• 1. Marmor M, Willeberg P, Glickman L, et al. Epizootiologic patterns of diabetes mellitus in dogs. Am J Vet Res 1982;43:465470.

  • 2. Hoenig M, Dawe DL. A qualitative assay for beta cell antibodies. Preliminary results in dogs with diabetes mellitus. Vet Immunol Immunopathol 1992;32:195203.

    • Search Google Scholar
    • Export Citation
  • 3. Davison LJ, Ristic JM, Herrtage ME, et al. Anti-insulin antibodies in dogs with naturally occurring diabetes mellitus. Vet Immunol Immunopathol 2003;91:5360.

    • Search Google Scholar
    • Export Citation
  • 4. Guptill L, Glickman L, Glickman N. Time trends and risk factors for diabetes mellitus in dogs: analysis of veterinary medical data base records (1970–1999). Vet J 2003;165:240247.

    • Search Google Scholar
    • Export Citation
  • 5. Nelson RW, Reusch CE. Animal models of disease: classification and etiology of diabetes in dogs and cats. J Endocrinol 2014;222:T1T9.

    • Search Google Scholar
    • Export Citation
  • 6. Nelson R. Canine diabetes mellitus. In: Feldman EC, Nelson RW, Reusch CE, et al, eds. Canine & feline endrocrinology. 4th ed. St Louis: Elsevier-Saunders, 2015;213257.

    • Search Google Scholar
    • Export Citation
  • 7. Beam S, Corea MT, Davidson MG. A retrospective-cohort study on the development of cataracts in dogs with diabetes mellitus: 200 cases. Vet Ophthalmol 1999;2:169172.

    • Search Google Scholar
    • Export Citation
  • 8. Basher AW, Roberts SM. Ocular manifestations of diabetes mellitus: diabetic cataracts in dogs. Vet Clin North Am Small Anim Pract 1995;25:661676.

    • Search Google Scholar
    • Export Citation
  • 9. Kador PF, Webb TR, Bras D, et al. Topical KINOSTAT ameliorates the clinical development and progression of cataracts in dogs with diabetes mellitus. Vet Ophthalmol 2010;13:363368.

    • Search Google Scholar
    • Export Citation
  • 10. Lee AY, Chung SK, Chung SS. Demonstration that polyol accumulation is responsible for diabetic cataract by the use of transgenic mice expressing the aldose reductase gene in the lens. Proc Natl Acad Sci U S A 1995;92:27802784.

    • Search Google Scholar
    • Export Citation
  • 11. van der Woerdt A, Nasisse MP, Davidson MG. Lens-induced uveitis in dogs: 151 cases 1985–1990. J Am Vet Med Assoc 1992;201:921926.

  • 12. Wilcock BP, Peiffer RL Jr. The pathology of lens-induced uveitis in dogs. Vet Pathol 1987;24:549553.

  • 13. Van Der Woerdt A. Lens-induced uveitis. Vet Ophthalmol 2000;3:227234.

  • 14. Simpson W, Wild G, Figg K, et al. Human T-cell mediated response to homologous lens antigen. Exp Eye Res 1989;48:4954.

  • 15. Patel M, Shine B, Murray PI. Antilens antibodies in cataract and inflammatory eye disease: an evaluation of a new technique. Int Ophthalmol 1990;14:97100.

    • Search Google Scholar
    • Export Citation
  • 16. Hendrix DVH. Diseases and surgery of the canine anterior uvea. In: Gelatt KN, Gilger BC, Kern TJ, eds. Veterinary ophthalmology. 5th ed. Ames, Iowa: Wiley-Blackwell, 2013;11641165.

    • Search Google Scholar
    • Export Citation
  • 17. Dziezyc J, Millichamp N, Smith W. Fluorescein concentrations in the aqueous of dogs with cataracts. Vet Comp Ophthalmol 1997;7:267270.

    • Search Google Scholar
    • Export Citation
  • 18. Paulsen M, Lavach J, Severin G, et al. The effect of lens-induced uveitis on the success of extracapsular cataract extraction: a retrospective study of 65 lens removals in the dog. J Am Anim Hosp Assoc 1986;22:4956.

    • Search Google Scholar
    • Export Citation
  • 19. Mille TR, Whitley RD, Meek LA, et al. Phacofragmentation and aspiration for cataract extraction in dogs: 56 cases (1980–1984). J Am Vet Med Assoc 1987;190:15771580.

    • Search Google Scholar
    • Export Citation
  • 20. Sigle KJ, Nasisse MP. Long-term complications after phacoemulsification for cataract removal in dogs: 172 cases (1995–2002). J Am Vet Med Assoc 2006;228:7479.

    • Search Google Scholar
    • Export Citation
  • 21. Cassuto H, Kochan K, Chakravarty K, et al. Glucocorticoids regulate transcription of the gene for phosphoenolpyruvate carboxykinase in the liver via an extended glucocorticoid regulatory unit. J Biol Chem 2005;280:3387333884.

