Raised Serum Thyroid-stimulating Hormone Research Articles

Clinical study to evaluate the efficacy of Commiphora muku (Muqil) on thyroid function in hypothyroidism

Background: Hypothyroidism is a common endocrine disorder in which there is deficient production of thyroid hormone. Even though hormone replacement therapy is the mainstay treatment of hypothyroidism, but due to adverse effects on long term use, safe and effective Unani herbal drugs need to be researched. A decrease in serum concentrations of thyroid hormone causes an increased secretion of thyroid stimulating hormone (TSH), thus resulting in elevated serum TSH concentration. Methods: The methods used to determine thyroid dysfunction are still serum thyroid stimulating hormone and the main circulating thyroid hormones thyroxine and triiodothyronine either as total or estimated free concentrations, and it is indeed the improved assay sensitivities and specificities that have made it possible to diagnose these milder forms. TSH, T3 and T4 with safety parameters tests were done before treatment and after completion of treatment in both the groups in order to make the proper diagnosis, to exclude other systemic ailments and to assess the efficacy/safety of the proposed herbal drug. Results: The effects of test drug on lowering the raised serum TSH are attributed to the thyroid activities of the test drug which shoes highly significance p<0.01 before and after intervention. In respect of thyroxin there were no significant results between the test and control group. Conclusions: The study concluded that the efficacy of Commiphora mukul (Muqil) on thyroid function was designed to explore the role of Unani herbal drugs in the management of hypothyroidism on Unani principles is effective, safe and cost effective.

DYSLIPIDEMIA IN SUBCLINICAL HYPOTHYROIDISM IN TERTIARY HEALTH CARE CENTRE

BACKGROUND: Subclinical hypothyroidism is dened as normal serum Total T4 /free T4 and Total T3 /free T3 levels in the presence of raised serum thyroid stimulating hormone (TSH) levels. The association between subclinical hypothyroidism and dyslipidemia has been widely investigated, but the ndings remain controversial. To assess lipid AIM AND OBJECTIVE: abnormalities in patients diagnosed with subclinical hypothyroidism. A cross se MATERIALS AND METHODS: ctional study was carried out in 100 patients of subclinical hypothyroidism at Rama Medical College Hospital and Research Centre. Blood samples were collected and analysed for thyroid-stimulating hormone (TSH), free thyroxine (FT4), total cholesterol, serum triglycerides, low-density lipoproteincholesterol (LDL), and high-density lipoprotein-cholesterol (HDL). In this study total RESULTS: cholesterol (TC) was signicantly elevated (p value <0.05) in patients with subclinical hypothyroidism. Triglycerides (TG) and low density lipoprotein cholesterol (LDL) were also high in these patients but the difference was not statistically signicant. High density lipoprotein cholesterol (HDL) was signicantly reduced. CONCLUSION: SCH is associated with dyslipidemia, increased total cholesterol, TG, LDL, and decreased HDL are observed. We strongly recommend biochemical screening for thyroid dysfunction for all patients with dyslipidemia.

Evidence of a Causal Relationship between Serum Thyroid-Stimulating Hormone and Osteoporotic Bone Fractures

