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Diagnosis and management of diabetes mellitus in a Bali mynah (Leucopsar rothschildi).

Abstract: An 18-year-old female Bali mynah (Leucopsar rothschildi) was presented for polyphagia, weight loss, and incoordination. Diabetes mellitus was diagnosed based on the history and clinical findings, including persistent hyperglycemia with concurrent hypoinsulinemia and glucosuria. A treatment protocol was developed that led to improvement of clinical signs and management of hyperglycemia over several months. Because of the advanced age of the animal, difficulty in maintaining euglycemia, and the stress of handling and treatment, euthanasia was elected 167 days after initial presentation. At postmortem examination, no pancreatic lesions were detected histologically that would account for the diabetes mellitus. To our knowledge this is the first reported case of diabetes mellitus and clinical management of this condition in a passerine species.

Key words: diabetes mellitus, insulin, avian, passerine bird, Bali mynah, Leucopsar rothschildi

Clinical Report

An 18-year-old female Bali mynah (Leucopsar rothschildi) was presented on day 0 with a history of polyphagia, weakness, and incoordination of several days' duration. The bird was housed in a mixed-species exhibit for approximately 1 month before the onset of clinical signs and was offered a diet of fresh fruits and greens, egg whites, insects (mealworms, wax worms, and crickets), and pellets (Tropical Bits, Marion Zoological, Wayzata, MN, USA). On examination, an immature cataract was visible in the right eye. The bird was in thin body condition and underweight (70 g; reference interval for female Bali mynahs 14.5-15.5 years old, 79.9 88.7 g). (1) Results of a complete blood cell count (CBC) revealed moderate anemia (packed cell volume [PCV] 28%; reference interval, 40.2-48.2%). (1) The sample was markedly lipemie; thus, no serum biochemical analysis was performed. Sodium sulfachlorpyridazine (0.3 mg/mL of water PO; Vetisulid, Fort Dodge Animal Health, Fort Dodge, IA, USA) was dispensed in the water as prophylaxis against Atoxoplasma.

A blood sample was collected on day 7 after fasting for 1 hour. The bird was treated with iron dextran (10 mg/kg IM) and parenteral fluids (4 mL SC; 2.5% dextrose and 0.45% sodium chloride). Although plasma remained lipemie, biochemical values revealed hyperglycemia (910 mg/dL [50.6 mmol/L]; reference interval, 267-391 mg/dL [14.8-21.7 mmol/L]), hypocalcemia (4.1 mg/dL [1.0 mmol/L]; reference interval 7.3-9.7 mg/dL [1.82.4 mmol/L]), hyponatremia (143 mEq/L [143 mmol/L]; reference interval 145-167 mEq/L [145-167 mmol/L]), hyperkalemia (6.2 mEq/L [6.2 mmol/L]; reference interval 2.1-3.9 mEq/L [2.1-3.9 mmol/L]), hypochloremia (98 mEq/L [98 mmol/L]; reference interval 111-127 mEq/L [111-127 mmol/L]), and increased activity of aspartate aminotransferase (AST) (468 U/L; reference interval 200-370 U/L). (1) The bile acid level was unremarkable (8.17 [micro]g/mL [20 [micro]mol/L]). The abnormal values of electrolytes and potassium were considered possible artifacts because of sample lipemia and hemolysis, respectively.

A urine sample collected on day 15 registered high glucose on the glucometer (TRUEtrack. Nipro Diagnostics, Fort Lauderdale, FL, USA). On a urine dipstick (Multistix, Siemens Healthcare Diagnostics Inc, Tarrytown, NY, USA), glucose concentration measured >2000 mg/dL [111 mmol/ L] with no ketones present. A blood sample collected on day 24 after overnight fasting revealed a normal amylase level, hyperglycemia (898 mg/dL [49.8 mmol/L]), and an insulin concentration of 2.93 [micro]U/mL [20.4 [micro]mol/L]. The insulin level from an apparently healthy conspecific with a normal blood glucose level was 5.16 [micro]U/mL [35.8 [micro]mol/L]. Repeat urinalysis revealed persistent glucosuria. Diabetes mellitus was diagnosed on the basis of clinical signs, glucosuria, and hyperglycemia with concurrent low insulin level, compared with the insulin concentration of the conspecific and reference intervals reported for psittacine birds (4.18-12.40 [micro]U/mL [29.0-86.1 [micro]mol/L). (2) Fruit was therefore removed from the diet to decrease access to simple sugars.

