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Journal articles on the topic 'STEROID-INDUCED HYPERTENSION'

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Published: 4 June 2021

Last updated: 5 February 2022

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1

Pingale, Dr Sushma Vijay. "Peri-Operative Steroid Induced Hypertension- A Case Report." Journal of Medical Science And clinical Research 05, no. 03 (March 18, 2017): 18999–9002. http://dx.doi.org/10.18535/jmscr/v5i3.112.

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2

Gerometta, Rosana, Steven M. Podos, John Danias, and Oscar A. Candia. "Steroid-Induced Ocular Hypertension in Normal Sheep." Investigative Opthalmology & Visual Science 50, no. 2 (February 1, 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, no. 10 (October 1, 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, and Nurullah Çağıl. "Corneal biomechanics in steroid induced ocular hypertension." Contact Lens and Anterior Eye 38, no. 3 (June 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, and Nicola Rosa. "Steroid-induced ocular hypertension after photorefractive keratectomy." Journal of Cataract & Refractive Surgery 44, no. 1 (January 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, and Khaled Mansour. "The value of prednisolone acetate provocative test before intravitreal triamcinolone acetonide injections." European Journal of Ophthalmology 30, no. 4 (April 12, 2019): 730–37. http://dx.doi.org/10.1177/1120672119842731.

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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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7

Zhan, Gui-Lin, Olivia CariÑo Miranda, and Laszlo Z. Bito. "Steroid glaucoma: Corticosteroid-induced ocular hypertension in cats." Experimental Eye Research 54, no. 2 (February 1992): 211–18. http://dx.doi.org/10.1016/s0014-4835(05)80210-6.

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8

Whitworth, Judith A., J. M. C. Connell, A. F. Lever, and R. Fraser. "PRESSOR RESPONSIVENESS IN STEROID-INDUCED HYPERTENSION IN MAN." Clinical and Experimental Pharmacology and Physiology 13, no. 4 (April 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, and Dong Wook Lee. "Steroid-Induced Ocular Hypertension Model in the Mice." Journal of the Korean Ophthalmological Society 55, no. 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, and I. E. Tareyeva. "Steroid-Induced Hypertension in Patients with Nephrotic Syndrome." Nephron 48, no. 4 (1988): 286–90. http://dx.doi.org/10.1159/000184944.

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11

Sejpal, Poonam, and Joni Scott-Weideman. "Surgical Intervention of Steroid-Induced Ocular Hypertension from Ozurdex." Optometry and Vision Science 90, no. 1 (January 2013): e24-e30. http://dx.doi.org/10.1097/opx.0b013e318279eba0.

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12

Al Hanaineh, Abeer T., Dina H. Hassanein, Sameh H. Abdelbaky, and Omar M. El Zawahry. "Steroid-induced ocular hypertension in the pediatric age group." European Journal of Ophthalmology 28, no. 4 (March 19, 2018): 372–77. http://dx.doi.org/10.1177/1120672118757434.

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Purpose: Comparing the effects of topical Rimexolone versus Dexamethasone and Rimexolone versus Fluorometholone on the intraocular pressure in children <13 years. Methods: A total of 40 patients (80 eyes) undergoing bilateral recession strabismus surgery were divided into two groups. Group A included 20 children (40 eyes); for each, one eye was randomized to receive 1% Rimexolone and the fellow eye received 0.1% Dexamethasone. Group B included 20 children (40 eyes); for each, one eye was randomized to receive 1% Rimexolone and the fellow eye received 0.1% Fluorometholone. Patients received eye drops for two consecutive weeks. Preoperative and postoperative intraocular pressure values for weeks 1, 2, 3, 4, and 6 were measured. The ocular-hypertensive response of all patients was categorized as either high, intermediate or low (Armaly–Becker Classification). Results: After a 2-week treatment for both groups, peak and maximal intraocular pressure changes were reached. Changes were significantly higher in the Dexamethasone-treated eyes than in the Rimexolone- and Fluorometholone-treated eyes, which had a comparable change. (Week 2 intraocular pressure Group A: 14.15 ± 3.23 mmHg vs 17.95 ± 4.27 mmHg; Group B: 15.1 ± 2.27 mmHg vs 15.2 ± 2.73 mmHg). In both groups, the increase was statistically significant compared to the baseline intraocular pressure (preoperative intraocular pressure Group A: 13.2 ± 3.53 mmHg vs 13.1 ± 3.43 mmHg; Group B: 12.55 ± 2.98 mmHg vs 12.15 ± 3.31 mmHg). Intraocular pressure returned to near preoperative values over the following four consecutive weeks (Week 6 intraocular pressure Group A: 12.25 ± 2.67 mmHg vs 12.55 ± 2.95 mmHg; Group B: 12.15 ± 2.8 mmHg vs 12.00 ± 2.75 mmHg). None of the patients were high responders. Conclusion: Dexamethasone caused a higher elevation in intraocular pressure than Rimexolone and Fluorometholone in children. The ocular-hypertensive response was transient after the 2-week course.

