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Letteratura scientifica selezionata sul tema "STEROID-INDUCED HYPERTENSION"

Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 5 febbraio 2022

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Articoli di riviste sul tema "STEROID-INDUCED HYPERTENSION"

1

Pingale, Dr Sushma Vijay. "Peri-Operative Steroid Induced Hypertension- A Case Report". Journal of Medical Science And clinical Research 05, n. 03 (18 marzo 2017): 18999–9002. http://dx.doi.org/10.18535/jmscr/v5i3.112.

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2

Gerometta, Rosana, Steven M. Podos, John Danias e Oscar A. Candia. "Steroid-Induced Ocular Hypertension in Normal Sheep". Investigative Opthalmology & Visual Science 50, n. 2 (1 febbraio 2009): 669. http://dx.doi.org/10.1167/iovs.08-2410.

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3

Gerometta, Rosana. "Steroid-Induced Ocular Hypertension in Normal Cattle". Archives of Ophthalmology 122, n. 10 (1 ottobre 2004): 1492. http://dx.doi.org/10.1001/archopht.122.10.1492.

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4

Yülek, Fatma, Sıdıka Gerçeker, Emine Akçay, Özge Saraç e Nurullah Çağıl. "Corneal biomechanics in steroid induced ocular hypertension". Contact Lens and Anterior Eye 38, n. 3 (giugno 2015): 181–84. http://dx.doi.org/10.1016/j.clae.2015.01.011.

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5

De Bernardo, Maddalena, Francesco Antonio Salzano e Nicola Rosa. "Steroid-induced ocular hypertension after photorefractive keratectomy". Journal of Cataract & Refractive Surgery 44, n. 1 (gennaio 2018): 118. http://dx.doi.org/10.1016/j.jcrs.2017.10.048.

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6

Saady, Aya Mohammed, Heba M. Fouad, Abdussalam M. Abdullatif, Youssef A. H. Helmy, Tamer A. Macky e Khaled Mansour. "The value of prednisolone acetate provocative test before intravitreal triamcinolone acetonide injections". European Journal of Ophthalmology 30, n. 4 (12 aprile 2019): 730–37. http://dx.doi.org/10.1177/1120672119842731.

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Abstract (sommario):
Purpose: The aim of this study was to investigate the diagnostic value of a topical prednisolone acetate 1% provocative test for steroid-induced ocular hypertension before intravitreal triamcinolone acetonide injection. Methods: This is a prospective, single-center, randomized controlled study at Kasr El Aini Hospital, Cairo University. Patients scheduled for intravitreal triamcinolone acetonide were enrolled and randomly allocated in a ratio 2:1 to either Group A: received prednisolone acetate provocative test and those who did not develop SIOH proceeded with intravitreal triamcinolone acetonide or Group B: did not receive prednisolone acetate provocative test and proceeded directly to intravitreal triamcinolone acetonide. Intraocular pressures were measured weekly for 4 weeks following intravitreal triamcinolone acetonide. Steroid-induced ocular hypertension is defined as intraocular pressure increase of 5 mmHg or more from baseline after prednisolone acetate provocative test or intravitreal triamcinolone acetonide. Results: A total of 66 eyes (66 patients) were included. Of which, 10 eyes (23.8%) showed prednisolone acetate provocative test steroid-induced ocular hypertension during the 4-week period. Intravitreal triamcinolone acetonide steroid-induced ocular hypertension was less likely to develop in Group A (prednisolone acetate provocative test non-steroid-induced ocular hypertension, n = 32, 31.25%) than in group B (n = 24, 54.2%) (p = 0.006, odds ratio: 0.178, 95% CI: 0.53–0.596). Our test achieved a negative predictive value of 68.75%. Conclusion: The topical prednisolone acetate provocative test may be a useful method to predict a steroid-induced ocular hypertension following intravitreal triamcinolone acetonide.
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Zhan, Gui-Lin, Olivia CariÑo Miranda e Laszlo Z. Bito. "Steroid glaucoma: Corticosteroid-induced ocular hypertension in cats". Experimental Eye Research 54, n. 2 (febbraio 1992): 211–18. http://dx.doi.org/10.1016/s0014-4835(05)80210-6.

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Whitworth, Judith A., J. M. C. Connell, A. F. Lever e R. Fraser. "PRESSOR RESPONSIVENESS IN STEROID-INDUCED HYPERTENSION IN MAN". Clinical and Experimental Pharmacology and Physiology 13, n. 4 (aprile 1986): 353–58. http://dx.doi.org/10.1111/j.1440-1681.1986.tb00362.x.

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9

Kim, You Ra, Wan Seok Kang, Eui Yong Kweon, Nam Chun Cho e Dong Wook Lee. "Steroid-Induced Ocular Hypertension Model in the Mice". Journal of the Korean Ophthalmological Society 55, n. 8 (2014): 1202. http://dx.doi.org/10.3341/jkos.2014.55.8.1202.

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10

Klepikov, P. V., I. M. Kutyrina e I. E. Tareyeva. "Steroid-Induced Hypertension in Patients with Nephrotic Syndrome". Nephron 48, n. 4 (1988): 286–90. http://dx.doi.org/10.1159/000184944.

