@article{dorshorst_molin_rubin_johansson_stromstedt_pham_chen_hallbook_ashwell_andersson_2011, title={A Complex Genomic Rearrangement Involving the Endothelin 3 Locus Causes Dermal Hyperpigmentation in the Chicken}, volume={7}, ISSN={["1553-7404"]}, DOI={10.1371/journal.pgen.1002412}, abstractNote={Dermal hyperpigmentation or Fibromelanosis (FM) is one of the few examples of skin pigmentation phenotypes in the chicken, where most other pigmentation variants influence feather color and patterning. The Silkie chicken is the most widespread and well-studied breed displaying this phenotype. The presence of the dominant FM allele results in extensive pigmentation of the dermal layer of skin and the majority of internal connective tissue. Here we identify the causal mutation of FM as an inverted duplication and junction of two genomic regions separated by more than 400 kb in wild-type individuals. One of these duplicated regions contains endothelin 3 (EDN3), a gene with a known role in promoting melanoblast proliferation. We show that EDN3 expression is increased in the developing Silkie embryo during the time in which melanoblasts are migrating, and elevated levels of expression are maintained in the adult skin tissue. We have examined four different chicken breeds from both Asia and Europe displaying dermal hyperpigmentation and conclude that the same structural variant underlies this phenotype in all chicken breeds. This complex genomic rearrangement causing a specific monogenic trait in the chicken illustrates how novel mutations with major phenotypic effects have been reused during breed formation in domestic animals.}, number={12}, journal={PLOS GENETICS}, author={Dorshorst, Ben and Molin, Anna-Maja and Rubin, Carl-Johan and Johansson, Anna M. and Stromstedt, Lina and Pham, Manh-Hung and Chen, Chih-Feng and Hallbook, Finn and Ashwell, Chris and Andersson, Leif}, year={2011}, month={Dec} }
 @article{johansson_gardner_atkins_lafevers_breuhaus_2007, title={Cardiovascular effects of acute pulmonary obstruction in horses with recurrent airway obstruction}, volume={21}, ISSN={["0891-6640"]}, DOI={10.1892/0891-6640(2007)21[302:CEOAPO]2.0.CO;2}, abstractNote={Recurrent airway obstruction (RAO) is common in horses. Although pulmonary artery (PA) pressure increases during RAO, cardiac function in horses with RAO has received limited attention.The purpose of this study was to noninvasively determine the cardiovascular effects of acute pulmonary obstruction (APO) in horses with RAO and their reversibility.Five geldings with RAO, inducible by exposure to moldy hay, were studied.Pulmonary mechanics, echocardiography, serum troponin I concentrations, arterial blood gases, and hematocrit were obtained before and after 7 days of APO. Heart rate, PA diameter and flow characteristics, right and left ventricular luminal dimensions and wall thicknesses, global cardiac performance, and evidence of myocardial damage were evaluated. Pulmonary mechanics and echocardiography were reevaluated during remission.[corrected] Severe, transient APO did not induce chronic cor pulmonale in horses, because cardiac anatomy and function were normal between episodes. An acute episode of APO produced anatomical and functional cardiac changes in both the right and left heart (including increased PA diameter, abnormal septal motion, and decreased left ventricular diameter and estimated stroke volume), possibly because of the development of pulmonary hypertension, without apparent myocardial damage. The decrease in stroke volume was offset by the increase in heart rate.With APO of 7 days' duration, cardiovascular abnormalities and the functional airway changes that produce them are reversible when the offending allergens are removed.}, number={2}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Johansson, Anna M. and Gardner, Sarah Y. and Atkins, Clarke E. and LaFevers, D. Heath and Breuhaus, Babetta A.}, year={2007}, pages={302–307} }