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13

Manzoor, Hina, Asma Batool, Saba Akram, Iqra Khalil, and Ammara Affi. "Relationship between post-op central corneal thickness and steroid-induced ocular hypertension following myopic photorefractive keratectomy." Advances in Ophthalmology & Visual System 10, no. 5 (November 23, 2020): 132–35. http://dx.doi.org/10.15406/aovs.2020.10.00398.

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Purpose: Purpose of this study is to determine the relationship between Post-op central corneal thickness and steroid-induced ocular hypertension following myopic photorefractive keratectomy. Methods: This longitudinal analytical study was carried on 50 patients, both gender and age ranging from 20-40 years who had undergone myopic PRK refractive surgery. The data collected from The Department of Ophthalmology in Madina Teaching Hospital Faisalabad in the duration of 11 months from July 2019 to May 2020. IOP measured by Goldmann applanation tonometer. Recorded IOP greater than 21mmHg was considered as Ocular hypertension (OHT). The post-Op follow-up was conducted 1 day, 1 week, 2-3 weeks, and 4-6 weeks. The CCT and IOP was evaluated carefully. Data was noted on Performa. Data was analyzed by using Descriptive and Repeated Measures ANOVA by using the latest version 21 of SPSS. Results: Out of 50 patients’ 46% were males and 54% were females. The mean score of CCT pre & post operatively for right eye and left eye was 529.28±34.74 & 462.56±40.20 and 529.18±37.2, 462.44±42.60 respectively. Statistically significant effect was seen on post-op central corneal thickness and steroid induced ocular hypertension, according to the results of repeated measure ANOVA. Thinner corneas were more susceptible to steroids induced OHT. In various post-op central corneal thickness, it was observed that patients with thinner corneal thickness ranges 413±4.24 to 449.33±48.29 in right eye and 455.8±56.42 to 456.83±50.52 are more affected by topical steroids used. Males were more affected than females due to decreased central corneal thickness. Elderly patients were more susceptible to steroid-induced ocular hypertension post-operatively. Conclusion: Post-op steroid induced ocular hypertension is affecting by central corneal thickness. Male and elderly individual are more susceptible to steroid-induced ocular hypertension following myopic PRK. Post-Op use of topical steroids cause ocular hypertension in thinner corneas

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14

Kim, Sang Myung, Hyoung Won Bae, Sung Yong Kang, Sa Min Hong, Gong Je Seong, and Chan Yun Kim. "Incidence of Steroid-Induced Ocular Hypertension Following Myopic Refractive Surgery." Journal of the Korean Ophthalmological Society 56, no. 7 (2015): 1081. http://dx.doi.org/10.3341/jkos.2015.56.7.1081.

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15

Busool, Yumna, Michael Mimouni, Igor Vainer, Shmuel Levartovsky, Tzahi Sela, Gur Munzer, and Igor Kaiserman. "Risk factors predicting steroid-induced ocular hypertension after photorefractive keratectomy." Journal of Cataract & Refractive Surgery 43, no. 3 (March 2017): 389–93. http://dx.doi.org/10.1016/j.jcrs.2016.12.030.

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16

MINATO, Masaya, Masanobu HONDA, and Michinobu HATANO. "A Comparative Study of C19 Steroid-Induced Hypertension and Deoxycorticosterone Acetate (DOCA)-Salt Hypertension." Folia Endocrinologica Japonica 66, no. 1 (1990): 29–41. http://dx.doi.org/10.1507/endocrine1927.66.1_29.

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17

Kalimi, M., J. Opoku, M. Agarwal, and K. Corley. "Effects of antimineralocorticoid RU 26752 on steroid-induced hypertension in rats." American Journal of Physiology-Endocrinology and Metabolism 258, no. 5 (May 1, 1990): E737—E739. http://dx.doi.org/10.1152/ajpendo.1990.258.5.e737.

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The effect of mineralocorticoid antagonist RU 26752 on the development and maintenance of hypertension produced by long-term administration of mineralocorticoid agonist aldosterone has been investigated. Uninephrectomized, saline-drinking male Sprague-Dawley rats were subcutaneously implanted with either placebo (control) pellets or pellets containing 100 micrograms aldosterone, 50 mg RU 26752, or 100 micrograms aldosterone plus 50 mg RU 26752. Aldosterone treatment resulted in an increase in blood pressure to 165 +/- 5 mmHg over the control value of 105 +/- 2 mmHg within 3 wk of experimental period. RU 26752 given alone had no observable hypertensinogenic effect. However, RU 26752 administered with aldosterone significantly prevented the hypertension produced by aldosterone alone. RU 26752 when given with aldosterone was able to prevent the aldosterone-induced increase in saline consumption, increase urine output, and reduce urinary Na+ excretion. The results presented suggest that long-term administration of antimineralocorticoid RU 26752 in vivo to Sprague-Dawley rats prevents the aldosterone-induced hypertension.

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18

Sheikh, Taha, Hina Shuja, Syeda Ramsha Zaidi, and Ayema Haque. "Glucocorticoid-induced cardiomyopathy: unexpected conclusion." BMJ Case Reports 13, no. 11 (November 2020): e237173. http://dx.doi.org/10.1136/bcr-2020-237173.

