This paper examines competing treatments—surgery and radioactive iodine (RAI, I131)—for hyperthyroidism in the context of post-colonial Cold War nuclear science in Taiwan. Although the U.S.-led Cold War Atoms for Peace project pushed for the globalization of nuclear medicine, it had to compete with the Japanese colonial legacy in Taiwan (Republic of China). This government-in-exile embraced nuclear science and ushered in RAI with staged rituals. However, this modern procedure failed to overtake the surgical approach (thyroidectomy); in fact, as late as the 1990s, well after RAI had become a standard procedure throughout the world, surgery was still the major treatment option for this common disease in Taiwan. The tension between the global and the local is rooted in infrastructure as well as the materiality, regulation and availability of the Iodine 131 isotope, and, finally, the customary practice of the surgical tradition, established since the colonial period. Thyroid diseases, especially endemic goiter, were an important issue in colonial medicine, and the study, diagnosis, and treatments of thyroid diseases were an integral part of colonial surgeons’ identity. Surgical clinics had been a fixture of institutional medicine throughout Taiwan by the mid-twentieth century. In contrast, with the exception of a few prestigious hospitals in Taipei such as the National Taiwan University Hospital, most medical institutions and clinicians were not equipped to use isotopes. The availability of I131 was also limited, as the nuclear reactor did not become active until the 1960s. The preference for surgery thus points to the significance of material and social conditions of medical practice in Taiwan, amid the backdrop of the haunting images of the atomic bombs dropped by the U.S. on nearby Japan which the Atoms for Peace Project had aimed to overcome.

Sinus tachycardia due to hyperthyroidism is generally treated with beta-blockers. But some patients do not respond to beta-blockers or may have non-tolerable side effects or have contraindications. We presented a case with persistent sinus tachycardia secondary to hyperthyroidism refractory to maximal doses of propranolol. After ivabradine treatment, her heart rate was < 100 bpm within 24 hours. There were no electrocardiogram changes or side effects. The use of ivabradine is promising and can be considered in cases where tachycardia cannot be controlled in children with hyperthyroidism.

In this overview of success stories in veterinary clinical nutrition topics in cats and dogs reviewed include the dietary management of chronic kidney disease, dissolution of urinary tract uroliths by dietary modification, the recognition that taurine and L-carnitine deficiencies can cause dilated cardiomyopathy; that clinical signs associated with feline hyperthyroidism (caused by a benign adenoma) can be controlled by a low-iodine diet alone; that dietary management of canine osteoarthritis can also reduce non-steroidal anti-inflammatory drug doses; and that disease-free intervals and survival times can be statistically longer in dogs with Stage III lymphoma managed with diet. As we discover more about nutrigenetics and nutrigenomics, and as we expand our basic understanding of idiopathic diseases we are bound to identify more nutritionally related causes, and be able to develop novel dietary strategies to manage disease processes, including the formulation of diets designed to alter gene expression to obtain beneficial clinical outcomes.

Hypokalemic periodic paralysis is the most common form of periodic paralysis and is characterized by attacks of muscle paralysis associated with a low serum potassium (K+) level due to an acute intracellular shifting. Thyrotoxic periodic paralysis (TPP), characterized by the triad of muscle paralysis, acute hypokalemia, and hyperthyroidism, is one cause of hypokalemic periodic paralysis. The triggering of an attack of undiagnosed TPP by β2-adrenergic bronchodilators has, to our knowledge, not been reported previously. We describe two young men who presented to the emergency department with the sudden onset of muscle paralysis after administration of inhaled β2-adrenergic bronchodilators for asthma. In both cases, the physical examination revealed an enlarged thyroid gland and symmetrical flaccid paralysis with areflexia of lower extremities. Hypokalemia with low urine K+ excretion and normal blood acid-base status was found on laboratory testing, suggestive of an intracellular shift of K+, and the patients' muscle strength recovered at serum K+ concentrations of 3.0 and 3.3 mmol/L. One patient developed hyperkalemia after a total potassium chloride supplementation of 110mmol. Thyroid function testing was diagnostic of primary hyperthyroidism due to Graves disease in both cases. These cases illustrate that β2-adrenergic bronchodilators should be considered a potential precipitant of TPP.

Thyroid disorders become more common with advancing age. Clinical features of hypothyroidism overlap with signs and symptoms often present in euthyroid older people and there is high likelihood of misdiagnosis. Conversely, there may be a relative paucity of signs and symptoms in hyperthyroid older people. A large number of patients may have subclinical disease. High suspicion and confirmation by laboratory assay is the key to correct diagnosis, though thyroid function tests should be interpreted with caution during acute illnesses. There is a reduced requirement for levothyroxine replacement in elderly hypothyroid patients and dosage should be titrated up cautiously as it can unmask symptoms of ischaemic heart disease. Drug interactions should be taken into account because a number of drugs interfere with levothyroxine absorption and metabolism. Radioactive iodine ablation of overactive thyroid tissue is the preferred treatment of hyperthyroidism in older people.