Selenium
| 證據等級: L5 | 預測適應症: 10 個 |
目錄
Selenium: From Trace Element Supplementation to Sclerosing Cholangitis
One-Sentence Summary
Selenium (DrugBank DB11135) is an essential trace element with no specific approved disease indication on file in this evidence pack. The TxGNN model predicts it may be relevant to Sclerosing Cholangitis, but the supporting literature shows selenium deficiency as a consequence of the disease’s cholestasis-driven malabsorption, not a validated treatment target — with 0 clinical trials and 5 publications currently available, none testing selenium supplementation as therapy.
Quick Overview
| Item | Content |
|---|---|
| Original Indication | No specific approved indication on file — Selenium is registered here as an essential trace element/nutritional supplement rather than a drug approved for a defined disease |
| Predicted New Indication | Sclerosing Cholangitis (primary sclerosing cholangitis, PSC) |
| TxGNN Prediction Score | 99.04% (global rank 4,662) |
| Evidence Level | L4 |
| South Africa Market Status | Not Marketed |
| Number of SAHPRA Registrations | 0 |
| Recommended Decision | Hold |
Why is This Prediction Reasonable?
Currently, detailed mechanism of action data is not available (Data Gap DG002). Based on known information, Selenium is a cofactor for glutathione peroxidase and other selenoproteins, giving it a general antioxidant role in human physiology.
Sclerosing cholangitis is a chronic cholestatic liver disease. The literature linking selenium to PSC describes hepatic retention of copper and selenium and poor fat-soluble micronutrient intake in PSC patients — findings that point to disease-driven trace-element derangement (malabsorption secondary to cholestasis), not a demonstrated benefit of selenium supplementation in treating PSC.
Critically, the evidence pack’s own mechanistic assessment flags this directly: selenium deficiency in PSC appears to be a result of the disease, not a treatment target, and there is no mechanistic hypothesis supporting selenium supplementation as PSC therapy. The TxGNN score should therefore be read as a knowledge-graph association (both entities co-occur in liver/trace-element literature) rather than evidence of therapeutic applicability.
Clinical Trial Evidence
Currently no related clinical trials registered.
Literature Evidence
| PMID | Year | Type | Journal | Key Findings |
|---|---|---|---|---|
| 9053974 | 1995 | Cohort | Scandinavian Journal of Gastroenterology | Hepatic copper and selenium retention studied in 32 PSC patients; indicates abnormal trace-element metabolism in PSC, not a treatment effect |
| 39601354 | 2025 | Cohort/Dietary survey | Liver International | PSC patients show poor dietary intake of fat-soluble vitamins and lower overall diet quality versus Nordic nutrition recommendations |
| 29148959 | 2017 | Case report | JPEN (J Parenter Enteral Nutr) | Case report on parenteral lipid emulsion in a patient with severe malabsorption and overlapping PSC/ulcerative colitis; discusses oxidative stress and antioxidant status in cholestatic disease |
| 17109383 | 2006 | Animal/Proteomic | Proteomics | Hepatic proteome changes in murine models of toxin-induced fibrosis and sclerosing cholangitis; mechanistic, not selenium-specific |
| 18941372 | 2008 | Review | European Journal of Cancer Prevention | Review of colorectal cancer chemoprevention agents (aspirin, NSAIDs); topic overlap with PSC/selenium is minimal — low relevance |
South Africa Market Information
Selenium is currently not marketed in South Africa under this evidence pack, with 0 SAHPRA registrations on file. No product/registration records are available to summarize.
Safety Considerations
Please refer to the SAHPRA-approved Professional Information (PI) for safety information. Report adverse drug reactions to SAHPRA.
Conclusion and Next Steps
Decision: Hold
Rationale:
- The available literature shows selenium/trace-element abnormalities as a downstream consequence of PSC-related cholestasis and malabsorption, not evidence that selenium supplementation treats the disease. No clinical trials have tested selenium in PSC, and no mechanistic rationale supports repurposing at this stage.
To proceed, the following is needed:
- Mechanism of action data for Selenium (Data Gap DG002)
- TFDA/SAHPRA-approved Professional Information — warnings, contraindications, DDI (Data Gap DG001)
- An interventional study specifically testing selenium supplementation as a therapeutic intervention in PSC patients (current data is observational/correlational only)
- Reassessment of causality: whether correcting selenium deficiency alters PSC disease course, versus deficiency being merely a biomarker of cholestasis severity
Note: Other TxGNN-predicted indications in this evidence pack carry stronger evidence than the top-ranked hit — notably congestive heart failure (Evidence Level L2, decision stage S2, 4 clinical trials including two large Phase 3 RCTs: NCT06694727 n=4,044 and NCT07234422 n=1,100) and rheumatoid arthritis (Evidence Level L3, decision stage S1, one Phase 1-tier RCT/meta-analysis plus multiple mechanistic studies). These may warrant separate evaluation reports given their comparatively stronger evidentiary base.
Disclaimer
This content is for research purposes only and does not constitute medical advice. Clinical validation is required before any clinical application.