Clinical Biochemistry of Domestic Animals (Sixth Edition) - UMK ...

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740 Chapter | 24 Lysosomal Storage Diseases N N N N N N N N N N N N N N N N N N Clinically normal male Clinically normal female Mannosidosis Heterozygous by assay N N Normal by assay Suspected mannosidosis Deceased Sex unknown FIGURE 24-14 The pedigree of a family of cats with alpha-mannosidosis. METABOLIC SCREENING OF URINE SAMPLES FIGURE 24-15 The scheme used to detect metabolic diseases, including some lysosomal storage disorders, by examining com- URINE pounds present in urine. SPOT TESTS PAPER CHROMATOGRAPHY THIN LAYER CHROMATOGRAPHY MPS spot Clinitest ketostix Nitroprusside Amino acid Organic acid Oligosaccharides Electrophoresis Carbohydrate chromatography Amino acid analyzer GC/Mass spectroscopy activity, there is overlap between the ranges for enzyme activity values from normal and obligate heterozygous animals ( Fig. 24-17 ). Thus, accurate determination of an asymptomatic individual as normal or a carrier may be difficult with an enzyme assay alone but can best be achieved by molecular DNA tests for the specific mutation in those diseases and families where the mutation has been identified. 2 An animal with clinical signs suspected of having an LSD that dies or requires euthanasia should have a complete postmortem examination, including the CNS, skeletal, and ocular 2 One such laboratory is the Josephine Deubler Genetic Disease Testing Laboratory, Section of Medical Genetics, Veterinary Hospital of the University of Pennsylvania, 3900 Delancy Street, Philadelphia, PA 19104- 6010 ( http://w3.vet.upenn.edu/research/centers/penngen/services ).
VI. Therapy 741 systems. Liver should be frozen as quickly as possible for subsequent determination of accumulated substrate, enzyme activities, and RNA and DNA analyses. Fibroblast cultures can be established from skin, linea alba, or pericardium (using sterile technique) for future studies that may require living cells. Liver, brain, and other tissues should be preserved in formalin, and samples should be taken for thin section and electron microscopy (in glutaraldehyde-paraformaldehyde), particularly from the liver and CNS. VI . THERAPY URINE SPOT TEST FOR GLYCOSAMINOGLYCANS NORMAL MPS AFFECTED FIGURE 24-16 The results of a urine spot test detecting abnormal amounts of glycosaminoglycans in the urine of animals with MPS. Enzyme activity 60 50 40 30 20 10 0 10 MEAN SERUM ALPHA-MANNOSIDASE ACTIVITY ±2 S.D. IN A COLONY OF RELATED CATS Affected Heterozygote Normal FIGURE 24-17 Serum alpha-mannosidase activity of a colony of cats illustrating the overlap that exists between normal and heterozygous animals. Although heterozygote detection is possible in a population, detection is difficult for an individual. Molecular techniques overcome these difficulties in carrier detection when the mutation is known. The combination of secretion of lysosomal enzymes by cells and uptake of enzymes by diseased cells via the M6P receptor system forms the basis for the present approaches to therapy for the LSDs. Providing a source of normal enzyme to abnormal cells will permit that enzyme to be taken up by the plasma membrane receptor, resulting in delivery of the normal enzyme to the lysosome where it can catabolize stored substrate (except for mucolipidoses). Fortunately, the amount of enzyme needed in the lysosome for sufficient function and, thus, phenotypic correction of an individual cell is only a small proportion of normal. The three approaches to providing normal enzyme to a patient’s cells are (1) enzyme replacement therapy (ERT), (2) bone marrow transplantation (BMT), and (3) gene therapy. In general, the most difficult target tissue in the LSDs is correction of the CNS lesions. Approximately 60% of LSDs have a CNS component, for which systemic therapy is limited by the blood-brain barrier. Successful treatment of the neuropathic LSDs will require direct therapy to the CNS or systemic therapy that crosses the blood-brain barrier. Animal models have been used extensively to evaluate these approaches