    • Search Google Scholar
    • Export Citation
  • 22. Scaroni C, Zilio M, Foti M, et al. Glucose metabolism abnormalities in Cushing syndrome: from molecular basis to clinical management. Endocr Rev 2017;38:189219.

    • Search Google Scholar
    • Export Citation
  • 23. Ferraù F, Korbonits M. Metabolic syndrome in Cushing's syndrome patients. Front Horm Res 2018;49:85103.

  • 24. Djurhuss CB, Gravholt CH, Nielsen S, et al. Effects of cortisol on lipolysis and regional interstitial glycerol levels in humans. Am J Physiol Endocrinol Metab 2002;283:E172E177.

    • Search Google Scholar
    • Export Citation
  • 25. Umeki D, Ohnuki Y, Mototani Y, et al. Protective effects of clenbuterol against dexamethasone-induced masseter muscle atrophy and myosin heavy chain transition. PLoS One 2015;10:e0128263.

    • Search Google Scholar
    • Export Citation
  • 26. Ruzzin J, Wagman AS, Jensen J. Glucocorticoid-induced insulin resistance in skeletal muscles: defects in insulin signaling and the effects on a selective glycogen synthase kinase-3 inhibitor. Diabetologia 2005;48:21192130.

    • Search Google Scholar
    • Export Citation
  • 27. Oliver JA, Clark L, Corletto F, et al. A comparison of anesthetic complications between diabetic and nondiabetic dogs undergoing phacoemulsification cataract surgery: a retrospective study. Vet Ophthalmol 2010;13:244250.

    • Search Google Scholar
    • Export Citation
  • 28. Briggs CE, Nelson RW, Feldman E, et al. Reliability of history and physical examination findings for assessing control of glycemia in dogs with diabetes mellitus: 53 cases (1995–1998). J Am Vet Med Assoc 2000;217:4853.

    • Search Google Scholar
    • Export Citation
  • 29. Armbruster DA. Fructosamine: structure, analysis, and clinical usefulness. Clin Chem 1987;33:21532163.

  • 30. Reusch CE, Liehs MR, Hoyer M, et al. Fructosamine. A new parameter for diagnosis and metabolic control in diabetic dogs and cats. J Vet Intern Med 1993;7:177182.

    • Search Google Scholar
    • Export Citation
  • 31. Gum G, MacKay EO. Physiology of the eye. In: Gelatt KN, Gilger BC, Kern TJ, eds. Veterinary ophthalmology. 5th ed. Ames, Iowa: Wiley-Blackwell, 2013;192196.

    • Search Google Scholar
    • Export Citation
  • 32. Richter M, Guscetti F, Spiess B. Aldose reductase activity and glucose-related opacities in incubated lenses from dogs and cats. Am J Vet Res 2002;63:15911597.

    • Search Google Scholar
    • Export Citation
  • 33. Pollreisz A, Schmidt-Erfurth U. Diabetic cataract–pathogenesis, epidemiology and treatment. J Ophthalmol 2010;2010:608751.

  • 34. Davidson M, Nelms S. Diseases of the lens and cataract formation. In: Gelatt KN, Gilger BC, Kern TJ, eds. Veterinary ophthalmology. 5th ed. Ames, Iowa: Wiley-Blackwell, 2013;12141215.

    • Search Google Scholar
    • Export Citation
  • 35. Lee AYW, Chung SSM. Contributions of polyol pathway to oxidative stress in diabetic cataract. FASEB J 1999;13:2330.

  • 36. Regnier A. Clinical pharmacology and therapeutics. Part 1 drug delivery and pharmacokinetics. In: Gelatt KN, Gilger BC, Kern TJ, eds. Veterinary ophthalmology. Ames, Iowa: Wiley-Blackwell, 2013;351380.

    • Search Google Scholar
    • Export Citation
  • 37. Eichenbaum J, Macy D, Severin G, et al. Effect in large dogs of ophthalmic prednisolone acetate on adrenal gland and hepatic function. J Am Anim Hosp Assoc 1988;24:705709.

    • Search Google Scholar
    • Export Citation
  • 38. Glaze MB, Crawford MA, Nachreiner RF, et al. Ophthalmic corticosteroid therapy: systemic effects in the dog. J Am Vet Med Assoc 1988;192:7375.

    • Search Google Scholar
    • Export Citation
  • 39. Roberts SM, Lavach JD, Macy DW, et al. Effect of ophthalmic prednisolone acetate on the canine adrenal gland and hepatic function. Am J Vet Res 1984;45:17111714.

    • Search Google Scholar
    • Export Citation
  • 40. Bahar I, Rosenblat I, Erenberg M, et al. Effect of dexamethasone eyedrops on blood glucose profile. Curr Eye Res 2007;32:739742.

  • 41. Kymionis GD, Panagiotoglou T, Tsilimbaris MK. The effect of intense, short-term topical dexamethasone disodium phosphate eyedrops on blood glucose level in diabetic patients. Ophthalmologica 2007;221:426429.

    • Search Google Scholar
    • Export Citation
  • 42. Habib GS, Abu-Ahmad R. Lack of effect of corticosteroid injection at the shoulder joint on blood glucose levels in diabetic patients. Clin Rheumatol 2007;26:566568.