Objective: We aimed to validate the association of genome-wide association study (GWAS)-identified loci and polygenic risk score with serum thyroid-stimulating hormone (TSH) concentrations and the diagnosis of hypothyroidism. Then, the causal relationship between serum TSH and osteoporotic bone fracture risk was tested. Methods: A cross-sectional study was done among patients of European Caucasian ethnicity recruited in Tayside (Scotland, UK). Electronic medical records (EMRs) were used to identify patients and average serum TSH concentration and linked to genetic biobank data. Genetic associations were performed by linear and logistic regression models. One-sample Mendelian randomization (MR) was used to test causality of serum TSH on bone fracture risk. Results: Replication in 9,452 euthyroid individuals confirmed known loci previously reported. The 58 polymorphisms accounted for 11.08% of the TSH variation (p < 1e−04). TSH-GRS was directly associated with the risk of hypothyroidism with an odds ratio (OR) of 1.98 for the highest quartile compared to the first quartile (p = 2.2e−12). MR analysis of 5,599 individuals showed that compared with those in the lowest tertile of the TSH-GRS, men in the highest tertile had a decreased risk of osteoporotic bone fracture (OR = 0.59, p = 2.4e−03), while no difference in a similar comparison was observed in women (OR = 0.93, p = 0.61). Sensitivity analysis yielded similar results. Conclusions: EMRs linked to genomic data in large populations allow replication of GWAS discoveries without additional genotyping costs. This study suggests that genetically raised serum TSH concentrations are causally associated with decreased bone fracture risk in men.

Subclinical hypothyroidism and its relation to obesity in patients before and after Roux-en-Y gastric bypass

BackgroundSubclinical hypothyroidism (SH), defined as a raised serum thyroid-stimulating hormone (TSH) with a normal free thyroxine (FT4), is occasionally observed in morbidly obese patients. ObjectivesIt is currently not known whether thyroid hormone treatment is indicated. The aim of the present study was to assess the changes in thyroid hormone levels in thyroxine-naïve patients with SH in response to weight loss induced by Roux-en-Y gastric bypass (RYGB). SettingGeneral hospital specialized in bariatric surgery. MethodsSerum levels of TSH and FT4 were measured at baseline in 503 patients presenting for RYGB. In patients diagnosed with SH, these measurements were repeated 12 months postoperatively. ResultsSH de novo was present in 71 out of 503 patients (14.1%). One-year follow-up was available in 61 out of 71 patients (86%). TSH level>10 mU/L was observed in 3 patients (.5%). RYGB induced a decrease in BMI from 47±8 kg/m2 to 33±6 kg/m2 at 12-month follow-up (P<.001), and this was associated with a decrease in TSH from 5.8±2.0 to 2.8±1.3 mU/L (P<.001) and a decrease in FT4 from 15.2±2.1 to 13.9±2.3 pmol/L (P<.001), respectively. SH completely resolved in 53 (87%) of the de novo cases. ConclusionThe prevalence of SH de novo is high in morbidly obese patients. After RYGB it resolves in about 90% of patients. This high degree of spontaneous recovery suggests that follow-up alone is sufficient in the majority of patients.

Management of Subclinical Hypothyroidism

Objective: To review current concepts in the management of subclinical hypothyroidism (SCH) in patients with non-specific symptoms.Data sources: A review of articles reported on overt hypothyroidism and subclinical hypothyroidism. Summary of review: In a patient with primary overt hypothyroidism, management is usually straightforward: treatment with thyroxine should be offered to anyone with characteristic clinical features, a raised serum thyroid stimulating hormone (TSH) concentration and a low serum thyroxine (T4) concentration. More difficult is the management of a patient with subclinical hypothyroidism (SCH), in whom serum TSH is slightly raised (5-20 mIU/L) but T3, T4 levels are normal, and who is either asymptomatic or has only non-specific symptoms. Left untreated, some of these patients will eventually develop overt hypothyroidism. This review will address the use of thyroxine in patients with subclinical hypothyroidism.DOI: http://dx.doi.org/10.3329/cmoshmcj.v13i3.21045

