INVESTIGATIONS INTO HYPERLIPIDEMIA AND ITS POSSIBLE ...

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181 90. Miller NE, Rao SN, Alaupovic P, et al. Familial apolipoprotein C-II deficiency: plasma lipoproteins and apolipoproteins in heterozygous and homozygous subjects and the effects of plasma infusion. Eur J Clin Invest 1981;11:69-76. 91. Stalenhoef AF, Casparie AF, Demacker PN, et al. Combined deficiency of apolipoprotein C-II and lipoprotein lipase in familial hyperchylomicronemia. Metabolism 1981;30:919-926. 92. Catapano AL, Mills GL, Roma P, et al. Plasma lipids, lipoproteins and apoproteins in a case of apo C-II deficiency. Clin Chim Acta 1983;130:317-327. 93. Saku K, Cedres C, Mcdonald B, et al. C-II anapolipoproteinemia and severe hypertriglyceridemia: report of a rare case with absence of C-II apolipoprotein isoforms and review of the literature. Am J Med 1984;77:457-462. 94. Baggio G, Manzato E, Gabelli C, et al. Apolipoprotein C-II deficiency syndrome: clinical features, lipoprotein characterization, lipase activity, and correction of hypertriglyceridemia after apolipoprotein C-II administration in 2 affected patients. J Clin Invest 1986;77:520-527. 95. Connelly PW, Maguire GF, Hofmann T, et al. Structure of apolipoprotein C- IIToronto: a nonfunctional human apolipoprotein. Proc Natl Acad Sci USA 1987;84:270-273. 96. Connelly PW, Maguire GF, Little JA. Apolipoprotein C-IISt. Michael. Familial apolipoprotein C-II deficiency associated with premature vascular disease. J Clin Invest 1987;80:1597-1606.
182 97. Fojo SS, Stalenhoef AF, Marr K, et al. A deletion mutation in the apo C-II gene (apo C-IINijmegen) of a patient with a deficiency of apolipoprotein C-II. J Biol Chem 1988;263:17913-17916. 98. Fojo SS, Beisiegel U, Beil U, et al. Donor splice site mutation in the apolipoprotein (apo) C-II gene (apo C-II Hamburg) of a patient with apo C-II deficiency. J Clin Invest 1988;82:1489-1494. 99. Cox DW, Wills DE, Quan F, et al. A Deletion of one nucleotide results in functional deficiency of apolipoprotein C-II (apo C-IIToronto). J Med Genet 1988;25:649-652. 100. Fojo SS, Degennes JL, Chapman J, et al. An initiation codon mutation in the apo C-II gene (apo C-IIParis) of a patient with a deficiency of apolipoprotein C-II. J Biol Chem 1989;264:20839-20842. 101. Fojo SS, Lohse P, Parrott C, et al. A nonsense mutation in the apolipoprotein C-II gene in a patient with apolipoprotein C-II deficiency. J Clin Invest 1989;84:1215- 219. 102. Crecchio C, Capurso A, Pepe G. Identification of the mutation responsible for a case of plasmatic apolipoprotein C-II deficiency (apo C-IIBari). Biochem Biophys Res Commun 1990;168:1118-1127. 103. Hegele RA, Connelly PW, Maguire GF, et al. An apolipoprotein C-II mutation, C-IILys19---Thr' identified in patients with hyperlipidemia. Dis Markers 1991;9:73-80.
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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
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115 The biochemical, metabolic, and
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117 Study design Each one of the do
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119 Questionnaires and consent form
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121 a target intensity of 30%, and
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123 might affect lipid metabolism (
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125 Figure 16. Serum triglyceride c
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127 Figure 18. Serum Spec cPL conce
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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 and 178: 164 peaks than dogs of other breeds
Page 179 and 180: 166 19.3; 95% CI, 2.0-184.0; P=0.00
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: 180 82. Yilmaz Z, Senturk S. Charac
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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