GOITRE TOXIQUE PDF

These images are a random sampling from a Bing search on the term "Multinodular Goiter. Search Bing for all related images. Started in , this collection now contains interlinked topic pages divided into a tree of 31 specialty books and chapters. Content is updated monthly with systematic literature reviews and conferences. Although access to this website is not restricted, the information found here is intended for use by medical providers.

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This review provides an update on recombinant human TSH rh-TSH augmented radioiodine I therapy and outlines its potential role in the treatment of symptomatic benign multinodular non-toxic goitre. In some countries, I has been used for three decades to reduce the size of nodular goitres. The feasibility of I therapy depends on an adequate thyroid I uptake. Although patient satisfaction is not improved at one-year, this approach facilitates tracheal decompression and is particularly promising in large goitres.

The majority of multinodular non-toxic goitre patients may not require amplified goitre reduction. The dose-reduction equality strategy is attractive in terms of minimizing post-therapeutic restrictions and in reducing the potential risk of radiation-induced malignancy. Adverse effects like temporary thyroid swelling and thyroid hormone excess are to a large extent dose-dependent and generally 0.

Based on these results we conclude that rh-TSH augmented I therapy is a promising new therapeutic principle allowing the tailoring of an optimal I therapy on the individual level. Radioactive iodine I has been used in the treatment of hyperthyroidism for more than 60 years. In large goitres i. Iodine prophylaxis intensification. In , Huysmans et al. Based on this observation, and the above-mentioned challenges, stimulation with rh-TSH before I therapy has been evaluated off-label during the last decade.

The aim has been to improve the efficacy of I therapy for MNG. Here, we provide an update on rh-TSH augmented I therapy with focus on potential strategies, eligibility criteria and directions for future research. Previously the only strategy, although not demonstrated in MNG patients, to optimize RAIU was to restrict dietary iodine intake, which is cumbersome. Data with rh-TSH doses below 0. Radioiodine plus recombinant human thyrotropin do not cause acute airway compression and are effective in reducing multinodular goiter.

Braz J Med Biol Res Click here to see the Library ], but the effect seems to decline. Theoretically, a second dose of rh-TSH could result in an even better retention of I within the thyroid gland. To clarify whether repetitive rh-TSH injections are beneficial in terms of improving the overall I kinetics during I therapy, well-controlled comparative studies, also focusing on alterations in the I half-life, are needed.

Absolute changes in mean hour radioiodine uptake RAIU in multinodular non-toxic goitre patients pretreated with rh-TSH or placebo at 24, 48 or 72 hours before a I tracer activity.

As a consequence of these limitations, we recommend that physicians who consider rh-TSH-augmented I therapy should evaluate the effect of rh-TSH in a patient sample representative of the potential treatment population. This approach is essential if a fixed dose regimen is considered and importantly it allows the physician to estimate whether a low iodine diet should also be instituted. Serum thyroxine and age - rather than thyroid volume and serum.

J Endocrinol Invest Click here to see the Library ]. Interestingly, rh-TSH appears to reverse this effect, since the increase in RAIU in relatively cold areas has been observed to be significantly higher in patients with a low s-TSH level i. Taken together, these findings indicate that patients with subclinical hyperthyroidism could be obvious candidates for rh-TSH stimulation before I therapy. Based on the marked increase in thyroid RAIU, the potential benefits of rh-TSH, when combined with I therapy, are those of increased absorbed thyroid dose without increasing the administered I activity superiority strategy or reduction of the administered activity with a maintained thyroid dose dose-reduction or equality strategy.

Improvement of goiter volume reduction after 0. Stimulation with 0. Facing these challenges rh-TSH was introduced as a method to increase the absorbed thyroid dose without increasing the administered I activity. Safety and efficacy of administering 0. Results from a multicenter international, randomized, placebo-controlled study. J Clin Endocrinol Metab in press. Interestingly, the gain is most pronounced in large goitres Fig. Comparison of the relative goitre volume one year after conventional placebo and rh-TSH augmented I therapy for multinodular non-toxic goitre, smaller and larger than mL.

