -- generation of active Oxygens.
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1. Adams N, Bestall JM, Jones PW. Fluticasone versus beclomethasone or budesonide for chronic asthma. Cochrane Database Systematic Reviews, 2002: CD002310. 2. Ganguly S, Dutta S, Chakraborty S, Ghosh J. Iatrogenic Cushing's syndrome. Indian Pediatr 1998; 35: 1236 Clevenbergh P, Corcostegui M, Gerard D, Hieronimus S, Mondain V, Chichmanian RM, et al. Iatrogenic Cushing's syndrome in an HIV-infected patient treated with inhaled corticosteroids fluticasone propionate ; and low dose ritonavir enhanced PI containing regimen. J Infect 2002; 44: 194 Skov M, Main KM, Sillesen IB, Muller J, Koch C, Lanng S. Iatrogenic adrenal insufficiency as a side-effect of combined treatment of itraconazole and budesonide. Eur Respir J 2002; 20: 12733. Neidel J. Intra-articular steroid therapy for inflammatory rheumatic diseases in children and adolescents. Orthopade 2002; 31: 1175 Nelson HS, Stricker W, Casale TB, Raff H, Fourre JA, Aron DC, et al. A comparison of methods for assessing hypothalamic-pituitaryadrenal HPA ; axis activity in asthma patients treated with inhaled corticosteroids. J Clin Pharmacol 2002; 42: 319 Casale TB, Nelson HS, Stricker WE, Raff H, Newman KB. Suppression of hypothalamic-pituitary-adrenal axis activity with inhaled flunisolide and fluticasone propionate in adult asthma patients. Ann Allergy Asthma Immunol 2001; 87: 379 Boner AL. Effects of intranasal corticosteroids on the hypothalamic-pituitary-adrenal axis in children. J Allergy Clin Immunol 2001; 108: S329. 9. Gupta D, Behera D, Lalrinmawia H, Dash RJ. Hypothalamopituitary-adrenal axis function in asthmatics taking low dose inhaled beclomethasone dipropionate. J Assoc Phys India 2000; 48: 682 Jarvis B, Faulds D. Inhaled fluticasone propionate: a review of its therapeutic efficacy at dosages 500 g day in adults and adolescents with mild to moderate asthma. Drugs 1999; 57: 769 Dluhy RG. Clinical relevance of inhaled corticosteroids and HPA axis suppression. J Allergy Clin Immunol 1998; 101: S44750. 12. Alsaeedi A, Sin DD, McAlister FA. The effects of inhaled corticosteroids in chronic obstructive pulmonary disease: a systematic review of randomized placebo-controlled trials. J Med 2002; 113: 59 Arthur KE, Wolff JC, Carrier DJ. Analysis of betamethasone, dexamethasone and related compounds by liquid chromatography electrospray mass spectrometry. Rapid Commun Mass Spectrom 2004; 18: 678 Guan F, Uboh C, Soma L, Hess A, Luo Y, Tsang DS. Sensitive liquid chromatographic tandem mass spectrometric method for the determination of beclomethasone dipropionate and its metabolites in equine plasma and urine. J Mass Spectrom 2003; 38: 82338. Noben JP, Gielen B, Royackers E, Missotten M, Jacobs A, Raus J. A high-performance liquid chromatography tandem mass spectrometric screening method for eight synthetic corticosteroids in bovine feces and the simultaneous differentiation between dexamethasone and betamethasone. Rapid Commun Mass Spectrom 2002; 16: 1590 Van Den Hauwe O, Perez JC, Claereboudt J, Van Peteghem C and urecholine.
