Severe Biochemical Thyrotoxicosis Without Clinical Hyperthyroidism in ESRF Following Parathyroidectomy: A Diagnostic and Therapeutic Pitfall
https://doi.org/10.15605/jafes.041.S1
- Author:
Ahmad Syahmi Yusof Zaki
1
;
Nur Izat Muhamad
2
;
Ezelea Elwina Walter Sandosam
2
;
Wan Mohd Izani Wan Mohamed
2
Author Information
1. Faculty of Medicine, University Sultan Zainal Abidin;Department of Internal Medicine, School of Medical Sciences, University Science Malaysia
2. Department of Internal Medicine, School of Medical Sciences, University Science Malaysia
- Publication Type:Journal Article
- MeSH:
Parathyroidectomy;
Hyperthyroidism;
Thyrotoxicosis
- From:
Journal of the ASEAN Federation of Endocrine Societies
2026;41(S1):116-117
- CountryPhilippines
- Language:English
-
Abstract:
Introduction:Thyrotoxicosis following neck surgery is typically
attributed to transient destructive thyroiditis from follicular
disruption. In end-stage renal failure (ESRF), however,
altered thyroid hormone kinetics, including reduced
protein binding, impaired peripheral metabolism, and
decreased clearance, can distort biochemical interpretation. This creates a high-risk scenario where laboratory
values overestimate tissue thyrotoxicity, predisposing
to inappropriate antithyroid therapy. We present a case
demonstrating marked clinical–biochemical dissociation,
reframing postoperative thyrotoxicosis in ESRF as a
disorder of hormone handling rather than hormone
overproduction.
Case:A 45-year-old female with ESRF on maintenance hemodialysis and tertiary hyperparathyroidism underwent total
parathyroidectomy. Preoperative thyroid function was
consistently euthyroid. Within 48 hours postoperatively,
she developed severe biochemical thyrotoxicosis (thyroidstimulating hormone 0.28 mIU/L, free thyroxine 4 [FT4] 68
pmol/L). Despite this, she remained clinically euthyroid,
with stable hemodynamics, absence of adrenergic or neuropsychiatric features, and no evidence of thyroid eye disease.
The temporal relationship strongly suggested destructive
thyroiditis secondary to surgical manipulation, with
passive release of preformed thyroid hormone. In the
context of ESRF, impaired hormone clearance and altered
binding likely amplified circulating free hormone levels
without proportional end-organ effect, resulting in striking
clinical–biochemical dissociation.
A conservative strategy was adopted. Antithyroid drugs
were withheld, given the non-synthetic mechanism of
hormone excess, and the patient was managed with close
monitoring and symptom-guided beta-blockade. Serial
thyroid function demonstrated spontaneous improvement
without complications.
Conclusion:Post-parathyroidectomy thyrotoxicosis in ESRF represents
exaggerated biochemical derangement without true tissue
toxicity. Management must prioritize physiology over
laboratory values, as misclassification risks iatrogenic
harm. This case demonstrates that in ESRF, elevated FT4
may not reflect true tissue thyrotoxicity, and reliance
on biochemical severity alone can lead to inappropriate
antithyroid therapy and iatrogenic harm.
- Full text:2026080509363018855EP_A174.pdf
