Thyroxine absorption test protocol for hypothyroid patients on high dose thyroxine replacement

presented at the Phillippine Nurses UK World Cafe Convention, 24 October 2020

STUDY OF THYROID DYSFUNCTION IN PATIENTS WITH METABOLIC SYNDROME

Introduction: Metabolic syndrome (MS) is described as insulin resistance, clusters of abnormalities including abdominal obesity, hypertension, hyperglycaemia, increased triglycerides, and decreased high-density lipoprotein cholesterol (HDL-C). In maintaining thermogenesis and metabolic homeostasis Thyroxine and Triidothryronine play an important role. Thyroid is established by thyroid stimulation hormone (TSH). Thyroid hormones up-regulate metabolic pathways relevant to resting energy expenditure, hence obesity and thyroid functions are often correlated. It is still not clear whether these alterations in thyroid hormones are a cause or an effect of obesity. Hypothyroidism is well known to cause diastolic hypertension, endothelial dysfunction, hyperlipidemia and cardiovascular disease. The functions of thyroid affect the components of metabolic syndrome including triglycerides (TG), HDL–cholesterol (HDL-C), blood pressure and plasma glucose. The impact of various degree of thyroid dysfunction on components of metabolic syndrome, however, continues to be debatable. On components of metabolic syndrome, Thyroid dysfunction is also risk factor for ASCVD mediated by the effects of thyroid hormones on glucose metabolism, lipid and blood pressure. In India about onethird of the urban population in large cities has metabolic syndrome with the overall prevalence varying between 11% and 56%. Worldwide Thyroid diseases are most prevalent endocrine disorders. According to various studies it showed that about 42 million people in India suffer from thyroid diseases. Aim: The main aim of this study was to study thyroid dysfunction in metabolic syndrome. Material and Methods: In this study 150 patients with different age group from 20 years to 60 years old were included with metabolic syndrome diagnosed as per IDF criteria. From all the patients who visit hospital as OPD and IPD patients’ detailed history was recorded and also laboratory examination were done. Result: In this study total 150 patients with metabolic syndrome were included in which there were 82 were males and 68 were females. In this study there were maximum numbers of male patients in comparing with female patients as 43.3% and 54.7% respectively with different age group from 20 years to 60 years old. Out of total patients age group of 35 to 50 years old shows maximum and the age group 50- 60 years old showed least as 37% and 23% respectively. In this study in the age group of 35-50 had abnormal TGL values, compared to the other age groups. While HDL values were low in the 50-60 age group compared to others. Conclusion: Thyroid dysfunction is common in metabolic syndrome patients. The prevalence of hypothyroidism is more common in metabolic syndrome. Therefore early detection and thyroxine replacement could reduce the significant cardiovascular risk. However, there is still a controversy whether the patients with subclinical hypothyroidism would be benefited from thyroxine replacement. Hence Subclinical hypothyroidism should be picked up and treated at the earliest. Keywords: Metabolic syndrome, Thyroid dysfunction, hypothyroidism, HDL

Routine free thyroxine reference intervals are suboptimal for monitoring children on thyroxine replacement therapy and target intervals need to be assay-specific

Central hypothyroidism is a condition where there is (qualitatively or quantitatively) TSH deficiency, leading to reduced thyroid hormone production. In such patients, serum TSH does not accurately reflect the adequacy of thyroxine replacement, as the log-linear relationship between thyrotropin (TSH) and free thyroxine (FT4) is lost. We aimed to prospectively determine the optimal physiological FT4 treatment range for children treated for primary hypothyroidism, based on their serum TSH concentrations. This information could be used to guide optimal therapy for all children on thyroxine replacement, including those with central hypothyroidism. In total, sixty children (median age: 11 years, range: 11 months to 18 years) were recruited over 21 months. They were prescribed a stable dose of thyroxine for at least 6–8 weeks prior to a thyroid function test that consisted of serum TSH, FT4 and free triiodothyronine (FT3) measurements. The serum sample for the thyroid function tests was collected before ingestion of the daily dose, i.e. the trough concentration, and measured using Beckman Coulter UniCel DxI 800 instrument, Siemens Advia Centaur, Roche Cobas, Abbott Architect, Ortho Clinical Diagnostics Vitros 5600 (Ortho-Clinical Diagnostics, Raritan, NJ) platforms. The FT4 and FT3 reference intervals showed significant inter-method difference. The lower limit of the FT4 reference intervals were generally shifted mildly higher when the TSH concentration of the children were restricted from 0.5–5.0 mIU/L to 0.5–2.5 mIU/L. By contrast, the upper limit of the FT3 and FT4 reference intervals were relatively stable for the different TSH concentrations. Assay-specific target ranges for optimal thyroxine therapy are required until FT4 assay standardisation is realised.

Double variants in TSHR and DUOX2 in a patient with hypothyroidism: case report

Thyroid dyshormonogenesis (TDH) is characterized by the defective synthesis of thyroid hormones. We present a patient with congenital hypothyroidism (CH) who presented in newborn screening with elevated serum thyroid-stimulating hormone (TSH), decreased free thyroxine (fT4) and increased thyroglobulin (Tg) concentrations. Ultrasound scan revealed a properly structured thyroid gland. Treatment with L-thyroxine was initiated. At the age of 2 years, thyroxine replacement was stopped. The patient remained untreated until 6 years of age when TSH levels progressively increased and L-thyroxine treatment was restarted at a dose of 12.5 μg/day. Genetic analysis revealed a double heterozygosity for likely pathogenic variants of dual oxidase 2 (DUOX2) and thyroid stimulating hormone receptor (TSHR). Both genes were earlier shown to be associated with CH. In a literature review, our patient was compared to previously published patients with similar clinical characteristics, and a good genotype-phenotype correlation was identified.