INVESTIGATIONS INTO HYPERLIPIDEMIA AND ITS POSSIBLE ...

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61 A serum triglyceride concentration of 862 mg/dL was selected based on ROC analysis, and this concentration was associated with a greater than 3-fold likelihood for having a serum cPLI concentration that is considered consistent with pancreatitis compared to the likelihood for dogs with triglyceride concentrations ≤ 862 mg/dL. The likelihood ratio for having a serum cPLI concentration that is consistent with pancreatitis was often higher (up to 8.5) when higher serum triglyceride concentrations were selected (Figure 2). Increases of serum triglyceride concentrations ≥ 862 mg/dL are generally considered to be rather severe. Results of the present study suggest that the severity of hypertriglyceridemia is an important factor affecting the risk for increased cPLI concentration consistent with pancreatitis in Miniature Schnauzers, and that only severely increased serum triglyceride concentrations are associated with an increased risk for an increased cPLI concentration consistent with pancreatitis in this breed. Mildly or moderately elevated serum triglyceride concentrations (e.g., < 800 mg/dL) did not appear to represent a risk factor for a serum cPLI concentration suggestive of pancreatitis in this study. These findings are in agreement with studies in humans, in which only severe hypertriglyceridemia is recognized as a cause of pancreatitis. 254,255 In humans, it has been reported that a serum triglyceride concentration above 1,000 mg/dL is an identifiable risk factor for pancreatitis. 255 In human patients, it has been described that hypertriglyceridemia can either be the cause or the result of pancreatitis, and the same has also been suggested for dogs. 19,165,255 When hypertriglyceridemia is the result of pancreatitis in humans it is usually mild to moderate, while hypertriglyceridemia that causes pancreatitis is usually
62 severe (typically ≥1,000 mg/dl). 255 In the present study, many dogs had serum triglyceride concentrations above the upper limit of the reference range and it is possible that some of these dogs might have had hypertriglyceridemia secondary to pancreatitis rather than the opposite. However, this speculation is not supported by the current literature. In 1 study where acute pancreatitis was experimentally induced in dogs, hypertriglyceridemia did not develop up to 96 hours after induction of pancreatitis. 19 Similar results were reported in another study where pancreatitis was experimentally induced in dogs by ligation of the major and minor pancreatic ducts. 18 In this study, pancreatitis did not result in hypertriglyceridemia or hypercholesterolemia up to 14 days after induction of pancreatitis. 18 In a more recent study, mild increases in serum triglyceride concentrations were noted in dogs after induction of pancreatitis. 20 Although serum triglyceride concentrations significantly increased, they remained within the reference range even after induction of pancreatitis. 20 However, this was not clearly discussed in this report. 20 Based on these studies, it can be concluded that hypertriglyceridemia is not a feature of experimentally induced pancreatitis in dogs. However, it remains unknown whether this is also the case for spontaneous canine pancreatitis. It should be mentioned that in another study of 56 dogs of different breeds (not including Miniature Schnauzers) with serum cPLI concentrations diagnostic for pancreatitis, only 14 (25%) had hypertriglyceridemia and of these only 1 (1.8%) had serum triglyceride concentration ≥862 mg/dL. g Collectively, the above data indicate that severe hypertriglyceridemia with triglyceride concentrations above 862 mg/dL, which in this study showed a significant association with serum cPLI concentrations consistent
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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
Page 23 and 24: 10 reach the vasculature, they acqu
Page 25 and 26: 12 Endocrine disease Most commonly,
Page 27 and 28: 14 with varying frequencies in dogs
Page 29 and 30: 16 hypercholesterolemia was found o
Page 31 and 32: 18 Primary hyperlipidemia with hype
Page 33 and 34: 20 Atherosclerosis Although dogs ap
Page 35 and 36: 22 Dietary management Typically, th
Page 37 and 38: 24 therapy when the latter fails to
Page 39 and 40: 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: 60 There was no significant differe
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 and 92: 78 Figure 7. Comparison of serum tr
Page 93: 80 pancreatitis as it cannot be pre
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
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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
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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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