On day 42, a blood glucagon level was measured by radioimmunoassay on an ethylenediaminetetra-acetic acid plasma sample (The Ohio State University Medical Center Clinical Laboratories, Columbus, OH, USA). Measured glucagon level was 280 [micro]g/mL [280 ng/L], which was slightly lower than that from a comparable plasma sample of an apparently healthy conspecific (372 [micro]g/mL [372 ng/L]). Although reference intervals for Bali mynahs have not been established, glucagon levels determined in 16 normal blue and gold macaws (Ara ararauna), a scarlet macaw (Ara macao), a hyacinth macaw (Anodorhynchus hyacinthinus), and a hybrid macaw species ranged from 299 to 1190 [micro]g/mL [299-1190 ng/L] compared with the levels in a diabetic blue and gold macaw that ranged from 684 to 2179 [micro]g/mL [684-2179 ng/L].3 The blood glucose (BG) level continued to register high on the glucometer, indicating BG > 600 mg/ dL [33.3 mmol/L]. The body weight had declined to 63 g, and appetite remained ravenous. Keepers reported that the bird's eyesight seemed to be worsening, and on recheck examination, cataracts were observed in both eyes.

On day 46, insulin therapy was initiated, starting at 0.2 IU/kg q 12h protamine zinc insulin (PZI), compounded to 1 lU/mL (Taylors Pharmacy, Winter Park, FL, USA) and delivered with U-100 insulin syringes. Treatment effectiveness was assessed by clinical response, body weight, BG levels, and urine glucose levels when possible. Blood glucose levels were usually measured 2-3 hours after morning treatments. Generally, while receiving the 1 IU/mL insulin, if the BG was confirmed as high, an additional 0.02-IU dose was given immediately, and the insulin dose was increased by 0.01 1U for each morning or afternoon treatment. By day 54, the bird was less ravenous, although the BG concentration continued to register from 582 mg/dL [32.3 mmol/L] to "HIGH" from day 46 to day 54, and the urine glucose concentration remained high. Glipizide (0.5 mg/kg PO q12h; Accord Healthcare Inc, Durham, NC, USA) was administered from day 58 to day 67, but no additional clinical benefit was observed. Glucosuria during treatment with glipizide was generally 500 mg/dL [27.8 mmol/L], Because of the incremental increases in the insulin dose over time, as the volume of insulin surpassed 0.12 mL, the doses were administered half subcutaneously and half intramuscularly to minimize muscle trauma. When the volume reached 0.18 mL, the entire dose was administered subcutaneously, and concentrated (40 IU/mL) insulin was ordered. A compounded formulation was used from days 65 to 91, until the commercial product was obtained on day 92.

Although some mild clinical improvement was seen with the insulin compounded at 1 IU/mL (maximum dose, 2.4 IU/kg), hyperglycemia and glucosuria persisted. When the bird received a dose of 8 IU/kg IM of insulin compounded at 40 IU/ mL, euglycemia was inconsistently achieved, and glucosuria was minimal. By day 72 (27 days after initiating insulin therapy), the anemia had resolved (PCY 42%), glucosuria was abated, and fair glycemie control was achieved for a few hours after insulin injection. A BG curve performed after the bird received compounded insulin at 10.7 IU/ kg IM (0.8 IU) showed mild to moderate hyperglycemia in the hours after the insulin injection and negative glucose on the urine dipstick (Table 1). However, within 3 hours, the BG again measured high by glucometer. An additional dose of 0.4 IU that day had similar results. For the next 20 days, the bird was maintained at a dosage of 10.7 IU/kg IM q12h of the compounded insulin (40 IU/mL). During this period, body weight averaged 78 g and glucosuria remained trace to negative.

