INVESTIGATIONS INTO HYPERLIPIDEMIA AND ITS POSSIBLE ...

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165 initial sample and to investigate the variability of the findings, the owners were instructed to have a second sample (sample 2) collected 1 to 2 months after the collection of the initial sample, and without making any changes to the diet of their dogs. If hypertriglyceridemia was confirmed in the second sample, the dogs were put on the study diet. Approximately 7 to 9 weeks after the dogs had been exclusively on the study diet a third blood sample (sample 3) was collected. Finally, a fourth sample (sample 4) was collected approximately 2 to 4 weeks after the third sample. Serum triglyceride concentrations before the diet change (median of sample 1: 480 mg/dL; median of sample 2: 493 mg/dL) were significantly higher than after the diet change (median of sample 3: 177 mg/dL; median of sample 4: 168 mg/dL; P=0.0001). Serum cholesterol concentrations before the diet change (mean of sample 1: 381 mg/dL; mean of sample 2: 380 mg/dL) were significantly higher than after the diet change (mean of sample 3: 257 mg/dL; mean of sample 4: 178 mg/dL; P
166 19.3; 95% CI, 2.0-184.0; P=0.006) were still classified as hyperlipidemic by lipoprotein profile analysis, while the majority of the dogs of this group (56%) were classified as normal. Logistic regression analysis of the baseline lipoprotein profiles (before the diet change) of dogs that eventually responded and dogs that did not respond to the diet change showed that dogs that responded to the diet change could be separated with 88% accuracy from the ones that did not respond, based on lipoprotein profile analysis even before the diet change. Dogs that did not respond to the diet change tended to have lower LDL fractions (mainly LDL 1 and LDL 2 ) and higher HDL fractions (mainly HDL 2a , HDL 3b , and HDL 3c ) than the ones that responded. The aims of the last part of the study were: a) to measure serum triglyceride and cholesterol concentrations in dogs with naturally occurring pancreatitis and compare them with those of healthy dogs, and b) to determine the lipoprotein profiles of dogs with naturally occurring pancreatitis and compare them with those of healthy dogs. Seventeen dogs with pancreatitis and 53 healthy control dogs were enrolled. There was no statistically significant difference in the proportion of dogs that had hypertriglyceridemia between dogs with pancreatitis (18%) and healthy controls (7.5%; P=0.35). However, there was a statistically significant difference in serum triglyceride concentrations between dogs with pancreatitis (median: 67 mg/dL; range: 48 – 324 mg/dL) and dogs healthy control dogs (median: 54 mg/dL; range: 26 – 257 mg/dL; P=0.0026). There was a statistically significant difference in the proportion of dogs that had hypercholesterolemia between dogs with pancreatitis (Group 1) and healthy control dogs (P=0.011). However, there was no statistically significant difference in serum
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INVESTIGATIONS INTO HYPERLIPIDEMIA
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INVESTIGATIONS INTO HYPERLIPIDEMIA
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iv was found to be useful for the s
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vi ACKNOWLEDGEMENTS I would like to
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viii TABLE OF CONTENTS Page ABSTRAC
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x LIST OF FIGURES FIGURE Page 1 Cor
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xii FIGURE Page 20 1-dimensional sl
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2 the results of these initial stud
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4 and HDL 1 concentrations and a de
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6 and, in smaller concentrations, L
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8 HDL molecules can be further subd
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10 reach the vasculature, they acqu
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12 Endocrine disease Most commonly,
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14 with varying frequencies in dogs
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16 hypercholesterolemia was found o
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18 Primary hyperlipidemia with hype
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20 Atherosclerosis Although dogs ap
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22 Dietary management Typically, th
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24 therapy when the latter fails to
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26 followed from the 1970s until to
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28 this theory, zymogen granules th
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30 be quite different, especially i
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32 Drugs As in humans, drug-induced
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34 Signalment Dogs of any age, bree
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36 erroneously direct the clinician
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38 of changes over time in serum Sp
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40 they have been shown to have a l
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42 revealed either a normal pancrea
