Our library of drug research abstracts drawn from the medical literature is updated on a regular schedule, and you can be assured that new levoxyl research articles will be listed here shortly after becoming available to us.
Related Sponsors
Medical research on levoxyl
Gynecol Endocrinol. 2008; 24(8): 459-464
Dei M, Seravalli V, Bruni V, Balzi D, Pasqua A
Objective. The aim of the present study was to investigate the anthropometric and endocrine characteristics of subjects with amenorrhea related to eating disorders after weight recovery, in order to identify factors connected with the resumption of menses. Methods. Clinical data, body composition parameters and serum levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), thyroid-stimulating hormone (TSH), free triiodothyronine, free thyroxine, cortisol, leptin and insulin were assessed in two groups of young women classified according to menstrual status after weight rehabilitation: 43 subjects who displayed persistent amenorrhea and 34 who resumed menses. Univariate and multivariate logistic regression analyses were used to examine the relationships between the different parameters and menstrual recovery. Results. The patients who resumed menses had low initial weight and BMI, and a greater difference between current and initial BMI (DeltaBMI), than those with amenorrhea. No differences were observed in lean mass, body fat or bone density between the two groups. Moreover, the reduction in FSH and the increase in LH, insulin and leptin emerged as significant predictors of menstrual recovery. Increased DeltaBMI and insulin continued to be positive predictors in the multivariate analysis. Conclusion. Following weight rehabilitation, the individual's metabolic set point before weight loss and the current insulin levels appear significant in predicting the reactivation of reproductive function.
J Anim Sci. 2008 Oct 10;
Waggoner JW, Löest CA, Mathis CP, Hallford DM, Petersen MK
Metabolic demand for sulfur-containing AA increases during inflammation in non-ruminants. Therefore, Met supplementation may alleviate negative effects of infection on N balance. Effects of gram(-) bacterial lipopolysaccharide (LPS) and supplemental dietary Met on N balance, serum hormones and haptoglobin, and plasma urea-N and AA were evaluated in 20 Angus-cross steers (BW = 262 +/- 6.3 kg). Treatments (2 x 2 factorial) were infusion of no LPS (-LPS) or prolonged low dose of LPS (+LPS) and dietary supplementation of no (-MET) or 14 g/d (+MET) rumen-protected Met (Smartamine M, Adisseo, Alpharetta, GA; providing 7.9 g/d DL-Met). Steers were adapted to a roughage-based diet (DMI = 1.4% of BW daily) and supplemental Met for 14 d, and were then infused (1 mL/min via i.v. catheter) with LPS on d 1 (2 microg/kg BW) and 3 (1 microg/kg BW) of a 5-d collection period. On d 1, blood was collected before LPS infusion and at 2, 4, 6, 8, 10, 12, and 24 h after LPS challenge. Diet samples, feed refusals, feces, and urine were collected daily for 5 d. Rectal temperature and serum concentrations of cortisol, prolactin, tumor necrosis factor alpha, and haptoglobin increased, whereas thyroxine and triiodothyronine decreased for +LPS vs -LPS steers (LPS x h, P < 0.01). Plasma urea-N was greater for +LPS than -LPS steers (LPS, P = 0.03), and serum IGF-1 was not affected (P >/= 0.26) by LPS or Met. Plasma concentrations of Thr, Lys, Leu, Ile, Phe, Trp, Asn, Glu, and Orn decreased, plasma Ala increased, and Gly and Ser initially increased, then declined in +LPS vs -LPS steers (LPS x h, P /= 0.24) N intake, fecal N excretion, or N digested, but resulted in greater (P < 0.01) urinary N excretion and lower (P < 0.01) N retention. The absence of an LPS x Met interaction (P = 0.26) for N retention indicates that supplemental Met does not improve N utilization of growing beef steers exposed to gram(-) bacterial endotoxin. Decreases in plasma concentrations of several essential AA in +LPS steers suggests that metabolic demand for these AA likely increased in steers exposed to endotoxin.
Prevalence of and risk factors for feline hyperthyroidism in Hong Kong.