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Glucocorticoid excess is an under-recognised cause of cardiovascular adverse effects. The sources can be either endogenous (Cushing’s syndrome) or exogenous (Anabolic steroid abuse). Cardiovascular complications due to excess glucocorticoid includes hypertension, left ventricular hypertrophy, myocardial infarction, and heart failure. Although anabolic steroid-induced cardiomyopathy is a well-recognised phenomenon, endogenous corticosteroid-induced cardiomyopathy and heart failure are rarely reported sequelae of glucocorticoid excess in the body. We report a glucocorticoid-induced dilated cardiomyopathy in a 26-year-old African–American man with cushingoid features and symptomatic heart failure.

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19

Pandav, SS, Savleen Kaur, Sushmita Kaushik, and Sonia Phulke. "Steroid-induced Glaucoma: An Avoidable Irreversible Blindness." Journal of Current Glaucoma Practice 11, no. 2 (2017): 67–72. http://dx.doi.org/10.5005/jp-journals-10028-1226.

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ABSTRACT Steroids are a group of anti-inflammatory drugs, commonly used to treat ocular and systemic conditions. Unmonitored use of steroids especially in eye drop formulations is common in situations when it is easily available over-the-counter, resulting in undesirable side effects. Among the ocular side effects, cataract and glaucoma are common. Steroid-induced ocular hypertension was reported in 1950, when long-term use of systemic steroid was shown to increase the intraocular pressure (IOP). Chronic administration of steroids in any form with raised IOP can cause optic neuropathy resulting in steroid-induced glaucoma. This review describes the pathophysiology and epidemiology of steroid-induced glaucoma, recognition of side effects, and principles of management. The purpose is to familiarize all clinicians with the potential dangers of administering steroids without monitoring the eye and the dangers of irreversible blindness in some instances of habitual self-prescription by patients. How to cite this article Phulke S, Kaushik S, Kaur S, Pandav SS. Steroid-induced Glaucoma: An Avoidable Irreversible Blindness. J Curr Glaucoma Pract 2017;11(2):67-72.

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20

Molinari, Joseph F. "Decrease Corneal Hysteresis in Steroid-Induced Ocular Hypertension: A Case Report." Military Medicine 178, no. 7 (July 2013): e862-e864. http://dx.doi.org/10.7205/milmed-d-12-00492.

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21

Badrinarayanan, Lakshmi. "Assessment of single nucleotide polymorphisms associated with steroid-induced ocular hypertension." International Journal of Ophthalmology 13, no. 8 (August 18, 2020): 1294–305. http://dx.doi.org/10.18240/ijo.2020.08.17.

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22

Geraghty, Dominic P., K. Bruce Byrne, Grant A. McPherson, and Elizabeth Burcher. "RENAL AND MYOCARDIAL ADRENOCEPTORS IN STEROID CONTRACEPTIVE-INDUCED HYPERTENSION IN RATS." Clinical and Experimental Pharmacology and Physiology 17, no. 8 (August 1990): 567–78. http://dx.doi.org/10.1111/j.1440-1681.1990.tb01357.x.

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23

Lu, Edeline, Lane T. Fujimoto, Paul A. Vejabul, and Russell L. Jew. "Steroid-induced ocular hypertension with loteprednol etabonate 0.2%—A case report." Optometry - Journal of the American Optometric Association 82, no. 7 (July 2011): 413–20. http://dx.doi.org/10.1016/j.optm.2010.10.011.

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24

Borrás, Teresa. "Gene therapy strategies in glaucoma and application for steroid-induced hypertension." Saudi Journal of Ophthalmology 25, no. 4 (October 2011): 353–62. http://dx.doi.org/10.1016/j.sjopt.2011.07.005.

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25

Lee, Ju Hyang, Min Cheol Seong, Hee Yoon Cho, and Yoon Jung Lee. "The Effectiveness of Selective Laser Trabeculoplasty in Steroid-Induced Ocular Hypertension." Journal of the Korean Ophthalmological Society 52, no. 7 (2011): 876. http://dx.doi.org/10.3341/jkos.2011.52.7.876.

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26

Bhattacherjee, Parimal. "Pharmacological Validation of a Feline Model of Steroid-Induced Ocular Hypertension." Archives of Ophthalmology 117, no. 3 (March 1, 1999): 361. http://dx.doi.org/10.1001/archopht.117.3.361.

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27

Reid, Amanda F., John P. Coghlan, Campbell D. Spence, Judith A. Whitworth, and Bruce A. Scoggins. "Studies on spirolactone steroid antagonists in ACTH-induced hypertension in sheep." Journal of Steroid Biochemistry 33, no. 6 (December 1989): 1213–21. http://dx.doi.org/10.1016/0022-4731(89)90432-9.