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Più fonti

Tesi sul tema "STEROID-INDUCED HYPERTENSION"

1

Lee, Yan-yee Jacinta. "Ultrastructural basis of steroid-induced ocular hypertension". Click to view the E-thesis via HKUTO, 2010. http://sunzi.lib.hku.hk/hkuto/record/B43957869.

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Lee, Yan-yee Jacinta, e 李茵怡. "Ultrastructural basis of steroid-induced ocular hypertension". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B43957869.

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3

Mangos, George Jack St George Clinical School UNSW. "MECHANISMS OF STEROID-INDUCED HYPERTENSION IN MAN AND RAT". Awarded by:University of New South Wales. St. George Clinical School, 1999. http://handle.unsw.edu.au/1959.4/32666.

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Abstract (sommario):
Models of steroid-induced hypertension in man and rat have been well characterized but the mechanisms by which ACTH and glucocorticoids raise blood pressure are not fully understood. Recently described paracrine (eg endothelial nitric oxide) and humoral (eg PHF) factors may be important in human essential hypertension. These factors were examined in cortisol-induced hypertension in man and ACTH-induced hypertension in the rat respectively. In man, the haemodynamic effects of ACTH can be attributed to the adrenal production of cortisol, but whether the major rodent glucocorticoid corticosterone is responsible for ACTH-induced hypertension in the rat has not been resolved. This question was examined in these studies. In male volunteers, exogenous cortisol raised blood pressure and suppressed endothelium-dependent vasodilatation, by a mechanism which may be nitric oxide synthase dependent. Although dexamethasone and fludrocortisone also raised blood pressure, attenuation of cholinergic vasodilatation was not observed. From these studies, the data suggest that the effect of cortisol on endothelium-dependent vasodilatation is unique to the endogenous hormone and not reproduced by synthetic agonists of GR or MR. Impaired endothelial vasodilator function may contribute to cortisol-induced hypertension in man. In the rat, exogenous corticosterone, administered in doses to achieve circulating concentrations similar to those observed in the experimental model of ACTH excess, reproduced the haemodynamic and some of the metabolic changes which characterize ACTH-induced hypertension. Further, like ACTH-induced hypertension, corticosterone-induced hypertension was prevented by L- but not D-arginine, and this effect was completely prevented by NOLA. It is likely that adrenal corticosterone mediates the hypertensive effects of ACTH excess. Parathyroidectomy had no significant effect on the rise in blood pressure secondary to ACTH excess. It is unlikely that PHF contributes to the model of ACTH-induced hypertension in the rat. The bioassay for the measurement of PHF could not be reproduced in our laboratory, leaving a question mark about the relevance of this putative factor in hypertension research.
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4

Opoku-Edusei, Justicia. "ROLE OF NEWLY SYNTHESIZED STEROID HORMONE ANTAGONISTS IN ADRENOCORTICO-STEROID HORMONE-INDUCED HYPERTENSION". VCU Scholars Compass, 1990. http://scholarscompass.vcu.edu/etd/4986.

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Abstract (sommario):
Excess adrenocorticosteroid hormones such as glucocorticoids and mineralocorticoids is well known to induce hypertension in several animal species as well as in humans. Therefore, the development of potent and specific glucocorticoid and mineralocorticoid antagonists with antihypertensive effects is clinically necessary. steroid hormone antagonists being used therapeutically present serious endocrinology side effects such as the widely used antimineralocorticoid, spironolactone. The antiglucocorticoids available so far have been active only in vitro or only weakly in viva. Recently, three new exciting adrenocorticosteroid hormone antagonists have been synthesized. RU 486 is a potent antiglucocorticoid (and antiprogesterone with potential as an abortifacient), RU 26752 and mespirenone, are novel mineralocorticoid antagonists. I studied the antihypertensive effect of RU 486, RU 26752 and mespirenone in Sprague- Dawley rats with dexamethasone- or aldosterone-induced hypertension. In addition, the effect of these antagonists on the hypertension developed by genetic model, spontaneously hypertensive rats (SHR) were also studied. The SHR is the closest animal model to human essential hypertension and it is believed that adrenocorticosteroid hormones are involved in the induction and maintenance of the hypertension. The results obtained from my studies showed that RU 486 administered simultaneously with dexamethasone prevented the hypertension induced by dexamethasone treatment. However, RU 486 had no effect on mineralocorticoid-induced hypertension. The administration of the antimineralocorticoid RU 26752 or mespirenone in combination with aldosterone successfully presented aldosterone-induced hypertension but not dexamethasone- induced hypertension. Surprisingly, RU 486 caused a significant increase in the blood pressure of the SHR whilst mespirenone caused a slight decrease in blood pressure as compared to control SHR. The effect of these antihormones on body/organ weights, fluid intake and urinary output was observed. Morphologically examination of the heart and kidney showed no abnormalities with treatment. These results suggest that 1) RU 486 is specific in preventing dexamethasone-induced hypertension; 2) RU 26752 and mespirenone are successful in preventing aldosterone-induced hypertension and 3) mineralocorticoids may be involved in the development and maintenance of hypertension in the SHR.
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Gerzenstein, Sabrina Melisa. "Pharmacogenomics of the Intraocular Pressure Response to Glucocorticoids". Scholarly Repository, 2009. http://scholarlyrepository.miami.edu/oa_theses/285.