J Feline Med Surg. 2008 Oct 9;
De Wet CS, Mooney CT, Thompson PN, Schoeman JP
A study was conducted to determine the prevalence of and potential risk factors for feline hyperthyroidism in Hong Kong. Serum total thyroxine (T(4)) was measured in 305 cats aged 10 years and older that presented at various veterinary clinics in Hong Kong. The prevalence of hyperthyroidism (T(4)>50nmol/l) within this population was 3.93% and there was no significant difference in prevalence between healthy (3.16%) and sick (4.37%) cats. Older cats (>15 years) were more likely to be affected and domestic shorthair cats were less likely to be diagnosed with hyperthyroidism than the other breeds combined. No specific association between the development of feline hyperthyroidism and food type was observed. The prevalence of feline hyperthyroidism in Hong Kong was less than that reported for most other parts of the world, despite the presence of previously identified risk factors.
J Feline Med Surg. 2008 Oct 8;
van Hoek IM, Peremans K, Vandermeulen E, Duchateau L, Gommeren K, Daminet S
This study investigated the thyroidal response to administration of recombinant human thyroid stimulating hormone (rhTSH) by means of serum total thyroxine (TT(4)) concentration and pertechnetate uptake by the thyroid gland in six healthy euthyroid spayed female cats. A pertechnetate scan was performed on day 1 to calculate thyroid/salivary gland (T/S) uptake ratio. On day 3, 25mug rhTSH was injected intravenously. Six hours later the thyroid scan was repeated as on day 1. Blood was drawn for serum TT(4) measurement prior to injection of rhTSH and performance of the pertechnetate scan. Statistically significant differences in mean serum TT(4) concentration, T/S uptake ratio before and 6h after rhTSH administration and T/S uptake ratio between left and right lobes were noted. We can conclude that 25mug rhTSH increases pertechnetate uptake in the thyroid glands of cats, this should be taken into account when thyroid scintigraphy after rhTSH administration is interpreted.
Isr Med Assoc J. 2008 Aug-Sep; 10(8-9): 603-6
Shuvy M, Arbelle JE, Grosbard A, Katz A
BACKGROUND: Heart rate variability is a sensitive marker of cardiac sympathetic activity. OBJECTIVES: To determine whether long-term hyperthyroidism induced by thyroxine suppressive therapy affects HRV. METHODS: Nineteen patients treated with suppressive doses of thyroxin for thyroid cancer and 19 age-matched controls were enrolled. Thyroid function tests and 1 minute HRV were performed on all subjects and the results were compared between the groups. The 1 minute HRV was analyzed during deep breathing and defined as the difference in beats/minute between the shortest and the longest heart rate interval measured by eletrocardiographic recording during six cycles of deep breathing. RESULTS: One minute HRV during deep breathing was significantly lower among thyroxine-treated patients compared to healthy controls (25.6 +/- 10.5 vs. 34.3 +/- 12.6 beats/min, P < 0.05). There were no significant differences in mean, maximal and minimal heart rate between the groups. CONCLUSIONS: Thyroxine therapy administered for epithelial thyroid cancer resulted in subclinical hyperthyroidism and significantly decreased HRV due to autonomic dysfunction rather than basic elevated heart rate.
Amiodarone-induced thyrotoxicosis. A review.
Minerva Endocrinol. 2008 Sep; 33(3): 213-28
Piga M, Serra A, Boi F, Tanda ML, Martino E, Mariotti S
Amiodarone (AM), a potent class III anti-arrhythmic drug, is an iodine-rich compound with a structural resemblance to thyroid hormones triiodothyronine (T3) and thyroxine (T4). At the commonly employed doses, AM causes iodine overlaod up to 50-100 times the optimal daily intake, which may be responsible of a spectrum of effects on thyroid function often counterbalancing its heart benefits. Although most patients on chronic AM treatment remain euthyroid, a consistent proportion may develop thyrotoxicosis (AM-induced thyrotoxicosis, AIT) or hypothyroidism. AIT is more prevalent in iodine-deficient areas and is currently subdivided in two different clinico-pathological forms (AIT I and AIT II). AIT I develops in subjects with underlying thyroid disease, and is caused by an exacerbation by iodine load of thyroid autonomous function; AIT II occurs in patients with no underlying thyroid disease and is probably consequent to a drug-induced destructive thyroiditis. Mixed or indeterminate forms of AIT encompassing several features of both AIT I and AIT II may be also observed. The differential diagnosis between AIT I and AIT II (which is important for the choice of the appropriate therapy) is currently made on radioiodine uptake (RAIU), which may be high, normal or low but detectable in AIT I, while is consistently very low or undetectable in AIT II and on colour-flow Doppler sonography (CFDS) showing normal or increased vascularity in AIT I and absent vascularity in AIT II. Quite recently, studies carried out in our Units at the University of Cagliari (Italy) showed that sestaMIBI thyroid scintigraphy may represent the best single test to differentiate AIT I (showing increased MIBI retention) from AIT II (displaying no significant uptake). Treatment of AIT is dependent from its etiology. AIT usually responds to combined thionamides and potassium perchlorate (KClO4) therapy, AIT II generally responds to glucorticoids, while indeterminate forms may require both therapeutic approaches. In patients with AIT I definitive treatment of hyperthyroidism by administration of (131)I, initially not feasible for the low RAIU and/or the risk of thyrotoxicosis exacerbation, is advised after normalization of iodine overload. To control severe AIT additional treatment with lithium carbonate, the use of short course of iopanoic acid and plasmapheresis have been also proposed. In cases resistant to medical treatment and/or in patients with severe cardiac diseases who cannot interrupt AM or require quick AM reintroduction, total thyroidectomy (possibly carried out by minimally invasive video-assisted technique) may be proposed after rapid correction of thyrotoxicosis with combination of thionamides, KClO4, corticosteroids and a short course of iopanoic acid.