On day 87, a BG curve was performed after subcutaneous administration of the insulin at the same dosage (Table 1) to compare administration routes. Results were similar to those achieved with intramuscular injection; thus, the bird was maintained on intramuscular injections because of ease of administration.

On day 92, the bird was switched to protamine zinc recombinant human insulin (ProZinc, Boehringer Ingelheim, St Joseph, MO, USA; 40 IU/mL) administered at the same dosage (Table 1). On day 94, the bird was found off the perch and depressed 4 hours after receiving insulin. Blood glucose level was 115 mg/dL [6.4 mmol/L]; thus, 2 drops of 50% dextrose solution were applied to the oral mucous membranes, followed by 2 mL of an elemental diet (Emeraid Carnivore, Lafeber Company, Cornell, IL, USA) by gavage. The afternoon BG level was 398 mg/dL [22.1 mmol/L], and no insulin was administered because of the risk of hypoglycemia with no overnight monitoring. The next day, a BG curve showed a longer period of euglycemia was achieved with the ProZinc than with the compounded insulin (Table 1). On day 96, the dose of ProZinc insulin was decreased to 5.3 IU/kg in the hopes that it would allow for twice daily administration with less extreme swings in the glucose levels and potentially allow the bird to be discharged back into the care of the zookeepers. The results of the BG tests performed on days 96 and 97 indicated fair to good glycemie control (Table 1).

On day 113, a blood sample was collected before treatment. Results of the CBC and serum biochemical analysis were unremarkable except for hyperglycemia (797 mg/dL [44.2 mmol/L]). The AST, cholesterol, and triglyceride concentrations were within reference intervals, and the bile acid level was 41.7 [micro]g/mL [102 [micro]mol/L]. Although no reference interval for bile acids in Bali mynahs was available, this level appeared to be at the high end of the reference interval to slightly elevated compared with levels in psittacine birds. (4) No lipemia was present.

To better manage the hyperglycemia, on day 117 the bird was transitioned to a pelleted diet with lower carbohydrate content (Low Iron Softbilled Bird-Pare, Reliable Protein Products, Rancho Mirage, CA, USA). Another glucose curve on day 129 showed that mild hypoglycemia to euglycemia was maintained for at least 3 hours, and mild to moderate hyperglycemia for an additional 3 hours (Table 1). Prom days 72 to 153, the bird's body weight, based on an every-other-day weight measurement, ranged from 76 to 81 g, averaging 78 g.

The bird was successfully maintained on ProZinc insulin (5.3 IU/kg q12h) until the morning of day 154, when the bird had episodes of hypoglycemia with depression, dullness, and ataxia. Results of blood tests performed on day 155 revealed a PCV of 30% and glucose concentration of 540 mg/dL [30.0 mmol/L], with normal amylase, AST, and bile acid levels. The glucose levels remained unregulated for several days, during which time the bird was treated with supportive care. Subsequently, the bird stabilized clinically for 1.5 weeks at the current insulin dosage (ProZinc, 5.3 IU/kg q12h). On day 167, the bird was found recumbent 2 hours after the morning insulin dose. The BG level measured 43 mg/dL [2.4 mmol/L], Because of the poor prognosis for establishing a reliable treatment protocol to return this bird into the care of the zookeepers or to the exhibit, euthanasia was elected.

