by Albert Yan Wo Chan. / Thesis (M.D.)--Chinese University of Hong Kong, 1995. / Includes bibliographical references (leaves 203-242). / Chapter CHAPTER1 --- INTRODUCTION --- p.1 / Chapter 1.1 --- Brief History of thyroid diseases --- p.2 / Chapter 1.2 --- Thyrotoxicosis and muscle diseases --- p.7 / Chapter 1.2.1 --- Thyrotoxic myopathy --- p.8 / Chapter 1.2.2 --- Exophthalmic ophthalmoplegia (Grave's ophthalmopathy) --- p.10 / Chapter 1.2.3 --- Myasthenia gravis --- p.10 / Chapter 1.2.4 --- Thyrotoxic periodic paralysis (TPP) --- p.11 / Chapter 1.2.4.1 --- Overview --- p.11 / Chapter 1.2.4.2 --- Prevalence --- p.13 / Chapter 1.3 --- Periodic paralysis syndromes in the Chinese --- p.16 / Chapter 1.4 --- Potassium homeostasis in TPP --- p.19 / Chapter 1.5 --- Cellular potassium transport --- p.24 / Chapter 1.5.1 --- Role of the sodium pump --- p.24 / Chapter 1.5.2 --- Hormonal control of the sodium pump --- p.26 / Chapter 1.5.3 --- Molecular biology of the sodium pump --- p.27 / Chapter 1.5.4 --- Na-K-Cl transporter --- p.30 / Chapter 1.5.5 --- Summary --- p.32 / Chapter 1.6 --- Mechanism of paralysis --- p.33 / Chapter 1.7 --- Aetiology of TPP --- p.37 / Chapter 1.7.1 --- Genetic predisposition --- p.37 / Chapter 1.7.2 --- Possible membrane defect --- p.38 / Chapter 1.7.3 --- The central role of the sodium pump in the pathogenesis of TPP --- p.39 / Chapter 1.7.4 --- Environmental factor --- p.40 / Chapter 1.7.5 --- Summary --- p.40 / Chapter 1.8 --- Aims of the thesis --- p.41 / Chapter CHAPTER2 --- A PILOT STUDY ON THE PATHOPHYSIOLOGY OF TPP --- p.44 / Chapter 2.1 --- Aim --- p.45 / Chapter 2.2 --- Background --- p.45 / Chapter 2.2.1 --- The measurement of Na-K ATPase/ sodium pump activity --- p.45 / Chapter 2.2.2 --- In vitro decline in plasma potassium concentration --- p.48 / Chapter 2.2.3 --- Catecholamines --- p.49 / Chapter 2.3 --- Subjects & methods --- p.50 / Chapter 2.4 --- Results --- p.51 / Chapter 2.5 --- Discussion --- p.56 / Chapter 2.6 --- Conclusion --- p.58 / Chapter CHAPTER3 --- PLATELET NA-K ATPASE AS A TISSUE MARKER OF HYPERTHYROIDISM --- p.59 / Chapter 3.1 --- Aim --- p.60 / Chapter 3.2 --- Background --- p.60 / Chapter 3.2.1 --- Thyroid function tests (TFTs) --- p.60 / Chapter 3.2.2 --- TFTs vs tissue markers as an index of hyperthyroidism --- p.61 / Chapter 3.2.3 --- Sodium pump activity as a tissue marker and TPP --- p.63 / Chapter 3.2.4 --- Choice of tissue for sodium pump study --- p.64 / Chapter 3.2.5 --- Rationale behind the aim of study --- p.65 / Chapter 3.3 --- Subjects & methods --- p.68 / Chapter 3.3.1 --- Chemicals --- p.68 / Chapter 3.3.2 --- Subjects --- p.68 / Chapter 3.3.3 --- Plasma thyroid hormones analysis --- p.69 / Chapter 3.3.4 --- Determination of platelet Na-K ATPase activity --- p.71 / Chapter 3.3.4.1 --- Principle --- p.71 / Chapter 3.3.4.2 --- Preparation of platelets --- p.73 / Chapter 3.3.4.3 --- Preparation of platelet lysate --- p.73 / Chapter 3.3.4.4 --- Measurement of Na-K ATPase activity --- p.74 / Chapter 3.3.4.5 --- Measurement of Pi --- p.76 / Chapter 3.3.4.6 --- Measurement of protein --- p.78 / Chapter 3.4 --- Statistics & data handling --- p.80 / Chapter 3.5 --- Results --- p.81 / Chapter 3.5.1 --- Development of the platelet Na-K ATPase assay --- p.81 / Chapter 3.5.1.1 --- Introduction --- p.81 / Chapter 3.5.1.2 --- Effect of saponin concentration on the Na-K ATPase activity --- p.81 / Chapter 3.5.1.3 --- Linearity of the Na-K ATPase assay --- p.83 / Chapter 3.5.1.4 --- Imprecision of the Na-K ATPase assay --- p.83 / Chapter 3.5.1.5 --- Linearity of the Pi assay --- p.86 / Chapter 3.5.1.6 --- Linearity of the protein assay --- p.86 / Chapter 3.5.2 --- Thyroid function tests --- p.89 / Chapter 3.5.3 --- Platelet Na-K ATPase activity --- p.92 / Chapter 3.5.4 --- Correlation between thyroid hormones concentrations and platelet Na-K ATPase activity --- p.95 / Chapter 3.5.5 --- Correlation between age and platelet Na-K ATPase activity --- p.95 / Chapter 3.5.6 --- Performance of platelet ATPase as an indicator of hyperthyroidism --- p.99 / Chapter 3.6 --- Discussion --- p.102 / Chapter CHAPTER4 --- BASAL NA-K ATPASE ACTIVITY IN THYROTOXIC SUBJECTS WITH AND WITHOUT HYPOKALAEMIC PERIODIC PARALYSIS --- p.107 / Chapter 4.1 --- Aim --- p.108 / Chapter 4.2 --- Introduction --- p.108 / Chapter 4.2.1 --- Background --- p.108 / Chapter 4.2.2 --- Difficulties and limitations in TPP study --- p.109 / Chapter 4.3 --- Subjects & methods --- p.112 / Chapter 4.3.1 --- Platelet Na-K ATPase --- p.112 / Chapter 4.3.2 --- Rubidium loading test --- p.114 / Chapter 4.4 --- Statistics & data handling --- p.115 / Chapter 4.5 --- Results --- p.117 / Chapter 4.5.1 --- Platelet Na-K ATPase activity --- p.117 / Chapter 4.5.1a --- Thyrotoxic vs TPP --- p.121 / Chapter 4.5.1b --- Thyrotoxic vs euthyroid and TPP vs EuTPP --- p.124 / Chapter 4.5.1c --- Control vs euthyroid and EuTPP --- p.126 / Chapter 4.5.2 --- Rubidium loading test --- p.127 / Chapter 4.6 --- Discussion --- p.129 / Chapter 4.6.1 --- Clinical marker of TPP --- p.129 / Chapter 4.6.2 --- RBC/ lymphocyte sodium pump activity --- p.130 / Chapter 4.6.3 --- Platelet Na-K ATPase activity --- p.135 / Chapter CHAPTER5 --- VALIDATION OF THE ORAL GLUCOSE TOLERANCE TEST --- p.142 / Chapter 5.1 --- Aim --- p.143 / Chapter 5.2 --- Background --- p.143 / Chapter 5.2.1 --- Need for a validated protocol for OGTT --- p.143 / Chapter 5.2.2 --- Effectiveness of sodium fluoride as a preservative of glucose in blood sample --- p.144 / Chapter 5.2.3 --- Effect of delay in sample handling --- p.146 / Chapter 5.2.4 --- Ideal concentration of NaF --- p.147 / Chapter 5.2.5 --- D-mannose as a preservative of blood glucose --- p.147 / Chapter 5.2.6 --- Rationale behind the aim of study --- p.148 / Chapter 5.3 --- Subjects & methods --- p.149 / Chapter 5.3.1 --- Effectiveness of NaF --- p.149 / Chapter 5.3.2 --- Effect of delay in sample handling --- p.150 / Chapter 5.3.3 --- Ideal concentration of NaF --- p.151 / Chapter 5.3.4 --- Evaluation of D-mannose as a preservative of blood glucose --- p.151 / Chapter 5.4 --- Results and discussion --- p.153 / Chapter 5.4.1 --- Effectiveness of NaF --- p.153 / Chapter 5.4.2 --- Effect of delay in sample handling --- p.157 / Chapter 5.4.3 --- Ideal concentration of NaF --- p.159 / Chapter 5.4.4 --- D-mannose as a preservative of glucosein blood --- p.161 / Chapter 5.4.5 --- Summary --- p.167 / Chapter CHAPTER6 --- HYPERINSULINAEMIA AND NA-K ATPASE ACTIVITY IN TPP --- p.168 / Chapter 6.1 --- Aim --- p.169 / Chapter 6.2 --- Background --- p.169 / Chapter 6.2.1 --- "Insulin, hypokalaemia and sodium pump" --- p.169 / Chapter 6.2.2 --- Insulin and skeletal muscle membrane potential --- p.170 / Chapter 6.2.3 --- Potential role of insulin in the pathogenesis of TPP --- p.172 / Chapter 6.2.4 --- Hyperinsulinaemia and thyrotoxicosis --- p.173 / Chapter 6.2.5 --- TPP vs uncomplicating thyrotoxic patients --- p.173 / Chapter 6.2.6 --- Catecholamines and insulin secretion --- p.175 / Chapter 6.3 --- Subjects and methods --- p.177 / Chapter 6.4 --- Statistics and data handling --- p.179 / Chapter 6.5 --- Results --- p.180 / Chapter 6.6 --- Discussion --- p.187 / Chapter CHAPTER7 --- OVERALL DISCUSSION AND CONCLUSION --- p.192 / Chapter 7.1 --- General discussion --- p.193 / Chapter 7.2 --- Role of sodium pump in the pathogenesis of TPP --- p.196 / Chapter 7.3 --- Strategy for further study --- p.201 / Chapter 7.4 --- Conclusion --- p.202 / REFERENCES --- p.203 / APPENDIX --- p.239 / (Selected publications)