To find whether the same results would be manifested in Saudi Arabia, growth hormone treatment affects must be observed. Concerning our research, a significant negative correlation between the duration of growth hormone treatment and the decrease in freethyroxine levels (FT4). With the results, we can verify that growth hormone treatment can play a key role in the hormonal secretions of the freethyroxine by the thyroid gland. Further explanations will be presented in the methods, results, discussion, and conclusion. METHODOLOGY
Thyroid hormones have a wide and important range of effects within the nervous system beginning from fetal life and continuing throughout the adult life [5, 6]. Thyroid dysfunction is common in auto- immune diseases of the nervous system, especially in neurological demyelinating disorders such as acute transverse myelitis, Guillain-Barré syndrome and multiple sclerosis [7–12]. Patients with acute trans- verse myelitis have lower levels of thyroid stimulat- ing hormones (TSH) and free triiodothyronine (FT3) and higher levels of freethyroxine (FT4) and FT4/ FT3 ratio than in healthy controls . A higher FT4 level and lower TSH level may be associated with the incidence and severity of Guillain-Barré syn- drome . In cerebrospinal fluid, the total T4 level (TT4) and the TT4/TT3 ratio in patients with mul- tiple sclerosis are significantly higher than those in normal controls .
A microplate chemiluminescence enzyme immunoassay (CLEIA) with high sensitivity, selectivity and repro- ducibility was developed for the determination of freethyroxine (FT4) in human serum. A competitive assay has been utilized with horseradish peroxidase (HRP) labeled thyroxine analog in the chemiluminescence (CL) detec- tion. The CL signal produced by the emission of photons from luminol was directly proportional to the amount of analyte. The linear range was 0.45-7.5 ng dL -1 and the detection limit was 0.09 ng dL -1 . Experimental conditions,
Because of contraction of the thyroxine distribution space the clearance of thyroxine was less markedly affected, increasing from 1.37 to 1.56 liters/day. Since the ratio of thyroxine turnover to freethyroxine concentration, i.e., the freethyroxine clearance, increased proportionately (4.79-5.55 liters × 10 3 /day) we conclude that triiodothyronine stimulates thyroxine clearance by a mechanism that is independent of effects on freethyroxine concentration.
As the maternal hypothyroidismhas been listed as one of the causes of high blood pressure i.e. the physiological changes in thyroidgland during pregnancy have been suggested asone of the patho-physiological cause ofpre-eclampsia (Endo, 1979). Some investigators reported no change in serum TSH and /or T 3 and T4 in pregnancy; while some found significant increases in TSH and /or T3 and T4 during pregnancy. Nahid et al., 2002-2004, in Iran, performed a prospective case-control study to identify the association between the maternal hypothyroidism and pre-eclampsia and they found that themean TSH levels was not significantly higher in pre- eclamptic group as compared to controls (p>0.05) (Nahid Mostaghel, 2008). Larijani et al., 2004, performed a study in maternal thyroid hormones and pre-eclampsia. They showed that serum levels of free T4 and TSH were increased in women with severe pre-eclampsia when compared with mild pre- eclampsia and normal pregnancy (Larijani, 2005). Kumar et al., 2005, as well, performed a study that showed significant elevation in mean serum TSH but FT3 and FT4 were without alterations in pre-eclampsia women (Kumar, 2005). Several studies done by Mostaghel et al, Kharb et al and Raoofi et al., (Mostaghel, 2008; Kharb, 2013; Raoofi, 2014), revealed similar result to Kumar et al study as increased level of TSH and decreased levels of T3 and T4 in pre-eclampsia women in compared with normal pregnant women. Ashoor et al., 2010, performed a study showed increase serum TSH and decreased in T4 with gestational age (Ashoor, 2010). Khadem et al., 2012, in Iran, performed similar study but with different result that showedno changes in FT3, FT4 and TSH levels and stated they do not support the hypothesis of thyroid hormones changes as apossible etiology of pre-eclampsia (Khadem, 2012). Sonali et al., 2012 - 2014, performed a case control study. They found that there was a significant association between pre-eclampsia and thyroid hypofunction (Sonali Deshpande, 2015). Hosen et al., 2014, in Bangladesh,
whether HVETL affect the bone metabolism, prevalence of the thyroid nodule, and oxidative stress levels in electrical work- ers. Furthermore, since biological effects of EMF are observed after a long period, the electrical workers are an appropriate group to search this effect. In the present study, we examined the effects of exposure to an EMF on bone mineral density (BMD), thyroid nodule formation, serum free triiodothyronine (FT3), freethyroxine (FT4), RANK, RANKL, osteoprotegerin (OPG), alkaline phosphatase (ALP), phosphor (P) levels, total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) of electrical workers.
