T levels when on transdermals peak and drop.
TSH levels indicate that your hypothalamus and pituitary are calling for more thyroid hormones. That can be mediated by poor T4–>T3 conversion. You should be taking some T3.
Find the references to T3 in this:
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L-thyroxine replacement
In view of the physiological, pharmacokinetic, and clinical biochemical considerations outlined above, ten tips can be given for clinical practice (2, 5â?? 8):
With regard to the frequency of TSH measurements after a change in the hormone dose or in the clinical circumstances, rechecking at four- to six-week intervals is recommended. For benign diseases of the thyroid gland, the target range for TSH is 1 to 2 mU/L (2, 8).
Blood drawing for fT4 should be done early in the morning before the daily dose of L-thyroxine.
Measuring fT3 is usually unnecessary for the monitoring of replacement therapy but can be useful for the detection of T3 hyperthyroidism in special situations, e.g., thyroid carcinoma.
L-thyroxine should be taken by mouth early in the morning, in the fasting state, 30 to 60 minutes before breakfast, with water. The standard dose is 15 μg/kg body weight (BW). If the patient forgets to take one daily dose, this can safely be neglected and should not be â??made up forâ?? by additional intake the next day (2, 8).
Giving T3 for replacement is unphysiological and less well tolerated and is thus not recommended as a routine measure. The mono-deiodization of T4 normally occurs as needed in the peripheral tissues, so that there is no need to take T3 (liothyronine) as well. In a total of 10 randomized double-blind clinical trials, including six crossover trials and four parallel-group trials (9, e10â?? e17), treatment with a combination of T3 and T4 was found to provide a convincing benefit with respect to well-being, cognitive functioning, or quality of life for some individual patients, but not in the overall group of patients studied, and this remained the case after multiple meta-analyses (e18, 10). There will be some patients who report having a better mental and cognitive state when receiving combination therapy and therefore want it. To this end, preparations are available that contain T3 and T4 in a fixed ratio of 10 or 20 μg of T3 to 100 μg of T4. If the clinical manifestations of hypothyroidism persist under L-thyroxine replacement therapy despite normalized TSH levels, this may be due to genetic variation (e19â?? e21) in the peripheral 5â??-deiodinases (e22â?? e24), which are selenoprotein enzymes that catalyze the conversion of T4 to active T3 as needed (11, e25). Patients with low peripheral 5â??-deiodinase activity may be unable to metabolize T4 to T3 in adequate amounts and may therefore respond better to combined replacement therapy than to T4 alone. There is, however, no routinely available clinical biochemical or genetic test to determine whether this is the case.
There is a widespread misconception that the various thyroid preparations on the market are identical in bioavailability. This is not so (e26), and therefore the preparation currently being taken should not be switched if the patient is tolerating it well. The area under the curve (AUC) of different preparationsâ?? absorption profiles can differ so greatly (e27) that their relative bioavailability varies from 0.8 to 1.25, and this is a clinically relevant variation (e28).
After thyroid hormone replacement is initiated at a low dose, the dose should be raised in individualized fashion. For patients who are elderly, suffer from heart disease, or have longstanding hypothyroidism, the dose should be raised slowly, e.g., in weekly increments of 25 μg, after an initial dose of 25 μg. On the other hand, patients in good general health who undergo thyroid surgery can have the dose rapidly raised to the target postoperative dose (within a maximum of five days after surgery) (1). The need for postoperative thyroid hormone replacement is a function of the residual volume of thyroid tissue (2). Hormone replacement is always necessary when less than 6 mL of thyroid tissue is left. A practical approach would be to start postoperatively at a dose of 1 μg/kgBW and then measure the TSH level again in four to six weeks.
Patients who are dysphagic or are receiving a special enteral diet can be given L-thyroxine as a liquid preparation (e.g., L-thyroxine drops [Henning], where 1 drop contains 5 μg of the hormone).
Note: In this review, we do not discuss the treatment of secondary or tertiary hypothyroidism caused by diseases affecting the hypothalamic-pituitary axis (12). Nevertheless, we take this opportunity to point out that TSH cannot be used as a guide to therapy in such cases, as the TSH concentration may be in the normal range, or low, despite peripheral hypothyroidism. Thus, treatment monitoring must be performed by measurement of fT4.
A potential pitfall: patients with other serious illnesses in addition to primary hypothyroidism can develop NTIS (â??non-thyroidal illness syndromeâ??) and therefore have low values of both fT3 and TSH. In such cases, too, hormone replacement therapy must be monitored by fT4 measurement.
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