Evaluation of exogenous glucocorticoid injection on preweaning growth performance of neonatal pigs under commercial conditions.
(1/6)
Three commercial trials were conducted to evaluate the use of dexamethasone (Dex) and/ or isoflupredone (Predef) in improving preweaning growth performance of neonatal pigs. The objectives of the commercial trials were threefold: 1) to evaluate Predef in comparison with Dex; 2) to address the sexual dimorphic growth response observed in a previous commercial trial; and 3) to determine whether there is any benefit of providing Dex treatment to pigs being fed supplemental milk. In Exp. 1, 276 pigs (Triumph 4 x PIC Camborough 22) were assigned according to birth weight and sex to three treatments. Treatments included saline (Control), Dex (2 mg/kg BW i.m. injection of Dex), or Predef (2 mg/kg BW i.m. injection of Predef 2X) within 24 h after birth. A treatment effect was observed for BW at weaning (P < 0.001), with pigs injected with Predef being 0.51 kg lighter than Control and Dex-treated pigs. The lower BW of Predef-treated pigs at weaning were a result of a lower ADG (P < 0.001) during the preweaning period compared with Control and Dex pigs. In Exp. 2, 703 pigs (Triumph 4 x PIC Camborough 22) were assigned according to birth weight and sex to three treatments. Treatments included either an i.m. injection of saline (Control), Dexl (1 mg/kg BW of Dex), or Dex2 (2 mg/kg BW of Dex) within 24 h after birth. No treatment effects were observed for BW at weaning (P = 0.24) or ADG (P = 0.19). In Exp. 3, 342 pigs (Genetiporc) were assigned according to birth weight and sex to two treatments. Treatments included either an i.m. injection of saline or Dex (2 mg/kg BW) within 24 h after birth. All pigs were provided supplemental milk from the time of treatment until weaning age. No treatment effects were observed for BW at weaning (P = 0.13) or ADG (P = 0.11). The negative response to Predef was similar to the growth-suppressive effects observed by others using chronic glucocorticoid treatment. In contrast to our previous findings, Dex did not improve preweaning growth performance regardless of dose or supplemental milk. (+info)
Effect of corticotherapy on proteomics of endometrial fluid from mares susceptible to persistent postbreeding endometritis.
(2/6)
A fifty-two-week chronic toxicity study of halopredone acetate (THS-201) in dogs.
(3/6)
In order to evaluate the long-term-safety of halopredone acetate (THS-201: 17 alpha, 21-diacetoxy-2-bromo-6 beta, 9 alpha-difluoro-11 beta-hydroxy-1, 4-pregnadiene-3, 20-dione), a 52-week chronic toxicity study was performed on the basis of its local accumulation in dogs. In doses of 0.1, 0.5 and 2.5 mg/kg, THS-201 was injected into the right knee joint in both sexes of dogs every 2 weeks for 39 weeks and withdrawn for 13 weeks. In this study, the below slight local changes were observed in both sexes of dogs treated with 2.5 mg/kg/2 weeks of THS-201: focal loss of hair of the injection site, lesser stain in cartilage matrix of articular cartilage and meniscus in light microscopic examinations, and irregular thickness and elongation of collagen fibers, roughness of fibrous density and decrement of proteoglycans in electron microscopic examinations. In conclusion, systemic adverse effects were not observed in any dogs treated with THS-201. (+info)
Glucocorticoid induced stress susceptibility in swine: adrenocortical pathology.
(4/6)
The studies reported here were undertaken to better characterize the role of the adrenal cortex in the increased susceptibility to stress observed in porcine stress syndrome. Since adrenal hypofunction was suggested during early studies as a factor in events leading to porcine stress syndrome it was decided to produce such a state by the exogenous administration of the glucocorticoids prednisolone and fluoroprednisolone.A total of 34 pigs (weighing 90 to 100 kg) received a series of graded doses (given intramuscularly) of one or the other of the foregoing compounds and were necropsied 48, 72, and 120 hours after the last treatment. The major adrenocortical changes produced by these treatments were atrophy, an accentuation of degenerative changes which could be observed in milder form in many of the 30 control pigs examined, a marked increase in stainable lipid 120 hours after the last fluoroprednisolone treatment and, ultrastructurally, an increase in lysosome-like bodies and cellular debris ("myelin bodies").Adrenocortical atrophy is not a feature of porcine stress syndrome nor were the localized depositions of stainable lipid within the zona reticularis, described in porcine stress syndrome, found in the glucocorticoid treated pigs. Consequently, the findings reported here bear a somewhat limited resemblance to those observed in pigs affected by porcine stress syndrome and cast some doubt on whether adrenal hypofunction plays a role in the pathogenesis of the latter condition. (+info)
Severe hypertension in childhood due to prolonged skin application of a mineralocorticoid ointment.
(5/6)
We report the case of a 9-year-old boy suffering from exzematous dermatitis who was treated for 6 years with a daily dose of 100 mg of a dermatological ointment containing 9 alpha-fluoroprednisolone-21-acetate. At examination the patient's blood pressure was persistently 230/160 mm Hg and was considered essential in origin after secondary forms of arterial hypertension had been excluded. Treatment with nifedipine and labetalol lowered the blood pressure to 150/100 mm Hg. When we became aware of the dermatological treatment, we advised its discontinuance. In the subsequent 7 days, the blood pressure fell to hypotensive levels (75/40 mm Hg) and then became normal a few days after discontinuance of the antihypertensive therapy. This case suggests that prolonged use of topical steroids, commonly prescribed for skin diseases, may cause hypertension, especially in childhood. (+info)
Cell membrane sialoglycopeptides of corticoid-sensitive and -resistant lymphosarcoma P1798.
(6/6)
Cells of corticoid-sensitive (CS) and corticoid-resistant (CR) lymphosarcoma P1798 were labeled in vivo with either [14C]- or [3H]fucose before and after treatment with 9-alpha-fluoroprednisolone (9-FP). Labeled glycopeptides, derived from isolated, Pronase-digested cell membranes of both tumors were separated by gel filtration on Bio-Gel P-10 by a double-label technique. Elution profiles of CS and CR fractions showed significant differences in early eluting material. Desialylation of glycopeptides by neuraminidase lowered the molecular weight of both CS and CR fractions, and altered 3H:14C ratios indicated that CS and CR sialoglycopeptides are different. 9-FP treatment for 7 hr increased the density of isolated P1798-CS and -CR cell membranes. All CS and CR glycopeptides from treated tumors eluted faster than did those of untreated preparations. Both CS and CR sialoglycopeptides were altered, although differences in CS and CR profiles persisted. Histochemical investigations indicated that negative charge, present on surfaces of untreated CS cells, is lost between 6 and 8 hr after exposure in vivo to 9-FP. CR cells had no or few anionic sites on their surfaces before and after steroid administration. We demonstrated that glycopeptides of both CS and CR tumors contain sialic acid, although only CS cells carry a surface-exposed negative charge that is lost after 9-FP treatment. Glucocorticoids alter both P1798-CS and -CR sialoglycopeptides, but the consistent differences between their chromatographic patterns suggest that steroid-induced changes in cell membranes of the two tumors are not identical. Cell death or survival of glucocorticoid-treated P1798 cells may, therefore, be influenced by specific structural characteristics involving cell surface sialoglycoproteins. (+info)