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This article is published by Yimaitong authorized by the author, please do not reprint without permission.
In recent years, the prevalence of thyroid disease in my country has shown an obvious upward trend, and it has become the second largest endocrine disease after diabetes, and "thyroid function examination" has been listed as a routine clinical examination item.
Due to the lack of relevant professional knowledge, many primary doctors just mechanically refer to the normal value range attached to the test sheet to draw conclusions when reading the thyroid function report, which often leads to clinical misjudgments.
The author has compiled 8 common mistakes in clinical practice, and I hope it will be helpful to everyone.
Mistake 1: Misunderstanding that the slight increase in thyroid function in pregnant women in early pregnancy is hyperthyroidism.
The physiological changes of certain hormones in pregnant women can affect thyroid function, the most important of which are human chorionic gonadotropin (hCG) and estrogen.
Hormone (E).
In the early pregnancy, the increase of hCG can stimulate the secretion of thyroxine, which causes a slight decrease in TSH through negative feedback (called "subclinical hyperthyroidism"), and TSH can gradually return to normal in the middle and late pregnancy.
Estrogen (E) can increase the content of thyroid hormone-binding protein (TBG) in the serum.
Because 99% of thyroid hormone in the blood is combined with thyroid-binding protein, the total thyroid hormone (TT3, TT4) levels may increase slightly, while free thyroid hormones (FT3, FT4) usually remain normal.
Therefore, if you find that TSH is slightly decreased and TT3 and TT4 are slightly increased when checking thyroid function in the early pregnancy, pregnant mothers do not need to worry, because this is a normal physiological change during pregnancy and not hyperthyroidism.
Mistake 2: Misunderstanding that the normal range of thyroid function in both "pregnancy period" and "non-pregnancy period" are the same.
As mentioned earlier, pregnancy is affected by physiological changes such as increased maternal estrogen levels, resulting in a slight decrease in pregnant women's TSH , Especially in the first trimester.
Therefore, the normal range of thyroid function is different during pregnancy and non-pregnancy.The 2011 ATA (American Thyroid Association) guidelines first proposed the specific TSH reference value during pregnancy: first trimester (T1 stage) 0.
1～2.
5mIU/L; second trimester (T2 stage) 0.
2～3.
0mIU/L; third trimester (T3 stage) ) 0.
3～3.
0mIU/L.
The study of Professor Teng Weiping in my country believes that the normal range of TSH during pregnancy proposed by ATA may not be suitable for Chinese pregnant women.
It is recommended that the region-specific TSH reference value during pregnancy should be used where conditions permit.
Hospitals that have unconditional access to pregnancy-specific reference values can be The reference value proposed by my country's "Guidelines for the Diagnosis and Treatment of Thyroid Diseases in Pregnancy and Postpartum" is adopted, that is, TSH<4.
0mIU/L.
From this, it can be seen that to judge whether the pregnant women's thyroid function is normal or not, the reference interval of ordinary adults cannot be mechanically applied, otherwise it is easy to draw wrong conclusions.
Mistake 3: Applying "adult hypothyroidism" standards to screen for "neonatal hypothyroidism" In order to detect "congenital hypothyroidism" early, newborns must be routinely screened for thyroid function (take foot blood to measure TSH).
TSH of normal full-term newborns rises rapidly to 60-80mIU/L 30 minutes after birth, drops to 20mIU/L after 24 hours, and slowly drops to 6-10mIU/L about 1 week after birth.
The screening of neonatal congenital hypothyroidism is usually arranged 48h to 72h after birth.
At this time, as long as the TSH does not exceed 10mIU/L, it can be considered normal.
If you do not understand this, blindly apply the diagnostic criteria for adult hypothyroidism (TSH>5mIU/L), it is bound to make a wrong judgment.
Mistake 4: The diagnosis is based on "reports", and the differential diagnosis is ignored.
In the early stages of pregnancy, some pregnant women often find that FT4 is slightly increased and TSH is slightly decreased during the thyroid function test.
If you encounter this situation in the clinic, do not diagnose it lightly.
"Graves disease", but also think of "HCG-related hyperthyroidism during pregnancy (also called hyperthyroidism syndrome of pregnancy)", its occurrence is related to the increased production of chorionic gonadotropin (hCG), because the chemical structure of hCG and TSH is similar, the same It can also promote the secretion of thyroid hormone (TH), causing a slight increase in FT4 and a slight decrease in TSH. If the pregnant woman has no previous history of hyperthyroidism, only a slight increase in FT4 and a decrease in TSH in the thyroid function test, thyroid-stimulating hormone receptor antibody (TRAb) is negative, and the HCG level is significantly increased, it can basically be determined as "HCG-related during pregnancy" "Hyperthyroidism", the course of the disease is transient and does not require antithyroid drugs (ATD) treatment, which is different from the treatment principle of "Graves' hyperthyroidism".
