Thyrotoxicosis: Stockigt JR

Stockigt JR. · No affiliation provided · Med J Aust. · Pubmed #10474600 No free full text.

This publication has no abstract.

Stockigt JR. · Epworth Hospital, Melbourne, Victoria, Australia. · Med J Aust. · Pubmed #17223768 links to  free full text

Abstract: Product information (PI) for thyroid-related medications endorsed by the Therapeutic Goods Administration, as reproduced in the commonly used compilation publications June 2006 MIMS (Monthly index of medical specialties) annual, MIMS Online and the Australian prescription products guide 2006, was evaluated to see whether it reflects contemporary therapeutic practice. Compared with current medical literature, these PI-based sources provide inadequate, inaccurate or outdated therapeutic directives. Examples include: Incorrect advice that thyroxine therapy should always begin at very low dosage. Failure to recommend increased thyroxine dosage early in pregnancy (thus placing the offspring of women being treated for hypothyroidism at risk of impaired fetal brain development). Incorrect and potentially unsafe advice to treat thyrotoxicosis with stable iodide in late pregnancy. Failure to advise serial adjustment of antithyroid drug dosage until after a patient becomes euthyroid (this can result in iatrogenic thyroid dysfunction). Outdated advice that antithyroid drugs are not compatible with breastfeeding. Recent initiatives to upgrade consumer medicine information (CMI) appear to accept PI-based sources as a reliable benchmark for CMI. That inference is not warranted for thyroid-related medications. Accountability for the updating of clinical information in PI needs to be defined, and the process for updating PI may need to be modified. Quality drug information, both PI and CMI, depends on fluent, evidence-based collaboration between suppliers, regulators, prescribers, specialist clinicians and consumers.

Stockigt JR. · Department of Endocrinology and Diabetes, Alfred Hospital, Prahran 3181, Victoria, Melbourne, Australia. · Clin Chim Acta. · Pubmed #11728414 No free full text.

Abstract: BACKGROUND: A case can be made for routine testing for thyroid dysfunction (TD) in women aged over 50 years once every 5 years when they present for medical care (case finding). This recommendation is based on: (i) the prevalence of TD, predominantly hypothyroidism, (ii) the insensitivity of standard clinical assessment in detecting even overt TD, (iii) the sensitivity of a single test, serum thyroid stimulating hormone (TSH), in identifying both over- and under-function, (iv) the probable adverse consequences of failure to recognize even mild TD, (v) the safety and effectiveness of treatment, and (vi) presumed lack of adverse effect from the testing program. METHODS: A normal serum TSH value has a high negative predictive value in ruling out primary TD; if TSH is abnormal, measurement of serum free thyroxine (T(4)) and further clinical assessment are both required to establish the degree of TD. RESULTS: Case finding identifies more "subclinical" or mild TD (abnormal TSH, normal T(4) and triiodothyronine (T(3))), than overt disease, but a major benefit of widespread testing is the earlier detection and treatment of unsuspected overt disease. There is now evidence that mild TD has adverse consequences and should not merely be regarded as a prognostic indicator, but there is still no consensus whether there is a causal relationship between mild thyroid failure and dyslipidemia. CONCLUSIONS: A case can be made for treatment of both mild thyrotoxicosis and hypothyroidism, but the therapeutic decision is generally simpler for hypothyroidism.

Stockigt JR. · Ewen Downie Metabolic Unit and, Department of Medicine, Monash University, Alfred Hospital, Melbourne, Victoria, Australia. · Endocrinol Metab Clin North Am. · Pubmed #11444163 No free full text.

Abstract: The main purpose of free T4 and free T3 assays is to distinguish reliably between thyrotoxicosis, hypothyroidism, and the euthyroid state, an objective that cannot be attained with assays of total T4 and T3 because of hereditary and acquired variations in the concentrations of binding proteins. Effective correction for changes in the serum concentration of TBG can be achieved with numerous types of free hormone estimate, but other changes in binding are not well accommodated. Despite remarkable methodologic ingenuity, no current method reflects the free T4 concentration in undiluted serum under in vivo conditions. Equilibrium dialysis, widely considered the reference method for free T4 measurement, is also subject to error, either preanalytic, owing to generation of NEFA in the sample leading to an overestimate of free T4, or analytic with underestimation of the effect of competitors to increase free T4. Current approaches to free T4 measurement are vulnerable to several method-dependent artifacts: abnormal albumin binding of T4 or of the assay tracer, the inhibition of T4 binding to TBG by medications, and the effects of critical illness, especially in heparin-treated patients, pregnancy, and the abnormalities in sick premature infants. Because of systematic variation between methods (i.e., whether a technique is albumin dependent or prone to incubation or dilution artifacts), it is essential to consider methodologic details in evaluating free T4 estimates in these situations and whenever estimates of free T4 are clinically discordant. False-positive abnormalities are more frequent than false-negative results. When free T4 results are correlated with the serum TSH concentration with attention to the assumptions that define this relationship, the majority of false-positive results can be readily identified. If a free T4 anomaly remains unexplained on repeat sampling, it is appropriate to use an alternative free T4 method that depends on a different assay principle and to correlate the result with an authentic total T4 measurement.

Wong R, Cheung W, Stockigt JR, Topliss DJ. · Department of Endocrinology and Diabetes, Alfred Hospital, Melbourne, Victoria, Australia. · Intern Med J. · Pubmed #14511194 No free full text.

Abstract: BACKGROUND: Amiodarone-induced thyrotoxicosis (AIT) presents a therapeutic challenge because of its resistance to standard antithyroid therapy. In iodine-deplete environments, colour-flow Doppler sonography (CFDS) has allowed distinction between two types of AIT: (i) Type I AIT, associated with increased vascularity (CFDS I-III) and response to thionamide antithyroid drug and (ii) type II AIT, with no/little thyroid vascularity (CFDS 0) and prednisolone responsiveness. AIM: To clarify if CFDS patterns correlated with treatment outcomes in a retrospective study of 24 patients with AIT in an iodine-replete environment. METHODS: Medical records of patients who presented to a teaching hospital between January 1998 to December 2000 were reviewed. Results of CFDS, ultrasound measurement of thyroid size and technetium scanning of the thyroid were correlated with treatment responses, especially prednisolone responsiveness. RESULTS: Thirteen of 24 patients showed CFDS 0. Twelve of these 13 were evaluable for prednisolone responsiveness, of whom seven (58%) were prednisolone-responsive. Of 11 patients with CFDS I-III, four (36%) responded to antithyroid medication alone and only one of seven (14%) was prednisolone-responsive. Euthyroidism was achieved twice as rapidly in patients with CFDS 0 than those with CFDS I-III. Because of medical treatment failure, seven patients, from both CFDS groups, required urgent near-total thyroidectomy which was successful and uncomplicated in all cases. CONCLUSIONS: CFDS is useful in the management of AIT because CFDS 0 correlates better with prednisolone response (58%) than CFDS I-III (14%). However, unlike experience in iodine-deficient regions, the results of the present study revealed that treatment responses to thionamide or prednisolone were heterogeneous within uniform CFDS patterns. Thus, prednisolone--responsiveness was not consistently predicted by CFDS 0, but the presence of flow appeared to correlate with non-response to prednisolone.

Stockigt JR, Ballok Z, Kalff V. · No affiliation provided · Med J Aust. · Pubmed #16296986 links to  free full text

This publication has no abstract.