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Kenalog Preoperative and therapeutic local anesthetics and steroids.
Shavelson D.
New York College of Podiatric Medicine, New York.
In a recent survey that the author conducted among podiatrists, the typical therapeutic injection for inflammatory lesions consisted of 2.25 or 2.5 mL of 1% lidocaine or plain bupivicaine (or, rarely, with epinephrine 1:200,000), 0.5 mL of hexadrol, and 0.25 mL of an insoluble cortisone such as triamcinolone acetonide (Kenalog). It is clear that variation exists and that each doctor has his or her own "cocktail" for therapeusis. The author finds that 1% lidocaine with epinephrine 1:200,000 therapeutic injections alone have a profound clinical effect when used in concert with biomechanic control. These injections are given as a series once a week and then the interphase is stretched out as needed. Because no steroids are used, there is no limit to the number of injections, and so, for chronic entities such as metatarsophalangeal (MTP) joint osteoarthritis, the author has been giving certain patients 6 to 10 therapeutic injections a year for 15 to 18 years, while controlling pain. Because all "cocktails" usually contain some amount of local anesthetic, maybe the podiatric community is using added medications such as steroids unnecessarily. Steroids mask poor diagnostic and technical skills and also infections. Clinicians also should spend time controlling the pedal sympathetics through "chemical sympathectomy." This posterior tibial nerve and artery therapeutic block was developed by Dr. Marvin Steinberg in the 1940s. Treatments are given in 1-week intervals with the first treatment giving 3 to 5 days' relief, the second 5 to 7 days, the third 7 to 10 days, and then 2- and 4-week intervals. Eventually, a comfortable interphase is selected, if necessary. In order for the blocks to work in summation, a vasoconstrictor such as epinephrine is mandatory. Lidocaine is the active ingredient of chemical sympathectomy; it blocks the artery and nerve, including the posterior tibial sympathetics. The posterior tibial sympathetics control 85% of the sympathetics to the foot, including all four muscle layers and the vital structures of the sole of the foot. Epinephrine works at the vasovasorum, nervonervorum, vasonervorum, and nervovasorum to maintain the active medication longer and make the block more effective. This chemical sympathectomy works even better than a lumbar paravertebral sympathectomy.(ABSTRACT TRUNCATED AT 400 WORDS)
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1586907&dopt=Abstract triamcinolone Kenalog
Kenalog The effect of combined daunorubicin and triamcinolone acetonide treatment on a refined experimental model of proliferative vitreoretinopathy.
Chen EP, Steinhorst UH, Samsa GP, Saloupis PT, Hatchell DL.
Department of Ophthalmology, Duke University, Durham, North Carolina.
Prior studies have shown that intravitreal daunorubicin (9-15 nmol) and triamcinolone acetonide (2 mg) are effective individually in preventing retinal detachment in experimental proliferative vitreoretinopathy. This report compares the efficacy of the combination of daunorubicin (15 nmol) and triamcinolone acetonide (2 mg) with that of daunorubicin alone in a refined experimental model of proliferative vitreoretinopathy. The degree of retinal detachment in each treatment group was graded, with the unequivocal absence or presence of retinal detachment used as an indicator of treatment success or failure. Both treatments (daunorubicin alone and in combination with triamcinolone acetonide) effectively prevented retinal detachment. However, there was no significant difference in the rate of retinal detachment between the two treatment groups. These results indicate that combination therapy with daunorubicin/triamcinolone is no more effective at preventing retinal detachment than daunorubicin alone.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1607226&dopt=Abstract triamcinolone Kenalog
Kenalog [Suppression of pituitary-adrenal axis by triamcinolone acetonide in asthmatics]
[Article in Chinese]
Li XH, Zhong NS.
Guangzhou Institute of Respiratory Diseases.
To assess the inhibitory effect of triamcinolone acetonide on pituitary-adrenal axis, we measured plasma cortisol, plasma ACTH and performed short ACTH stimulation test before and after injection of 40 mg of triamcinolone acetonide intramuscularly in 34 asthmatic patients. At the same time salivary cortisol levels had been followed up for four weeks in ten of the 34 patients. Maximum adrenal suppression was found in two to three days after the administration. The suppression rates of salivary cortisol, plasma cortisol, plasma ACTH and ACTH stimulation test were 81.5%, 53.2%, 70% and 45.6% respectively. Such suppression lasted for two weeks. Afterwards the secretion of pituitary and adrenal glands recovered gradually. The secretion of plasma ACTH and salivary cortisol returned to normal in four weeks and that of plasma cortisol in five weeks. Triamcinolone acetonide, 40 mg monthly, is comparable with prednisone 10 mg daily, or oral dexamethasone 0.75 mg daily. The inhibitory effect of the steroids on pituitary-adrenal axis was in the order of dexamethasone, triamcinolone acetonide and prednisone.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1666866&dopt=Abstract triamcinolone Kenalog
Kenalog An approach to management of keloids.
Stucker FJ, Shaw GY.
Department of Otolaryngology-Head and Neck Surgery, Louisiana State University Medical Center, Shreveport 71130.