Mistake 5: As long as the thyroid hormone is lowered, it is considered "hypothyroidism.
" Generally speaking, hypothyroidism often has a lowered thyroid hormone (such as FT3, FT4) level, but conversely, if there is a lowered thyroid hormone level, it may not be It must be hypothyroidism.
This is because the elderly, severely malnourished, and patients with advanced cachexia often have a slight decrease in T3 (or T3, T4) during the thyroid function test, while TSH is normal or slightly decreased (this is different In "hypothyroidism"), anti-T3 (rT3) is elevated, it is clinically called "low T3 syndrome" (also called "normal thyroid sick syndrome", ESS).
It should be pointed out that this is not hypothyroidism, but a protective response of the body to adapt to the critically ill state.
If this situation is mistaken for "hypothyroidism" and given thyroid hormone replacement therapy, it will be counterproductive and make the condition worse.
Mistake 6: Completely rely on "thyroid autoantibody examination" to determine the cause.
Thyroid autoantibodies (such as TPOAb, TGAb, etc.
) are mainly seen in various "autoimmune thyroid diseases (AITD)", and Graves hyperthyroidism, Hashimoto's thyroiditis, etc.
Belongs to the category of AITD.
Therefore, the above-mentioned thyroid autoantibodies can be detected in these patients.
The difference between the two is: patients with Hashimoto's thyroiditis have higher titers of TPOAb and TGAb, while patients with Graves hyperthyroidism can also detect TPOAb and TGAb, but their antibody levels are relatively low.
Because thyroid autoantibodies are not specific in disease diagnosis, and there is no clear boundary for the antibody titers of the above two diseases.
Therefore, in clinical diagnosis, antibody titer can only be used as an important reference, sometimes combined with thyroid function, 131 iodine uptake rate or thyroid fine needle aspiration cytology for comprehensive judgment.
Mistake 7: Misunderstanding that the changes of thyroid hormone (TH) and thyroid stimulating hormone (TSH) are always synchronized.
Thyroid hormones (TH, including T3 and T4) and thyroid stimulating hormone (TSH) are finally realized through feedback adjustment to "hypothalamus-pituitary gland" -The dynamic balance of the "thyroid axis", but this requires a process of several weeks.
During this period, the changes between TSH and T3 and T4 are not completely synchronized: Generally speaking, after hypothyroidism is replaced with TH preparations, It takes 4 to 6 weeks for the blood TSH to return to normal; and after hyperthyroidism is treated with ATD, it takes 2 to 6 months for the blood TSH to return to normal.
Before this, the blood T3, T4 and TSH concentrations will appear contradictory.
T3 and T4 are normal, but TSH is still high (such as hypothyroidism) or low (such as hyperthyroidism).
This seemingly contradictory result, It is not that the laboratory test results are inaccurate, but because there is a time difference between the two to reach a balance.
Understanding this point is of great significance for evaluating the effect of treatment and guiding drug adjustment.
For example, after a period of drug treatment in patients with hyperthyroidism, FT3 and FT4 have fallen to normal, but the test results are still low due to the obvious lag in TSH changes.
At this stage, the adjustment of drugs should not only look at TSH, but should be based on FT3 and FT4.
Make a decision based on the level of clinical symptoms.
Mistake 8: Inadequate understanding of the limitations of the clinical application of TSH TSH is the most sensitive indicator of thyroid function.
When a patient's thyroid function is abnormal, TSH often changes before T3 and T4.
Therefore, the determination of TSH is of great value in the diagnosis of "subclinical hyperthyroidism" or "subclinical hypothyroidism".
However, TSH also has certain limitations in reflecting thyroid function.
Serum TSH is not suitable for central thyroid abnormalities secondary to the pituitary or hypothalamus (such as "central hyperthyroidism" or "central hypothyroidism").
An index to evaluate thyroid function. In short, as a clinician, you must understand the scope and limitations of the various indicators of thyroid function.
When interpreting the thyroid function report, you must pay attention to combining the patient’s medical history and other related examinations to make a comprehensive analysis and judgment, not just based on the laboratory laboratory.