to therapy for LSDs in humans. Although these novel therapies could be adapted for domestic animals, supportive care is generally used in clinical practice and emphasis is placed on prevention of the production of affected animals in future generations. A . Enzyme Replacement Therapy (ERT) The efficacy of the parenteral injection of purified recombinant enzyme has been tested in various animal models of LSDs, including MPS VII mice, MPS I dogs and cats, MPS VI cats, and glycogen storage disease in Japanese quail (Ellinwood et al. , 2004 ; Haskins et al. , 2002 ). In knockout mice, enzyme derived from rabbit milk or from Chinese hamster ovary cells has been shown to be useful ( Ioannou, 2000 ; Kakkis et al. , 1996, 2001 ; Wraith, 2001 ). Today, ERT by intravenous infusion is the standard therapy for non-neuronopathic Gaucher disease in human patients and is available or under evaluation for the treatment of Fabry disease, Pompe disease, MPS I, MPS II, and MPS VI. B . Bone Marrow Transplant (BMT) Heterologous BMT as therapy for LSDs has been performed for decades (reviewed in Brochstein [1992] , Haskins et al. [1991] , Hoogerbrugge and Valerio [1998 ], Krivit et al. [1999] , and O’Marcaigh and Cowan [1997] ). This approach provides both normal bone marrow and bone marrow-derived cells, which are available to release enzyme continuously for uptake by other deficient cells. In addition, some monocyte-derived cells can cross the bloodbrain barrier, becoming microglia and secreting an enzyme that can be available to neurons. BMT in animal models of LSDs has been carried out in MPS VII mice, mannosidosis, and mucolipidoses II cats, GM2 gangliosidosis mice, MPS VI cats, and the MPS VII dog, among others ( Haskins, 1996 ; Haskins et al. , 1991 ). A combination of neonatal ERT followed by BMT at 5 weeks of age in MPS VII mice had positive long-term effects ( Sands et al. , 1997 ).
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Preface It has been more than a dec
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viii Contributors Björn P. Meij (5
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2 Chapter | 1 Concepts of Normality
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10 Chapter | 1 Concepts of Normalit
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Chapter 2 Comparative Medical Genet
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I. Introduction 29 Green Red Green
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I. Introduction 31 A1 genetic map d
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I. Introduction 33 of genomes of va
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36 Chapter | 2 Comparative Medical
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46 Chapter | 3 Carbohydrate Metabol
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IX. Disorders of Carbohydrate Metab
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X. Disorders of Ruminants Associate
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X. Disorders of Ruminants Associate
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References 79 Kaneko , J. J. , Luic
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Chapter 4 Lipids and Ketones Michae
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II. Long Chain Fatty Acids 83 FIGUR
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II. Long Chain Fatty Acids 85 Plasm
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IV. Phospholipids 87 The regulation
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V. Cholesterol 89 V. CHOLESTEROL A.
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VI. Lipoproteins 91 TABLE 4-1 Compo
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VI. Lipoproteins 93 TABLE 4-2 Apoli
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96 Chapter | 4 Lipids and Ketones B
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98 Chapter | 4 Lipids and Ketones
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Chapter 5 Proteins, Proteomics, and
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III. Metabolism of Proteins 119 C .
