Kenalog
In vivo protective effects of prophylactic treatment with tiaprofenic acid or intraarticular corticosteroids on osteoarthritic lesions in the experimental dog model.

Pelletier JP, Martel-Pelletier J.

University of Montreal, Rheumatic Diseases Unit Research Laboratory, Notre-Dame Hospital Research Center, PQ, Canada.

We examined the in vivo effects of prophylactic intraarticular corticosteroid injections and nonsteroidal antiinflammatory drugs (NSAID) (tiaprofenic acid) oral administration on cartilage lesions of osteoarthritis (OA) and osteophyte formation in 18 dogs in which the anterior cruciate ligament had been sectioned. Six of the dogs received no treatment; 5 had 3 injections of 5 mg triamcinolone hexacetonide at 0, 4 and 8 weeks postsurgery; and 7 were treated orally with 5 mg/kg/day tiaprofenic acid. The untreated dogs developed cartilage lesions on the tibial plateaus and femoral condyles with prominent osteophytes on both lateral and medial condyles. The number and size of the osteophytes were significantly reduced in the triamcinolone treated dogs (p less than 0.0001). Moreover, both triamcinolone and tiaprofenic acid treated groups showed a decrease in the grade and size of tibial plateau lesions, compared to the untreated dogs. There was a similar and statistically significant decrease in lesion size when the treated dogs (about 50 mm2) were compared to the untreated dogs (77 mm2). Histological studies revealed that both drugs also significantly decreased the severity of OA structural changes of the cartilage on both femoral condyles and tibial plateaus, although the response to triamcinolone was more pronounced. Our data confirm the effectiveness of prophylactic treatment with corticosteroids and tiaprofenic acid in preventing the progression of OA lesions in the dog model.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2027112&dopt=Abstract triamcinolone Kenalog



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Studies of variant palatal rugae in normal and corticosteroid-treated mouse embryos.

Sakamoto MK, Nakamura K, Handa J, Kihara T, Tanimura T.

Department of Anatomy, Kinki University School of Medicine, Osaka, Japan.

Fourteen- and 15-day mouse embryos treated with triamcinolone on day 11 of gestation were examined for the presence of variant rugae. Nontreated mouse embryos served as controls. Variant rugae found were classified into five types. All five types of variations (bifurcation, division, supernumerary, shortness and cross) were observed in triamcinolone-treated embryos, and shortness was most frequently seen. Supernumerary, bifurcation and division were ranked next, following by cross. Variant, rugae, except the cross, were also observed in non-treated embryos in low frequencies, but more than one-half of them were the bifurcation of the second ruga. Divided rugae ranked next, and supernumerary and shortness were found occasionally. Except for the bifurcated and supernumerary rugae, the greater part of the variant rugae were found in the fifth and fourth ruga in the triamcinolone-treated groups and in the fifth ruga in the nontreated groups. As the incidence of variant rugae in the triamcinolone-treated embryos was significantly higher than that in the nontreated, it was regarded as one of the changes induced by the corticoid. Based on the characteristic features of the rugal region, it is speculated that the formation of variant rugae is associated with the disturbance of normal epithelial-mesenchymal interaction which may be controlled by the nerve fibers appearing at the time of rugal formation. The relationship between the increased appearance of variant rugae and the failure of palatal shelf elevation was examined, but no direct evidence was obtained.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2064023&dopt=Abstract triamcinolone Kenalog



Kenalog
[The effect of triamcinolone acetonide on the liver mitochondria in endotoxemia]

[Article in Russian]

Natanzon LV, Artiukhina AI.

Endotoxin Salmonella typhimurium (LD50) was administered intraperitoneally to mice. It was shown that triamcinolone acetonide in a dose of 1 mg/kg living weight administered to mice 1 hour before endotoxin administration completely prevents the death of the animals and decreases the level of changes in the activities of enzymes of glutamate dehydrogenase, succinate dehydrogenase, monoaminoxidase, cytochrome oxidase in the liver mitochondria in endotoxemia. The level of lipid peroxidation in mitochondria during endotoxemia against the background of triamcinolone acetonide action is close to control. The use of triamcinolone acetonide in the absence of the effect of endotoxin results in an insignificant damage of mitochondrial membranes.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2081570&dopt=Abstract triamcinolone Kenalog



Kenalog
The effect of various steroid treatment regimens on cold-induced brain swelling.

Unterberg A, Schmidt W, Dautermann C, Baethmann A.

Department of Neurosurgery, Universitatsklinikum Rudolf Virchow, Free University of Berlin, Federal Republic of Germany.