 @article{fogle_gerard_johansson_breuhaus_blikslager_jones_2007, title={Spontaneous rupture of the guttural pouch as a complication of treatment for guttural pouch empyema}, volume={19}, ISSN={["0957-7734"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-34547981740&partnerID=MN8TOARS}, DOI={10.2746/095777307X196900}, abstractNote={Equine Veterinary EducationVolume 19, Issue 7 p. 351-355 Spontaneous rupture of the guttural pouch as a complication of treatment for guttural pouch empyema C. A. Fogle, Corresponding Author C. A. Fogle Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.*Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorM. P. Gerard, M. P. Gerard Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorA. M. Johansson, A. M. Johansson Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorB. A. Breuhaus, B. A. Breuhaus Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorA. T. Blikslager, A. T. Blikslager Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorS. L. Jones, S. L. Jones Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this author C. A. Fogle, Corresponding Author C. A. Fogle Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.*Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorM. P. Gerard, M. P. Gerard Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorA. M. Johansson, A. M. Johansson Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorB. A. Breuhaus, B. A. Breuhaus Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorA. T. Blikslager, A. T. Blikslager Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorS. L. Jones, S. L. Jones Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this author First published: 05 January 2010 https://doi.org/10.2746/095777307X196900Citations: 14AboutPDF ToolsExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat References Adkins, A.R., Yovich, J.V. and Colbourne, C.M. (1997) Nonsurgical treatment of chondroids of the guttural pouch in a horse. Aust. vet. J. 75, 332–333. 10.1111/j.1751-0813.1997.tb15703.x CASPubMedWeb of Science®Google Scholar Bentz, B.G., Dowd, A.L. and Freeman, D.E. (1996) Treatment of guttural pouch empyema with acetylcysteine irrigation. Equine Pract. 18, 33–35. Web of Science®Google Scholar Freeman, D.E. (1991) Guttural pouches. In: Equine Respiratory Disorders, Ed: J. Beech, Lea and Febiger, Philadelphia. pp 305–328. Web of Science®Google Scholar Freeman, D.E. (1999) Guttural pouch. In: Equine Surgery, Eds: J.A. Auer and J.A. Stick, W.B. Saunders, Philadelphia. pp 368–375. Google Scholar Hawkins, J.F., Frank, N., Sojka, J.E. and Levy, M. (2001) Fistulation of the auditory tube diverticulum (guttural pouch) with a neodymiumyttrium-aluminum-garnet laser for treatment of chronic empyema in two horses. J. Am. vet. med. Ass. 218, 405–407. 10.2460/javma.2001.218.405 CASPubMedWeb of Science®Google Scholar Judy, C.E., Chaffin, M.K. and Cohen, N.D. (1999) Empyema of the guttural pouch (auditory tube diverticulum) in horses: 91 cases (1977–1997). J. Am. vet. med. Ass. 215, 1666–1670. CASPubMedWeb of Science®Google Scholar McAllister, E.S. (1978) Guttural pouch disease. Proc. Am. Ass. equine Practnrs. 23, 251–256. Web of Science®Google Scholar Perkins, G.A., Pease, A., Crotty, E. and Fubini, S.L. (2003) Diagnosing guttural pouch disorders and managing guttural pouch empyema in adult horses. Comp. cont. Educ. pract. Vet. 25, 966–973. Web of Science®Google Scholar Citing Literature Volume19, Issue7August 2007Pages 351-355 ReferencesRelatedInformation}, number={7}, journal={EQUINE VETERINARY EDUCATION}, author={Fogle, C. A. and Gerard, M. P. and Johansson, A. M. and Breuhaus, B. A. and Blikslager, A. T. and Jones, S. L.}, year={2007}, month={Aug}, pages={351–355} }
 @article{johansson_gardner_levine_papich_lafevers_goldman_sheets_atkins_2004, title={Pharmacokinetics and pharmacodynamics of furosemide after oral administration to horses}, volume={18}, ISSN={["1939-1676"]}, DOI={10.1892/0891-6640(2004)18<739:PAPOFA>2.0.CO;2}, abstractNote={Furosemide is the most common diuretic drug used in horses. Furosemide is routinely administered as IV or IM bolus doses 3-4 times a day. Administration PO is often suggested as an alternative, even though documentation of absorption and efficacy in horses is lacking. This study was carried out in a randomized, crossover design and compared 8-hour urine volume among control horses that received placebo, horses that received furosemide at 1 mg/kg PO, and horses that received furosemide at 1 mg/kg IV. Blood samples for analysis of plasma furosemide concentrations, PCV, and total solids were obtained at specific time points from treated horses. Furosemide