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同样患有原发性甲状旁腺功能亢进症(PHPT),为什么有些患者只是轻度骨量减少,有些患者却会发展为明显骨质疏松,甚至面临更高骨折风险?

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同样患有原发性甲状旁腺功能亢进症(PHPT),为什么有些患者只是轻度骨量减少,有些患者却会发展为明显骨质疏松,甚至面临更高骨折风险?

. 从肠道到骨髓:一种细菌牵动骨吸收. 科技导报, 2026 , 44 (11) : 4 -4 .
. Science & Technology Review, 2026 , 44 (11) : 4 -4 .
同样患有原发性甲状旁腺功能亢进症(PHPT),为什么有些患者只是轻度骨量减少,有些患者却会发展为明显骨质疏松,甚至面临更高骨折风险?
过去,人们通常把目光集中在甲状旁腺激素(PTH)本身:持续偏高的PTH会打破骨骼重建平衡、促进骨吸收,是PHPT诱发骨丢失的核心诱因。然而,一个长期困扰临床的问题是:PTH水平并不能完全解释患者之间骨损伤程度的巨大差异。换句话说,在“激素升高”和“骨头变脆”之间,身体里可能还存在其他关键“放大器”。
2026年5月25日,美国埃默里大学Roberto Pacifici团队发现,特定肠道细菌的丰度,可独立于PTH水平,预测患者的骨密度和骨微结构破坏程度。
研究纳入50例PHPT受试者,同步开展肠道菌群测序、免疫细胞分析和骨密度检测,发现长双歧杆菌(Bifidobacterium longum)是连接肠道菌群与骨丢失的关键节点。数据显示,B. longum丰度与患者体内的肿瘤坏死因子(TNF)和白细胞介素-17(IL-17)水平呈显著正相关,而这些炎症因子与骨吸收指标密切相关。
进一步机制研究提示,在PHPT背景下,B. longum可能通过以下路径加剧骨丢失:促进肠道中TNF+ T细胞和Th17细胞的扩增,并驱动这些免疫细胞向骨髓迁移;在骨髓微环境中,TNF和IL-17协同增强破骨细胞生成信号,从而加速骨吸收。研究团队还通过粪菌移植实验验证了因果关系:将PHPT患者的肠道微生物移植给无菌小鼠后,受体小鼠出现了与供体患者相似的骨结构破坏表型。
这一发现为理解PHPT患者骨骼表型异质性提供了新解释:不是所有患者的肠道菌群都以相同方式“配合”PTH发挥作用。某些患者之所以更易发生骨质疏松,可能部分归因于其肠道内B. longum等菌群更易激活炎症性T细胞反应。
(来源于中国科技期刊卓越行动计划入选期刊:《Bone Research》,2026,14,57)
2026年第44卷第11期
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  • 首发时间:2026-06-23
  • 出版时间:2026-06-13
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2种不同金属材料的力学参数

Family
属数
Number of
genus
种数
Number of
species
占总种数比例
Percentage of
total species (%)

Genus
种数
Number of
species
占总种数比例
Percentage of total
species (%)
鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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