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Sixteen pregnant Border LeicesterMerino crossbred ewes of known gestational age were used in this study. The animal experiments were approved by the Monash University Standing Committee on Ethics in animal experimentation. Ewes underwent surgery between 118 and 125 days of gestation to implant electromyogram electrodes. Electrodes were implanted into the myometrium to enable labour onset to be identified Harding et al., 1982 ; . A paired treatmentcontrol experimental paradigm was used in the first part of the study to determine the effects of glucocorticoid on PGHS expression. Fetal sheep were injected using guided ultrasonography via maternal transabdominal injection ; with either glucocorticoid betamethasone; Celestone Chronodose, Schering Plough Pharmaceuticals, Baulkham Hills, NSW; 5.7 mg ml1 in 1 ml total volume; n 5 ; or an equivalent volume of sterile isotonic saline control; n 5 ; on day 131 of gestation. Animals that received betamethasone were killed by i.v. barbiturate injection when labour was established. Labour onset occurred 56.6 0.8 h after glucocorticoid injection and was determined from increased uterine electromyogram activity and clinical factors such as swelling of the maternal Immunohistochemistry was performed using the DAKO ENVISIONTM System DAKO Corporation, Carpinteria, CA ; . After paraffin wax was removed from the tissue sections, they were incubated with 0.03% w v ; H2O2 for 5 min to quench endogenous peroxidase activity. Tissue sections were incubated for 1 h at room temperature with PGHS-1 or PGHS-2 antibody at 1: 1000 dilution. PGHS-1 antiserum was raised in rabbits against ram seminal vesicle PGHS McLaren et al., 1996 ; . PGHS used for injection 99% purity ; was purchased from the Oxford Biochemicals Company Oxford, MI ; . The crossreactivity of the antibody with the PGHS-2 isozyme was estimated to be 0.1%, as determined from laser densitometry McLaren et al., 1996 ; . The polyclonal PGHS-2 antiserum, raised in rabbits against murine PGHS-2, was purchased from the Cayman Chemical Company Ann Arbor, MI ; . There was no detectable crossreactivity of the PGHS-2 antibody with PGHS-1 protein at amounts up to 2.5 mg as determined from western blot analysis; McLaren et al., 1996 ; . After washing with Tris-buffered saline TBS ; pH 7.5 ; , the sections were incubated with peroxidaselabelled polymer conjugated to goat anti-rabbit IgG second antibody for 30 min. Slides were rinsed once and the substratechromogen solution was added for 10 min. Specific immunostaining was identified using diaminobenzidine. The sections were counterstained with Harris' and bicalutamide.
Effects of betamethasone on HO-2 expression in cerebral microvessels in vivo. To investigate whether glucocorticoids affect HO expression in the cerebral microcirculation in vivo, newborn pigs were treated with two doses of betamethasone 0.2 and 5.0 mg kg ; administered intramuscularly two times over a 48-h period. We found that HO-2 expression in cerebral microvessels was increased by 3060% in piglets treated with both low and high doses of betamethasone Fig. 4 ; . HO-1 and HO-2 localization in quiescent endothelial cells. HO localization was investigated using indirect immunofluorescence with isoform-specific antibodies. For these purposes, we used antibodies raised against a purified recombinant HO-1 ; or native HO-2 ; protein StressGen ; followed by FITCconjugated anti-rabbit IgG dilution, 1: 100 ; . In quiescent endothelial cells, HO-2 has multiple localization sites that include the nuclear envelope, the perinuclear zone of the cytoplasm, and a wide area of the cytoplasm around the nucleus Fig. 5B ; . In the cytoplasm, a.
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The assumption that local references normally convey only one single hierarchical level, as in "this chapter", which would be inappropriate for the present analysis. The difficulties in identifying books with the desired structure and layout, and the low frequency of descriptions with the required characteristics makes this method a rather labour-intensive task. We manually examined hundreds of books, most of which simply did not meet our criteria. Among the suitable candidates, it was often the case that we could not identify non-local references, since many authors seemed to avoid reference across chapters etc. As a result, the identified referring expressions below ; were taken from twelve books written by different authors on various fields of knowledge, from Psychology to Economics, and released between the years of 1967 and 1999 by different publishers. These books are listed in Appendix 2. In the twelve books meeting the above criteria, we identified 41 instances of Document.