concentrations were determined by reversed-phase high-performance liquid chromatography with fluorescent detection. Systemic availability of furosemide PO was poor, erratic, and variable among horses. Median systemic bioavailability was 5.4% (25th percentile, 75th percentile: 3.5, 9.6). Horses that received furosemide IV produced 7.4 L (7.1, 7.7) of urine over the 8-hour period. The maximum plasma concentration of 0.03 microg/mL after administration PO was not sufficient to increase urine volume compared with control horses (1.2 L [1.0, 1.4] PO versus 1.2 L [1.0, 1.4] control). There was a mild decrease in urine specific gravity within 1-2 hours after administration of furosemide PO, and urine specific gravity was significantly lower in horses treated with furosemide PO compared with control horses at the 2-hour time point. Systemic availability of furosemide PO was poor and variable. Furosemide at 1 mg/kg PO did not induce diuresis in horses.}, number={5}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Johansson, AM and Gardner, SY and Levine, JF and Papich, MG and LaFevers, DH and Goldman, RB and Sheets, MK and Atkins, CE}, year={2004}, pages={739–743} }
 @article{johansson_gardner_levine_papich_lafevers_fuquay_reagan_atkins_2003, title={Furosemide continuous rate infusion in the horse: Evaluation of enhanced efficacy and reduced side effects}, volume={17}, ISSN={["1939-1676"]}, DOI={10.1892/0891-6640(2003)017<0887:FCRIIT>2.3.CO;2}, abstractNote={Journal of Veterinary Internal MedicineVolume 17, Issue 6 p. 887-895 Open Access Furosemide Continuous Rate Infusion in the Horse: Evaluation of Enhanced Efficacy and Reduced Side Effects Anna M. Johansson, Anna M. Johansson Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorSarah Y. Gardner, Corresponding Author Sarah Y. Gardner Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NC DVM, PhD, Department of Clinical Sciences, College of Veterinary Medicine, Hillsborough Street 4700, Raleigh, NC 27606; e-mail: [email protected].Search for more papers by this authorJay F. Levine, Jay F. Levine Department of Farm Animal Health and Resource Management, College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorMark G. Papich, Mark G. Papich Department of Anatomy, Physiological Sciences, and Radiology, College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorVirginia H. Reagan, Virginia H. Reagan Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorClarke E. Atkins, Clarke E. Atkins Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this author Anna M. Johansson, Anna M. Johansson Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorSarah Y. Gardner, Corresponding Author Sarah Y. Gardner Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NC DVM, PhD, Department of Clinical Sciences, College of Veterinary Medicine, Hillsborough Street 4700, Raleigh, NC 27606; e-mail: [email protected].Search for more papers by this authorJay F. Levine, Jay F. Levine Department of Farm Animal Health and Resource Management, College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorMark G. Papich, Mark G. Papich Department of Anatomy, Physiological Sciences, and Radiology, College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorVirginia H. Reagan, Virginia H. Reagan Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorClarke E. Atkins, Clarke E. Atkins Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this author First published: 28 June 2008 https://doi.org/10.1111/j.1939-1676.2003.tb02529.xCitations: 32AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat Abstract Continuous rate infusion (CRI) of furosemide in humans is considered superior to intermittent administration (IA). This study examined whether furosemide CRI, compared with IA, would increase diuretic efficacy with decreased fluid and electrolyte fluctuations and activation of the renin-angiotensin-aldosterone system (RAAS) in the horse. Five mares were used in a crossover-design study. During a 24-hour period, each horse received a total of 3 mg/kg furosemide by either CRI (0.12 mg/kg/h preceded by a loading dose of 0.12 mg/kg IV) or IA (1 mg/kg IV q8h). There was not a statistically significant difference in urine volume over 24 hours between methods; however, urine volume was significantly greater after CRI compared