Hypothyroidism

<h2>Abstract</h2> Hypothyroidism is common, affecting 1–2% of women. The onset is often insidious and symptoms and signs are vague. It is essential to confirm the diagnosis biochemically before initiating treatment. Measurement of serum thyroid-stimulating hormone (TSH) is a highly sensitive and specific test for primary thyroid failure. Elevation of TSH with normal serum T4 is termed ‘subclinical' hypothyroidism. If free T4 is low, with raised serum TSH, the biochemical diagnosis is overt hypothyroidism. In the UK, hypothyroidism is usually autoimmune (characterized by positive antithyroid antibodies) or iatrogenic (secondary to treatment for hyperthyroidism). Worldwide, iodine deficiency remains a major cause. Overt hypothyroidism is treated with T4 replacement; the aim is to restore serum TSH and free T4 to the normal range and hence abolish relevant symptoms and signs. The starting T4 dose is 100 <i>µ</i>g/day, though lower doses should be used in those with a history of ischaemic heart disease. Serum TSH should be checked no sooner than 6–8 weeks after initiating T4, to prompt dose adjustment. The T4 dose required to restore biochemical euthryoidism is usually 100–125 <i>µ</i>g per day. Over-treatment with T4 (indicated by suppression of serum TSH) should be avoided, because of potential long-term risks. After euthyroidism has been restored, TSH should be checked annually to ensure ongoing compliance. There is little evidence that mild, subclinical hypothyroidism is associated with symptoms or adverse events, so if TSH is less than 10 mU/litre conservative management is reasonable, with annual monitoring of TSH to identify biochemical progression.

Subclinical hypothyroidism: the case against treatment

Controversy exists regarding the management of spontaneous subclinical hypothyroidism, defined as a raised serum thyroid-stimulating hormone (TSH) but a normal serum thyroxine (T 4) level in an asymptomatic patient. It is claimed that T 4 therapy improves non-specific symptoms, prevents progression to overt hypothyroidism and reduces the cardiovascular risk by improving the atherogenic lipid profile. However, there are few data to suggest a positive benefit of T 4 therapy in those documented to have a serum TSH between 5 and 10 mU l −1. Normalization of serum TSH with T 4 is often not achieved in clinical practice, and detrimental effects on the skeleton, the cardiovascular system and even mortality have been suggested by subclinical hyperthyroidism, which can be a consequence of overtreatment with T 4 therapy. Many patients will not progress to overt hypothyroidism in 20 years, and adopting a ‘wait and see’ policy rather than intervention will avoid unnecessary treatment and the potential for harm in a significant number of patients.

Subclinical thyroid disease

Widespread use of improved measurements for serum thyroid hormones and thyroid-stimulating hormone (TSH) has resulted in characterization of the syndromes of subclinical hypothyroidism, characterized by normal free T4 estimate and raised serum TSH, and subclinical hyperthyroidism, in which patients have normal serum free T4 estimate and decreased serum TSH. Therapy for these two disorders in generally recommended but must be individualized according to the patient's general medical condition. Additional studies are needed to assess the benefits of treatment. This report reviews subclinical hypothyroidism and subclinical hyperthyroidism, describing their causes, diagnostic criteria, complications, and indications for treatment. A brief review of testing for thyroid function is presented, and each of the subclinical disorders is compared with the classic syndromes of hypothyroidism and hyperthyroidism.

In Vitro Testing of Thyroid Function: a review

Triiodothyronine (T(3)) is the major thyroid hormone and thyroxine (T(4)) may be only a "prohormone". A normal serum T(3) concentration can compensate for a low serum T(4) to maintain euthyroidism and on the other hand hyperthyroidism can exist in spite of a normal T(4) if the T(3) concentration is increased ("T(3)-toxicosis"). A raised serum thyroid stimulating hormone (TSH) concentration is the present most sensitive indicator of thyroidal hypothyroidism and the level can be used to titrate replacement therapy to the individual's own requirements. TSH concentration is classically low in hypothyroidism secondary to pituitary or to hypothalamic disorder and synthetic thyrotrophin release hormone can then be used to identify which of these two sites is at fault. Thyroxine is the best form of thyroid replacement for hypothyroidism because it produces more consistently physiological concentrations of T(3). Full replacement is achieved with 0.1 - 0.2 mg of T(4)/day and doses above this, as formerly widely used, may cause over-replacement. New reliable kit tests are available which give in one quick procedure a measure of free-thyroxine even in the presence of abnormalities of protein-binding. These kit tests are suitable for the routine screening of the whole spectrum of thyroid dysfunction and when combined, in appropriate instances, with radioimmunoassay procedures for serum T(3) and TSH, provide a battery of tests which will help in the diagnosis of the great majority of causes of thyroid dysfunction.

