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Journal articles on the topic 'Desoxycorticosterone pivalate'

Author: Grafiati

Published: 10 September 2021

Last updated: 13 February 2022

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1

Albers, M., P. Defauw, F. Mortier, and S. Daminet. "The use of desoxycorticosterone pivalate in dogs with hypoadrenocorticism: a retrospective study of eight cases." Vlaams Diergeneeskundig Tijdschrift 87, no. 6 (December 28, 2018): 309–13. http://dx.doi.org/10.21825/vdt.v87i6.16048.

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In this article, the use of desoxycorticosterone pivalate is retrospectively reviewed in eight dogs with primary hypoadrenocorticism, presented at the Small Animal Department of Ghent University. The results showed that desoxycorticosterone pivalate provided adequate mineralocorticoid replacement in all cases, also in the dogs that had previously been treated with fludrocortisone acetate. A starting dosage of 1.5 – 2.2 mg/kg SC was used, with a fixed dosing interval of 28 days in most of the cases. Each time, prednisolone was added to the therapy as glucocorticoid supplementation. No side effects related to desoxycorticosterone pivalate therapy were noted and all owners were satisfied with the treatment consisting of desoxycorticosterone pivalate and prednisolone.

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2

McCabe, MD, EC Feldman, RC Lynn, and PH Kass. "Subcutaneous administration of desoxycorticosterone pivalate for the treatment of canine hypoadrenocorticism." Journal of the American Animal Hospital Association 31, no. 2 (March 1, 1995): 151–55. http://dx.doi.org/10.5326/15473317-31-2-151.

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Twelve dogs with hypoadrenocorticism were treated with subcutaneous desoxycorticosterone pivalate (DOCP). Eight of these dogs were recently diagnosed and had not yet been treated. Four dogs previously had been diagnosed and treated (three with intramuscular DOCP, one with oral fludrocortisone acetate). History, physical examination, serum electrolytes, and blood urea nitrogen (BUN) were evaluated. Desoxycorticosterone pivalate (2.2 mg/kg body weight) was administered every 25 days. On day 0, recently diagnosed dogs had a median serum sodium concentration of 131.5 mEq/L, median serum potassium concentration of 6.6 mEq/L, and median BUN of 41.5 mg/dl. All subsequent median serum electrolyte and BUN concentrations were normal. All previously treated dogs had normal blood values which were maintained throughout the study.

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3

Lynn, Randy C., and E. C. Feldman. "Treatment of canine hypoadrenocorticism with microcrystalline desoxycorticosterone pivalate." British Veterinary Journal 147, no. 5 (September 1991): 478–83. http://dx.doi.org/10.1016/0007-1935(91)90091-z.

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4

Reimann, Franziska, Stefanie Siol, Charlotte Schlüter, and Reto Neiger. "Hypoadrenocorticism in two cats successfully treated with desoxycorticosterone pivalate." Veterinary Record Case Reports 6, no. 3 (September 2018): e000600. http://dx.doi.org/10.1136/vetreccr-2018-000600.

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Two cats were presented with lethargy and anorexia. Clinically, the cats showed hypothermia and dehydration. Blood examination in both cats showed hyponatraemia, hyperkalaemia and additionally azotaemia in case 1 and hypercalcaemia in case 2. In both cats, an adrenocorticotropic hormone (ACTH) stimulation test showed an insufficient stimulation of the adrenal glands. In case 1, markedly elevated endogenous ACTH was additionally measured. Both cats were successfully treated with a combination of desoxycorticosterone pivalate (DOCP) and prednisolone (0.15 mg/kg daily). Case 1 received a final concentration of 2.6 mg/kg DOCP every 30 days, while case 2 was successfully managed with 2.2 mg/kg every 28 days. These rare cases of feline hypoadrenocorticism demonstrate that DOCP can be used similarly as in dogs.

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5

Bates, JA, S. Shott, and WD Schall. "Lower initial dose desoxycorticosterone pivalate for treatment of canine primary hypoadrenocorticism." Australian Veterinary Journal 91, no. 3 (February 26, 2013): 77–82. http://dx.doi.org/10.1111/avj.12019.

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6

White, Constance N. "Use of desoxycorticosterone pivalate (DOCP) in the treatment of canine hypoadrenocorticism." Companion Animal 23, no. 2 (February 2, 2018): 82–88. http://dx.doi.org/10.12968/coan.2018.23.2.82.