Demographic and clinical variables were obtained from participant report and electronic medical records. Demo- graphic inclued age, sex, body mass index (BMI) and edu- cation. BMI was calculated as weight (kg)/squared height (m 2 ). A fasting morning venous blood sample was ob- tained from each participant. Levels of serum thyroid-stimulating hormone (TSH), free-triiodothyronine (FT3), freethyroxine (FT4), TgAbs, and TPOAbs were de- termined with automated immuno chemiluminescent assay (ICMA) kits (Abbott Laboratories, IL, USA). Levels of serum 25-hydroxyvitamin D (25(OH)D) were deter- mined using a competitive protein-binding assay (Roche Diagnostics, Mannheim, Germany). The inter-assay vari- ation coefficient for 25(OH)D measurement was 8.5%. Serum 25(OH)D levels in HT patients were divided into four quartiles (≤ 34.0, 34.1–40.0, 40.1–47.0 and ≥ 47.1 nmol/L), as the raw data of 25(OH)D were skewed. The median 25-hydroxyvitamin D values for all quartiles were 30.8, 36.6, 43.7 and 53.1 nmol/L, respectively.
We ascertained three patients with syndromic symptoms associated with CPHD. An informed written consent was used to recruit the patients and their family mem- bers. All affected patients underwent detailed examin- ation at the departments of clinical genetics and pediatrics of King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia. Laboratory testing, radio- logical investigation (X-ray) and audiologic assessments were performed. Pituitary examination was made by multisequential multiplanar magnetic resonance imaging (MRI) by applying standard scanning protocols . The hormonal tests were measured by radioimmunoassay techniques by Roche Diagnostics, USA. Hormonal evalu- ation included basal levels for GH response to glucagon stimulation, TSH, PRL, LH, FSH, cortisol, ACTH and freethyroxine (FT4) levels. Growth biochemical markers including insulin growth factor 1 (IGF1) and insulin
A non-fasting venous blood sample was drawn from each participant. Concentrations of TSH, freethyroxine (fT4) and total triiodothyronine (T3) in HUNT2 were measured at the Hormone Laboratory, Aker University Hospital, Oslo, using DELFIA hTSH Ultra (sensitivity, 0.03 mU/L; and total analytic variation <5%), DELFIA fT4 (total analytic variation <7%), and AutoDELFIA T3 (total analytic variation <5%), all from Wallac Oy, Turku, Finland. In HUNT3, serum TSH and fT4 were measured at Levanger Hospital, Levanger, Norway, using Architect cSystems ci8200 (sensitivity, 0.01 mU/l; and a total ana- lytic variation <5%), and Architect cSystems ci8200 (total analytic variation <6%), respectively, both from Abbott, Clinical Chemistry, USA. The measurement methods of TSH in HUNT2 and HUNT3 have previously been compared, with similar results , and agreement expressed by Bland-Altman  did not reveal any ob- vious pattern or deviations. The Norwegian population is considered to have sufficient iodine intake , and reference range for clinically normal TSH was defined as 0.50 to 3.5 mU/l based on previous publications from this population .
Main body: The historical developments and motivation leading to that decision and its potential implications are explored from pathophysiological, clinical and statistical viewpoints. An increasing frequency of hypothyroid-like complaints is noted in patients in the wake of this directional shift, together with relaxation of treatment targets. Recent prospective and retrospective studies suggested a changing pattern in patient complaints associated with recent guideline-led low-dose policies. A resulting dramatic rise has ensued in patients, expressing in various ways dissatisfaction with the standard treatment. Contributing factors may include raised problem awareness, overlap of thyroid-related complaints with numerous non-specific symptoms, and apparent deficiencies in the diagnostic process itself. Assuming that maintaining TSH anywhere within its broad reference limits may achieve a satisfactory outcome is challenged. The interrelationship between TSH, freethyroxine (FT4) and free triiodothyronine (FT3) is patient specific and highly individual. Population-based statistical analysis is therefore subject to amalgamation problems (Simpson ’ s paradox, collider stratification bias). This invalidates group-averaged and range-bound approaches, rather demanding a subject-related statistical approach. Randomised clinical trial (RCT) outcomes may be equally distorted by intra-class clustering. Analytical distinction between an averaged versus typical outcome becomes clinically relevant, because doctors and patients are more interested in the latter. It follows that
The rate of appearance of labeled thyroxine (T4) and albumin in lymph from various areas after simultaneous i.v. injection of the labeled substances in conscious ambulatory sheep has been used to estimate the relative rates of transcapillary movement of stable T4 and albumin. Labeled T4 appeared in hepatic lymph at the same rate as albumin. In intestinal and leg lymph, labeled T4 appeared eight and four times as rapidly as albumin indicating that T4 crosses capillaries in these areas independently of and much more rapidly than albumin and other proteins having similar distribution kinetics. The lymph:plasma ratios for all the T4-binding proteins including albumin were very similar in any one area showing that the relative fractional rates of transcapillary movement of these proteins were very similar. Therefore in extrahepatic areas, transcapillary movement of T4 in the protein-bound form was quantitatively much less important than in the free form. The findings support earlier views, recently questioned, that free T4 is of considerable physiological significance.
