Voorkomen en beheer van een afwijkende vrij T4 in combinatie met een normale TSH
Geplaatst: 21 sep 2018, 13:29
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Voorkomen en beheer van een afwijkende vrij T4 in combinatie met een normale TSH
K.M. van Veggel1*, J.M. Rondeel2, S. Anten3
1Department of Internal Medicine, Isala Hospital (previously employed by Department of Internal Medicine, Alrijne Hospital), Zwolle, the Netherlands, 2Department of Clinical Chemistry, Isala Hospital, Zwolle, the Netherlands,3Department of Internal Medicine, Alrijne Hospital, Leiderdorp, the Netherlands,
*corresponding author: email: k.m.van.veggel@isala.nl
Abstract
Background:
Thyroid function tests may show the combination of a normal concentration of serum thyroidstimulating hormone (TSH) and an increased or decreased level of free thyroxine (free T4). How often this occurs is unclear and not everyone is familiar with how it should be adressed.
Methods:
We conducted a retrospective cohort study of all adult patients who presented at a non-academic general hospital in the Netherlands between 1 January 2010 and 31 December 2014 and yielded an increased or decreased free T4 in combination with a normal TSH.
Exclusion criteria included the use of thyroid medication, pregnancy, a history of thyroid surgery and treatment with radioactive iodine. The medical records of the patients included were retrieved and evaluated.
Results:
Of the 30,143 combined TSH and free T4 measurements in 23,199 individual patients, 1005 measurements (3.33%) in 775 patients (3.34%) yielded an aberrant free T4 in combination with a normal TSH.
398 patients (1.72%) had a persistent aberrant free T4, 349 (87.7%) of whom had a decreased free T4 and 49 (12.3%) an increased free T4.
In 58 of the 398 patients (14.6%) with a persistent abberant free T4 a possible cause was established by the treating physician.
However, upon re-examination of medical files a possible causative factor could be identified in 123 patients (30.9%).
Conclusion:
In our study population the prevalence of hyperthyroxinemia or hypothyroxinemia in combination with a normal TSH was 334 per 10.000 patients.
When records were thoroughly searched, identification of potential causative factors increased substantially. Clinicians should be encouraged to check for underlying causes.
Table 1.
Causes of hypothyroxinemia and hyperthyroxinemia in combination with a normal TSH and corresponding data that have been evaluated in patients’ medical records
- Causes of a normal TSH in combination with a decreased free T4
Causes of a normal TSH in combination with a decreased free T4 - Increased concentrations of TBG: hepatitis, porphyria, estrogen, heroin, methadone, mitotane, 5-fluorouracil, selective estrogen receptor modulators (e.g. tamoxifen, raloxifene), perphenazine
- Increased clearance of thyroxine therapy: phenobarbital, primidone, phenytoin, carbamazepine, oxcarbazepine, rifampicin, growth hormone, sertraline, tyrosine kinase inhibitors (e.g. imatinib, sunitinib), quetiapine, stavudine, nevirapine
- Decreased release of thyroid hormone by the thyroid: lithium
- Critical illness
- Central hypothyroidism: decreased pituitary function due to pituitary adenomas, compressive lesions, cranial surgery or irradiation, empty sella, auto-immune disease, vascular accidents, infiltrative lesions (e.g. hemochromatosis), infections (e.g. tuberculosis), inherited disease
- Causes of a normal TSH in combination with an increased free T4
Causes of a normal TSH in combination with an increased free T4 - Decreased concentrations of TBG: liver failure, nephrotic syndrome, androgens, anabolic steroids, glucocorticoids, nicotinic acid, L-asparginase
- Inhibition of T4 binding to TBG: salicylates, furosemide, free fatty acids, phenytoin, carbamazepine, non-steroidal anti-inflammatory drugs, heparin
- Inhibition of thyroid hormone transport through the plasma membrane: amiodarone
- Critical illness
- Pituitary TSH adenoma (e.g. TSHoma)
- Thyroid hormone resistance
- Assay error (TSH / free T4)
Table 2.
Patient characteristics at baseline
Table 3.
Occurrence of known associated factors (‘risk factors’) for developing an aberrant free T4 concentration in combination with a normal TSH concentration among 504 evaluated patients at baseline
Figure 1.
Summary of the results
Figure 2.
Suggested analysis of hyperthyroxinemia and hypothyroxinemia in combination with a normal TSH
CONCLUSION
This study demonstrates that in our population of patients screened for thyroid dysfunction in a non-university general hospital 334 per 10,000 patients had a normal TSH in combination with an aberrant free T4.
We also found that many physicians do not follow-up on this condition or record a causative factor.
When medical files are searched thoroughly however, identification of a possible causative factor increases from 14.6% to 30.9%.
Therefore, clinicians should be encouraged to check for additional causes of these aberrant free T4 entities. The largest challenge is not to miss serious underlying conditions like secundary hypothyroidism.
We present a possible strategy for analyse hyperthyroxinemia and hypothyroxinemia in combination with a normal TSH. We believe it is important to deploy a similar strategy in guidelines about thyroid disorders.
Future studies on this topic should be performed to gain more insight about the best way to follow-up on this condition.
Volledig artikel
http://www.njmonline.nl/getpdf.php?id=2021
.
