School of Biotechnology, Kalinga Institute of Industrial Technology (Deemed University), Bhubaneswar, 751024, India.
Technology Business Incubator, Kalinga Institute of Industrial Technology (Deemed University), Bhubaneswar, 751024, India.
Biosci Rep. 2024 Nov 27;44(11). doi: 10.1042/BSR20240482.
Human malaria, caused by Plasmodium parasites, is a fatal disease that disrupts the host's physiological balance and affects the neuroendocrine system. This review explores how malaria influences and is influenced by hormones. Malaria activates the Hypothalamus-Pituitary-Adrenal axis, leading to increased cortisol, aldosterone, and epinephrine. Cortisol, while reducing inflammation, aids parasite survival, whereas epinephrine helps manage hypoglycemia. The Hypothalamus-Pituitary-Gonad and Hypothalamus-Pituitary-Thyroid axes are also impacted, resulting in lower sex and thyroid hormone levels. Malaria disrupts the renin-angiotensin-aldosterone system (RAAS), causing higher angiotensin-II and aldosterone levels, contributing to edema, hyponatremia and hypertension. Malaria-induced anemia is exacerbated by increased hepcidin, which impairs iron absorption, reducing both iron availability for the parasite and red blood cell formation, despite elevated erythropoietin. Hypoglycemia is common due to decreased glucose production and hyperinsulinemia, although some cases show hyperglycemia due to stress hormones and inflammation. Hypocalcemia, and hypophosphatemia are associated with low Vitamin D3 and parathyroid hormone but high calcitonin. Hormones such as DHEA, melatonin, PTH, Vitamin D3, hepcidin, progesterone, and erythropoietin protects against malaria. Furthermore, synthetic analogs, receptor agonists and antagonists or mimics of hormones like DHEA, melatonin, serotonin, PTH, vitamin D3, estrogen, progesterone, angiotensin, and somatostatin are being explored as potential antimalarial treatments or adjunct therapies. Additionally, hormones like leptin and PCT are being studied as probable markers of malaria infection.
人类疟疾是由疟原虫引起的，是一种致命疾病，会破坏宿主的生理平衡并影响神经内分泌系统。本综述探讨了疟疾如何影响和受激素影响。疟疾激活下丘脑-垂体-肾上腺轴，导致皮质醇、醛固酮和肾上腺素增加。皮质醇虽然能减轻炎症，但有助于寄生虫存活，而肾上腺素有助于控制低血糖。下丘脑-垂体-性腺轴和下丘脑-垂体-甲状腺轴也受到影响，导致性激素和甲状腺激素水平降低。疟疾还会破坏肾素-血管紧张素-醛固酮系统（RAAS），导致血管紧张素 II 和醛固酮水平升高，引起水肿、低钠血症和高血压。疟原虫引起的贫血会因铁调素增加而加重，铁调素会抑制铁吸收，减少寄生虫和红细胞形成所需的铁量，尽管促红细胞生成素水平升高。由于葡萄糖生成减少和高胰岛素血症，低血糖很常见，尽管有些病例由于应激激素和炎症而出现高血糖。低钙血症和低磷血症与维生素 D3 和甲状旁腺激素降低有关，但降钙素升高。脱氢表雄酮、褪黑素、甲状旁腺激素、维生素 D3、铁调素、孕酮和促红细胞生成素等激素具有抗疟作用。此外，正在探索脱氢表雄酮、褪黑素、5-羟色胺、甲状旁腺激素、维生素 D3、雌激素、孕酮、血管紧张素和生长抑素等激素的合成类似物、受体激动剂和拮抗剂或模拟物，作为潜在的抗疟治疗或辅助治疗方法。此外，瘦素和 PCT 等激素也被研究作为疟疾感染的可能标志物。