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44 At present, a definitive diagnos
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46 factors should always be investi
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48 associated pancreatitis is much
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50 clear whether hyperlipidemia was
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52 hepatobiliary disease in both Mi
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54 the reference range, while Group
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56 ROC analysis and calculation of
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58 Figure 3. Serum cPLI concentrati
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60 There was no significant differe
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62 severe (typically ≥1,000 mg/dl
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64 gastrointestinal signs or suspec
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66 CHAPTER III SERUM TRIGLYCERIDE C
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68 logical assumption that a defect
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70 pancreatitis. For the same reaso
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72 Spec cPL concentrations were mea
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74 were significantly more likely t
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76 Figure 5. Comparison of serum tr
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78 Figure 7. Comparison of serum tr
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80 pancreatitis as it cannot be pre
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83 Although serum cholesterol conce
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85 Footnotes a Spec cPL ® , IDEXX
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87 several subfractions, with diffe
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89 Miniature Schnauzers (Group 2) T
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91 Assays Serum triglyceride (refer
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93 Figure 8. Custom-built fluoresce
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95 range HDL 1 has not been accurat
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97 mg/dL) were significantly higher
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99 Figure 10: Serum cholesterol con
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101 (Eigenvalues=0.5455; P=0.00017;
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103 Figure 12: Representative lipop
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105 Figures 14A and 14B: Representa
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107 Specifically, 97% of non-hypert
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109 The fraction of TRLs was a sign
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111 Schnauzers without hyperlipidem
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113 Footnotes a Roche/Hitachi MODUL
Page 128 and 129: 115 The biochemical, metabolic, and
Page 130 and 131: 117 Study design Each one of the do
Page 132 and 133: 119 Questionnaires and consent form
Page 134 and 135: 121 a target intensity of 30%, and
Page 136 and 137: 123 might affect lipid metabolism (
Page 138 and 139: 125 Figure 16. Serum triglyceride c
Page 140 and 141: 127 Figure 18. Serum Spec cPL conce
Page 142 and 143: 129 Figure 19. 1-dimensional sliced
Page 144 and 145: 131 Dogs that did not respond to th
Page 146 and 147: 133 Hypertriglyceridemia has been l
Page 148 and 149: 135 degrees. One possible explanati
Page 150 and 151: 137 Footnotes a Royal Canin Gastroi
Page 152 and 153: 139 concentrations and lipoprotein
Page 154 and 155: 141 inclusion criteria for the stud
Page 156 and 157: 143 light source j , located in a d
Page 159 and 160: 146 Serum triglyceride and choleste
Page 161 and 162: 148 Figure 22. Serum triglyceride c
Page 163 and 164: 150 Figure 24. 1-dimensional sliced
Page 165 and 166: 152 Discussion The purpose of the p
Page 167 and 168: 154 fraction of these dogs (about 3
Page 169 and 170: 156 of lipoproteins might also have
Page 171 and 172: 158 Footnotes a Roche/Hitachi MODUL
Page 173 and 174: 160 the etiology of pancreatitis, b
Page 175 and 176: 162 times (P=0.0343) for a serum cP
Page 177: 164 peaks than dogs of other breeds
Page 181 and 182: 168 4) Specific lipoprotein classes
Page 183 and 184: 170 REFERENCES 1949;8:96-97. 1. Lew
Page 185 and 186: 172 17. Whitney MS, Boon GD, Rebar
Page 187 and 188: 174 33. Ford RB. Clinical managemen
Page 189 and 190: 176 50. Nelson RW, Turnwald GH, Wil
Page 191 and 192: 178 66. Williams DA, Steiner JM. Ca
Page 193 and 194: 180 82. Yilmaz Z, Senturk S. Charac
Page 195 and 196: 182 97. Fojo SS, Stalenhoef AF, Mar
Page 197 and 198: 184 111. Lam CW, Yuen YP, Cheng WF,
Page 199 and 200: 186 127. Crispin SM. Ocular manifes
Page 201 and 202: 188 144. Lindsay S, Entenmann C, Ch
Page 203 and 204: 190 161. Steiner JM. Canine pancrea
Page 205 and 206: 192 176. Steiner JM, Teague SR, Wil
Page 207 and 208: 194 191. Steiner JM. Diagnosis of p
Page 209 and 210: 196 208. Talukdar R, Vege S. Recent
Page 211 and 212: 198 224. Koch K, Drewelow B, Liebe
Page 213 and 214: 200 241. Petrov MS, van Santvoort H
Page 215 and 216: 202 258. Ewald N, Hardt PD, Kloer H
Page 217 and 218: 204 274. Otvos JD, Jeyarajah EJ, Be
Page 219 and 220: 206 289. Carpentier YA, Scruel O. C
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