Endocrine GR: 1st yr fellow Dr Andrew Barr discussed pancytopenia 2/2 #thyrotoxicosis & how to manage it. Often improves w/in months of euthyroidism. Can use ATDs; monitor closely. If not resolving, consider other etiologies. @cudeptofmedicine.bsky.social
Plot: Thyrotoxic symptoms in patients with resistance to thyroid hormone β (RTHβ) decrease under therapy with TRIAC
Plot: Resting energy expenditure decreases in patients with resistance to thyroid hormone β (RTHβ) under therapy with TRIAC
Therapy with #TRIAC, a non-classical #thyroid hormone, relieves peripheral #thyrotoxicosis and hypermetabolism in patients with resistance to thyroid hormone β (RTHβ).
pubmed.ncbi.nlm.nih.gov/41131705/
www.livivo.de/doc/M41131705
doi.org/10.1210/clin...
🧪 🩺 #MedSky
The following drugs are suitable for the treatment of thyrotoxicosis #thyroid #thyrotoxicosis ... Continue to: www.facebook.com/reel/1550244...
Minerals necessary in case of thyrotoxicosis
Thus, the body consumes more mineral elements such as phosphorus, calcium and potassium and there is also a deficiency of vitamins.
To avoid this disease, it is very important to always consume iodized salt.
#thyrotoxicosis #minerals #Phosphorus
Only boiled meat and fish in case of thyrotoxicosis
It is recommended to eat meat and fish only boiled.
If you follow these rules, then the rest of the rules for processing food are the same as for a normal person.
#thyroid #thyrotoxicosis #meat #fish
Exciting news, my first publication is out in #JIM !
#Amiodarone induced thyroid dysfunction: A high cumulative incidence in a nationwide cohort study in Iceland
We found a very high incidence of both #thyrotoxicosis and #hypothyroidism among amiodarone users
doi.org/10.1111/joim...
An integrated model for the association between thyroid homeostasis and major cardiovascular events. In the dyshomeostatic type of thyrogenic arrhythmia elevated FT4 concentration, caused by primary thyrotoxicosis, increases the risk for severe arrhythmia as a major cause for cardiovascular mortality. The TSH concentration is reduced in this case, represented by the left, declining, branch of the U-shaped relation between TSH level and risk (A). In the allostatic type, mainly caused by type 2 allostatic load and genetic traits, the set point of thyroid homeostasis is raised, resulting in increased TSH and FT4 concentration and subsequently elevated risk for arrhythmia. This situation is mirrored in the right, rising, branch of the relation between TSH concentration and cardiovascular risk (B). In any case, elevated concentrations of T3, T4 and other T3-agonistic thyroid hormones increase the sensitivity to catecholamines and sympathetic signaling (via upregulated expression of beta1 and beta2 adrenoceptors), thereby contributing to reduced stress tolerance. SPINA-GT, “gain of thyroid,” i.e., thyroid’s secretory capacity.
Interestingly, both subclinical #hypothyroidism and #thyrotoxicosis predict #MACE. The free thyroxine (FT4) concentration is more associated with the HR for cardiovascular events than thyrotropin (TSH) levels. Our observations yield an integrated model including psychosocial and somatic mechanisms.
Fig. 1. Simplified block diagram of the pituitary-thyroid feedback loop. The thyroid produces the hormones T3 and T4. On the one hand, this process is stimulated by TSH, a hormone secreted from the pituitary. On the other hand, this process is inhibited by Methimazole (MMI), an antithyroid agent (i.e., a medication), which constitutes the control input in this work. The hormone T4 gets converted into T3 by the enzymes 5’-deiodinase type I (D1) and 5’-deiodinase type II (D2). Finally, TRH (which is a natural hormone, and not a medication) stimulates the production of TSH.
Fig. 2. Illustration of the guidelines given by the American Thyroid association (ATA) (Ross et al., 2016). The treating physician may encounter many difficulties to select one precise dosage using these (rather vague) recommendations.
Fig. 3. Simulation results of an exemplary treatment based on the guidelines introduced in Ross et al. (2016). We apply the mean medication dosage for each interval, e.g., if the concentration of FT4 (which is proportional to T4) is within 27−42 pmol/L, we apply 7.5 mg. As disturbances, we consider forgotten dosages and measurement noise as explained in Section 3.
Fig. 4. Course of the hormone concentrations and the corresponding MMI dosages that are taken orally once per day. The dosages are determined by the MPC scheme introduced in Subsection 2.2. As explained in Section 3, we consider forgotten dosages, a model-plant mismatch, and some measurement noise as disturbances.
Medical treatment of #hyperthyroidism, i.e. #thyrotoxicosis due to overproduction of #thyroid hormone, remains a challenge. We developed a new dosage methodology based on model predictive control (MPC), which is faster and more stable than the usual trial-and-error approach. doi.org/10.1016/j.if...
Enhance your clinical knowledge with the next ESE Clinical Update on Management of #Thyrotoxicosis (online), endorsed by the European Thyroid Association (ETA).
#Endocrinology #ThyroidHealth
Register today! 👉 bit.ly/4jd2W8B
Last chance to save on your registration fee for ESE Clinical Update on Management of #Thyrotoxicosis - endorsed by the European Thyroid Association.
📅Early Bird deadline - 18 March 2025
Register today! #Endocrinology #ThyroidHealth
ow.ly/NMGU50UBqx0
🩺🧩 A 64 y/o man with ischemic #cardiomyopathy & ICD presents with #thyrotoxicosis, new-onset AF & VT. Amiodarone was stopped 3 months ago. What’s the best management?
▶️ Watch Dr. Tariq Ramtoola at Best Case Report Contest 2024: empendium.com/mcmtextbook/...
#YoungTalents #CaseReport #MedEd #FOAMEd
🧪 In #thyrotoxicosis, it is both essential and difficult to identify its pathogenesis (e.g. exogenous thyrotoxicosis, subacute thyroiditis or true hyperthyroidism). #SPINA_GD may be helpful to speed up the diagnostic work-up. This may be especially helpful in life-threatening thyroid storm.
Thyroid parameters and body mass index in subclinically or overtly hyperthyroid patients (TSH < 0.4 mIU/l) with toxic adenoma, Graves’ disease or LT4-treated carcinoma, stratified by their FT4 concentration (euthyroid vs hyperthyroid). The hormonal patterns differed between the treatment categories. FT4 concentrations were higher in the treated patients, deiodinase activity was markedly lower, but FT3 concentrations similar. Body mass index was also different between diagnostic categories despite “normal” FT4. Statistical comparison between etiological groups overall and in FT4-subgroups is based on Kruskal-Wallis test
🧪 With a cut-off value of about 28 nmol/s, total step-up #deiodinase activity (#SPINA_GD) may be used for differential diagnosis between exogenous (factitious) #thyrotoxicosis and true #hyperthyroidism.
doi.org/10.1016/j.jc...
pubmed.ncbi.nlm.nih.gov/32099819/