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Abstract (sommario):
Glucocorticoids (GCs) have been widely used as a therapeutic agent for diverse inflammatory ocular diseases. However, a high percentage of patients undergoing this treatment develop high intraocular pressure (IOP), which if left unsupervised may lead to glaucoma. It is believed that the IOP elevation in response to GC treatment has a genetic determinant. In order to test this hypothesis, we analyzed in 52 patients the presence of single nucleotide polymorphisms (SNPs) in the glucocorticoid receptor gene (GR), the principal mediator of GCs uptake by the cells. We studied six GR SNPs previously reported to be associated with sensitivity and resistance to GCs: GluArg22/23GluLys (codon 22-23), Asn363Ser (codon 363), IVS2+646C>G (intron 2/BclI), IVS3-46G>C (intron 3), IVS4-16G>T (intron 4), Asn766Asn (Codon 766). Nevertheless, the results of this preliminary study did not show any specific correlation between SNPs in the GR gene and IOP elevation. Therefore, we proceeded to perform a whole genome SNP screen with the DNA samples of these patients to search for possible target genes responsible for the elevated IOP after GC treatment. As a result, we identified forty-eight SNPs in thirty-three genes that correlate with the high IOP response. The gene showing the strongest association is a poorly known G-protein coupled receptor. In addition, four SNPs hit a single transporter gene. Other candidate genes identified are a translation elongation factor, an F-box protein, an oxysterol binding protein, and a solute carrier family gene. These results support our hypothesis that IOP elevation following GC treatment is a genetically determined response. GCs are a common treatment for innumerable medical conditions; we believe that a genetic association between GC treatment and its physiological response may be important for improving treatment management and drug development for retinal diseases as well as for other medical ailments. However, further studies need to be performed to analyze in depth the association between the candidate genes identified in this study and the steroid response.
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Mangos, George Jack. "Mechanisms of steroid-induced hypertension in man and rat /". 1999. http://www.library.unsw.edu.au/~thesis/adt-NUN/public/adt-NUN20001113.155853/index.html.

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Libri sul tema "STEROID-INDUCED HYPERTENSION"

1

Huntbach, Julie, e Amar Alwitry. Glaucoma. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199237593.003.0007.

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Abstract (sommario):
The chapter begins by discussing optic nerve head anatomy and aqueous fluid dynamics, before covering the key clinical skills, namely optic nerve head assessment in glaucoma, tonometry and pachymetry , gonioscopy, and perimetry. It also covers the key areas of clinical knowledge, including ocular hypertension, primary open-angle glaucoma, acute angle closure, normal-tension glaucoma, steroid-induced glaucoma, traumatic glaucoma, inflammatory glaucomas, pseudoexfoliative and pigmentary glaucoma, neovascular glaucoma, malignant glaucoma, iridocorneal endothelial syndrome and iridocorneal dysgenesis, ocular hypotensive agents, laser therapy for glaucoma, and glaucoma surgery. The chapter concludes with three case-based discussions, on open-angle glaucoma, angle closure glaucoma, and steroid glaucoma.
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Tatham, Andrew, e Peng Tee Khaw. Glaucoma. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199672516.003.0008.

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Abstract (sommario):
This chapter explores glaucoma. It starts off with an outline of optic nerve head anatomy and then describes aqueous fluid dynamics and the pathogenesis of glaucoma. It then goes on to discuss the clinical skill areas of optic nerve head assessment in glaucoma, glaucoma imaging devices, tonometry and tachymetry, gonioscopy, and perimetry. The chapter also details ocular hypertension, primary open-angle glaucoma, primary angle closure, and secondary angle closure. In addition, it discusses normal tension glaucoma, steroid-induced glaucoma, traumatic glaucoma, inflammatory glaucomas, pseudoexfoliative glaucoma, pigmentary glaucoma, and neovascular glaucoma. It then covers aqueous misdirection, iridocorneal endothelial syndrome and iridocorneal dysgenesis, ocular hypotensive agents, laser therapy for glaucoma, and glaucoma surgery.
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Capitoli di libri sul tema "STEROID-INDUCED HYPERTENSION"

1

Clark, A. F. "Steroid-Induced Ocular Hypertension and Effects of Glucocorticoids on the Trabecular Meshwork". In Encyclopedia of the Eye, 219–23. Elsevier, 2010. http://dx.doi.org/10.1016/b978-0-12-374203-2.00099-3.

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Sethi, A., e A. F. Clark. "Steroid-Induced Ocular Hypertension and Effects of Glucocorticoids on the Trabecular Meshwork☆". In Reference Module in Neuroscience and Biobehavioral Psychology. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-12-809324-5.01523-6.

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