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IV. Plasma Proteins 121 NH 4 HCO
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V. Methodology 123 molecule. The gl
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V. Methodology 125 has occurred wil
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V. Methodology 127 Although attempt
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V. Methodology 129 kD 94 67 43 2 2
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V. Methodology 131 D . Specific Pro
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VI. Normal Plasma and Serum Protein
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VII. Interpretation of Serum Protei
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References 149 Andersson , M. , Ste
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References 151 response of haptoglo
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References 153 dogs with metastasiz
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References 155 Watson , T. D. G. (
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158 Chapter | 6 Clinical Veterinary
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V. Methods for Evaluation of the Im
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VI. Laboratory Diagnosis of Disease
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Chapter 7 The Erythrocyte: Physiolo
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II. Hematopoiesis 175 progenitor ce
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III. Developing Erythroid Cells 177
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IV. Mature RBC 185 immune-mediated
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IV. Mature RBC 187 TABLE 7-3 Erythr
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IV. Mature RBC 189 TABLE 7.5 Erythr
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IV. Mature RBC 191 Echinocyte forma
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IV. Mature RBC 193 Pig RBC isoantig
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IV. Mature RBC 195 occurs in chicke
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IV. Mature RBC 197 inorganic phosph
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IV. Mature RBC 199 (a) FIGURE 7-6 T
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IV. Mature RBC 201 RBC 2,3DPG incre
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IV. Mature RBC 203 mechanisms would
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IV. Mature RBC 205 released during
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IV. Mature RBC 207 reduced by ascor
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V. Determinants of RBC Survival 209
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V. Determinants of RBC Survival 211
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VI. Inherited Disorders of RBCs 213
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described in people. They include a
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References 221 Boas , F. E. , Forma
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References 223 Della Rovere , F. ,
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References 225 Gedde , M. M. , Davi
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References 227 phosphofructokinase-
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References 231 Martinovich , D. , a
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References 235 Shadduck , R. K. ( 1
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References 237 Tennant , B. , Dill
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References 239 Williams , D. M. , L
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Chapter 8 Porphyrins and the Porphy
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II. Porphyrins 243 two vinyl groups
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II. Porphyrins 245 TABLE 8-2 Nomenc
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IV. Porphyrias 247 6. Uroporphyrins
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IV. Porphyrias 249 i . Urine It is
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IV. Porphyrias 251 to localize the
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IV. Porphyrias 253 FIGURE 8-6 Metab
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IV. Porphyrias 255 estrogens. The d
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References 257 and hexachlorobenzen
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Chapter 9 Iron Metabolism and Its D
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II. Iron Distribution 261 plasma of
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IV. Plasma Iron Transport 263 pathw
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VI. Iron Metabolism in Cells 265 of
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VI. Iron Metabolism in Cells 267 in
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VII. Tests for Evaluating Iron Meta
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VII. Tests for Evaluating Iron Meta
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VIII. Disorders of Iron Metabolism
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References 279 ( Norrdin et al ., 2
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References 281 Fresco , R. ( 1981 )
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References 283 Moore , C. V. , Duba
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References 285 Weiden , P. L. , Hac
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288 Chapter | 10 Hemostasis TABLE 1
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292 Chapter | 10 Hemostasis The pro
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294 Chapter | 10 Hemostasis exhibit
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298 Chapter | 10 Hemostasis that is
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302 Chapter | 10 Hemostasis However
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304 Chapter | 10 Hemostasis 2. Comp
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306 Chapter | 10 Hemostasis is a re
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308 Chapter | 10 Hemostasis 2. Asse
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310 Chapter | 10 Hemostasis necessi
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312 Chapter | 10 Hemostasis disease
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314 Chapter | 10 Hemostasis concent
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316 Chapter | 10 Hemostasis the rol
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318 Chapter | 10 Hemostasis proport
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320 Chapter | 10 Hemostasis a consi
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322 Chapter | 10 Hemostasis Bakhtia
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324 Chapter | 10 Hemostasis Dowd ,
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326 Chapter | 10 Hemostasis Kier ,
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328 Chapter | 10 Hemostasis Nielsen
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330 Chapter | 10 Hemostasis Tablin
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332 Chapter | 11 Neutrophil Functio
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352 Chapter | 12 Diagnostic Enzymol
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380 Chapter | 13 Hepatic Function L
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382 Chapter | 13 Hepatic Function e
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384 Chapter | 13 Hepatic Function p
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386 Chapter | 13 Hepatic Function m
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388 Chapter | 13 Hepatic Function s
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390 Chapter | 13 Hepatic Function f
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394 Chapter | 13 Hepatic Function 2