Endocrinology. 2008 Oct 9;
Westholm DE, Stenehjem DD, Rumbley JN, Drewes LR, Anderson GW
The organic anion transporter Oatp1c1 is a high affinity thyroxine (T4) transporter with narrow substrate specificity expressed at the blood-brain barrier. A transport model using cells over-expressing Oatp1c1 was created to identify novel Oatp1c1 substrates and inhibitors. Rat Oatp1c1 was cloned and stably expressed in HEK293 cells. Oatp1c1-transfected HEK293 cells transported (125)I-labeled T4 in a time dependent manner which was completely abolished in the presence of excess unlabeled T4. Next, various compounds including inhibitors of thyroid hormone uptake were screened for inhibitory effects on Oatp1c1-mediated T4 uptake. Phenytoin (64%), indocyanine green (17%) and fenamic acid (68%) diclofenac (51%) and meclofenamic acid (33%) all reduced T4 uptake by Oatp1c1 when assayed at concentrations of 10microM. Dose response assays for the fenamic acids, iopanoic acid, indocyanine green and phenytoin revealed IC50s for Oatp1c1 T4 uptake below or near the blood plasma levels after therapeutic doses. Further kinetic assays and reciprocal plot analyses demonstrated that the fenamic acid diclofenac inhibited in a competitive manner. Finally, microvessels were isolated from adult rat brain and assessed for T4 uptake. 10microM fenamate concentrations inhibited T4 microvessel uptake with a similar hierarchical inhibition profile (fenamic acid (43%), diclofenac (78%) and meclofenamic acid (85%) as observed for Oatp1c1 transfected cells. Oatp1c1 is expressed luminally and abluminally in the BBB endothelial cell and exhibits bidirectional transport capabilities. Together, these data suggest that Oatp1c1 transports fenamates into, and perhaps across, brain barrier cells.
J Laryngol Otol. 2008 Oct 10; 1-5
Tunca F, Senyurek YG, Terzioglu T, Tanakol R, Tezelman S
Objective:This study aimed to compare the impact of total versus subtotal thyroidectomy on calcium metabolism and bone mineral density in euthyroid, premenopausal women.Subjects:The study included 24 premenopausal women who had undergone total (n = 10) or subtotal (n = 14) thyroidectomy and who were receiving nonsuppressive doses of thyroxine. The median post-operative period was four years. We determined, in all patients, the following parameters associated with calcium metabolism: total serum calcium, inorganic phosphate, intact parathormone, calcitonin and alkaline phosphatase. The bone mineral density of the spine and hip were measured using a Hologic QDR 4500C bone densitometer and were compared with controls matched for age and peak bone mineral density (using the t-test).Results:The measured calcium metabolism parameters were normal in all patients, and none had osteoporosis. There was no significant difference in the bone mineral density measurements for the spine and hip, comparing patients who had undergone total versus subtotal thyroidectomy (using the t-test).Conclusion:The impact of total thyroidectomy on bone mineral metabolism is not significantly different from that of subtotal thyroidectomy, in premenopausal women with normal thyroid-stimulating hormone values.