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28

Jeong, Shinwu, Nitin Patel, Christopher K. Edlund, Jaana Hartiala, Dennis J. Hazelett, Tatsuo Itakura, Pei-Chang Wu, et al. "Identification of a Novel Mucin GeneHCG22Associated With Steroid-Induced Ocular Hypertension." Investigative Opthalmology & Visual Science 56, no. 4 (April 30, 2015): 2737. http://dx.doi.org/10.1167/iovs.14-14803.

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29

Gomez-Sanchez, Elise P., Jacqueline Samuel, Gaston Vergara, and Naveed Ahmad. "Effect of 3β-hydroxysteroid dehydrogenase inhibition by trilostane on blood pressure in the Dahl salt-sensitive rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, no. 2 (February 2005): R389—R393. http://dx.doi.org/10.1152/ajpregu.00441.2004.

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The brains of rats and humans express the enzymes required for the synthesis of aldosterone from cholesterol, including the 3β-steroid dehydrogenase that catalyzes the conversion of pregnenolone to progesterone in the pathway of adrenal steroid synthesis. Salt-induced hypertension in the Dahl inbred salt-sensitive (SS/jr) rat is associated with normal to low levels of circulating aldosterone, yet it is abrogated by the central infusion of mineralocorticoid receptor antagonists. To test the hypothesis that de novo synthesis of aldosterone in the brain has a pathophysiological role in the salt-induced hypertension of the SS rat, the 3β-steroid dehydrogenase antagonist trilostane was infused continuously intracerebroventricularly or subcutaneously in two different cohorts of Dahl SS/jr rats, one female, the other male, during and after the development of salt-induced hypertension. The doses of trilostane used had no effect on blood pressure when infused subcutaneously. Animals receiving vehicle intracerebroventricularly experienced a 30- to 45-mmHg increase in systolic blood pressure measured by tail cuff. The intracerebroventricular, but not subcutaneous, infusion of 0.3 μg/h trilostane effectively blocked the increase in systolic blood pressure and reversed the hypertension produced by drinking 0.9% saline. Trilostane was equally effective in female and male rats. Weight gain, serum aldosterone and corticosterone concentrations, and behavior assessed subjectively and by elevated plus maze were unchanged by the trilostane treatment. These studies suggest that the synthesis in the brain of a mineralocorticoid receptor agonist, probably aldosterone, is responsible in part for the salt-induced hypertension of the inbred Dahl SS/jr rat.

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30

Betul, Oran, Hun Lee, Marcos de Lima, Daniel Couriel, Sergio Giralt, and Rima Saliba. "Steroid Complications in Patients with Acute Graft Versus Host Disease." Blood 106, no. 11 (November 16, 2005): 5338. http://dx.doi.org/10.1182/blood.v106.11.5338.5338.

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Abstract Background: High dose steroid treatment remains to be the first line therapy for acute graft versus host disease (aGVHD) after allogeneic hematopoietic stem cell transplantation (HSCT). Although effective in controlling aGVHD, high dose steroids can cause multiple serious complications which can result in increased morbidity and mortality. Purpose: Our aim was to determine the frequency of steroid induced complications and to analyze risk factors for steroid-myopathy in patients with AML who developed grade 2 aGVHD after allogeneic HSCT. Patients and Methods: Inclusion criteria were: 1) AML/MDS patients who received allogeneic HSCT between 1/1996 and 12/2001 2) grade 2 aGVHD treated with at least 2mg/kg of methylprednisolone 3) post transplantation overall survival at least 100 days. Steroid induced complications reviewed were: cataracts, headaches, mood swings, hypertension, gastritis, hyperglycemia, osteopenia, myopathy, avascular necrosis, edema, hypokalemia and infections. Pre- and post-transplantation characteristics analyzed as risk factors for steroid-myopathy were: age, gender, race, history of diabetes, body mass index, HLA types, steroid use after HSCT prior to grade 2 acute GVHD and duration of steroid use for acute GVHD. Logistic regression analysis was used for risk factor evaluation. Steroid-myopathy was defined as proximal muscle weakness, atrophy and myalgia in the absence of genetic, inflammatory or drug-induced etiologies other than steroid use. Results: 178 AML /MDS patients were transplanted during the study period. 70 patients (37 males and 33 females) with a median age of 43 (range, 21–66) were eligible for our study. Median duration of follow-up and median duration of steroid use after grade 2 aGVHD were 269 days and 127 days respectively. The number of patients and their frequency distribution of steroid induced complications were as follows: hyperglycemia, 43 (61.4%); hypertension, 35 (50%); cataracts, 10(14.3%); headaches, 7 (10%); mood swings,12(17.1%); gastritis, 7 (10%); myopathy, 32(45.7%); avascular necrosis, 1 (1.4%); edema, 22 (31.4%); hypokalemia, 52 (74.3%); bacterial infections, 55 (78.6%); viral infections, 39(55.7%); and fungal infections, 22(31.4%). For steroid-induced myopathy, male gender (RR=4.0, 95% CI=1.01–16.4, p=0.05), steroid use before acute GVHD grade II (RR=5.5, 95% CI=1.35–22.14, p=0.02) or steroid use more than 4 months after developing acute GVHD grade II (HR=6.4, 95% CI=1.38–29.94, p=0.02) were independent risk factors. 47 of 70 patients died with median overall survival of 10 months. 22 of 47 (46.8%) had steroid-myopathy and there was no increased mortality with steroid induced myopathy. Conclusion: Steroid therapy for aGVHD after allogeneic HSCT in AML/MDS patients is associated with frequent toxicities. The possibility of identifying prognostic factors for steroid toxicities support the study and development of strategies that may ameliorate or prevent steroid induced complications.

