The role of inflammatory cytokines in Meigs' syndrome

Case report OA: closed CC0
View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by qwen3.7-flash, 2026-10-10 ⓘ

Analysis of fluids from a Meigs' syndrome patient revealed elevated inflammatory cytokines that declined after tumor removal, suggesting these mediators contribute to the disorder's ascites and hydrothorax.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

BACKGROUND: Inflammatory cytokines are known to induce capillary leakage and third-space fluid accumulation in numerous gynecologic and nongynecologic disorders. This study aimed to assess their role in Meigs' syndrome. CASE: Evaluation of serum, peritoneal, and pleural fluids retrieved from a patient suffering from Meigs' syndrome revealed high interleukin (IL)-1beta, IL-6, IL-8, and tumor necrosis factor (TNF)-alpha levels. After surgical removal of the ovarian tumor and with resolution of ascites and hydrothorax, serum levels of IL-1beta, IL-6, and IL-8 declined, whereas tumor necrosis factor-alpha levels remained high. CONCLUSION: The correlation between these inflammatory cytokines and the clinical course of Meigs' syndrome suggests their involvement in the formation of ascites and hydrothorax in this disorder.

My notes (saved in your browser only)

MeSH descriptors

Cytokines Meigs Syndrome Cytokines Female Humans Interleukin-1 Interleukin-1 Interleukin-6 Interleukin-6 Interleukin-8 Interleukin-8 Meigs Syndrome Meigs Syndrome Postmenopause Tumor Necrosis Factor-alpha Tumor Necrosis Factor-alpha

Citation neighborhood (no data yet)

We don't have any in-corpus citations linked to this paper yet. The paper's references may be in our DB but unresolved to ``paper_id`` (resolution happens at ingest when the cited DOI matches a row we already have). Run the cross-source citation reconcile pass to retry.

References (8)

Source provenance

openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-10-08T21:00:31.392641+00:00
License: CC0 · commercial use OK