    • Search Google Scholar
    • Export Citation
  • 43. Habib G, Safia A. The effect of intra-articular injection of bethamethasone acetate/betamethasone sodium phosphate on blood glucose levels in controlled diabetic patients with symptomatic osteoarthritis of the knee. Clin Rheumatol 2009;28:8587.

    • Search Google Scholar
    • Export Citation
  • 44. Toda J, Fukushima H, Kato S. Systemic complications of posterior subtenon injection of triamcinolone acetonide in type 2 diabetes patients. Diabetes Res Clin Pract 2009;84:e38e40.

    • Search Google Scholar
    • Export Citation

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Evaluation of diabetes mellitus regulation in dogs treated with ophthalmic preparations of prednisolone acetate versus diclofenac sodium

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  • 1 1Department of Clinical Sciences, College of Veterinary Medicine, Kansas State University, Manhattan, KS 66506.
  • | 2 2Department of Statistics, Department of Arts and Sciences, Kansas State University, Manhattan, KS 66506.

Abstract

OBJECTIVE

To evaluate and compare regulation of diabetes mellitus (DM) in dogs with cataracts and well-controlled DM that received an ophthalmic preparation of prednisolone acetate versus diclofenac sodium.

ANIMALS

22 client-owned dogs with cataracts and well-controlled DM.

PROCEDURES

A prospective, randomized, double-masked, experimental study was conducted. On days 0 and 32, serum fructosamine concentrations (SFCs), clinical scores, and body weights were determined. Dogs were assigned to receive a topically administered ophthalmic preparation of either prednisolone acetate 1% or diclofenac sodium 0.1% in each eye 4 times daily for 28 days. Data analysis was conducted with generalized linear mixed models.

RESULTS

Findings indicated no meaningful differences in SFCs, clinical scores, or body weights between the treatment groups on days 0 or 32. Clinical score on day 0 was positively associated with SFC, as indicated by the corresponding rate of change such that each 1 -unit increase in clinical score was associated with an approximately 45.6 ± 9.4 μmol/L increase in SFC. In addition, the least squares mean ± SEM SFC was higher in spayed females (539.20 ± 19.23 μmol/L; n = 12) than in castrated males (458.83 ± 23.70 μmol/L; 8) but did not substantially differ between sexually intact males (446.27 ± 49.72 μmol/L; 2) and spayed females or castrated males regardless of the treatment group assigned.

CONCLUSIONS AND CLINICAL RELEVANCE

Findings indicated no evidence for any differential effect on DM regulation (assessed on the basis of SFCs, clinical scores, and body weights) in dogs treated topically with an ophthalmic preparation of prednisolone versus an ophthalmic preparation of diclofenac. Additional research investigating plasma concentrations of topically applied ophthalmic glucocorticoid medications is warranted. (Am J Vet Res 2019;80:1129-1135)

Abstract

OBJECTIVE

To evaluate and compare regulation of diabetes mellitus (DM) in dogs with cataracts and well-controlled DM that received an ophthalmic preparation of prednisolone acetate versus diclofenac sodium.

ANIMALS

22 client-owned dogs with cataracts and well-controlled DM.

PROCEDURES

A prospective, randomized, double-masked, experimental study was conducted. On days 0 and 32, serum fructosamine concentrations (SFCs), clinical scores, and body weights were determined. Dogs were assigned to receive a topically administered ophthalmic preparation of either prednisolone acetate 1% or diclofenac sodium 0.1% in each eye 4 times daily for 28 days. Data analysis was conducted with generalized linear mixed models.

RESULTS

Findings indicated no meaningful differences in SFCs, clinical scores, or body weights between the treatment groups on days 0 or 32. Clinical score on day 0 was positively associated with SFC, as indicated by the corresponding rate of change such that each 1 -unit increase in clinical score was associated with an approximately 45.6 ± 9.4 μmol/L increase in SFC. In addition, the least squares mean ± SEM SFC was higher in spayed females (539.20 ± 19.23 μmol/L; n = 12) than in castrated males (458.83 ± 23.70 μmol/L; 8) but did not substantially differ between sexually intact males (446.27 ± 49.72 μmol/L; 2) and spayed females or castrated males regardless of the treatment group assigned.

CONCLUSIONS AND CLINICAL RELEVANCE

Findings indicated no evidence for any differential effect on DM regulation (assessed on the basis of SFCs, clinical scores, and body weights) in dogs treated topically with an ophthalmic preparation of prednisolone versus an ophthalmic preparation of diclofenac. Additional research investigating plasma concentrations of topically applied ophthalmic glucocorticoid medications is warranted. (Am J Vet Res 2019;80:1129-1135)

Contributor Notes

Dr. Huey's present address is Memphis Veterinary Specialists, 555 Trinity Creek Cove, Cordova, TN 38018.

Dr. Fentiman's present address is Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Oklahoma State University, Stillwater, OK 74078.

Address correspondence to Dr. Rankin (arankin@vet.k-state.edu).