Postmortem examination revealed good body condition. The pancreas in the duodenal loop had a yellow translucent mass that was 5 mm in greatest dimension. Histologically, the pancreas had a few variably sized ductular cysts, mild multifocal nodular acinar cell hypoplasia, and focal mild islet cell hyperplasia. Numerous islets were observed that were histologically normal. Islet size and density were otherwise comparable to those of archived conspecifics that had unrelated disease processes, including 2 neonates and 4 geriatric adults. Histologically, no functional mass was identified, and the discrete pancreatic mass visible on gross examination was not appreciated. Additional histologic findings included moderate mesangioproliferative glomerulopathy with glomerulosclerosis, mild proliferative bronchitis, mild pneumoconiosis, mild splenic arteriosclerosis, mild hepatic hemosiderosis, mild endocardiosis, mild proliferative enterocolitis, ductular adenitis of the uropygial gland, an ovarian cystadenoma, mild rhabdomyolysis, and cataracts. Most of these abnormal findings were mild and considered secondary to aging and diabetes mellitus. The proventriculus, ventriculus, ganglia, brain, adipose, oviduct, and trachea were histologically normal.

Discussion

Naturally occurring diabetes mellitus (DM) has been documented in various psittacine birds and toucans, as well as in pigeons (Columba livia) and a red-tailed hawk (Buteo jamaicensis). (2,3,5-12 This is the first report of DM in a passerine species to our knowledge. Typical clinical signs in avian species include polyuria, polydipsia, polyphagia with weight loss, weakness, and lethargy. (2,7-9)

Glucagon, a catabolic hormone produced by the pancreatic islet A cells, is considered the dominant glucose regulator in birds, with levels typically ranging from 1000 to 4000 [micro]g/mL [1000-4000 ng/ L]. (2,7,13) Glucagon stimulates gluconeogenesis, glycogenolysis, and lipolysis in birds. Insulin, an anabolic hormone secreted by pancreatic islet B cells, stimulates glycogenesis. Somatostatin, produced by pancreatic D cells, inhibits secretion of glucagon and insulin. (13) Whereas in mammals hyperglycemia induces insulin production and release, in birds insulin can be released in response to a variety of factors, including glucagon, glucose, amino acids, and cholecystokinin. (2,13,14) The pathophysiology of DM in birds appears to be influenced somewhat by the taxonomic classification and feeding strategy. Experimentally, granivorous birds appear relatively insensitive to insulin, relying more on glucagon for primary regulation of glucose levels. Thus they are hypothesized to develop DM associated with an overproduction of glucagon. (2) Regulation of glucose in carnivorous birds, however, appears more dependent on insulin. (2,8)

Because DM has not previously been characterized in passerine birds, documenting the underlying hormonal imbalance in this case was important, but also led to delays in initiating treatment because of the difficulty in finding a laboratory to perform the glucagon test. The diabetic Bali mynah did not have evidence of excessive glucagon production when compared with a normal conspecific, as well as with other avian orders. The glucagon levels in both of these passerine birds (280-372 [micro]g/mL [280-372 ng/L]) was significantly lower than those in most other avian orders, which typically range from 2000 to 4000 [micro]g/mL (2000-4000 ng/L) in chickens, ducks, pigeons, and geese and from 299 to 1190 [micro]g/mL (299-1190 ng/L) in macaws (A. ararauna, A. macao, A. hyacinthinus) (3,14) The methodology for testing the glucagon in this mynah was similar to that used in macaws, except that aprotinin was not added to the whole blood. Aprotinin can prevent degradation of glucagon, although studies have shown this step to be unnecessary with advanced radioimmunoassay techniques and tracers currently used. (15,16) Lurthermore, any degradation of glucagon that may occur actually causes spurious elevation, by up to 26% in one study, because hormone fragments may be recognized as intact molecules. (17,18) The diabetic Bali mynah we describe had a lower insulin level compared with that of a healthy conspecific and with reference intervals for psittacine birds, although reference intervals for passerine birds have not been established. Considering the apparently low glucagon level and an insulin value lower than a healthy conspecific despite concurrent hyperglycemia, we concluded that the bird had an insulin deficiency.