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DR. FRIEDMAN: But a couple of other points. One, can these particular drugs, their primary use, we are dealing with chronic conditions, conditions that last years, sometimes many years, and so the drugs are intended for use over those many years potentially. Yet, most of the clinical trials we heard reported yesterday are 12, 18 weeks, a few of them go longer. You mentioned that one of the reasons we didn't see the problems early on may be numbers, and I agree that is potentially it, but the fact is we didn't see problems arise in the studies until 14, 18 months. We often see analyses by patient years of exposure. In this particular setting, I don't know whether patient years are always equal to patient years, and therefore, I guess I would say why aren't we doing more bigger, longer randomized clinical trials for these chronic conditions?.
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TABLE 2 use corticosteroids if they are indicated for him or her ; at the RAS * THERAPY: COMMON ADVERSE EFFECTS OF prodromal stage to abort the DRUGS TO BE USED SYSTEMICALLY ONLY BY attacks. Treatment often includes the ORAL MEDICINE SPECIALISTS. use of a chlorhexidine mouthDRUG POSSIBLE ADVERSE EFFECT S ; wash without alcohol base ; , and a short course of topical corticosPainful gastrointestinal symptoms, diarrhea, male infertility Colchicine teroids as soon as the ulcers Methemoglobinemia Dapsone appear. Because of the consistent Decreased white blood cell count Levamisole recurrent pattern, these patients may need a maintenance treatNausea Pentoxifylline ment protocol. Teratogenicity, polyneuropathy, mood change Thalidomide Alternative regimens include dexamethasone 0.05 milligrams * RAS: Recurrent aphthous stomatitis. 5 mL rinse and spit three times per day ; or a high-potency topical corticosteroid such as clobetasol ointment 0.05 courses of RAS in which by the time one ulcer percent in Orabase 1: ; Colgate Oral Pharmaheals, another develops. ceuticals, Canton, Mass. ; or fluocinonide ointThese patients are best treated by an oral ment 0.05 percent in Orabase 1: ; if the ulcer s ; medicine specialist, who often will use potent recur on the same site, used three times daily topical corticosteroids such as betamethasone, Figure 5 ; . If corticosteroids are used, patients beclomethasone, clobetasol, fluticasone or fluocishould be monitored for yeast superinfection.49 In nonide ; , systemic corticosteroids, azathioprine or patients with poor oral hygiene, professional help other immunosuppressants such as dapsone, from a dental hygienist should be considered once pentoxifylline and sometimes thalidomide.50 ulcers heal. Table 2 shows the potential adverse effects of In patients with recalcitrant RAS, a short these agents. course of systemic corticosteroid therapy may be In addition, oral medicine specialists may required, never exceeding more than 50 mg per administer intralesional injections of a corticosday preferably in the morning ; for five days. This teroid such as betamethasone, dexamathasone or course of treatment is best left to a physician or triamcinolone to enhance or boost the local oral medicine specialist. response, thus allowing for shorter systemic Type C. Type C RAS involves painful, chronic treatment. In patients with poor oral hygiene.
