INVESTIGATIONS INTO HYPERLIPIDEMIA AND ITS POSSIBLE ...

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79 Discussion In the present study, Miniature Schnauzers with a history of pancreatitis were 5 times more likely to have hypertriglyceridemia and almost 15 times more likely to have moderate to severe hypertriglyceridemia (defined as >500 mg/dL) than age-matched Miniature Schnauzers with no history of pancreatitis. The majority of Miniature Schnauzers with a history of pancreatitis (58.8%) had moderate to severe hypertriglyceridemia as compared to only 8.8% in the control group. The presence of hypertriglyceridemia after resolution of pancreatitis is considered to provide retrospective evidence of a pre-existing disorder in lipid metabolism. 256,267,268,270 Knowing whether severe hypertriglyceridemia is a risk factor or even a cause of pancreatitis is of major importance in dogs, because control of hypertriglyceridemia might prevent the development or recurrence of pancreatitis. This has been confirmed in human patients with severe hypertriglyceridemia and pancreatitis, in whom control of hypertriglyceridemia limits the risk of recurrence of pancreatitis. 267,272 People with uncontrolled severe hypertriglyceridemia commonly have recurrent pancreatitis. 257,272 It remains to be determined whether pre-existing hypertriglyceridemia in this group of Miniature Schnauzers predisposed them to develop pancreatitis. A clear causal association between hypertriglyceridemia and pancreatitis in Miniature Schnauzers is very challenging to illustrate in clinical studies. Ideally, samples before, during, and after resolution of pancreatitis should be collected in order to clearly determine the association between hypertriglyceridemia and pancreatitis. Although this is possible to do in experimental models of pancreatitis, it is impossible in cases of naturally occurring
80 pancreatitis as it cannot be predicted which dogs will develop pancreatitis. Therefore, evidence of pre-existing hypertriglyceridemia in this study was based on the presence of hypertriglyceridemia after recovery from pancreatitis. Most follow-up samples were collected soon after pancreatitis was diagnosed (within 1-4 months) and thus it is very likely that hypertriglyceridemia was present before the development of pancreatitis. This has been shown in a large number of human studies using different methods, in which disorders of lipid metabolism that persist after recovery from pancreatitis were considered to be pre-existing. 256,267,268,270 Due to the fact that follow-up samples in Group 1 were collected after resolution of pancreatitis (based on both clinical and biochemical evidence), it is unlikely that hypertriglyceridemia in these samples was the result of pancreatitis. There is a theoretical possibility that pancreatitis could have permanently changed lipid metabolism in those dogs but, to the authors’ knowledge, this has not been reported or even hypothesized in dogs or any other species. It needs to be pointed out that, in this study, Miniature Schnauzers with a history of pancreatitis were significantly more likely to be on diets labeled as low-fat than dogs of the same breed without such a history. This is very important because the reported serum triglyceride concentrations after recovery from pancreatitis likely underestimate the true prevalence and severity of serum triglyceride concentrations before the development of pancreatitis. Despite that, Miniature Schnauzers with a history of pancreatitis were significantly more likely to have hypertriglyceridemia than agematched Miniature Schnauzers with no history of pancreatitis. It is very important to note, however, that the diets were considered to be low-fat only based on their label and
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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
Page 41 and 42: 28 this theory, zymogen granules th
Page 43 and 44: 30 be quite different, especially i
Page 45 and 46: 32 Drugs As in humans, drug-induced
Page 47 and 48: 34 Signalment Dogs of any age, bree
Page 49 and 50: 36 erroneously direct the clinician
Page 51 and 52: 38 of changes over time in serum Sp
Page 53 and 54: 40 they have been shown to have a l
Page 55 and 56: 42 revealed either a normal pancrea
Page 57 and 58: 44 At present, a definitive diagnos
Page 59 and 60: 46 factors should always be investi
Page 61 and 62: 48 associated pancreatitis is much
Page 63 and 64: 50 clear whether hyperlipidemia was
Page 65 and 66: 52 hepatobiliary disease in both Mi
Page 67 and 68: 54 the reference range, while Group
Page 69 and 70: 56 ROC analysis and calculation of
Page 71 and 72: 58 Figure 3. Serum cPLI concentrati
Page 73 and 74: 60 There was no significant differe
Page 75 and 76: 62 severe (typically ≥1,000 mg/dl