Bars represent the relative mean goitre volume before therapy and one year after therapy. Adapted with permission from Nielsen et al. Lacking a subjective benefit of rh-TSH-augmented I therapy, objective measures to demonstrate the superiority of rh-TSH-augmented I therapy over conventional I therapy are important. Monitoring alterations in pulmonary function and smallest cross-sectional area of the trachea SCAT are obvious methods to demonstrate a positive effect of I therapy.

The failure to demonstrate a subjective benefit of the superiority strategy within the first year raises the question whether increased GVR is worth pursuing in the majority of patients, with moderate sized oligo-symptomatic goitre.

Furthermore, the radiation protection principle As Low As Reasonably Achievable ALARA implies that the goal of I therapy should be pursued with the lowest possible radiation burden to the patient as well as to the environment. As long as the long-term risk of thyroidal and particularly extrathyroidal malignancy is not clarified, it is obvious that strategies reducing the radiation burden are worth exploring.

In an uncontrolled study, Nieuwlaat et al. Pre-treatment with 0. Importantly, that study also included a dosimetric evaluation, which demonstrated that when the target was a thyroid dose of Gy, prestimulation with rh-TSH resulted in a 2—3 fold lower absorbed dose i. The combination of 0.

Cervical compression symptoms, as determined by a VAS-score, were effectively and equally reduced in the placebo and the rh-TSH group. Consequently, the need for hospitalization and post-therapeutic restrictions were dramatically reduced. Our motivation to evaluate a lower absorbed thyroid dose than what is usually the aim i. Perhaps the preconditioning effect of rh-TSH results in a parallel shift of the dose-response curve.

Goitre volume reduction at three and 12 months follow-up in patients treated with 0. The use of rh-TSH in subjects with an intact thyroid gland is off-label and carries significant risks related to thyroid hyperfunction and acute thyroid swelling. During the last decade, focus has been on establishing whether these side effects are dose-dependent. Depending on the dose of rh-TSH thyroid hormones peak at 24—48 hours after rh-TSH injection, followed by normalization within three weeks.

With rh-TSH doses at or below 0. However, when used in combination with I therapy the rise in thyroid hormones caused by rh-TSH per se may not be the only factor determining the increase in thyroid hormones.

This results in increased thyroid tissue destruction, which in theory could also increase the release of thyroid hormones into the circulation. Consequently, increased efficacy, in terms of GVR, may be inevitably related to a higher risk of thyroid hormone excess, even if using low doses of rh-TSH.

Reassuringly, studies using rh-TSH doses at or below 0. When applying the dose-reduction strategy, 0. This observation is in line with the finding by Romao et al. Parallel to the finding that subclinical hyperthyroidism is associated with a higher increase in RAIU upon rh-TSH stimulation, this likely reflects the reactivation of down-regulated TSH-responsive thyrocytes in large areas of the nodular thyroid gland. Effects of 0. Transient goiter enlargement after administration of 0. The only comparative study, in healthy individuals, indicate that acute thyroid swelling, at least to some extent, is dose-dependent and is less pronounced and less likely to occur with rh-TSH doses at or below 0.

However, only studies evaluating the combined effect of rh-TSH and I on thyroid volume may reassure us that these factors do not act in a synergistic way. On average thyroid volume was not altered to any greater extent 96 hours after I therapy preceded by 0. Click here to see the Library ], demonstrating that thyroid volume and tracheal cross-sectional area were unaltered on days 2 and 7 after I therapy combined with placebo, 0.

Taken together, the current evidence suggests that clinically relevant acute thyroid swelling is uncommon following rh-TSH-augmented I therapy, at least when using doses below 0. However, variation in the individual sensitivity to rh-TSH suggests that a clinically significant thyroid enlargement occasionally may occur.

Importantly, with regard to keeping the above mentioned side effects to a minimum, it is promising that a considerable increase in thyroid RAIU can be achieved with rh-TSH doses in the range of 0.

It is unclear whether this is solely caused by the increased absorbed thyroid dose or if the use of, and perhaps the dose of, rh-TSH is an independent determinant of hypothyroidism. In the only controlled equality study, 0. Thus, it seems that the risk of hypothyroidism is closely related to the GVR obtained. Based on the existing literature, we may draw some conclusions regarding the benefit and future use of rh-TSH in the context of I therapy for MNG. Before rh-TSH-augmented I therapy is widely implemented, this issue deserves further attention.