The typical pancreatic lesions associated with insulin-responsive DM, such as islet cell depletion, islet fibrosis, or islet amyloidosis, were not present in this case. Islet cell morphology and islet density were judged to be within normal limits on the basis of examination of archival conspecifics of varying age and with disease processes that did not include DM. The ductular cysts and acinar cell hyperplasia in this bird are common age-related incidental findings and would not be expected to result in derangements of glucose metabolism or islet function. The cause for the DM in this case could not be determined from the tissues that were examined histologically. The pituitary gland, which can indirectly influence glucose metabolism, was not available. Pituitary tumors in budgerigars (Melopsittacus undulatus) secrete somatostatin, and somatostatinomas in some species, including humans and bearded dragons (Pogona vitticeps), may be associated with hyperglycemia.

Because of the high metabolic rate of passerine birds, a long-acting insulin was desired. Initially insulin glargine was investigated, but because of the high concentration and manufacturer's warnings not to dilute the insulin, other options were pursued. A blue and gold macaw was managed well with neutral protamine Hagedorn insulin (0.2 IU/kg SC q12h) for at least 7 months. (3) A diabetic nanday conure (Nandayus nenday) was managed for approximately 1 month; it was treated for approximately 1.5 weeks with a diluted formulation of an intermediate-acting porcine insulin (Caninsulin, Merck, Sharp, & Dohme Animal Health, Kenilworth, NJ, USA; 0.4 IU/kg q12h), which produced unsatisfactory results, and for approximately 2.5 weeks with diluted, long-acting human insulin (Humulin U, 0.25-0.35 IU/kg q12h) before its death. (5) However, a chestnut-fronted macaw (Ara severa) was managed for 22 months on Caninsulin (0.5-0.67 IU/kg q12h), and a military macaw (Ara militaris) was managed for over 2 years with bovine PZI (0.1-0.15 IU/kg IM q12h). (11) In this case, we decided to treat the Bali mynah with PZI, and for several months the bird responded well to insulin therapy once an appropriate dosage was established. However, after switching from compounded to commercially produced 40 IU/mL insulin, the dose of insulin had to be decreased and the bird had more frequent episodes of hypoglycemia. Possible causes for this are several. The pelleted diet was changed to one with a lower carbohydrate content, which may have precipitated a need to decrease the insulin dose. Although specific testing was not performed on the compounded insulin, studies have documented that compounded insulin frequently does not meet United States Pharmacopeia specifications, including concentration of insulin and zinc, pH, and endotoxin levels. (19) Finally, histologically normal islets were documented. There are multiple reports of diabetic birds that improved with treatment and were successfully maintained with decreasing doses of insulin or completely weaned off the insulin. (9,11,12) Histopathologic results from birds diagnosed with DM may reveal no histologic lesions of the pancreas or may show lesions including pancreatitis, multifocal islet cell hyperplasia and hypertrophy, islet atrophy, and neoplasia. (5,10,12) The histopathologic results of the pancreas in this Bali mynah showed many normal islets with some foci of hyperplasia.

Without conclusive histopathologic lesions, further conjecture on the pathophysiology behind the development of DM in this bird is difficult. Birds with hemosiderosis appear to be predisposed to developing DM. (11,12) Bali mynahs are predisposed to hemosiderosis, but only a mild amount was appreciated histologically in the liver of this bird. The original diet did contain simple sugars, and this bird was in a mixed species exhibit at the time of the onset of diabetes. Possibly the bird was preferentially selecting fruit from available diets. In people, vitamin D deficiency is associated with DM. (20) In a diabetic toucan (Ramphastos toco), urine glucose levels consistently decreased when the bird was exposed to natural sunlight. (12) The Bali mynah in this report was housed solely indoors. While it is possible that an association exists between vitamin D and DM in birds, controlled studies need to be performed.