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7

Saito, Miyoko, Natasha J. Olby, Leticia Obledo, and Jody L. Gookin. "Muscle Cramps in Two Standard Poodles With Hypoadrenocorticism." Journal of the American Animal Hospital Association 38, no. 5 (September 1, 2002): 437–43. http://dx.doi.org/10.5326/0380437.

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Two standard poodles were evaluated for painful, episodic muscle cramps affecting their thoracic and pelvic limbs. Both dogs had been diagnosed with hypoadrenocorticism and were being treated with fludrocortisone acetate and prednisone when evaluated for muscle cramps. However, the muscle cramping started approximately 1 month prior to the diagnosis of hypoadrenocorticism. Findings on general physical examination included lethargy and dehydration. Neurological examination was normal between episodes. Serum biochemical abnormalities included hyperalbuminemia, azotemia, hyponatremia, hypochloremia, and hyperkalemia. Altering treatment to desoxycorticosterone pivalate resolved the electrolyte abnormalities and the episodes of muscle cramping in both dogs. The authors conclude that hypoadrenocorticism can be associated with episodes of painful muscle cramping in standard poodles.

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8

Solocinski, K., M. Holzworth, X. Wen, K. Y. Cheng, I. J. Lynch, B. D. Cain, C. S. Wingo, and M. L. Gumz. "Desoxycorticosterone pivalate-salt treatment leads to non-dipping hypertension in Per1 knockout mice." Acta Physiologica 220, no. 1 (October 3, 2016): 72–82. http://dx.doi.org/10.1111/apha.12804.

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9

Jaffey, J. A., P. Nurre, A. B. Cannon, and A. E. DeClue. "Desoxycorticosterone Pivalate Duration of Action and Individualized Dosing Intervals in Dogs with Primary Hypoadrenocorticism." Journal of Veterinary Internal Medicine 31, no. 6 (September 11, 2017): 1649–57. http://dx.doi.org/10.1111/jvim.14828.

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10

Vincent, Alysha M., Linda K. Okonkowski, Jean M. Brudvig, Kent R. Refsal, Nora Berghoff, N. Bari Olivier, and Daniel K. Langlois. "Low‐dose desoxycorticosterone pivalate treatment of hypoadrenocorticism in dogs: A randomized controlled clinical trial." Journal of Veterinary Internal Medicine 35, no. 4 (June 10, 2021): 1720–28. http://dx.doi.org/10.1111/jvim.16195.

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11

Sieber‐Ruckstuhl, Nadia S., Claudia E. Reusch, Nathalie Hofer‐Inteeworn, Claudia Kuemmerle‐Fraune, Claudia Müller, Regina Hofmann‐Lehmann, and Felicitas S. Boretti. "Evaluation of a low‐dose desoxycorticosterone pivalate treatment protocol for long‐term management of dogs with primary hypoadrenocorticism." Journal of Veterinary Internal Medicine 33, no. 3 (March 13, 2019): 1266–71. http://dx.doi.org/10.1111/jvim.15475.

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12

Furukawa, Sho, Natsuko Meguri, Kazue Koura, Hiroyuki Koura, and Akira Matsuda. "A Case of Canine Polyglandular Deficiency Syndrome with Diabetes Mellitus and Hypoadrenocorticism." Veterinary Sciences 8, no. 3 (March 7, 2021): 43. http://dx.doi.org/10.3390/vetsci8030043.

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This report describes the first clinical case, to our knowledge, of a dog with polyglandular deficiency syndrome with diabetes mellitus and hypoadrenocorticism. A six-year-old female Cavalier King Charles Spaniel presented with a history of lethargy and appetite loss. The dog was diagnosed with diabetic ketoacidosis based on hyperglycemia and renal glucose and ketone body loss. The dog’s condition improved on intensive treatment of diabetes mellitus; daily subcutaneous insulin detemir injection maintained an appropriate blood glucose level over half a year. However, the dog’s body weight gradually decreased from day 207, and on day 501, it presented with a decreased appetite; the precise cause could not be determined. Based on mild hyponatremia and hyperkalemia, hypoadrenocorticism was suggested; the diagnosis was made using an adrenocorticotropic hormone stimulation test. Daily fludrocortisone with low-dose prednisolone oral administration resulted in poor recovery of the blood chemistry abnormalities; however, monthly desoxycorticosterone pivalate (DOCP) subcutaneous injection with daily low-dose prednisolone oral administration helped in the significant recovery of the abnormalities. Therefore, clinicians should consider the possibility of coexistence of hypoadrenocorticism in dogs with diabetes mellitus presenting with undifferentiated weight loss. Additionally, DOCP (not fludrocortisone) may be useful in treating dogs with diabetes mellitus complicated with hypoadrenocorticism.