with IA during the first 8 hours ([median 25th percentile, 75th percentile]: 9.6 L [8.9, 14.4] for CRI versus 5.9 L [5.3, 6.0] for IA). CRI produced a more uniform urine flow, decreased fluctuations in plasma volume, and suppressed renal concentrating ability throughout the infusion period. Potassium, Ca, and Cl excretion was greater during CRI than IA (1,133 mmol [1,110, 1,229] versus 764 mmol [709, 904], 102.7 mmol [96.0, 117.2] versus 73.3 mmol [65.0, 73.5], and 1,776 mmol [1,657, 2,378] versus 1,596 mmol [1,457, 1,767], respectively). Elimination half-lives of furosemide were 1.35 and 0.47 hours for CRI and IA, respectively. The area under the excretion rate curve was 1,285.7 and 184.2 mL mg/mL for CRI and IA, respectively. Furosemide CRI (0.12 mg/kg/h) for 8 hours, preceded by a loading dose (0.12 mg/kg), is recommended when profound diuresis is needed acutely in horses. References 1 Jackson EK. Diuretics. In: JG Hardman, LE Limbird, PB Molinoff, RW Ruddon, AG Gilman, eds. Goodman & Gilman's The Pharmacological Basis of Therapeutics. New York , NY : The McGraw-Hills Companies; 1995: 685–715. Web of Science®Google Scholar 2 Rose BD. Diuretics. Kidney Int 1991; 39: 336–352. 10.1038/ki.1991.43 CASPubMedWeb of Science®Google Scholar 3 Tobin T, Roberts BL, Swerczek TW, et al. The pharmacology of furosemide in the horse. III. Dose and time response relationships, effects of repeated dosing, and performance effects. J Equine Med Surg 1978; 2: 216–226. CASWeb of Science®Google Scholar 4 Hinchcliff KW, McKeever KH, Muir WW, 3rd. Furosemide-in-duced changes in plasma and blood volume of horses. J Vet Pharmacol Ther 1991; 14: 411–417. 10.1111/j.1365-2885.1991.tb00855.x CASPubMedWeb of Science®Google Scholar 5 Muir WW, McGuirk SM. Pharmacology and pharmacokinetics of drugs used to treat cardiac disease in horses. Vet Clin North Am Equine Pract 1985; 1: 335–352. 10.1016/S0749-0739(17)30759-9 CASPubMedWeb of Science®Google Scholar 6 Muir WW, Kohn CW, Sams R. Effects of furosemide on plasma volume and extracellular fluid volume in horses. Am J Vet Res 1978; 39: 1688–1691. CASPubMedWeb of Science®Google Scholar 7 Freestone JF, Carlson GP, Harrold DR, et al. Influence of furo-semide treatment on fluid and electrolyte balance in horses. Am J Vet Res 1988; 49: 1899–1902. CASPubMedWeb of Science®Google Scholar 8 Van Meyel JJ, Smits P, Russel FG, et al. Diuretic efficiency of furosemide during continuous administration versus bolus injection in healthy volunteers. Clin Pharmacol Ther 1992; 51: 440–444. 10.1038/clpt.1992.44 PubMedWeb of Science®Google Scholar 9 Lahav M, Regev A, Ra'anani P, et al. Intermittent administration of furosemide vs continuous infusion preceded by a loading dose for congestive heart failure. Chest 1992; 102: 725–731. 10.1378/chest.102.3.725 CASPubMedWeb of Science®Google Scholar 10 Acara MA. Renal pharmacology–Diuresis. In: CM Smith, AM Reynard, eds. Textbook of Pharmacology. Philadelphia , PA : WB Saunders Company; 1992: 554–588. Google Scholar 11 Baggot JD. The pharmacological basis of cardiac drug selection for use in horses. Equine Vet J Suppl 1995: 97–100. CASPubMedGoogle Scholar 12 Guthrie GP Jr, Cecil SG, Darden ED, et al. Dynamics of renin and aldosterone in the thoroughbred horse. Gen Comp Endocrinol 1982; 48: 296–299. 10.1016/0016-6480(82)90140-X CASPubMedWeb of Science®Google Scholar 13 Lee MG, Li T, Chiou WL. Effect of intravenous infusion time on the pharmacokinetics and pharmacodynamics of the same total dose of furosemide. Biopharm Drug Dispos 1986; 7: 537–547. 10.1002/bdd.2510070603 CASPubMedWeb of Science®Google Scholar 14 Pivac N, Rumboldt Z, Sardelic S, et al. Diuretic effects of fu-rosemide infusion versus bolus injection in congestive heart failure. Int J Clin Pharmacol Res 1998; 18: 121–128. CASPubMedWeb of Science®Google Scholar 15 Yelton SL, Gaylor MA, Murray KM. The role of continuous infusion loop diuretics. Ann Pharmacother 1995; 29: 1010–1014; quiz 1060–1011. 10.1177/106002809502901011 CASPubMedWeb of Science®Google Scholar 16 Gwilt PR. Pharmacokinetics. In: CR Craig, RE Stitzel, eds. Modern Pharmacology. Boston , MA : Little, Brown and Company; 1990: 68–81. Google Scholar 17 Chay S, Woods WE, Rowse K, et al. The pharmacology of furosemide in the horse. V. Pharmacokinetics and blood levels of fu-rosemide after intravenous administration. Drug Metab Dispos 1983; 11: 226–231. CASPubMedWeb of Science®Google Scholar 18 Harrison MH. Effects on thermal stress and exercise on blood volume in humans. Physiol Rev 1985; 65: 149–209. 