One challenge in the management of DM in this bird was monitoring its glycemie status because of its small size, which limited the amount of blood that could be collected, particularly when it was anemic. Monitoring for glucosuria can be useful, but somewhat unreliable because of potential contamination of urine with fecal matter in the cloaca. Normal avian urine should be negative or have trace amounts of glucose if there is contamination of the urine by feces or uric acid. (2,7) Glucosuria may occur with blood glucose levels exceeding 600 mg/dL [33.3 mmol/L]. (4) As a passerine bird with a high metabolic rate, the insulin was likely rapidly metabolized. Although published dosages for psittacine birds are 0.002-3 IU/kg IM q 12h of neutral protamine Hagedorn insulin, and a toco toucan was treated with [is less than or equal to] 2 IU IM of PZI, this Bali mynah did not approach euglycemia until it received 8-10 IU/kg of compounded PZI. (3,11,12,21) Even then, it only maintained euglycemia for a few hours after treatment. Slightly lower doses of a commercial product, however, may be more effective.

As the first report of DM in a passerine bird, this case begins to describe potential management strategies for this avian order. Compared with cases described in other orders of birds, it appears that both the insulin dose and treatment frequency need to be much higher. Further investigation of normal insulin and glucagon levels in passerine species is needed.

Acknowledgments: We thank Dr Michael Gamer of Northwest ZooPath for the histologic examination and archival comparisons, and the veterinary technicians for their dedication in caring for and treating this bird.

References

(1.) Teare JA. Bali mynah (Leucopsar rothschildi)-reference ranges for physiologic data values. In: International Species Information System Physiologic Data Reference Values. Apple Valley, MN: International Species Information System; 2002.

(2.) Rae M. Avian endocrine disorders. In: Fudge AM, ed. Laboratory Medicine: Avian and Exotic Pets. Philadelphia, PA: WB Saunders; 2000:76-89.

(3.) Bonda M. Plasma glucagon, serum insulin, and serum amylase levels in normal and a hyperglycemic macaw. Proc Amu Conf Assoc Avian Vet. 1996;77 88.

(4.) Hochleithner M. Biochemistries. In: Ritchie BW, Harrison GJ, Harrison LR, eds. Avian Medicine: Principles and Application. Lake Worth, FL: Wingers Publishing Inc; 1994:223-245.

(5.) Desmarchelier M, Langlois I. Diabetes mellitus in a nanday conure (Nandayus nendav). J Avian Med Surg. 2008;22(3):246-254.

(6.) Kahler J. Sandostatin (synthetic somatostatin) treatment for diabetes mellitus in a sulfur-breasted toucan (Ramphastos sulfur atus sulfura tus). Proc Annu Conf Assoc Avian Vet. 1994;269-273.

(7.) Pilny AA. The avian pancreas in health and disease. Vet Clin North Am Exot Anim Pract. 2008; 11(1):25-34.

(8.) Wallner-Pendleton EA, Rogers D. Epple A. Diabetes mellitus in a red-tailed hawk (Buteo jamaicensis). Avian Pathol. 1993;22(3):631-635.

(9.) Oglesbee BL. Diseases of the endocrine system. In: Altman RB. Clubb SL, Dorrestein GM, Quesenberry K, eds. Avian Medicine and Surgery. Philadelphia, PA: WB Saunders Company; 1997:482-488.

(10.) Candeletta SC, Homer BL, Garner MM, Isaza R. Diabetes mellitus associated with chronic lymphocytic pancreatitis in an African grey parrot (Psittacus erithacus erithacus). J Assoc Avian Vet. 1993;7(1):39-43.

(11.) Gancz AY, Wellehan JFX, Boutette J, et al. Diabetes mellitus concurrent with hepatic hemosiderosis in two macaws (Ara severa, Ara militaris). Avian Pathol. 2007;36(4):331-336.

(12.) Murphy J. Diabetes in toucans. Proc Annu Conf Assoc Avian Vet. 1992:165-170.