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31

HESTER, D. E., P. N. TRITES, R. L. PEIFFER, and V. PETROW. "Steroid-Induced Ocular Hypertension in the Rabbit: A Model Using Subconjunctival Injections." Journal of Ocular Pharmacology and Therapeutics 3, no. 3 (January 1987): 185–89. http://dx.doi.org/10.1089/jop.1987.3.185.

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32

Muecke, James, and Garry Brian. "Steroid-induced ocular hypertension in the presence of a functioning Molteno seton." Australian and New Zealand Journal of Ophthalmology 23, no. 1 (February 1995): 67–68. http://dx.doi.org/10.1111/j.1442-9071.1995.tb01649.x.

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33

Lee, Kyoung Min, Mee Kum Kim, Won Ryang Wee, and Jin Hak Lee. "Risk Factors of the Steroid Induced Ocular Hypertension After Corneal Refractive Surgery." Journal of the Korean Ophthalmological Society 51, no. 10 (2010): 1333. http://dx.doi.org/10.3341/jkos.2010.51.10.1333.

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34

Epstein, Rebecca, Michael Taravella, and Mina B. Pantcheva. "Kahook Dual Blade goniotomy in post penetrating keratoplasty steroid-induced ocular hypertension." American Journal of Ophthalmology Case Reports 19 (September 2020): 100826. http://dx.doi.org/10.1016/j.ajoc.2020.100826.

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35

Tasaki, Anne. "Case Report: Steroid-induced Ocular Hypertension in a 6-year-old Boy." Optometry and Vision Science 98, no. 8 (August 2021): 867–69. http://dx.doi.org/10.1097/opx.0000000000001747.

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36

Bakk, Ian, Sarah O'Brien, Suzanne Reed, and Terah Koch. "Steroid-Induced Hypertension during Induction Chemotherapy for Acute Lymphoblastic Leukemia in US Children's Hospitals." Blood 124, no. 21 (December 6, 2014): 3651. http://dx.doi.org/10.1182/blood.v124.21.3651.3651.

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Abstract Background: Acute lymphoblastic leukemia (ALL) is the most common pediatric cancer. The induction phase of chemotherapy, including high-dose corticosteroids, is critical and effective as 98% of patients achieve remission after induction. It is generally understood that most non-life threatening side effects of chemotherapy during induction should be tolerated and treated with additional medication (if necessary) rather than reducing or discontinuing chemotherapeutic medication. Although hypertension (HTN) is a known possible complication of high-dose corticosteroids, the actual incidence and risk factors for this adverse event are poorly understood. Our objective was to utilize a national administrative data source to begin to answer these uncertainties. Methods: The Pediatric Health Information System (PHIS) database consists of inpatient information from 43 US free-standing pediatric hospitals representing 25% of US pediatric centers and the majority of tertiary care pediatric hospitals. The PHIS database includes de-identified demographic data, discharge diagnoses, and medications prescribed among other data. Our study examined all new cases of ALL from age 0 to 28 years from Jan 1, 2009 to Dec 31, 2013. We defined our population of ALL patients receiving induction chemotherapy as those who: 1) had a non-relapse ALL ICD-9 code (204.0, 204.00, 204.01) and 2) received induction chemotherapy medications within the first 14 days of admission. Patients receiving antihypertensive medication before or on the date of chemotherapy initiation were excluded from our population. Due to the unknown sensitivity and specificity of ICD-9 codes for hypertension in this patient population, we elected to define hypertension based on recorded use of anti-hypertensive medications rather than diagnostic codes. Results: We identified 4,917 unique patients who received induction chemotherapy for ALL. Of these patients, 13.0% received anti-hypertensive drugs during their admission. Adjusted logistic regression demonstrated increased odds of developing steroid-induced hypertension in obese patients [2.3; 95% CI: (1.42-3.71)] and those receiving anthracycline drugs [1.3; 95% CI: (1.004-1.67)]. Decreased odds of developing steroid-induced hypertension were independently associated with the 5 to 9 year age group [0.61; 95% CI: (0.49-0.76)] as compared to the 0 to 4 year age group. To assess the reliability of using ICD-9 codes to identify patients with hypertension, sensitivity and specificity were calculated. Using receipt of anti-hypertensive drugs as the gold standard, the sensitivity of ICD-9 codes to detect hypertension was 0.60 [95% CI: (0.56-0.64)] and specificity was 0.96 [95% CI: (0.96-0.97)]. Conclusion: To our knowledge, this was the first study of steroid-induced HTN in pediatric ALL patients using a national data source. We found that HTN is a common complication of induction ALL therapy. Increased risk for HTN was independently associated with obesity and anthracycline use. Although ICD-9 codes are very useful in ruling out hypertension, they are significantly less accurate in detecting those patients with hypertension. The lack of sensitivity of the HTN ICD-9 codes was notable and suggests underreporting of HTN by physicians. This study is limited as patient information is from a single inpatient admission. As cure rates of pediatric ALL approach 85%, the long-term effects of steroid-induced HTN deserves further study. Disclosures No relevant conflicts of interest to declare.

