Journal of hypertension · 2013
Procalcitonin and the inflammatory response to salt in essential hypertension: a randomized cross-over clinical trial.
СтатьяРандомизированное исследованиеНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Mallamaci Francesca, Leonardis Daniela, Pizzini Patrizia, Cutrupi Sebastiano, Tripepi Giovanni, Zoccali Carmine
Аннотация
OBJECTIVES: Inflammation is considered as a major effector of arterial damage brought about by salt excess in animal models. In a randomized, single masked, cross-over study in 32 uncomplicated essential hypertensive patients, we assessed the effect of a short-term low-salt diet on biomarkers of innate immunity [procalcitonin (PCT), interleukin-6, C-reactive protein, and tumor necrosis factor-α (TNF-α)], adiponectin (ADPN, an anti-inflammatory cytokine), and leptin.
METHODS: Patients were randomized to either a 10-20 mmol sodium diet and sodium tablets (180 mEq/day) to achieve a 200 mmol intake per day or the same diet and identical placebo tablets, each for 2 weeks. At the end of each of these periods, all patients underwent a 24-h urine collection, a fasting blood sampling, and a 24 h ambulatory blood pressure monitoring.
RESULTS: In parallel with expected increase in plasma renin activity and aldosterone (P<0.001), both PCT (+33%) and TNF-α (9%) rose at low salt intake (P≤0.007) while ADPN underwent an opposite change (- 17%, P<0.001). In a linear regression analysis for repeated measurements, PCT was significantly and inversely related to urinary salt (weighted r=-0.27, P=0.03). Changes in inflammation biomarkers did not differ in salt-sensitive (n=7) and salt-resistant (n=25) patients.
CONCLUSION: In essential hypertensive patients, a very low salt diet generates a pro-inflammatory phenotype characterized by an increase in PCT and TNF-α and an opposite effect on an anti-inflammatory cytokine like ADPN.
METHODS: Patients were randomized to either a 10-20 mmol sodium diet and sodium tablets (180 mEq/day) to achieve a 200 mmol intake per day or the same diet and identical placebo tablets, each for 2 weeks. At the end of each of these periods, all patients underwent a 24-h urine collection, a fasting blood sampling, and a 24 h ambulatory blood pressure monitoring.
RESULTS: In parallel with expected increase in plasma renin activity and aldosterone (P<0.001), both PCT (+33%) and TNF-α (9%) rose at low salt intake (P≤0.007) while ADPN underwent an opposite change (- 17%, P<0.001). In a linear regression analysis for repeated measurements, PCT was significantly and inversely related to urinary salt (weighted r=-0.27, P=0.03). Changes in inflammation biomarkers did not differ in salt-sensitive (n=7) and salt-resistant (n=25) patients.
CONCLUSION: In essential hypertensive patients, a very low salt diet generates a pro-inflammatory phenotype characterized by an increase in PCT and TNF-α and an opposite effect on an anti-inflammatory cytokine like ADPN.