In principle, increased GVR could translate into sustained relief of goitre related symptoms and perhaps reduce the need for additional therapy. Although radiation regulations may differ between countries, an important clinical implication of the equality strategy is that the substantial reduction of the necessary I activity dramatically reduces the need for hospitalization.

In most countries, as an additional benefit, patient restrictions are less rigorous with lower I activities. Although cost-effectiveness analyses have not been performed, these results imply that the dose-reduction strategy may also prove cost-effective.

Some patients are reluctant to receive I therapy because of fear of developing radiation-induced cancer, a concern also shared by some physicians. When rh-TSH is used to enhance GVR superiority strategy the absorbed thyroid dose is increased and it is unclear whether this results in a higher or perhaps a lower risk of subsequent thyroid malignancy, as well as whether rh-TSH influences this risk per se. The optimal strategy in a given MNG patient depends on goitre size, the degree of symptoms, the wish to maintain normal thyroid function, the age of the patient, the risks associated with radiation exposure and the therapeutic alternatives.

Subjects with a large compressive goitre, in whom the only therapeutic alternative is near total thyroidectomy, are obvious candidates for the superiority strategy. In these patients destroying enough goitre tissue to cause, hypothyroidism may be seen as analogous to near total thyroidectomy, which also leaves the patient with life-long LT4 replacement therapy.

On the other hand, patients with small to moderate sized oligo-symptomatic goitres may not require extensive GVR. Long-term follow-up studies should establish the outcome of the superiority strategy, focusing on whether the difference in GVR is maintained and whether this reduces the need for additional therapy.

This approach should increase the chance of demonstrating a positive patient outcome. Comparative studies evaluating the dependency of GVR on the retained I dose, both with and without rh-TSH stimulation are still lacking, but it may be questioned whether such a study is ethical. It follows that the optimal dose of rh-TSH is still not established and to answer this question we need RCTs comparing the effect of different doses of rh-TSH between 0. Click here to see the Library ] in combination with an adjusted thyroid dose.

This could translate into a more favourable balance between destruction of goitre nodules and normal thyroid tissue. Critics of conventional I therapy have argued that most of the GVR observed is caused by the destruction of normal paranodular thyroid tissue.

Finally, large studies should confirm the safety of using rh-TSH in this context and focus on preventing and treating acute thyroid swelling. This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.

ASTM D1748 PDF

Nodular goiter: Effects of surgery and thyroxine medication

This review provides an update on recombinant human TSH rh-TSH augmented radioiodine I therapy and outlines its potential role in the treatment of symptomatic benign multinodular non-toxic goitre. In some countries, I has been used for three decades to reduce the size of nodular goitres. The feasibility of I therapy depends on an adequate thyroid I uptake. Although patient satisfaction is not improved at one-year, this approach facilitates tracheal decompression and is particularly promising in large goitres. The majority of multinodular non-toxic goitre patients may not require amplified goitre reduction.

GRUNDFOS UPS 32-80 PDF

We'd like to understand how you use our websites in order to improve them. Register your interest. In a prospective investigation, thyroid function was studied in 43 patients before and after surgery on a nontoxic nodular goiter. Prior to surgery, 11 patients displayed a flat thyroid-stimulating hormone TSH response to thyrotropin-releasing hormone TRH , suggesting subclinical hyperthyroidism. Three months following surgery, 32 patients were chemically euthyroid and 11 patients had elevated TSH values. Seven of the latter had additional signs of hypothyroidism and were given continuous thyroxine substitution.

ICAO DOC 9694 PDF

Basedow struma. Calls on the Commission to promote the sustainable management of the world's forests by ensuring ecological processes and forest biodiversity and productivity and by respecting the rights of indigenous people to sustain forest resources; calls, in addition, on the Commission to prohibit the destruction of natural forests, to safeguard endangered species and to ban toxic pesticides and the planting of genetically modified trees;. Believes that the technical measures should ensure that destructive and non-selective fishing gear is not used, and that the general use of explosive and poisonous substances should be prohibited;. Most air quality problems in affected urban areas appear to be related to toxic NOx and direct NO2 emissions. We assume no liability for the accuracy, completeness or timeliness of this information.

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