Thyroid. 2008 Oct; 18(10): 1087-94
Sørensen HG, van der Deure WM, Hansen PS, Peeters RP, Breteler MM, Kyvik KO, Sørensen TI, Hegedüs L, Visser TJ
OBJECTIVE: Genetic factors exert considerable influence on thyroid function variables. Single nucleotide polymorphisms (SNPs) in thyroid hormone pathway genes have been associated with serum thyroid parameters implying small alterations in the hypothalamus-pituitary-thyroid axis. However, little is known about SNPs in the THRA (17q11.2) and THRB (3p24.2) genes. The aim of this study was to map THRA and THRB for the occurrence and frequencies of SNPs and relate these to thyroid parameters. DESIGN AND METHODS: SNPs were identified by sequencing all THRA and THRB exons and flanking regions in 52 randomly selected subjects. SNPs were genotyped in 1116 healthy Danish twins by TaqMan assays and related to thyroid parameters. One SNP in THRB was additionally genotyped in the elderly population of the Rotterdam Scan Study (n = 940). MAIN OUTCOME: 15 SNPs (7 novel) in THRA and THRB were identified. Two SNPs in the 3' untranslated region of THRA were genotyped: a novel SNP (2390A/G) and 1895C/A (rs12939700). In THRB, a synonymous (735C/T; rs3752874) and an intronic SNP (in9-G/A; rs13063628) were genotyped. No associations between SNPs and thyroid hormone levels (total and free 3,3',5-triiodo-L-thyronine [T3] and thyroxine, reverse T3) were found. THRB-in9-G/A was significantly associated with higher serum thyroid stimulating hormone (TSH) (p(lnTSH) = 0.01) in the Danish twins, but not in subjects of the Rotterdam Scan Study, although it showed a similar trend. CONCLUSIONS: Analysis of the T3 receptor genes revealed 15 SNPs, including 7 novel. Only THRB-in9-G/A was associated with higher serum TSH in a large population of Danish twins.
Thyroid. 2008 Oct; 18(10): 1071-85
Eisenberg M, Samuels M, DiStefano JJ
BACKGROUND: We upgraded our recent feedback control system (FBCS) simulation model of human thyroid hormone (TH) regulation to include explicit representation of hypothalamic and pituitary dynamics, and updated TH distribution and elimination (D&E) parameters. This new model greatly expands the range of clinical and basic science scenarios explorable by computer simulation. METHODS: We quantified the model from pharmacokinetic (PK) and physiological human data and validated it comparatively against several independent clinical data sets. We then explored three contemporary clinical issues with the new model: combined triiodothyronine (T(3))/thyroxine (T(4)) versus T(4)-only treatment, parenteral levothyroxine (L-T(4)) administration, and central hypothyroidism. RESULTS: Combined T(3)/T(4) therapy--In thyroidectomized patients, the L-T(4)-only replacement doses needed to normalize plasma T(3) or average tissue T(3) were 145 microg L-T(4)/day or 165 microg L-T(4)/day, respectively. The combined T(4) + T(3) dosing needed to normalize both plasma and tissue T(3) levels was 105 microg L-T(4) + 9 microg T(3) per day. For all three regimens, simulated mean steady-state plasma thyroid-stimulating hormone (TSH), T(3), and T(4) was within normal ranges (TSH: 0.5-5 mU/L; T(4): 5-12 microg/dL; T(3): 0.8-1.9 ng/mL). Parenteral T(4) administration--800 microg weekly or 400 microg twice weekly normalized average tissue T(3) levels both for subcutaneous (SC) and intramuscular (IM) routes of administration. TSH, T(3), and T(4) levels were maintained within normal ranges for all four of these dosing schemes (1x vs. 2x weekly, SC vs. IM). Central hypothyroidism--We simulated steady-state plasma T(3), T(4), and TSH concentrations in response to varying degrees of central hypothyroidism, reducing TSH secretion from 50% down to 0.1% of normal. Surprisingly, TSH, T(3), and T(4) plasma concentrations remained within normal ranges for TSH secretion as low as 25% of normal. CONCLUSIONS: Combined T(3)/T(4) treatment--Simulated standard L-T(4)-only therapy was sufficient to renormalize average tissue T(3) levels and maintain normal TSH, T(3), and T(4) plasma levels, supporting adequacy of standard L-T(4)-only treatment. Parenteral T(4) administration-TSH, T(3), and T(4) levels were maintained within normal ranges for all four of these dosing schemes (1x vs. 2x weekly, SC vs. IM), supporting these therapeutic alternatives for patients with compromised L-T(4) gut absorption. Central hypothyroidism--These results highlight how highly nonlinear feedback in the hypothalamic-pituitary-thyroid axis acts to maintain normal hormone levels, even with severely reduced TSH secretion.
