Frontiers of Hormone Research最新文献

Exercise-associated hyponatremia (EAH) refers to below-normal serum sodium concentrations [Na+] that develop during exercise. The pathogenesis of EAH is best described as a spectrum ranging between profound polydipsia to modest sweat sodium losses with hypovolemia and relative dilution. Non-osmotic arginine vasopressin (AVP) remains the unifying pathogenic stimulus to abnormal renal water retention in acute symptomatic EAH. Cases of hyponatremia are mostly reported after endurance sports, but are also observed after shorter duration events and in team sport athletes. The signs and symptoms of EAH are vague, and include bloating, vomiting, headache, and altered mental status. A diagnosis of EAH can only be confirmed by a blood test, whereas signs/symptoms guide the most appropriate treatment strategy. Mild-to-moderate EAH (without encephalopathy) can be treated with either fluid restriction or an oral bolus of a hypertonic saline solution. Severe EAH (with encephalopathy) is a life-threatening emergency and should be urgently treated with intravenous 100 mL boluses of 3% saline until the resolution of encephalopathy symptoms. The prevention of EAH is evolutionarily rooted in preventing overdrinking during exercise. Drinking according to the dictates of thirst is the most individualized strategy to prevent life-threatening dysnatremia during exercise, regardless of sport.

In the evolutionary process, the successful adaptation of living organisms initially to an aqueous and thereafter to an arid terrestrial environment posed radically different challenges to the maintenance of water balance. Whereas the former required defense against water excess, the latter called for water conservation. To meet such challenges, the mammalian nephron evolved mechanisms for increasing both water excretion by diluting and water conservation by concentrating the urine. This chapter reviews the process whereby the osmosensors control thirst and the secretion of the antidiuretic hormone (vasopressin) to allow for either urinary dilution or concentration and thereby delicately maintain tonicity of body fluids within a very narrow range. Central to this process is the now well-defined cellular pathway whereby vasopressin renders the collecting duct, water permeable. Disorders of vasopressin secretion and action result in disturbances of body fluids tonicity, which are clinically recognized as abnormalities in reduced plasma sodium concentration or hyponatremia.

A time-dependent loss of cell solute protects against lethal cerebral edema in hyponatremia. This adaptation, which makes survival possible when the serum sodium concentration is extremely low, also makes the brain vulnerable to injury if chronic (>48 hours) hyponatremia is corrected more rapidly than lost brain solutes can be recovered. Rapid correction of chronic hyponatremia results in programmed cell death of astrocytes and oligodendrocytes and presents clinically with a delayed onset of neurological findings, known as the osmotic demyelination syndrome. This iatrogenic complication can be avoided by limiting correction of hyponatremia to <8 mEq/L per day.

Asymptomatic primary hyperparathyroidism has become the most common presentation of primary hyperparathyroidism in Europe and North America, and an increasingly common presentation in other parts of the world. As many as 25% of asymptomatic patients may develop indications for parathyroidectomy when followed long-term for up to 15 years. Patients who remain asymptomatic should be monitored for the development of complications that justify surgery. Patients who become symptomatic should be referred for surgery. Surgery may improve quality of life even in patients who remain asymptomatic.