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En-18-al ; , beclomethasone dipropionate 9ac-chlorolII, - hydroxy - 16fi - methyl - 17, 21 - dipropionyloxypregna-1, 4-diene-3, 20-dione ; , betamethasone 9axfluoro - 1 , 17, 21 - trihydroxy - 16, B methylpregna1, 4-diene-3, 20-dione ; , chlormadinone acetate 17acetoxy-6-chloropregna-4, 6-diene-3, 20-dione ; , corticosterone 1 lfl, 21-dihydroxypregn-4-ene-3, 20-dione ; , cortisol 1 , 17, 21-trihydroxypregn-4-ene-3, 20dione ; , cortisone 17, 21-dihydroxypregn-4-ene-3, 1 ; , equilenin [3-hydroxyoestra-1, 3, 5 10 ; , 6, 8pentaen-17-one], fludrocortisone 9x-fluoro-1Ifl, 17, 21-trihydroxypregn-4-ene-3, ; , flumethasone 6a, 9a difluoro 1 , 17, 21 trihydroxy 16a methylpregna-1, 4-diene-3, 20-dione ; , fluocinolone 6a, 9adifluoro - Ill, 21 - dihydroxy- 16a, 17a- isopropylidenedioxypregna-1, 4-diene-3, 20-dione ; , fluocortolone 6a-fluoro- 1 Bfl, 21 -dihydroxy-I 6a-methylpregna1, 4-diene-3, 20-dione ; , fluorometholone 9a-fluoro1 1 17 dihydroxy 6ac methylpregna 1, 4 diene3, 20-dione ; , fluperolone acetate 21-acetoxy-9afluoro - 1 , B17 - dihydroxy - 21 methylpregna 1, 4diene-3, 20-dione ; , fluprednisolone 6a-fluoro-1 Ifl, 17, 21-trihydroxypregna-1, 4-diene-3, ; , flurandrenolone 6a-fluoro-11, 21-dihydroxy-16a, ; , paramethasone acetate 21-acetoxy-6a-fluoro-1lfl, 17-dihydroxy-16a-methylpregna-1, 4-diene-3, ; , prednisone 17, 21 -dihydroxypregna-1, 4-diene-3, 11, 20trione ; , progesterone pregn-4-ene-3, 20-dione ; , testosterone 17fl-hydroxyandrost-4-en-3-one ; and triamcinolone 9ac-fluoro- 1l, 16oc, ; . Preparation of dexamethasone 21-hemisuccinate. Dexamethasone 21-hemisuccinate was prepared by a method similar to that used by Erlanger et al. 1959 ; for deoxycorticosterone 21-hemisuccinate 21-hydroxypregn-4-ene-3, 20-dione ; . The compound was recrystallized from aqueous methanol to give white needles, m.p. 137-139C. The yield was 33% of theoretical. The purity and identity of the compound were confirmed by t.l.c., i.r. spectroscopy.
A study has been performed comparing the ability of a foam formulation to release the active ingredient betamethasone benzoate ; with ointment, gel, and cream formulations.[5] It was found that the release of betamethasone benzoate from the ointment, gel, and foam formulations was similar, but better than the release from the cream. This was one of the first investigations into the use of foams in dermatology and illustrates the usefulness of this type of formulation. A foam formulation of the superpotent corticosteroid, clobetasol propionate, has demonstrated anti-inflammatory, antipruritic, and vasoconstrictive properties.[9, 11] In patients with moderate to severe scalp psoriasis, topical application of clobetasol propionate foam 0.05% ; twice daily for 2 weeks resulted in significant improvement of all signs and symptoms of the disease compared with placebo and clobetasol propionate solution 0.05% ; . Furthermore, patients who received clobetasol propionate foam demonstrated greater improvement of scaling after 2 weeks of treatment, and after 2 weeks of follow-up. There are only a limited number of reports in the literature concerning the use of foam formulations in other fields of dermatology or nondermatological fields. Nonsteroidal anti-inflammatory and antifungal agents are among the other drug families that have been formulated into foam products, while nonoxynol-9 foam[12] has been used vaginally as a contraceptive, and chlorhexidine gluconate foam has been used as a preoperative application.[13] If one considers that drug delivery to the alimentary canal and mucosae may be classified as `topical' delivery in the classical sense, then one may include rectal foam products in this discussion of dermatological foams. Prednisolone, hydrocortisone, beclomethasone dipropionate, and mesalazine foams have been applied rectally in ulcerative colitis and the treatment of postepisiotomy pain and erythema. A.