The role of steroid therapy in brain oedema following acute cerebral lesions is still unsolved. This study was conducted to compare the efficacy of dexamethasone and triamcinolone, and to analyze the influence of timing and duration of treatment on cold-induced brain swelling. In rabbits, a cryogenic lesion of the left parietal cortex was induced. 24, or 48 hrs after trauma, hemispheric swelling, water- and electrolyte-contents were measured. A first series of animals received dexamethasone, triamcinolone or saline for 24 hrs, starting treatment 10 min after trauma. In a second series, steroid treatment lasted 48 hrs and in a third series the animals were additionally pretreated for 24 hrs. Dexamethasone and triamcinolone slightly decreased posttraumatic hemispheric swelling, from 7.7% in controls to 7.0% in treated animals. There was no significant difference between dexamethasone and triamcinolone. Reduction of swelling was most pronounced in animals with 48 hrs treatment. Pretreatment with steroids was not superior to early posttraumatic treatment. On the other hand, dexamethasone and triamcinolone significantly decreased cerebral water content in the traumatized and contralateral hemisphere, as well as in non-traumatized animals. The unspecific reduction of water content by steroids in rabbits might explain the moderate therapeutical effect on brain swelling. This effect might be beneficial, nevertheless, with respect to an improvement of the intracranial compliance.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2089872&dopt=Abstract triamcinolone Kenalog



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Corticosteroid regulation of gonadotropin and prolactin secretion in the rat.

Brann DW, Putnam CD, Mahesh VB.

Department of Physiology and Endocrinology, Medical College of Georgia, Augusta 30912-3000.

The purpose of this study was to determine if glucocorticoids had any direct effects on the release of gonadotropin. In estrogen-primed ovariectomized immature rats, triamcinolone acetonide and deoxycorticosterone (1 mg/kg BW) caused a surge in both serum LH and FSH levels. Dexamethasone treatment (0.05 mg/kg BW) resulted in a highly significant selective release of FSH. Cortisol (1 mg/kg BW) suppressed serum FSH levels. A systematic dose-response study showed that triamcinolone acetonide significantly released LH and FSH and suppressed PRL at all doses tested (range, 0.25-4 mg/kg BW). Deoxycorticosterone was not as potent as triamcinolone acetonide and only doses greater than 0.8-1 mg/kg BW significantly released LH and FSH. Dexamethasone selectively released FSH at low doses (0.01, 0.02, 0.05, and 0.1 mg/kg BW) and inhibited LH at higher doses (0.5 and 1.0 mg/kg BW). A single low dose of dexamethasone (0.02 mg/kg BW) was found to significantly release LH. With respect to PRL secretion, a biphasic effect of dexamethasone was observed in that the lowest dose (0.01 mg/kg BW) stimulated PRL release while the highest dose (1.0 mg/kg BW) significantly inhibited PRL release. Triamicolone acetonide and deoxycorticosterone were found to require estrogen priming for their effects on gonadotropin secretion. The findings in this study raise the possibility that the beneficial effects seen with corticosteroids in inducing ovulation in polycystic ovarian syndrome may be due, in part, to their direct effects upon the release of gonadotropins.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2104585&dopt=Abstract triamcinolone Kenalog



Kenalog
Corticosteroid regulation of gonadotropin secretion and induction of ovulation in the rat.

Brann DW, Putnam CD, Mahesh VB.

Department of Physiology and Endocrinology, Medical College of Georgia, Augusta 30912-3000.

In the human polycystic ovarian syndrome, glucocorticoids have been demonstrated to have beneficial effects in inducing ovulation in a number of cases. These beneficial effects were assumed to be due to suppression of adrenal overproduction of androgens. However, the possibility exists that glucocorticoids may directly regulate gonadotropin secretion and thereby improve menstrual rhythm and ovulatory activity. Herein, we report that the corticoid, deoxycorticosterone, and the synthetic glucocorticoid, triamcinolone acetonide, like progesterone (P4), are able to induce luteinizing hormone and follicle-stimulating hormone surges and facilitate ovulation in the pregnant mare serum gonadotropin-primed rat. This effect is not shared by cortisol. Prolactin release was also stimulated by deoxycorticosterone, cortisol, and progesterone, but not by triamcinolone acetonide. Similar to progesterone, triamcinolone acetonide and deoxycorticosterone administration caused a loss of fluid retention in the uterus. This effect of triamcinolone acetonide and deoxycorticosterone may be related to progesterone action as opposed to anti-inflammatory action since cortisol had no effect on uterine fluid retention. These findings raise the possibility that the beneficial effects seen with glucocorticoids in inducing ovulation in polycystic ovarian syndrome may be due in part to their direct effects upon the release of gonadotropins.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2106139&dopt=Abstract triamcinolone Kenalog