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37

Shafagoj, Y., J. Opoku, D. Qureshi, W. Regelson, and M. Kalimi. "Dehydroepiandrosterone prevents dexamethasone-induced hypertension in rats." American Journal of Physiology-Endocrinology and Metabolism 263, no. 2 (August 1, 1992): E210—E213. http://dx.doi.org/10.1152/ajpendo.1992.263.2.e210.

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Dehydroepiandrosterone (DHEA) is an endogenous steroid having a wide variety of biological and biochemical effects. In the present study, we have examined the role of DHEA on various rodent models of experimental hypertension. Sprague-Dawley rats were given subcutaneous injections of 1.5 mg dexamethasone every alternate day, resulting in an increase in systolic blood pressure within 1 wk. Interestingly, administration of a pharmacological dose of 1.5, 3, or 7.5 mg DHEA along with dexamethasone prevented dexamethasone-induced hypertension in a dose-dependent manner. DHEA had no effect on the hypertension induced by deoxycorticosterone acetate (DOCA)-salt administration using uninephrectomized rats or on the genetic model of spontaneously hypertensive rats. Dexamethasone administration resulted in a significant weight loss in rats, which was not prevented by simultaneous administration of DHEA. These results indicate that dexamethasone-mediated weight loss may involve mechanisms separate from its hypertensive action. Dexamethasone treatment resulted in a significant decrease in food consumption that was not reversed by DHEA. It is concluded that DHEA at doses above physiological levels when given subcutaneously has no effect on DOCA-salt or a genetic model of hypertension but has a beneficial effect on dexamethasone-induced hypertension.

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Opoku, Justicia, and Mohammed Kalimi. "Role of the antiglucocorticoid RU 486 in the prevention of steroid-induced hypertension." Acta Endocrinologica 127, no. 3 (September 1992): 258–61. http://dx.doi.org/10.1530/acta.0.1270258.

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In the present study, we determined the effect of RU 486 on two experimental models of hypertension in the rat, deoxycorticosterone acetate (DOCA)-salt in nephrectomized rats and spontaneously hypertensive rats. Uni-nephrectomized saline-drinking male Sprague-Dawley rats were divided into three groups and each animal was given either 0.2ml olive oil (control), 1 mg DOCA, or 1 mg DOCA +10 mg RU 486 dissolved in 0.2 ml olive oil every third day for a period of three weeks. Within a week of steroid administration, there was a significant increase in the systolic blood pressure (SBP) in the DOCA-salt (157±3.8 mmHg) and DOCA+RU 486 (155±2.1 mmHg) treated rats over the control (116±2.6 mmHg) rats, which remained elevated throughout the experimental period. There was significant increase in the water intake and urine output in DOCA or DOCA+RU 486 treated rats as compared to the control untreated rats. In the experiment involving the spontaneously hypertensive rats, the rats were divided into three groups and each animal given 0.2 ml olive oil (control), 1 mg RU 486, or 5 mg RU 486 dissolved in 0.2 ml olive oil for six weeks. Instead of the expected decrease in the blood pressure, RU 486 significantly elevated blood pressure during the six weeks of drug administration. Water intake, urine output, and weights remained comparable in both groups. We conclude that RU 486 has no effect on the DOCA-salt model of hypertension but, surprisingly, elevates hypertension in the spontaneously hypertensive rats.

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Fini, M. Elizabeth, Stephen G. Schwartz, Xiaoyi Gao, Shinwu Jeong, Nitin Patel, Tatsuo Itakura, Marianne O. Price, Francis W. Price, Rohit Varma, and W. Daniel Stamer. "Steroid-induced ocular hypertension/glaucoma: Focus on pharmacogenomics and implications for precision medicine." Progress in Retinal and Eye Research 56 (January 2017): 58–83. http://dx.doi.org/10.1016/j.preteyeres.2016.09.003.

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Yülek, Fatma. "Reply to “Corneal biomechanics in steroid induced ocular hypertension” by Yülek et al." Contact Lens and Anterior Eye 38, no. 5 (October 2015): 390. http://dx.doi.org/10.1016/j.clae.2015.05.009.

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41

Senthil, Sirisha, Monica Thakur, Harsha Laxmana Rao, Ashik Mohamed, Ganesh Babu Jonnadula, Virender Sangwan, and Chandra Sekhar Garudadri. "Steroid-induced glaucoma and blindness in vernal keratoconjunctivitis." British Journal of Ophthalmology 104, no. 2 (May 4, 2019): 265–69. http://dx.doi.org/10.1136/bjophthalmol-2019-313988.