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Betamethasone beyond 8 to 10 has led to erroneous conclusions about the acetate prodrug. In contrast, studies conducted by Ballard et al. 1975 ; have examined the clinical dosing regimen of two doses of 12-mg betamethasone phosphate acetate 24 h apart. Based on the half-life obtained from this study and information from betamethasone phosphate studies in nonpregnant subjects, Ballard has stated that the dual formulation does have sustained-release properties Ballard, 1986; Ballard and Ballard, 1995 ; . The terminal half-life of 6 h reported by Ballard is the widely accepted half-life for betamethasone after administration of the dual formulation Padbury et al., 1996; Dudley et al., 2003 ; . Although Ballard made an insightful and accurate conclusion about the dual-release properties of the phosphate acetate formulation, the commonly accepted half-life is probably incorrect. Based on the data in Fig. 2, it is obvious that the true terminal decline phase of betamethasone from the acetate prodrug will be missed if the profile is followed for any duration less than 2 to 3 days. In light of this new finding, dosing recommendations for betamethasone formulations need to be reassessed. This finding is particularly important because, in the United States, the only injectable form of betamethasone recommended and available for antenatal use is the dual formulation. Betamethasone sodium phosphate injection now appears in the "discontinued" section of Food and Drug Administration's Orange Book because Schering-Plough discontinued the manufacture of this product in May 2002. Furthermore, many clinicians have adopted the practice of giving multiple doses as many as 11 repeat courses ; of betamethasone to enhance fetal lung maturation Andrews and Matthews, 2003 ; . The prolonged half-life for betamethasone from the intramuscular depot combined with multiple dosing can have accumulative and unfavorable effects in the mother and fetus, and this will be discussed below. Implications of a Prolonged Half-Life on Fetal and Maternal Health. Results from Fig. 4 indicate that both betamethasone formulations produce similar early exposures, but the dual formulation could have a lower safety index. This is supported by the fact that efficacy of both formulations has been demonstrated in pregnancy trials. However, a recently conducted meta-analysis Jobe and Soll, 2004 ; has shown that betamethasone use in pregnancy might be associated with a higher incidence of maternal infections as compared with dexamethasone. The majority of the betamethasone trials in the meta-analysis used the dual formulation, whereas dexamethasone was exclusively used as the phosphate prodrug. The mother serves as a delivery mode and reservoir for the steroid and is exposed to betamethasone levels 3 times higher than that in the fetus. The practice of exposing the parturient mother to steroid levels that are of no therapeutic benefit to her and probably lead to adverse effects is unfortunate. Reassessment of use of this dual-formulation regimen during pregnancy is warranted. Several assumptions have been made in arriving at the conclusion regarding the reassessment of corticosteroid dosing regimens during pregnancy. These conclusions need to be supported by additional long-duration experimental data on corticosteroid pharmacokinetics, adrenal suppression, and fetal drug exposure from different formulations during pregnancy. Corticosteroids have been used for precocious induction of fetal lung maturation for over 30 years. However, the pharmacokinetic, pharmacodynamic, and toxicodynamic properties of corticosteroids in pregnancy are poorly understood and can be improved by well designed mechanistic studies using modern analytical tools. Acknowledgments. We thank Donna Ruszaj for helpful discussions and technical assistance with LC MS MS assay development.
