Thiamine

證據等級: L5 預測適應症: 10

目錄

  1. Thiamine
  2. Thiamine: From Vitamin B1 Deficiency to Hyperthyroidism
    1. One-Sentence Summary
    2. Quick Overview
    3. Why is This Prediction Reasonable?
    4. Clinical Trial Evidence
    5. Literature Evidence
    6. South Africa Market Information
    7. Safety Considerations
    8. Conclusion and Next Steps
    9. Disclaimer

## 藥師評估報告

Thiamine: From Vitamin B1 Deficiency to Hyperthyroidism

One-Sentence Summary

Thiamine (Vitamin B1, DrugBank DB00152) is classically used to treat thiamine deficiency states such as beriberi and Wernicke’s encephalopathy. The TxGNN model predicts it may also be effective for Hyperthyroidism, specifically for managing the cardiovascular consequences of the hypermetabolic thyrotoxic state, with 1 completed pilot clinical trial and 20 related publications currently supporting this direction — though the evidence base remains preliminary.


Quick Overview

Item Content
Original Indication Thiamine (Vitamin B1) deficiency (e.g., beriberi, Wernicke’s encephalopathy) — no SAHPRA-approved indication text is on file, as the product is not currently registered in South Africa
Predicted New Indication Hyperthyroidism (cardiovascular dysfunction associated with thyrotoxicosis)
TxGNN Prediction Score 99.44%
Evidence Level L3
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 for this candidate (data gap DG002). Based on known pharmacology, thiamine is an essential water-soluble vitamin that functions as a cofactor for pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, and transketolase — enzymes central to carbohydrate metabolism and cellular energy production. Its efficacy in correcting thiamine deficiency (beriberi, Wernicke’s encephalopathy) is well established.

The proposed link between thiamine and hyperthyroidism is physiological rather than a shared disease category: thyrotoxicosis is a hypermetabolic state that increases tissue oxygen consumption and substrate turnover, which in turn raises the body’s thiamine requirement. Older biochemical studies (1940s–1960s) documented altered thiamine turnover and tissue storage in hyperthyroid animals and patients, and multiple modern case reports describe hyperthyroid or thyrotoxic patients developing beriberi-like high-output heart failure or Wernicke’s encephalopathy — conditions that are classically thiamine-responsive.

Mechanistically, this suggests that in a subset of severely hyperthyroid patients, a relative or functional thiamine deficiency may develop and contribute to cardiovascular strain, which could theoretically be improved by thiamine supplementation. This hypothesis has been tested directly in one small prospective pilot study, giving the prediction some early clinical grounding, though it does not establish thiamine as a treatment for hyperthyroidism itself (the underlying thyroid disease still requires standard antithyroid therapy).


Clinical Trial Evidence

Trial Number Phase Status Enrollment Key Findings
NCT02767245 Phase NA Completed 12 Pilot study evaluating prevalence of thiamine deficiency and thiamine supplementation’s effect on cardiovascular function in patients with severe hyperthyroidism/thyrotoxicosis; small uncontrolled cohort.

Literature Evidence

PMID Year Type Journal Key Findings
21064291 1946 Mechanistic study Federation proceedings Thiamine deficiency, quinidine, hyper- and hypothyroidism alter cardiac muscle ATP content and ATPase activity in rats.
13305517 1955 Clinical mechanistic study Endocrinologia e scienza della costituzione Urinary thiamine excretion after IV cocarboxylase loading differs in hyperthyroid vs. normal subjects.
13934469 1963 Animal study Annals of biochemistry and experimental medicine Tissue thiamine storage and intestinal synthesis altered in hypo- and hyper-thyroid rats.
13168067 1954 Mechanistic study La Riforma medica Behavior of free thiamine and thiamine ester differs across thyroid disease states.
13588400 1958 Animal study The Journal of nutrition Thyroprotein and penicillin affect thiamine requirement and growth in hyperthyroid rats.
26567494 2015 Case report Critical care nursing clinics of North America High-output heart failure caused by thyrotoxicosis and beriberi (thiamine deficiency); reviews shared hemodynamic mechanism.
18026802 2008 Case report Journal of general internal medicine Thyrotoxicosis-associated Wernicke’s encephalopathy responsive to thiamine repletion.
32983708 2020 Case report Cureus Wernicke’s encephalopathy associated with transient gestational hyperthyroidism and hyperemesis gravidarum.
22436368 2013 Case report Neurologia (Barcelona, Spain) Wernicke’s encephalopathy secondary to hyperthyroidism and ingestion of thiaminase-rich foods.
36176825 2022 Case report Cureus Uncommon presentation of hyperthyroidism culminating in severe neurological (Wernicke-type) consequences.

South Africa Market Information

Thiamine currently holds no SAHPRA registration on record for this candidate (taiwan_regulatory.total_licenses = 0, market status: Not marketed). No licensed product entries are available to summarize dosage form or approved indication text in South Africa.


Safety Considerations

Please refer to the SAHPRA-approved Professional Information (PI) for safety information. Report adverse drug reactions to SAHPRA.

Note: A Blocking data gap (DG001) has been identified — TFDA/SAHPRA label warnings and contraindications are not yet available, which prevents this candidate from completing the S1 safety pre-screen.


Conclusion and Next Steps

Decision: Hold

Rationale: Evidence for thiamine in hyperthyroidism-related cardiovascular dysfunction is currently limited to one small, uncontrolled pilot study (n=12) supported mainly by historical mechanistic research and case reports of thiamine-responsive complications (beriberi-like heart failure, Wernicke’s encephalopathy) occurring in thyrotoxic patients — this is suggestive but not yet actionable evidence. Combined with the product having zero SAHPRA registrations in South Africa and a Blocking safety data gap (no TFDA/SAHPRA label data available), the candidate is not ready to proceed.

To proceed, the following is needed:

  • TFDA/SAHPRA-approved Professional Information (warnings, contraindications, dosing) to resolve the Blocking data gap (DG001)
  • Confirmed mechanism of action data (DG002)
  • Larger controlled trials directly testing thiamine supplementation for cardiovascular outcomes in hyperthyroid/thyrotoxic patients
  • Clarification of target population (e.g., severe thyrotoxicosis vs. general hyperthyroidism) and dosing/route feasibility given the product is not currently marketed in South Africa

    Disclaimer

This content is for research purposes only and does not constitute medical advice. Clinical validation is required before any clinical application.



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