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        <identifier>oai:figshare.com:article/34004085</identifier>
        <datestamp>2026-09-27T00:47:01Z</datestamp>
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          <dc:title>&lt;i&gt;Helicobacter pylori&lt;/i&gt; Management During Alendronate Therapy, Cell-Free DNA Levels, and Gastrointestinal Safety in Osteoporosis</dc:title>
          <dc:creator>Xuemei Huang (170562)</dc:creator>
          <dc:creator>Qingshan Liu (1286793)</dc:creator>
          <dc:creator>Xu Li (23864)</dc:creator>
          <dc:creator>Chengchui He (25115215)</dc:creator>
          <dc:creator>Xiaoli Xie (4496059)</dc:creator>
          <dc:creator>Qi Gou (10791362)</dc:creator>
          <dc:subject>Clinical microbiology</dc:subject>
          <dc:subject>Osteoporosis</dc:subject>
          <dc:subject>Helicobacter pylori</dc:subject>
          <dc:subject>alendronate</dc:subject>
          <dc:subject>DNA</dc:subject>
          <dc:description>&lt;p dir="ltr"&gt;Oral alendronate is widely used for osteoporosis, but upper gastrointestinal symptoms may complicate treatment initiation in patients with pre-existing gastric vulnerability. Helicobacter pylori infection contributes to chronic gastric inflammation, yet evidence is limited on whether infection management around alendronate initiation is associated with early biological or gastrointestinal outcomes. We therefore conducted a prospective, single-center, routine-care-based cohort study in 90 patients aged 50–85 years: 34 H. pylori-positive patients receiving eradication management, 26 H. pylori-positive patients with delayed, declined, incomplete, or unconfirmed management, and 30 H. pylori-negative reference patients. Plasma cfDNA was measured at baseline and week 24, and gastrointestinal adverse events, alendronate administration behavior, treatment interruption, and eradication confirmation were assessed during follow-up. Valid week-24 cfDNA data were available for 81 participants. Mean cfDNA change was −5.2 ± 3.5 ng/mL in the eradication-management cohort, −0.8 ± 4.0 ng/mL in the delayed-management cohort, and −1.7 ± 3.6 ng/mL in the reference cohort (overall P &lt; 0.001). Upper gastrointestinal adverse events occurred in 7/34 (20.6%), 11/26 (42.3%), and 4/30 (13.3%) participants, respectively (overall P = 0.034); serious gastrointestinal events were uncommon (0, 1, and 1 event, respectively). Total cfDNA was interpreted only as a non-specific circulating marker of inflammatory or tissue-stress burden and cannot identify a gastric or H. pylori-specific tissue source. These exploratory findings support structured H. pylori assessment, eradication confirmation, correct alendronate administration, and gastrointestinal safety monitoring during early osteoporosis treatment, while requiring confirmation in larger studies.&lt;/p&gt;</dc:description>
          <dc:date>2026-09-27T00:47:01Z</dc:date>
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          <dc:identifier>10.6084/m9.figshare.34004085.v1</dc:identifier>
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          <dc:rights>CC BY 4.0</dc:rights>
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