Keloids present a major therapeutic dilemma for the surgeon because of frequent recurrences. We use a new protocol for management of large primary or recalcitrant keloids. The technique employs carbon dioxide laser resection of the keloid and then allows the open wound bed to heal by secondary intention. The open wound is treated as though it were a third-degree skin burn. The wounds invariably orient their long axis parallel to the relaxed skin tension lines. No keloid has ever been noted to recur before epithelial migration is complete. Careful follow-up detects early recurrences that are then treated with injection consisting of 40 mg/mL of triamcinolone acetonide (Kenalog), 150 mg of hyaluronidase (Wydase), and 2% lidocaine via a dermajet. Thirty-seven patients were treated with this protocol and have been followed up for at least 2 years. A control rate of 84% has been achieved with compliant patients.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1728280&dopt=Abstract triamcinolone Kenalog
Kenalog The effect of budesonide and triamcinolone acetonide on hepatic microsomal testosterone metabolism in the rat.
Edwards RJ, Freeling AB, Watson D, Davies DS.
Department of Clinical Pharmacology, Royal Postgraduate Medical School, London, U.K.
The hepatic microsomal metabolism of testosterone was studied in male rats after treatment with either budesonide or triamcinolone acetonide for 13 weeks. The in vitro metabolism was determined using a testosterone concentration of 35 nM which is comparable to the levels found in plasma. It was shown that the total microsomal testosterone metabolism was decreased in budesonide-treated rats and increased in rats treated with triamcinolone acetonide. The testosterone metabolites produced were measured and thus it was revealed that budesonide treatment brought about its effect through a 50% decrease in the activity of steroid 5 alpha-reductase, but did not affect other reductive enzymes, or the oxidation of testosterone. Triamcinolone acetonide treatment decreased steroid 5 alpha-reductase activity by 95% and also decreased the activities of steroid 3 alpha- and 3 beta-reductases by more than 90%. In addition, treatment with triamcinolone acetonide caused a 50% increase in the oxidative metabolism of testosterone, which resulted in the observed increase in total testosterone metabolism. The presence of 0.1 microM budesonide in the microsomal incubations was without effect on testosterone metabolism. However, 0.1 microM triamcinolone acetonide inhibited testosterone oxidation by 65%, without affecting the reductive pathway of testosterone metabolism.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1739415&dopt=Abstract triamcinolone Kenalog
Kenalog Reversible effects of triamcinolone and lack of effects with aspirin or L-656,224 on external genitalia of male Sprague-Dawley rats exposed in utero.
Wise LD, Vetter CM, Anderson CA, Antonello JM, Clark RL.
Merck Sharp & Dohme Research Laboratories, Department of Safety Assessment, West Point, Pennsylvania 19486.
Inhibitors of the arachidonic acid cascade were given to pregnant rats during the critical period for morphogenesis of the external genitalia. Groups treated subcutaneously (s.c.) with 0.1 or 0.25 mg/kg/day of triamcinolone acetonide (TA) on gestational days (GD) 14-19 had male fetuses on GD 20 with moderate decreases in absolute anogenital distance (AGD), but gross and histological examinations revealed no alterations to the genital tubercle (i.e., no hypospadias). The s.c. coadministration of arachidonic acid at 100 mg/kg/day had minimal to no effect on AGD in the TA-exposed groups. No effect on AGD was observed in male fetuses from groups administered aspirin orally at 150 mg/kg/day, and only a 6% decrease was observed in the 300-mg/kg/day group. Neither TA nor aspirin adversely affected AGD of female fetuses. In another study, TA was administered on GD 11-19 at dose levels of 0.05 and 0.1 mg/kg/day, and dams were allowed to deliver. High-dose male offspring examined on postcoitum day (PCD) 23, had moderate decreases in AGD. In both studies with TA, there were also significant decreases in offspring weights. The contribution of the decreased weight to the decrease in absolute AGD was examined by a variety of methods (ratio of AGD to cube root of weight or biparietal distance, comparison to weight-matched controls, and covariance analysis). We conclude that TA caused a specific decrease in AGD on GD 20 that was largely reversed by PCD 23. When examined as adults (8 weeks old), the external genitalia of TA-exposed offspring were normal. Thus, the TA-induced decreases in AGD on GD 20 did not predict irreversible malformation. TA also caused other effects, which included a somewhat flattened genital tubercle and apparently thinned and glossy skin between the tubercle and the anus in both sexes on GD 20 and PCD 23, but not as adults. In addition, there were high pup mortality and high incidences of micrognathia and omphalocele (in the 0.25-mg/kg/day group only). Aspirin at 75 or 150 mg/kg/day and a specific lipoxygenase inhibitor (L-656,224) at 1,000 or 2,000 mg/kg/day were also administered from GD 14 to 19, and no offspring effects were observed. Thus, of the three agents that potentially inhibit the arachidonic acid cascade, only triamcinolone produced moderate effects on rat external genitalia that were largely reversible.(ABSTRACT TRUNCATED AT 400 WORDS)
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1771593&dopt=Abstract triamcinolone Kenalog
Kenalog (triamcinolone) References
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