INVESTIGATIONS INTO HYPERLIPIDEMIA AND ITS POSSIBLE ...

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17 apolipoprotein C-II, which is an activator of lipoprotein lipase, was evaluated for the presence of possible mutations in Miniature Schnauzers with primary hypertriglyceridemia. However, no variants of the apo-CII gene were found to be associated with hypertriglyceridemia. 112 Further studies are warranted to identify the genetic basis of primary hypertriglyceridemia in Miniature Schnauzers. Until recently, primary hypertriglyceridemia was considered to be a relatively benign condition in Miniature Schnauzers. However, recent studies indicate that hypertriglyceridemia in Miniature Schnauzers might be associated with pancreatitis, hepatobiliary disease, ocular disease, seizures, or possibly other conditions (for further discussion on this topic please see “Clinical signs and complications of hyperlipidemia” on page 18). Primary hyperlipidemia in other dog breeds Primary hypercholesterolemia without hypertriglyceridemia has been documented in 15 Briards from the United Kingdom (UK). 35 A similar condition has also been described in a family of rough-coated Collies also from the UK. 16 A slightly different condition of primary hypercholesterolemia with or without concurrent hypertriglyceridemia has been reported in Shetland Sheepdogs. 113 The cause of these lipid abnormalities that mainly involve cholesterol metabolism has not yet been determined, but hereditary factors were suspected. 16,35,113 In addition, primary hypercholesterolemia has been reported anecdotally in Doberman Pinschers and Rottweilers. 114
18 Primary hyperlipidemia with hypercholesterolemia and hypertriglyceridemia has been reported in 2 related Beagles. 115 Finally, primary hypertriglyceridemia has been reported in 2 related Brittany Spaniels and 1 mixed-breed 28-day old puppy. 116,117 Clinical signs and complications of hyperlipidemia In general, dogs with secondary hyperlipidemia display clinical signs associated with the primary disorder. In contrast, dogs with primary lipid disorders are often asymptomatic for long periods or throughout their lives, depending on many factors, including the type and severity of hyperlipidemia. However, some dogs with hyperlipidemia develop secondary diseases as a result of hyperlipidemia that may account for the development of specific clinical signs. Pancreatitis For a detail discussion on this topic please see “Relationship between hyperlipidemia and pancreatitis” on page 47. Hepatobiliary disease Clinical studies and anecdotal observations suggest that 2 hepatic disorders might be associated with hypertriglyceridemia in dogs: vacuolar hepatopathy and gallbladder mucocele. 118,119 Hyperlipidemia-associated vacuolar hepatopathy has been anecdotally associated with hyperlipidemia in Miniature Schnauzers. Also, a gallbladder mucocele has been commonly reported in dog breeds that are predisposed to idiopathic
Page 1 and 2: INVESTIGATIONS INTO HYPERLIPIDEMIA
Page 3 and 4: INVESTIGATIONS INTO HYPERLIPIDEMIA
Page 5 and 6: iv was found to be useful for the s
Page 7 and 8: vi ACKNOWLEDGEMENTS I would like to
Page 9 and 10: viii TABLE OF CONTENTS Page ABSTRAC
Page 11 and 12: x LIST OF FIGURES FIGURE Page 1 Cor
Page 13 and 14: xii FIGURE Page 20 1-dimensional sl
Page 15 and 16: 2 the results of these initial stud
Page 17 and 18: 4 and HDL 1 concentrations and a de
Page 19 and 20: 6 and, in smaller concentrations, L
Page 21 and 22: 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: 16 hypercholesterolemia was found o
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 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
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72 Spec cPL concentrations were mea
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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
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87 several subfractions, with diffe
Page 102 and 103:
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
Page 112 and 113:
99 Figure 10: Serum cholesterol con
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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
Page 130 and 131:
117 Study design Each one of the do
Page 132 and 133:
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 (
Page 138 and 139:
125 Figure 16. Serum triglyceride c
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127 Figure 18. Serum Spec cPL conce
Page 142 and 143:
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
Page 150 and 151:
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
Page 171 and 172:
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
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
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182 97. Fojo SS, Stalenhoef AF, Mar
Page 197 and 198:
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
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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