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Free access

Kristien Boelaert, W. Edward Visser, Peter Nicholas Taylor, Carla Moran, Juliane Leger and Luca Persani

This manuscript provides guidance on the management of thyroid dysfunction during the COVID-19 pandemic. Auto-immune thyroid diseases are not linked to increased risks of COVID-19. Uncontrolled thyrotoxicosis may result in more severe complications from SARS-CoV-2 infection, including thyroid storm.

The management of patients with a new diagnosis of hyperthyroidism is best undertaken with a block and replace regimen due to limited biochemical testing availability. Antithyroid drug (ATD)-induced neutropenia may favour the progression of COVID-19 and symptoms of infection may be confused with SARS-CoV-2 infection. The withdrawal of ATDs and urgent measurement of neutrophils should be considered in case of flu-like manifestations occurring in the initial months of treatment. Urgent surgery or 131-I may be undertaken in selected cases of uncontrolled thyrotoxicosis. Patients with COVID-19 infection may present with conjunctivitis, which could cause diagnostic difficulties in patients with new or existing Graves’ ophthalmopathy.

Patients who are on replacement treatment with thyroid hormones should ensure they have sufficient supply of medication. The usual advice to increase dosage of levothyroxine during pregnancy should be adhered to.

Many newly presenting and previously diagnosed patients with thyroid dysfunction can be managed through virtual telephone or video clinics supported by a dedicated nurse-led service, depending on available facilities.

Free access

Laura P B Elbers, Carla Moran, Victor E A Gerdes, Bregje van Zaane, Joost C M Meijers, Erik Endert, Greta Lyons, Krishna Chatterjee, Peter H Bisschop and Eric Fliers

Objective

Hyperthyroidism is associated with a hypercoagulable state, but the underlying mechanism is unknown. Patients with resistance to thyroid hormone (RTH) due to defective thyroid hormone receptor β (THRB or THRB) exhibit elevated circulating thyroid hormones (TH) with refractoriness to TH action in THRB-expressing tissues. We tested the hypothesis that the hypercoagulable state in hyperthyroidism is mediated via the THRB.

Design

We conducted a cross-sectional study from November 2013 to January 2015 in 3 hospitals in the Netherlands and the United Kingdom.

Methods

Patients with RTH due to defective THRB (n=18), patients with hyperthyroidism (n=16) and euthyroid subjects (n=18) were included. TH concentrations and markers of coagulation and fibrinolysis were measured. Data are expressed as median (interquartile range).

Results

Free thyroxine (FT4) levels were slightly higher in hyperthyroid patients than in RTH patients (53.9 (30.5–70.0) and 34.9 (28.4–42.2)pmol/L, respectively, P=0.042). Both groups had raised FT4 levels compared with euthyroid subjects (14.0 (13.0–15.8)pmol/L, P≤0.001). Levels of von Willebrand factor (VWF), factor (F) VIII, fibrinogen and d-dimer were significantly higher in hyperthyroid patients than in RTH patients (VWF 231 (195–296) vs 111 (82–140)%, FVIII 215 (192–228) vs 145 (97–158)%, fibrinogen 3.6 (3.0–4.4) vs 2.8 (2.5–3.2)g/L, d-dimer 0.41 (0.31–0.88) vs 0.20 (0.17–0.26)mg/L, respectively, P≤0.001), while there were no differences between RTH patients and euthyroid controls.

Conclusions

Parameters of coagulation and fibrinolysis were elevated in hyperthyroid patients compared with patients with RTH due to defective THRB, whereas these parameters were not different between euthyroid controls and RTH patients, despite elevated FT4 concentrations in RTH patients. This indicates that the procoagulant effects observed in hyperthyroidism are mediated via the THRB.

Open access

Serena Khoo, Greta Lyons, Anne McGowan, Mark Gurnell, Susan Oddy, W Edward Visser, Sjoerd van den Berg, David Halsall, Kevin Taylor, Krishna Chatterjee and Carla Moran

Objective

Familial dysalbuminaemic hyperthyroxinaemia (FDH), most commonly due to an Arginine to Histidine mutation at residue 218 (R218H) in the albumin gene, causes artefactual elevation of free thyroid hormones in euthyroid individuals. We have evaluated the susceptibility of most current free thyroid hormone immunoassay methods used in the United Kingdom, Europe and Far East to interference by R218H FDH.

Methods

Different, one- and two-step immunoassay methods were tested, measuring free T4 (FT4) and free T3 (FT3) in 37 individuals with genetically proven R218H FDH.

Results

With the exception of Ortho VITROS, FT4 measurements were raised in all assays, with greatest to lowest susceptibility to interference being Beckman ACCESS > Roche ELECSYS > FUJIREBIO Lumipulse > Siemens CENTAUR > Abbott ARCHITECT > Perkin-Elmer DELFIA. Five different assays recorded high FT3 levels, with the Siemens CENTAUR method measuring high FT3 values in up to 30% of cases. However, depending on the assay method, FT4 measurements were unexpectedly normal in some, genetically confirmed, affected relatives of index FDH cases.

Conclusions

All FT4 immunoassays evaluated are prone to interference by R218H FDH, with their varying susceptibility not being related to assay architecture but likely due to differing assay conditions or buffer composition. Added susceptibility of many FT3 assays to measurement interference, resulting in high FT4 and FT3 with non-suppressed TSH levels, raises the possibility of R218H FDH being misdiagnosed as resistance to thyroid hormone beta or TSH-secreting pituitary tumour, potentially leading to unnecessary investigation and inappropriate treatment.