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In a follow-up program; no patient has reported an allergic reaction to a drug that we had exonerated on the basis of a negative drug provocation result. If not included in the diagnostic procedure, important cofactors, such as exercise or sunlight, may sometimes explain the negative results 6 ; . Tolerance induction during the provocation, although never documented in the literature, may also explain a false-negative result. In our hands, drug provocation tests were effective and safe. With careful selection of patients, the progressive administration of the drug with a very small starting dose Table 1 ; , and strict medical surveillance, no positive reaction was too severe to respond promptly to treatment. We could reproduce the initial episode with the same chronology but with milder clinical symptoms and signs. Drug provocation tests are still serious and potentially dangerous procedures 6 ; . Documenting the patient's personal details, medical history, and concomitant drug therapy and the availability of full resuscitation facilities during the tests are important. Generally, drug provocation tests with a suspected drug should not be performed on patients with severe comorbid illnesses that is, underlying cardiac, hepatic, renal, or other diseases ; 6 ; . We excluded these patients from our present study, but exceptions may be permissible if the suspected drug is essential to the patient. Conversely, absolute contraindications to rechallenge with medication include patients who have had severe lifethreatening reactions, such as vasculitis, the StevensJohnson syndrome, toxic epidermal necrolysis, drug reaction with eosinophilia and systemic symptoms, and organ involvement. Although very rare, these reactions, if reactivated, may not be controlled medically. We excluded 230 patients. Among them, 125 patients had clinical histories that were not compatible with immediate drug hypersensitivity reactions nonimmediate reaction, suspected drugs not stopped, chronology, and clinical symptoms and signs not compatible ; . To exclude hypersensitivity in a patient whose history does not suggest drug allergy, the European Academy of Allergology and Clinical Immunology 6 ; proposes drug provocation tests. Most patients excluded were so convinced that they were drug allergic that they underwent drug provocation tests 148 patients ; . The test results were all negative. Among patients excluded from the study were 92 patients who received a positive result on a skin test for -lactams and later had drug provocation tests performed with other -lactam alternatives. These test results were also negative data not shown ; . These results demonstrate the utility of drug provocation tests in diagnosing suspected drug hypersensitivity reactions and in searching for appropriate alternative drugs.
Aerosols containing greater amounts of medicament may be administered more rapidly.
Chronic Diseases Flavonoids - Disease Prevention Oxidative Stress Date: June 30, 2003 Effects of Flavonoid Intake on Oxidative Stress-related Chronic Diseases Knekt P, Kumpulainen J, Jarvinen R, et al. Flavonoid intake and risk of chronic diseases. American Journal of Clinical Nutrition. 2002; 76: 560-568. Free oxygen radicals may be involved in the development of atherosclerosis, cancer, diabetes, asthma, rheumatoid arthritis, and cataract. Flavonoids are products of plant metabolism and are effective antioxidants; thus, they protect tissues against free oxygen radicals. Different flavonoids have different chemical structures and may have different effects on health. This study evaluated the effects of flavonoid intake on chronic diseases associated with oxidative stress. The Finnish Mobile Clinic Health Examination Survey collected questionnaires from 65, 440 people from 1966 to 1972. A thorough dietary history of each participant was collected. In 1997, intakes of flavonoids and nutrients were evaluated for all food items by collecting fruits, berries, vegetables, and beverages as well as performing chemical analyses. Incidence of cerebrovascular disease, cancer, asthma, type 2 diabetes, cataract, and rheumatoid arthritis were assessed 28-30 years later. People with a higher flavonoid intake tended to have a lower total mortality. The association was mainly due to quercetin intake, especially from apples, onions, and oranges. Ischemic heart disease tended to be lower at higher quercetin and kaempferol intakes. Apple and onion intakes were significantly associated with a decrease in ischemic heart disease mortality. The incidence of cerebrovascular disease leading to hospitalization or death was lower at higher intakes of kaempferol, hesperetin, and naringenin. Orange, white cabbage, and grapefruit intakes showed the strongest associations with cerebrovascular occurrence. Apple intake showed a significant association for thrombotic stroke. The total cancer incidence was significantly lower at higher quercetin intakes, especially for lung cancer risk in men. Prostate cancer risk was lower at higher myricetin intakes, and breast cancer risk tended to be lower at higher quercetin intakes. There was no association between flavonoid intake and occurrence of cancers of the stomach, colorectum, or urinary organs. Apple intake was strongly associated with a lower risk of lung cancer. A higher intake of kaempferol was related to a high risk of rheumatoid arthritis. Intake of white cabbage was strongly associated with an increase in rheumatoid factor-positive disease.
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