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PurposeTo report the clinical features, treatment outcomes and blindness associated with steroid-induced glaucoma in vernal keratoconjunctivitis (VKC).Materials and methodsRecords of patients with VKC, who visited our tertiary centre from 1992 and 2009, were reviewed and those with steroid-induced glaucoma were included in the study. Glaucoma was diagnosed based on intraocular pressure (IOP) ≥22 mm Hg on two consecutive visits (ocular hypertension) and/or glaucomatous optic disc damage. Blindness was defined as best corrected visual acuity of ≤20/400 or visual field <10°.ResultsOf the 4062 VKC subjects, 91 (157 eyes) had steroid-induced glaucoma (SIG), showing a prevalence of 2.24%. Of these 87% were men. The median (IQR) age at onset of VKC was 12 years (7–17). At presentation, the median duration of VKC was 48 months (24–72) and the median duration of steroid usage was 24 months (12–36). The median cup-to-disc ratio (CDR) was 0.9 (0.7–0.9) and median mean deviation was −21.9 dB (−30.0 to –10.2). IOP was medically controlled in 66% eyes (104/157) and 34% eyes (53/157) needed glaucoma surgery. High presenting IOP (OR: 1.04; p=0.05) and increased duration of steroid usage (OR: 1.07; p=0.02) were significantly associated with need for glaucoma surgery. At presentation, 29/91 subjects (31.8%) were bilaterally blind due to SIG. Higher CDR at presentation was significantly associated with blindness in this cohort (p=0.02).ConclusionIn this cohort of VKC with SIG, the disease predominantly affected adolescent males. Glaucoma was severe with one-third needing surgery and one-third blind due to SIG.

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Razali, Norhafiza, Renu Agarwal, Puneet Agarwal, Sunil Kumar, Minaketan Tripathy, Sushil Vasudevan, Jonathan G. Crowston, and Nafeeza M. Ismail. "Role of adenosine receptors in resveratrol-induced intraocular pressure lowering in rats with steroid-induced ocular hypertension." Clinical & Experimental Ophthalmology 43, no. 1 (November 20, 2014): 54–66. http://dx.doi.org/10.1111/ceo.12375.

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Thompson, George R., Katharina R. Beck, Melanie Patt, Denise V. Kratschmar, and Alex Odermatt. "Posaconazole-Induced Hypertension Due to Inhibition of 11β-Hydroxylase and 11β-Hydroxysteroid Dehydrogenase 2." Journal of the Endocrine Society 3, no. 7 (June 6, 2019): 1361–66. http://dx.doi.org/10.1210/js.2019-00189.

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Abstract We describe two cases of hypertension and hypokalemia due to mineralocorticoid excess caused by posaconazole treatment of coccidioidomycosis and rhinocerebral mucormycosis infections, respectively. Clinical laboratory evaluations, including a comprehensive analysis of blood and urine steroid profiles, revealed low renin and aldosterone and indicated as the underlying mechanism primarily a block of 11β-hydroxylase activity in patient 1, whereas patient 2 displayed weaker 11β-hydroxylase but more pronounced 11β-hydroxysteroid dehydrogenase 2 inhibition. The results show that both previously suggested mechanisms must be considered and emphasize significant interindividual differences in the contribution of each enzyme to the observed mineralocorticoid excess phenotype. The mineralocorticoid symptoms of patient 1 resolved after replacement of posaconazole therapy by isavoconazole, and posaconazole dosage de-escalation ameliorated the effects in patient 2. By providing a thorough analysis of the patients’ blood and urine steroid metabolites, this report adds further evidence for two individually pronounced mechanisms of posaconazole-induced hypertension and hypokalemia. The elucidation of the factors responsible for the individual phenotype warrants further research.

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Agarwal, Renu, SK Gupta, Sushma Srivastava, and Rohit Saxena. "IOP Lowering Effects of Ocimum basilicum Seed Extract in Two Rabbit Models of Ocular Hypertension." Journal of Clinical and Health Sciences 4, no. 1 (June 30, 2019): 39. http://dx.doi.org/10.24191/jchs.v4i1.7281.

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Introduction: Ocimum basilicum (OB), a herb known for its antihypertensive, anticholinesterase and antioxidant properties was investigated for possible intraocular pressure (IOP) lowering effects in rabbits with ocular hypertension (OHT). Methods: The IOP lowering effect of a single drop of OB extract (OBE) was evaluated in oculonormotensive rabbits using three concentrations (0.25, 0.5 and 1% w/v). The concentration showing maximum IOP reduction was further evaluated in rabbits with water-loading and steroid-induced OHT. Results: IOP lowering effect of OBE 0.5% in oculonormotensive rabbit eyes was significantly greater compared to OBE 0.25% (p<0.05) but was comparable (p>0.05) to OBE 1%. Therefore, 0.5% concentration was selected for further evaluation. Pretreatment with OBE (0.5%) caused significantly lower increase in IOP after water loading amounting to 23.39% above baseline as compared to 54.00% in control eye, 15 minutes post water loading. At 60 minutes, post water loading, mean IOP rise was 95.12% and 63.58% in control and test eyes, respectively. Significant difference between the mean IOP of two eyes persisted during the 2nd hr. In rabbits with steroid induced OHT, OBE 0.5% produced a mean IOP reduction of 24.73% at the end of first hr and the mean peak IOP reduction of 31.63% was observed at the end of 2 hr. A significant difference between the IOP of test and control eyes persisted from 1 to 6 hr. Conclusions: Ocimum basilicum seed extract showed significant IOP lowering effect in rabbits with water loading and steroid induced OHT, however, its utility as an effective antiglaucoma medication needs further investigations.