The attached range of normal values makes a diagnosis indiscreetly.
In recent years, the prevalence of thyroid disease in my country has shown an obvious upward trend, and it has become the second largest endocrine disease after diabetes, and "thyroid function examination" has been listed as a routine clinical examination item.
Due to the lack of relevant professional knowledge, many primary doctors just mechanically refer to the normal value range attached to the test sheet to draw conclusions when reading the thyroid function report, which often leads to clinical misjudgments.
The author has compiled 8 common mistakes in clinical practice, and I hope it will be helpful to everyone.
Mistake 1: Misunderstanding that the slight increase in thyroid function in pregnant women in early pregnancy is hyperthyroidism.
The physiological changes of certain hormones in pregnant women can affect thyroid function, the most important of which are human chorionic gonadotropin (hCG) and estrogen.
Hormone (E).
In the early pregnancy, the increase of hCG can stimulate the secretion of thyroxine, which causes a slight decrease in TSH through negative feedback (called "subclinical hyperthyroidism"), and TSH can gradually return to normal in the middle and late pregnancy.
Estrogen (E) can increase the content of thyroid hormone-binding protein (TBG) in the serum.
Because 99% of thyroid hormone in the blood is combined with thyroid-binding protein, the total thyroid hormone (TT3, TT4) levels may increase slightly, while free thyroid hormones (FT3, FT4) usually remain normal.
Therefore, if you find that TSH is slightly decreased and TT3 and TT4 are slightly increased when checking thyroid function in the early pregnancy, pregnant mothers do not need to worry, because this is a normal physiological change during pregnancy and not hyperthyroidism.
Mistake 2: Misunderstanding that the normal range of thyroid function in both "pregnancy period" and "non-pregnancy period" are the same.
As mentioned earlier, pregnancy is affected by physiological changes such as increased maternal estrogen levels, resulting in a slight decrease in pregnant women's TSH , Especially in the first trimester.
Therefore, the normal range of thyroid function is different during pregnancy and non-pregnancy.The 2011 ATA (American Thyroid Association) guidelines first proposed the specific TSH reference value during pregnancy: first trimester (T1 stage) 0.
1～2.
5mIU/L; second trimester (T2 stage) 0.
2～3.
0mIU/L; third trimester (T3 stage) ) 0.
3～3.
0mIU/L.
The study of Professor Teng Weiping in my country believes that the normal range of TSH during pregnancy proposed by ATA may not be suitable for Chinese pregnant women.
It is recommended that the region-specific TSH reference value during pregnancy should be used where conditions permit.
Hospitals that have unconditional access to pregnancy-specific reference values can be The reference value proposed by my country's "Guidelines for the Diagnosis and Treatment of Thyroid Diseases in Pregnancy and Postpartum" is adopted, that is, TSH<4.
0mIU/L.
From this, it can be seen that to judge whether the pregnant women's thyroid function is normal or not, the reference interval of ordinary adults cannot be mechanically applied, otherwise it is easy to draw wrong conclusions.
Mistake 3: Applying "adult hypothyroidism" standards to screen for "neonatal hypothyroidism" In order to detect "congenital hypothyroidism" early, newborns must be routinely screened for thyroid function (take foot blood to measure TSH).
TSH of normal full-term newborns rises rapidly to 60-80mIU/L 30 minutes after birth, drops to 20mIU/L after 24 hours, and slowly drops to 6-10mIU/L about 1 week after birth.
The screening of neonatal congenital hypothyroidism is usually arranged 48h to 72h after birth.
At this time, as long as the TSH does not exceed 10mIU/L, it can be considered normal.
If you do not understand this, blindly apply the diagnostic criteria for adult hypothyroidism (TSH>5mIU/L), it is bound to make a wrong judgment.
Mistake 4: The diagnosis is based on "reports", and the differential diagnosis is ignored.
In the early stages of pregnancy, some pregnant women often find that FT4 is slightly increased and TSH is slightly decreased during the thyroid function test.
If you encounter this situation in the clinic, do not diagnose it lightly.
"Graves disease", but also think of "HCG-related hyperthyroidism during pregnancy (also called hyperthyroidism syndrome of pregnancy)", its occurrence is related to the increased production of chorionic gonadotropin (hCG), because the chemical structure of hCG and TSH is similar, the same It can also promote the secretion of thyroid hormone (TH), causing a slight increase in FT4 and a slight decrease in TSH. If the pregnant woman has no previous history of hyperthyroidism, only a slight increase in FT4 and a decrease in TSH in the thyroid function test, thyroid-stimulating hormone receptor antibody (TRAb) is negative, and the HCG level is significantly increased, it can basically be determined as "HCG-related during pregnancy" "Hyperthyroidism", the course of the disease is transient and does not require antithyroid drugs (ATD) treatment, which is different from the treatment principle of "Graves' hyperthyroidism".