Thyroid function in patients treated with radioactive iodine for thyrotoxicosis.

A series of 105 patients treated at least two years earlier with radioactive iodine for thyrotoxicosis have been surveyed. Eighty-five patients (81%) were euthyroid clinically and on the basis of routine thyroid function tests. Of the euthyroid patients 46 (54%) had normal thyroid-stimulating hormone (TSH) levels and 39 (46%) had raised TSH levels. There was no difference in serum triiodothyronine levels between these two groups but the serum protein bound iodine and serum thyroxine, though still well within the normal range, were significantly lower in the group with raised TSH levels. The serum cholesterol was also significantly higher in this latter group.Most of the euthyroid patients were seen again a year later. None had become hypothyroid and neither those with normal nor those with raised TSH levels showed any evidence of a decline in the level of serum thyroxine.It is concluded that raised serum TSH levels in patients treated with iodine-131 are not necessarily indicative of hypothyroidism. There is no indication that patients who have this abnormality become overtly hypothyroid over a 12-month follow up.

Grades of hypothyroidism.

Seventy-nine patients with hypothyroidism and autoimmune thyroid disease were studied, and allotted to one of four categories on the basis of clinical and biochemical features. Firstly, patients with overt hypothyroidism had obvious clinical features of hypothyroidism and abnormal results from routine tests of thyroid function. Secondly, those with mild hypothyroidism, however, had minor and non-specific symptoms, but the routine measurements of circulating thyroid hormone concentration generally lay within the normal range, although they were significantly lower than those seen in subclinical hypothyroidism or in normal subjects. The serum concentration of thyroid-stimulating hormone (TSH) was raised in this group and their symptoms resolve with treatment. Thirdly, patients with subclinical hypothyroidism were asymptomatic, had a raised serum TSH concentration, but all other measurements of thyroid function are indistinguishable from those recorded in people with autoimmune thyroid disease without disturbance of thyroid function and in normal subjects. Lastly, subjects with circulating thyroid antibodies, normal indices of thyroid function, and a normal serum TSH concentration were indistinguishable biochemically from normal subjects. Thus hypothyroidism is a graded phenomenon, the most valuable features for defining the individual grade being the clinical manifestations, the serum TSH concentration, and the presence of circulating antibodies to thyroid tissue.

Grades of hypothyroidism.

Seventy-nine patients with hypothyroidism and autoimmune thyroid disease were studied, and allotted to one of four categories on the basis of clinical and biochemical features. Firstly, patients with overt hypothyroidism had obvious clinical features of hypothyroidism and abnormal results from routine tests of thyroid function. Secondly, those with mild hypothyroidism, however, had minor and non-specific symptoms, but the routine measurements of circulating thyroid hormone concentration generally lay within the normal range, although they were significantly lower than those seen in subclinical hypothyroidism or in normal subjects. The serum concentration of thyroid-stimulating hormone (TSH) was raised in this group and their symptoms resolve with treatment. Thirdly, patients with subclinical hypothyroidism were asymptomatic, had a raised serum TSH concentration, but all other measurements of thyroid function are indistinguishable from those recorded in people with autoimmune thyroid disease without disturbance of thyroid function and in normal subjects. Lastly, subjects with circulating thyroid antibodies, normal indices of thyroid function, and a normal serum TSH concentration were indistinguishable biochemically from normal subjects.Thus hypothyroidism is a graded phenomenon, the most valuable features for defining the individual grade being the clinical manifestations, the serum TSH concentration, and the presence of circulating antibodies to thyroid tissue.