10.1152/physrev.1985.65.1.149 CASPubMedWeb of Science®Google Scholar 19 Yamaoka K, Nakagawa T, Uno T. Application of Akaike's information criterion (AIC) in the evaluation of linear pharmacokinetic equations. J Pharmacokinet Biopharm 1978; 6: 165–175. 10.1007/BF01117450 CASPubMedWeb of Science®Google Scholar 20 Campbell MJ, Machin D. Non-parametric tests. In: MJ Campbell, D Machin, eds. Medical Statistics–A Commonsense Approach, 3rd ed. Chichester , UK : John Wiley & Sons Ltd; 1999: 163–165. Web of Science®Google Scholar 21 Chennavasin P, Seiwell R, Brater DC, et al. Pharmacodynamic analysis of the furosemide-probenecid interaction in man. Kidney Int 1979; 16: 187–195. 10.1038/ki.1979.120 CASPubMedWeb of Science®Google Scholar 22 Kaojarern S, Day B, Brater DC. The time course of delivery of furosemide into urine: An independent determinant of overall response. Kidney Int 1982; 22: 69–74. 10.1038/ki.1982.134 CASPubMedWeb of Science®Google Scholar 23 Hammarlund MM, Odlind B, Paalzow LK. Acute tolerance to furosemide diuresis in humans. Pharmacokinetic-pharmacodynamic modeling. J Pharmacol Exp Ther 1985; 233: 447–453. CASPubMedWeb of Science®Google Scholar 24 Streeten DH, Tomycz N, Anderson GH. Reliability of screening methods for the diagnosis of primary aldosteronism. Am J Med 1979; 67: 403–413. 10.1016/0002-9343(79)90786-1 CASPubMedWeb of Science®Google Scholar 25 Roberts BL, Blake JW, Tobin T. The pharmacology of furose-mide in the horse. II. Its detection, pharmacokinetics, and clearance from urine. J Equine Med Surg 1978; 2: 185–194. CASWeb of Science®Google Scholar Citing Literature Volume17, Issue6November 2003Pages 887-895 ReferencesRelatedInformation}, number={6}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Johansson, AM and Gardner, SY and Levine, JF and Papich, MG and LaFevers, DH and Fuquay, LR and Reagan, VH and Atkins, CE}, year={2003}, pages={887–895} }
 @article{johansson_gardner_jones_fuquay_reagan_levine_2003, title={Hypomagnesemia in hospitalized horses}, volume={17}, ISSN={["1939-1676"]}, DOI={10.1892/0891-6640(2003)017<0860:HIHH>2.3.CO;2}, abstractNote={This study was initiated to identify the signalment and clinical variables potentially associated with hypomagnesemia in horses evaluated at the North Carolina State University, College of Veterinary Medicine (NCSU-CVM) veterinary teaching hospital between January 1999 and May 2001. A nested case reference study (nested case-control study) was conducted to examine the potential relationship between hypomagnesemia and signalment, serum chemistry panel analyses, number of hospitalization days, discharge status, and diagnosis. A series of independent and multivariable logistic regression models were used to assess the potential association of each variable with low total serum magnesium concentrations. Four hundred one of 823 (48.7%) horses had serum total magnesium concentrations below the normal reference range. Hypomagnesemia was more likely to occur in horses older than 1 month of age. Colic (odds ratio [OR]: 2.96, 95% confidence intervals [CI]: 2.14–4.08), acute diarrhea (OR: 5.91, 95% CI: 2.32–15.06), other gastrointestinal disease (OR: 2.07, 95% CI: 1.15–3.71), infectious respiratory disease (OR: 5.07, 95% CI: 2.09–12.28), and multiorgan system disease (OR: 2.31, 95% CI: 1.24–4.28) were associated with hypomagnesemia in adult horses, whereas foals with diarrhea (excluding septic foals) (OR: 0.11, 95% CI: 0.01–0.84) were less likely to have hypomagne-semia. Overall, there was no relationship between hypomagnesemia and mortality (OR: 1.00, 95% CI: 0.72–1.41), but horses with colic and hypomagnesemia were less likely to die than horses with colic and normal or high total magnesium (OR: 0.53, 95% CI: 0.30–0.95). Among horses that survived, hypomagnesemia at admission was associated with a longer hospitalization period (OR: 1.45, 95% CI: 1.00–2.11).}, number={6}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Johansson, AM and Gardner, SY and Jones, SL and Fuquay, LR and Reagan, VH and Levine, JF}, year={2003}, pages={860–867} }