Mistake 5: As long as the thyroid hormone is lowered, it is considered "hypothyroidism.
" Generally speaking, hypothyroidism often has a lowered thyroid hormone (such as FT3, FT4) level, but conversely, if there is a lowered thyroid hormone level, it may not be It must be hypothyroidism.
This is because the elderly, severely malnourished, and patients with advanced cachexia often have a slight decrease in T3 (or T3, T4) during the thyroid function test, while TSH is normal or slightly decreased (this is different In "hypothyroidism"), anti-T3 (rT3) is elevated, it is clinically called "low T3 syndrome" (also called "normal thyroid sick syndrome", ESS).
It should be pointed out that this is not hypothyroidism, but a protective response of the body to adapt to the critically ill state.
If this situation is mistaken for "hypothyroidism" and given thyroid hormone replacement therapy, it will be counterproductive and make the condition worse.
Mistake 6: Completely rely on "thyroid autoantibody examination" to determine the cause.
Thyroid autoantibodies (such as TPOAb, TGAb, etc.
) are mainly seen in various "autoimmune thyroid diseases (AITD)", and Graves hyperthyroidism, Hashimoto's thyroiditis, etc.
Belongs to the category of AITD.
Therefore, the above-mentioned thyroid autoantibodies can be detected in these patients.
The difference between the two is: patients with Hashimoto's thyroiditis have higher titers of TPOAb and TGAb, while patients with Graves hyperthyroidism can also detect TPOAb and TGAb, but their antibody levels are relatively low.
Because thyroid autoantibodies are not specific in disease diagnosis, and there is no clear boundary for the antibody titers of the above two diseases.
Therefore, in clinical diagnosis, antibody titer can only be used as an important reference, sometimes combined with thyroid function, 131 iodine uptake rate or thyroid fine needle aspiration cytology for comprehensive judgment.
Mistake 7: Misunderstanding that the changes of thyroid hormone (TH) and thyroid stimulating hormone (TSH) are always synchronized.
Thyroid hormones (TH, including T3 and T4) and thyroid stimulating hormone (TSH) are finally realized through feedback adjustment to "hypothalamus-pituitary gland" -The dynamic balance of the "thyroid axis", but this requires a process of several weeks.
During this period, the changes between TSH and T3 and T4 are not completely synchronized: Generally speaking, after hypothyroidism is replaced with TH preparations, It takes 4 to 6 weeks for the blood TSH to return to normal; and after hyperthyroidism is treated with ATD, it takes 2 to 6 months for the blood TSH to return to normal.
Before this, the blood T3, T4 and TSH concentrations will appear contradictory.
T3 and T4 are normal, but TSH is still high (such as hypothyroidism) or low (such as hyperthyroidism).
This seemingly contradictory result, It is not that the laboratory test results are inaccurate, but because there is a time difference between the two to reach a balance.
Understanding this point is of great significance for evaluating the effect of treatment and guiding drug adjustment.
For example, after a period of drug treatment in patients with hyperthyroidism, FT3 and FT4 have fallen to normal, but the test results are still low due to the obvious lag in TSH changes.
At this stage, the adjustment of drugs should not only look at TSH, but should be based on FT3 and FT4.
Make a decision based on the level of clinical symptoms.
Mistake 8: Inadequate understanding of the limitations of the clinical application of TSH TSH is the most sensitive indicator of thyroid function.
When a patient's thyroid function is abnormal, TSH often changes before T3 and T4.
Therefore, the determination of TSH is of great value in the diagnosis of "subclinical hyperthyroidism" or "subclinical hypothyroidism".
However, TSH also has certain limitations in reflecting thyroid function.
Serum TSH is not suitable for central thyroid abnormalities secondary to the pituitary or hypothalamus (such as "central hyperthyroidism" or "central hypothyroidism").
An index to evaluate thyroid function. In short, as a clinician, you must understand the scope and limitations of the various indicators of thyroid function.
When interpreting the thyroid function report, you must pay attention to combining the patient’s medical history and other related examinations to make a comprehensive analysis and judgment, not just based on the laboratory laboratory.
The attached range of normal values makes a diagnosis indiscreetly.