Page 77 and 78: 64 gastrointestinal signs or suspec
Page 79 and 80: 66 CHAPTER III SERUM TRIGLYCERIDE C
Page 81 and 82: 68 logical assumption that a defect
Page 83 and 84: 70 pancreatitis. For the same reaso
Page 85 and 86: 72 Spec cPL concentrations were mea
Page 87 and 88: 74 were significantly more likely t
Page 89 and 90: 76 Figure 5. Comparison of serum tr
Page 91: 78 Figure 7. Comparison of serum tr
Page 96 and 97: 83 Although serum cholesterol conce
Page 98 and 99: 85 Footnotes a Spec cPL ® , IDEXX
Page 100 and 101: 87 several subfractions, with diffe
Page 102 and 103: 89 Miniature Schnauzers (Group 2) T
Page 104 and 105: 91 Assays Serum triglyceride (refer
Page 106 and 107: 93 Figure 8. Custom-built fluoresce
Page 108 and 109: 95 range HDL 1 has not been accurat
Page 110 and 111: 97 mg/dL) were significantly higher
Page 112 and 113: 99 Figure 10: Serum cholesterol con
Page 114 and 115: 101 (Eigenvalues=0.5455; P=0.00017;
Page 116 and 117: 103 Figure 12: Representative lipop
Page 118 and 119: 105 Figures 14A and 14B: Representa
Page 120 and 121: 107 Specifically, 97% of non-hypert
Page 122 and 123: 109 The fraction of TRLs was a sign
Page 124 and 125: 111 Schnauzers without hyperlipidem
Page 126 and 127: 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
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129 Figure 19. 1-dimensional sliced
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131 Dogs that did not respond to th
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133 Hypertriglyceridemia has been l
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135 degrees. One possible explanati
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137 Footnotes a Royal Canin Gastroi
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139 concentrations and lipoprotein
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141 inclusion criteria for the stud
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143 light source j , located in a d
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146 Serum triglyceride and choleste
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148 Figure 22. Serum triglyceride c
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150 Figure 24. 1-dimensional sliced
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152 Discussion The purpose of the p
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154 fraction of these dogs (about 3
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156 of lipoproteins might also have
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158 Footnotes a Roche/Hitachi MODUL
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160 the etiology of pancreatitis, b
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162 times (P=0.0343) for a serum cP
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164 peaks than dogs of other breeds
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166 19.3; 95% CI, 2.0-184.0; P=0.00
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168 4) Specific lipoprotein classes
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170 REFERENCES 1949;8:96-97. 1. Lew
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172 17. Whitney MS, Boon GD, Rebar
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174 33. Ford RB. Clinical managemen
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176 50. Nelson RW, Turnwald GH, Wil
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178 66. Williams DA, Steiner JM. Ca
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180 82. Yilmaz Z, Senturk S. Charac
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182 97. Fojo SS, Stalenhoef AF, Mar
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184 111. Lam CW, Yuen YP, Cheng WF,
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186 127. Crispin SM. Ocular manifes
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188 144. Lindsay S, Entenmann C, Ch
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190 161. Steiner JM. Canine pancrea
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192 176. Steiner JM, Teague SR, Wil
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194 191. Steiner JM. Diagnosis of p
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196 208. Talukdar R, Vege S. Recent
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198 224. Koch K, Drewelow B, Liebe
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200 241. Petrov MS, van Santvoort H
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202 258. Ewald N, Hardt PD, Kloer H
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204 274. Otvos JD, Jeyarajah EJ, Be
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206 289. Carpentier YA, Scruel O. C
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