Google-vertaling;
Voorkomen en beheer van een afwijkende vrij T4 in combinatie met een normale TSH
K.M. van Veggel1*, J.M. Rondeel2, S. Anten3
1Department of Internal Medicine, Isala Hospital (previously employed by Department of Internal Medicine, Alrijne Hospital), Zwolle, the Netherlands, 2Department of Clinical Chemistry, Isala Hospital, Zwolle, the Netherlands,3Department of Internal Medicine, Alrijne Hospital, Leiderdorp, the Netherlands,
*corresponding author: email: k.m.van.veggel@isala.nl
Abstract
Background:
Thyroid function tests may show the combination of a normal concentration of serum thyroidstimulating hormone (TSH) and an increased or decreased level of free thyroxine (free T4). How often this occurs is unclear and not everyone is familiar with how it should be adressed.
Methods:
We conducted a retrospective cohort study of all adult patients who presented at a non-academic general hospital in the Netherlands between 1 January 2010 and 31 December 2014 and yielded an increased or decreased free T4 in combination with a normal TSH.
Exclusion criteria included the use of thyroid medication, pregnancy, a history of thyroid surgery and treatment with radioactive iodine. The medical records of the patients included were retrieved and evaluated.
Results:
Of the 30,143 combined TSH and free T4 measurements in 23,199 individual patients, 1005 measurements (3.33%) in 775 patients (3.34%) yielded an aberrant free T4 in combination with a normal TSH.
398 patients (1.72%) had a persistent aberrant free T4, 349 (87.7%) of whom had a decreased free T4 and 49 (12.3%) an increased free T4.
In 58 of the 398 patients (14.6%) with a persistent abberant free T4 a possible cause was established by the treating physician.
However, upon re-examination of medical files a possible causative factor could be identified in 123 patients (30.9%).
Conclusion:
In our study population the prevalence of hyperthyroxinemia or hypothyroxinemia in combination with a normal TSH was 334 per 10.000 patients.
When records were thoroughly searched, identification of potential causative factors increased substantially. Clinicians should be encouraged to check for underlying causes.
Assays
Prior to 13 May 2014 concentrations of free T4 and TSH were determined by a Siemens Immulite 1000 immuno-assay analyser. Maximal total coefficients of variation for free T4 and TSH were 12.1% and 17.5%.
Reference values of free T4 and TSH were 10.3-24.5 pmol/l and 0.4-4.0 mU/l. As of 13 May 2014 the laboratory used a chemiluminescent microparticle immunoassay (CMIA; Architect, Abbott Diagnostics USA). The Abbot assay has a dilution factor of 75 before measuring FT4. Maximal total coefficients of variation were 7.8% and 5.3% for free T4 and TSH respectively.
Reference values of free T4 and TSH were 10-19 pmol/l and 0.27-4.2 mU/l, respectively. Concentrations outside the reference range were considered abnormal.
Table 1.
Causes of hypothyroxinemia and hyperthyroxinemia in combination with a normal TSH and corresponding data that have been evaluated in patients’ medical records
- Causes of a normal TSH in combination with a decreased free T4
Causes of a normal TSH in combination with a decreased free T4 - Increased concentrations of TBG: hepatitis, porphyria, estrogen, heroin, methadone, mitotane, 5-fluorouracil, selective estrogen receptor modulators (e.g. tamoxifen, raloxifene), perphenazine
- Increased clearance of thyroxine therapy: phenobarbital, primidone, phenytoin, carbamazepine, oxcarbazepine, rifampicin, growth hormone, sertraline, tyrosine kinase inhibitors (e.g. imatinib, sunitinib), quetiapine, stavudine, nevirapine
- Decreased release of thyroid hormone by the thyroid: lithium
- Critical illness
- Central hypothyroidism: decreased pituitary function due to pituitary adenomas, compressive lesions, cranial surgery or irradiation, empty sella, auto-immune disease, vascular accidents, infiltrative lesions (e.g. hemochromatosis), infections (e.g. tuberculosis), inherited disease
- Causes of a normal TSH in combination with an increased free T4
Causes of a normal TSH in combination with an increased free T4 - Decreased concentrations of TBG: liver failure, nephrotic syndrome, androgens, anabolic steroids, glucocorticoids, nicotinic acid, L-asparginase
- Inhibition of T4 binding to TBG: salicylates, furosemide, free fatty acids, phenytoin, carbamazepine, non-steroidal anti-inflammatory drugs, heparin
- Inhibition of thyroid hormone transport through the plasma membrane: amiodarone
- Critical illness
- Pituitary TSH adenoma (e.g. TSHoma)
- Thyroid hormone resistance
- Assay error (TSH / free T4)
Table 2.
Patient characteristics at baseline
Table 3.
Occurrence of known associated factors (‘risk factors’) for developing an aberrant free T4 concentration in combination with a normal TSH concentration among 504 evaluated patients at baseline
Figure 1.
Summary of the results
Figure 2.
Suggested analysis of hyperthyroxinemia and hypothyroxinemia in combination with a normal TSH
CONCLUSION
This study demonstrates that in our population of patients screened for thyroid dysfunction in a non-university general hospital 334 per 10,000 patients had a normal TSH in combination with an aberrant free T4.
We also found that many physicians do not follow-up on this condition or record a causative factor.
When medical files are searched thoroughly however, identification of a possible causative factor increases from 14.6% to 30.9%.
Therefore, clinicians should be encouraged to check for additional causes of these aberrant free T4 entities. The largest challenge is not to miss serious underlying conditions like secundary hypothyroidism.
We present a possible strategy for analyse hyperthyroxinemia and hypothyroxinemia in combination with a normal TSH. We believe it is important to deploy a similar strategy in guidelines about thyroid disorders.
Future studies on this topic should be performed to gain more insight about the best way to follow-up on this condition.
Volledig artikel
http://www.njmonline.nl/getpdf.php?id=2021
.