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Abu Samra, Khawla, Sandra Fernando Sieminski, and Vimal Sarup. "Decompression Retinopathy after ExPRESS Shunt Implantation for Steroid-Induced Ocular Hypertension: A Case Report." Case Reports in Ophthalmological Medicine 2011 (2011): 1–4. http://dx.doi.org/10.1155/2011/303287.

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Purpose. To present a unique case of decompression retinopathy after the implantation of ExPRESS drainage device.Method. A 25-year-old female patient underwent implantation of ExPRESS drainage device in the left eye for the management of steroid-induced ocular hypertension.Results. On the postoperative day one, best-corrected visual acuity in the left eye was 20/50. Fundus examination revealed diffuse intraretinal hemorrhages, some white-centered, throughout the retina. There was also marked tortuosity to the retinal vasculature and no evidence of choroidal effusion. Intravenous fluorescein angiography and indocyanine green did not contribute to the aetiopathogenesis.Conclusion. Decompression retinopathy can occur following the implantation of ExPRESS drainage device. It is very important to be aware of this complication in patients with relatively high intraocular pressure who is planned for filtration surgery, including the ExPRESS implant.

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Jeng, Karen W., Howard F. Fine, H. Matthew Wheatley, Daniel Roth, Daniel B. Connors, and Jonathan L. Prenner. "INCIDENCE OF STEROID-INDUCED OCULAR HYPERTENSION AFTER VITREORETINAL SURGERY WITH DIFLUPREDNATE VERSUS PREDNISOLONE ACETATE." Retina 34, no. 10 (October 2014): 1990–96. http://dx.doi.org/10.1097/iae.0000000000000215.

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Bakk, Ian, Terah Koch, Joseph Stanek, Sarah H. O’Brien, and Suzanne Reed. "Steroid-induced Hypertension During Induction Chemotherapy for Acute Lymphoblastic Leukemia in US Children’s Hospitals." Journal of Pediatric Hematology/Oncology 40, no. 1 (January 2018): 27–30. http://dx.doi.org/10.1097/mph.0000000000000997.

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Miyai, Takashi, Takaharu Yonemura, Ryohei Nejima, Shinichiro Otani, Kazunori Miyata, and Shiro Amano. "Interlamellar Flap Edema Due to Steroid-Induced Ocular Hypertension After Laser In Situ Keratomileusis." Japanese Journal of Ophthalmology 51, no. 3 (June 7, 2007): 228–30. http://dx.doi.org/10.1007/s10384-006-0441-y.

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Takeda, R., T. Yamazaki, Y. Ito, H. Koshida, T. Morise, I. Miyamori, T. Hashimoto, and S. Morimoto. "Twenty-four year spironolactone therapy in an aged patient with aldosterone-producing adenoma." Acta Endocrinologica 126, no. 2 (February 1992): 186–90. http://dx.doi.org/10.1530/acta.0.1260186.

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A case of primary aldosteronism treated with spironolactone therapy has been followed up for 24 years. This is probably the longest case of spironolactone therapy for primary aldosteronism that has ever been reported. Long-term treatment with spironolactone controlled the hypertension and prevented hypokalemic alkalosis in this patient, without any deleterious effects on steroid biosynthesis. Based on data obtained during dose reduction and subsequent withdrawal of spironolactone, it is suggested that the suppressed plasma renin activity associated with adenoma-induced aldosteronism develops prior to hypokalemia and hypertension.

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Gruener, Anna Maria, Pranev Sharma, Sally Ameen, and Faisal Ahmed. "Severe Corticosteroid-Induced Ocular Hypertension Requiring Bilateral Trabeculectomies in a Patient with Takayasu’s Arteritis." Case Reports in Ophthalmological Medicine 2016 (2016): 1–4. http://dx.doi.org/10.1155/2016/5253029.

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We present a rare case of severe corticosteroid-induced ocular hypertension (OHT) after prolonged systemic corticosteroid use in a young woman with Takayasu’s arteritis. As she did not sufficiently respond to ocular antihypertensive therapies, bilateral enhanced trabeculectomies were required to normalize her intraocular pressures. The systemic side effects of corticosteroids are well known, yet steroid-induced OHT and glaucoma remain silent causes of ocular morbidity. This case highlights the importance of IOP-monitoring in visually asymptomatic patients on systemic corticosteroids. It further emphasizes the need to raise awareness of the potential ocular side effects of steroids amongst physicians, in particular those looking after patients with autoimmune and inflammatory diseases.

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