International journal of women's health · 2026
Gut and Gastric Dysbiosis in Hyperemesis Gravidarum: A Scoping Review of Microbiome-Targeted Evidence and Translational Pathways.
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Ratnadewi Neilvy, Husin Farid, Mose Johanes Cornelius, Syamsunarno Mas Rizky Anggun Adipurna, Irianti Setyorini
Аннотация
BACKGROUND: Hyperemesis gravidarum (HG) is defined by severe nausea and/or vomiting beginning in early pregnancy, impaired ability to eat or drink normally, and a marked restriction of daily activities. Although gastrointestinal dysbiosis has been proposed in HG, its role remains uncertain within the emerging growth differentiation factor 15 (GDF15)-centered model of susceptibility.
METHODS: Guided by PRISMA-ScR, this scoping review searched PubMed/MEDLINE, Scopus, Web of Science, publisher websites, and reference lists for contemporary evidence published between 1 January 2021 and 2 May 2026. Pre-2021 foundational publications were excluded from the charted evidence map and included-study count and were cited only as methodological or biological background.
RESULTS: Thirty-six sources of evidence were synthesized across five thematic domains. Direct human studies identified associations between HG and altered microbial diversity or composition, as well as gastric Helicobacter pylori exposure, but taxonomic findings were inconsistent and no reproducible diagnostic signature emerged. Mendelian randomization implicated Coprococcus 2, Ruminococcus, and Turicibacter, whereas observational studies could not resolve whether dysbiosis preceded symptoms or followed vomiting, dietary restriction, medication exposure, or hospitalization. Pregnancy-context and mechanistic studies supported plausible pathways involving bile acids, short-chain fatty acids, intestinal barrier function, inflammation, and gut-brain signaling, but these remain indirect for HG. GDF15-centered endocrine susceptibility had the strongest mechanistic support. Pregnancy probiotic and prebiotic studies provided safety and proof-of-concept data, while HG-specific efficacy evidence remained insufficient.
CONCLUSION: Current evidence supports dysbiosis as an associated modifier, consequence, or endotype marker rather than an established independent cause of HG. Priority studies should use Windsor-compatible definitions, early longitudinal sampling, harmonized sequencing and metabolomic methods, concurrent assessment of GDF15 and nutritional status, and biologically stratified trials of confirmed H. pylori infection or reproducible functional dysbiosis.
METHODS: Guided by PRISMA-ScR, this scoping review searched PubMed/MEDLINE, Scopus, Web of Science, publisher websites, and reference lists for contemporary evidence published between 1 January 2021 and 2 May 2026. Pre-2021 foundational publications were excluded from the charted evidence map and included-study count and were cited only as methodological or biological background.
RESULTS: Thirty-six sources of evidence were synthesized across five thematic domains. Direct human studies identified associations between HG and altered microbial diversity or composition, as well as gastric Helicobacter pylori exposure, but taxonomic findings were inconsistent and no reproducible diagnostic signature emerged. Mendelian randomization implicated Coprococcus 2, Ruminococcus, and Turicibacter, whereas observational studies could not resolve whether dysbiosis preceded symptoms or followed vomiting, dietary restriction, medication exposure, or hospitalization. Pregnancy-context and mechanistic studies supported plausible pathways involving bile acids, short-chain fatty acids, intestinal barrier function, inflammation, and gut-brain signaling, but these remain indirect for HG. GDF15-centered endocrine susceptibility had the strongest mechanistic support. Pregnancy probiotic and prebiotic studies provided safety and proof-of-concept data, while HG-specific efficacy evidence remained insufficient.
CONCLUSION: Current evidence supports dysbiosis as an associated modifier, consequence, or endotype marker rather than an established independent cause of HG. Priority studies should use Windsor-compatible definitions, early longitudinal sampling, harmonized sequencing and metabolomic methods, concurrent assessment of GDF15 and nutritional status, and biologically stratified trials of confirmed H. pylori infection or reproducible functional dysbiosis.