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398 Chapter | 13 Hepatic Function 2
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400 Chapter | 13 Hepatic Function c
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402 Chapter | 13 Hepatic Function F
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404 Chapter | 13 Hepatic Function A
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406 Chapter | 13 Hepatic Function E
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408 Chapter | 13 Hepatic Function K
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410 Chapter | 13 Hepatic Function R
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412 Chapter | 13 Hepatic Function W
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414 Chapter | 14 Gastrointestinal F
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Chapter 15 Skeletal Muscle Function
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II. Specialization of the Sarcolemm
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II. Specialization of the Sarcolemm
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III. Heterogeneity of Skeletal Musc
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III. Heterogeneity of Skeletal Musc
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V. Exercise and Adaptations to Trai
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VI. Diagnostic Laboratory Methods f
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VI. Diagnostic Laboratory Methods f
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IX. Selected Neuromuscular Disorder
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IX. Selected Neuromuscular Disorder
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References 479 and, recently, there
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References 481 Engel , A. G. ( 2004
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Chapter 16 Kidney Function and Dama
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II. Kidney Morphology and Function
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II. Kidney Morphology and Function
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III. Tests of Kidney Function 491 (
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III. Tests of Kidney Function 493 T
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III. Tests of Kidney Function 495 B
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6 5 4 3 2 1 0 Dog Cat Equine Cattle
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III. Tests of Kidney Function 499 d
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IV. Tests of Kidney Damage 501 1000
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IV. Tests of Kidney Damage 503 and
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IV. Tests of Kidney Damage 505 Enzy
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V. Biochemical Changes in Kidney Di
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V. Biochemical Changes in Kidney Di
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References 511 were reported to occ
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References 513 Bovee , K. C. ( 1969
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References 515 Deguchi , E. , and A
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References 521 Kühl , S. , Mischke
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References 523 creatinine measureme
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Chapter 17 Fluid, Electrolyte, and
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532 Chapter | 17 Fluid, Electrolyte
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VIII. Clinicopathological Indicator
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References 555 plasma water, electr
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References 557 Krzywanek , H. ( 197
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562 Chapter | 18 Pituitary Function
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606 Chapter | 19 Adrenocortical Fun
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624 Chapter | 20 Thyroid Function a
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628 Chapter | 20 Thyroid Function A
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630 Chapter | 20 Thyroid Function S
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632 Chapter | 20 Thyroid Function a
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634 Chapter | 20 Thyroid Function O
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636 Chapter | 21 Clinical Reproduct
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664 Chapter | 22 Trace Minerals the
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666 Chapter | 22 Trace Minerals the
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668 Chapter | 22 Trace Minerals P i
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670 Chapter | 22 Trace Minerals be
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Copper Cuproreductase Cytochromes C
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674 Chapter | 22 Trace Minerals 2 .
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676 Chapter | 22 Trace Minerals Cor
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678 Chapter | 22 Trace Minerals inf
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680 Chapter | 22 Trace Minerals tis
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682 Chapter | 22 Trace Minerals VI
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684 Chapter | 22 Trace Minerals red
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686 Chapter | 22 Trace Minerals of
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Page 691 and 692: Chapter 23 Vitamins Robert B. Rucke
Page 693 and 694: III. Fat-Soluble Vitamins 697 TABLE
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Page 762 and 763: References 767 Walter , J. ( 2000 )
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792 Chapter | 26 Cerebrospinal Flui
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Chapter 27 Clinical Biochemistry in
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II. Hepatotoxicity 823 Therefore, A
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III. Nephrotoxicity 825 suggested a
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IV. Toxins Affecting Skeletal and C
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VII. Toxins Affecting Erythrocytes
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VIII. Toxins Affecting Hemoglobin a
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IX. Toxins Affecting the Nervous Sy
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References 835 Plants classified as
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References 837 Solaiman , S. G. , M
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840 Chapter | 28 Avian Clinical Bio
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Budgerigar ALAT (IU/g tissue) Budge
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874 Appendix | I SI Units TABLE E S
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Appendix II Conversion Factors of S
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Appendix IV Stability of Serum Enzy
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Appendix VI Nomogram for Computing
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t0100 Appendix VIII Blood Analyte R
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884 Appendix | VIII Blood Analyte R
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890 Appendix | IX Blood Analyte Ref
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Appendix X Blood Analyte Reference
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Appendix XI Blood Analyte Reference
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Appendix XII Urine Analyte Referenc
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902 Appendix | XIII Cerebrospinal F
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904 Appendix | XIV Cerebrospinal Fl
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