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13

Lynch, I. Jeanette, Amanda K. Welch, Michelle L. Gumz, Donald E. Kohan, Brian D. Cain, and Charles S. Wingo. "Effect of mineralocorticoid treatment in mice with collecting duct-specific knockout of endothelin-1." American Journal of Physiology-Renal Physiology 309, no. 12 (December 15, 2015): F1026—F1034. http://dx.doi.org/10.1152/ajprenal.00220.2015.

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Aldosterone increases blood pressure (BP) by stimulating sodium (Na) reabsorption within the distal nephron and collecting duct (CD). Aldosterone also stimulates endothelin-1 (ET-1) production that acts within the CD to inhibit Na reabsorption via a negative feedback mechanism. We tested the hypothesis that this renal aldosterone-endothelin feedback system regulates electrolyte balance and BP by comparing the effect of a high-salt (NaCl) diet and mineralocorticoid stimulation in control and CD-specific ET-1 knockout (CD ET-1 KO) mice. Metabolic balance and radiotelemetric BP were measured before and after treatment with desoxycorticosterone pivalate (DOCP) in mice fed a high-salt diet with saline to drink. CD ET-1 KO mice consumed more high-salt diet and saline and had greater urine output than controls. CD ET-1 KO mice exhibited increased BP and greater fluid retention and body weight than controls on a high-salt diet. DOCP with high-salt feeding further increased BP in CD ET-1 KO mice, and by the end of the study the CD ET-1 KO mice were substantially hypernatremic. Unlike controls, CD ET-1 KO mice failed to respond acutely or escape from DOCP treatment. We conclude that local ET-1 production in the CD is required for the appropriate renal response to Na loading and that lack of local ET-1 results in abnormal fluid and electrolyte handling when challenged with a high-salt diet and with DOCP treatment. Additionally, local ET-1 production is necessary, under these experimental conditions, for renal compensation to and escape from the chronic effects of mineralocorticoids.

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14

"Lower initial dose of desoxycorticosterone pivalate." Advances in Small Animal Medicine and Surgery 26, no. 7 (June 2013): 4–5. http://dx.doi.org/10.1016/j.asams.2013.06.004.

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15

Deng, Yan, Maodi Xie, Qian Li, Xuewen Xu, Wei Ou, Yabing Zhang, Haitao Xiao, et al. "Targeting Mitochondria-Inflammation Circuit by β-Hydroxybutyrate Mitigates HFpEF." Circulation Research, November 12, 2020. http://dx.doi.org/10.1161/circresaha.120.317933.

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Rationale: Over 50% of heart failure patients have preserved, rather than reduced ejection fraction (HFpEF vs. HFrEF). Complexity of its pathophysiology and the lack of animal models hamper the development of effective therapy for HFpEF. Objective: This study was designed to investigate the metabolic mechanisms of HFpEF and test therapeutic interventions using a novel animal model.Methods and Results: By combining the age, long-term high-fat diet and desoxycorticosterone pivalate challenge in a mouse model we were able to recapture the myriad features of HFpEF. In these mice, mitochondrial hyperacetylation exacerbated while increasing ketone body availability rescued the phenotypes. The HFpEF mice exhibited overproduction of interleukin (IL)-1β/IL-18, and tissue fibrosis due to increased assembly of NLPR3 inflammasome on hyperacetylated mitochondria. Increasing β-hydroxybutyrate (β-OHB) level attenuated NLPR3 inflammasome formation and antagonized proinflammatory cytokines-triggered mitochondrial dysfunction and fibrosis. Moreover, β-OHB downregulated the acetyl-CoA pool and mitochondrial acetylation, partially via activation of citrate synthase and inhibition of fatty acid uptake. Conclusions: Therefore, we identify the interplay of mitochondrial hyperacetylation and inflammation as a key driver in HFpEF pathogenesis which can be ameliorated by promoting β-OHB abundance.

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