(13.) Pollock C. Carbohydrate regulation in avian species. Semin Avian Exot Pet Med. 2002; 11 (2):57-64.

(14.) Hazelwood RL. Pancreas. In: Whittow GC, ed. Sturkie's Avian Physiology. 5th ed. San Diego, CA: Academic Press; 1999:539-555.

(15.) Bak MJ, Albrechtsen NW, Hartmann B, et al. No effect of aprotinin (Trasylol(tm)) on degradation of exogenous and endogenous glucagon in human, mouse and rat plasma. J Endocrinol Diabetes. 2014;1(1):5.

(16.) Hendriks T, Benraad TJ. On the stability of immunoreactive glucagon in plasma samples. Diabetologia. 1981 ;20(5):553-557.

(17.) Guder WG, Narayanan S, Wisser H, Zawta B. Diagnostic Samples: From the Patient to the Laboratory: The Impact of Preanalytical Variables on the Quality of Laboratory Results. 4th ed. Darmstadt, Germany: Wiley-Blackwell; 2009.

(18.) Eisentraut AM, Whissen N, Unger RH. Incubation damage in the radioimmunoassay for human plasma glucagon and its prevention with "Trasylol." Am J Med Sci. 1968;255(Feb): 137-142.

(19.) Scott-Moncrieff JCR, Moore GE, Coe J, et al. Characteristics of commercially manufactured and compounded protamine zinc insulin. J Am Vet Med Assoc. 2012;240(5):600-605.

(20.) Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357(3):266-281.

(21.) Pollock C, Carpenter JW, Antinoff N. Birds. In: Carpenter JW, ed. Exotic Animal Formulary. 3rd ed. St Louis, MO: Elsevier Saunders; 2005:135-344.

Susan L. Bartlett, DVM, Dipl ACZM, Ryan Bailey, DVM, and Eric Baitchman, DVM, Dipl ACZM

From Zoo New England, One Franklin Park Road, Boston, MA 02121, USA (Bartlett, Baitchman); and the College of Veterinary Medicine. University of Illinois at Urbana-Champaign, 2001 South Lincoln Avenue, Urbana. IL 61802, USA (Bailey). Present address (Bailey): School of Veterinary Medicine, University of California, Davis, One Shields Avenue, Davis, CA 95616, USA.
Table 1. Blood glucose curves and urine glucose test results performed
after administration of insulin to a Bali mynah with hypoglycemia.
Insulin was administered IM except on day 87.

                          Blood glucose concentration
                             after treatment, mg/dL
           Insulin
            dose,        Initial        0     1 h    2 h
Day         IU/kg     treatment time

72         10.7 (a)      8:10 AM        --    428    451
72          5.3         11:00 AM        --    337    438
87 (b)     10.7          8:18 AM        --    578    381
92         10.7 (c)      8:45 AM        --    494    450
95         10.7          8:00 AM        --    High   183
96          5.3          8:30 AM        --    --     326
97          5.3          8:30 AM        --    High   581
129         5.3          8:20 AM       High   237    189

           Blood glucose concentration
            after treatment, mg/dL
                                           Urine glucose
           3 h    4 h    6 h   8 h           (dipstick)
Day

72         High   --     --    --        --
72         High   --     --    --        Negative at 2:30 PM
87 (b)     591    High   --    --        Trace at 12:15 PM
92         High   --     --    --        Trace at 10:00 AM
95         --     324    --    584       --
96         --     332    --    --        --
97         381    349    575   592       --
129        381    491    549   High      --

(a) Compounded 40 IU/mL insulin used from days 65 to 91.

(b) Insulin was administered subcutaneously.

(c) ProZinc 40 IU/mL insulin used from day 92 to end of treatment.
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Title Annotation:Clinical Report
Author:Bartlett, Susan L.; Bailey, Ryan; Baitchman, Eric
Publication:Journal of Avian Medicine and Surgery
Article Type:Clinical report
Date:Jun 1, 2016
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