Subclinical hypothyroidism (SCH) is defined by increase in serum thyroid stimulating hormone (TSH) and freethyroxine (FT4) and free triiodothyronine (FT3) levels within normal range, coupled with absence of typical clinical symptoms. 1 It shows much higher predilection for
Swarna Sindura (SS) is an ayurvedic preparation used as a traditional medicine in the treatment of neurasthenia. In this study, effect of SS on thyroid hormone profile was evaluated after chronic administration of this drug to male Sprague-Dawley rats. The acute pharmacological test of SS recorded no death or any signs of toxicity even at the highest dose of 4000 mg/Kg body weight. For chronic pharmacological evaluation, the animals were divided into two groups. The first group was given SS preparation at a dose of 40 mg/kg body weight for 28 days while the second group that served as the control received water for the same period. After 28 days of chronic administration of the SS preparation the following effects on the thyroid hormone profile were noted. There was a statistically highly significant (p=0.008, 15.62 % increase) increase in the serum circulating free Triiodothyronine (fT3) level. The drug (SS) did not affect serum circulating total Thyroxine (tT4) level, total Triiodothyronine (tT3) level, freeThyroxine (fT4) level and Thyroid stimulating hormone (TSH) significantly.
was followed yearly with MRI to determine whether it was growing. In September 2009, periodic MRI showed that the pituitary tumor had become larger. She was re- ferred to our hospital for further evaluation. She had no remarkable history or medications. She had a family his- tory of rheumatoid arthritis. On physical examination, her blood pressure was 127/75 mmHg, and her pulse was regular at 105 beats/minute. Her body temperature was 36.8 °C, height was 163.7 cm, body weight was 53.8 kg, and body mass index was 20.1 kg/m 2 . Her con- sciousness was alert. She had no neck goiter or leg edema. Both Achilles’ tendon reflexes were moderately increased. She had mild exophthalmos. She denied any headaches or visual field defect. Her other clinical symp- toms were not notable. An endocrinological examination and thyroid echocardiography were performed because of hyperthyroidism; in particular, Graves’ disease was suspected. Her serum free triiodothyronine (FT3) level was 6.3 pg/mL (normal 2.3 to 4.0 pg/mL), freethyroxine (FT4) level was 2.3 ng/dL (normal 0.9 to 1.7 ng/dL), thyroid-stimulating hormone (TSH) level was 0.27 μIU/ mL (normal 0.5 to 5.0 μIU/mL), anti-TSH receptor anti- body (TRAb) was positive (5.0 IU/L, normal <1.0 IU/L), anti-thyroglobulin antibody (TgAb) was positive (2.3 IU/ mL, normal <0.3 IU/mL), and anti-thyroid peroxidase antibody (TPOAb) was positive (4.6 IU/mL, normal <0.3 IU/mL). Ultrasonography showed a moderately hypervascular thyroid without any nodes. Due to the in- crease in her FT3 and FT4 levels, and the decrease in her TSH level and TRAb positivity, Graves’ disease was diagnosed, and anti-thyroid drug therapy was started in April 2010. Subsequently, she stopped taking her medi- cation because she felt that the headache and sweating were exacerbated. In Graves’ disease, the TSH level is normally suppressed by negative feedback due to an in- crease in the FT3 and FT4 levels; the TSH value falls
The binding proteins appeared to be determinants of the freethyroxine fraction, which in turn, appeared to be a direct determinant of the half-time of turnover. These inferences did not exclude other possible factors including diminished hepatic uptake and metabolism of the hormone in liver disease.
increases with age , in other countries with borderline sufficient iodine intake, it declines . In this study, a serum TSH of 4.0 µIU/L better distinguished the two TSH distribution curves (population with hypothyroidism on the right side of figure 1). As Völzke H et al.  concluded, normal TSH ranges in formerly iodine deficient regions are different than those without a scarcity of iodine. Moreover, the TSH value of 4.0 µIU/L is in accord with the 97.5 percentile of the NHANES III Mexican-American reference group of 3.9 µIU/mL . Indeed, the mean total thyroxine and freethyroxine were significantly lower in the group with SH (TSH ≥ 4.0 µIU/L) than the group with TSH (between 0.4 to 3.99 µIU/L inclusive). Thus, evaluations for association use the 4.0 µIU/L cutoff point for SH.