Predictors of euthyreosis in hyperthyroid patients treated with radioiodine 131I-: a retrospective study.

BACKGROUND: Radioiodine (RAI) treatment for hyperthyroidism is a very common modality, chosen by physicians worldwide. The outcome of the therapy, however, is not always predictable. While rendering a patient hypo- or euthyroid is meant as a therapeutic success, the latter does not require lifelong hormonal supplementation. The aim of our study is to determine predictors of euthyreosis in patients who underwent RAI treatment. METHODS: Medical records of 144 patients who had undergone RAI therapy were examined. Laboratory and clinical data were analyzed statistically. Ultrasonography findings, such as thyroid volume, nodules' size and characteristics had been collected at the beginning of treatment and 6 months after the administration of radioiodine 131I-. Moreover, scintigraphy results were taken into account. Multivariate logistic regression analysis model has been used to find predictors of euthyroidism after 12 months of follow-up. The predictors of normal thyroid function have also been analyzed separately for patients with GD (Graves' disease) and TMNG (toxic multinodular goiter). RESULTS: The analysis showed that age (OR 1,06; 95%CI 1.025-1.096, p = 0,001), thyroid gland volume (OR 1,04; 95%CI 1,02-1,06; p < 0.001) and iodine uptake level (OR 0,952; 95%CI 0,91-0,98; p = 0,004) were significant factors of achieving normal thyroid function after RAI therapy. According to multivariate logistic regression analysis, in GD patients only age has been shown to be a significant factor (OR 1,06; 95%CI 1,001-1,13; p = 0.047), while in TMNG patients' age (OR 1,04; 95%CI 1-1,09; p = 0.048), thyroid gland volume (OR 1.038; 95%CI 1.009-1.068; p = 0.009) and iodine uptake level (OR 0.95; 95%CI 0.9-0.99; p = 0.02) all have been proven to be significant predictors of achieving euthyroidism. CONCLUSIONS: The more advanced age, larger volume of thyroid gland and lower iodine uptake level are predictors of euthyreosis after RAI treatment.

Hyperactive thyroid nodules treated by radiofrequency ablation: a Dutch single-centre experience.

BACKGROUND: Hyperactive thyroid nodules (HTN) are usually treated with radioactive iodine (RAI). However, as RAI is associated with a 30-60% long-term risk of permanent hypothyroidism, radiofrequency ablation (RFA) may be a good alternative. Primary aim of this study was to assess the percentage of patients achieving euthyroidism after RFA. PATIENTS AND METHODS: Patients with a symptomatic HTN were treated by ultrasound-guided RFA, using the trans-isthmic approach and moving-shot technique, in an outpatient setting under local anaesthesia. RESULTS: Twenty-one patients were included, ranging in age from 37-75 years. Follow-up was at least one year. All patients had a suppressed serum thyroid-stimulating hormone (TSH), with free thyroxine (FT4) and free triiodothyronine (FT3) concentrations mildly elevated in 33% and 43% of cases, respectively. RFA was not associated with clinically meaningful adverse effects. TSH normalisation was achieved in 11/21 patients (52%) after first RFA. A partial response, defined as a normalisation of FT4 and FT3, but incomplete improvement of TSH, was observed in 6/21 patients (29%). Three patients had no response (14%), and one patient developed mild, asymptomatic subclinical hypothyroidism. Five patients underwent a second RFA and this led to TSH normalisation in four, thereby raising the rate of complete remission to 71%. Recurrence of TSH suppression did not occur during the study period. CONCLUSION: These data suggest that RFA is a safe and promising treatment for symptomatic hyperactive thyroid nodules, with a low risk of permanent hypothyroidism. Long-term studies are needed to identify the recurrence risk of hyperthyroidism.

Transient Hyperthyroidism following the ingestion of complementary medications containing kelp seaweed: A case-report.

RATIONALE: The prevalence of obesity has increased over the past few years, becoming a public health problem. Generally, the primary therapeutic remedies are diet, physical exercise, medication, and bariatric surgery. However, an increased number of obese and overweight people are using complementary and herbal slimming supplements. PATIENT CONCERNS: A 70-years-old Caucasian woman presented to the outpatient clinic with tachycardia (>100 bpm), insomnia, anxiety, and recent weight loss (6 kilos in 3 months). She had no previous thyroid disease, but she presented transient hyperthyroidism at 3 months after ingestion of tablets containing kelp seaweeds. DIAGNOSES: Hypertensive and obese patient, without previous thyroid disease, presented with transient hyperthyroidism at 3 months following ingestion of tablets containing kelp seaweed. INTERVENTIONS: The kelp-containing tablets were discontinued, and antithyroid therapy with Methimazole was initiated as follows: Methimazole at 15 mg/day for 1 month, at 10 mg/day in the second month, and 5 mg/day for the third month. OUTCOMES: After 3 months of antithyroid therapy and without the consumption of kelp - containing tablets, normal thyroid function was regained. Further analysis revealed normal thyroid function, so the hyperthyroidism reversed completely. LESSONS: Adults who consume complementary medication based on kelp seaweed should be informed of the risk of developing thyroid dysfunction also in the absence of any pre-existing thyroid disease. Due to the high iodine content, supplements containing kelp should be taken with the supervision of a physician and with monitoring of thyroid function.

Excess iodine intake: sources, assessment, and effects on thyroid function.

Iodine is essential for thyroid hormone synthesis. High iodine intakes are well tolerated by most healthy individuals, but in some people, excess iodine intakes may precipitate hyperthyroidism, hypothyroidism, goiter, and/or thyroid autoimmunity. Individuals with preexisting thyroid disease or those previously exposed to iodine deficiency may be more susceptible to thyroid disorders due to an increase in iodine intake, in some cases at intakes only slightly above physiological needs. Thyroid dysfunction due to excess iodine intake is usually mild and transient, but iodine-induced hyperthyroidism can be life-threatening in some individuals. At the population level, excess iodine intakes may arise from consumption of overiodized salt, drinking water, animal milk rich in iodine, certain seaweeds, iodine-containing dietary supplements, and from a combination of these sources. The median urinary iodine concentration (UIC) of a population reflects the total iodine intake from all sources and can accurately identify populations with excessive iodine intakes. Our review describes the association between excess iodine intake and thyroid function. We outline potential sources of excess iodine intake and the physiological responses and consequences of excess iodine intakes. We provide guidance on choice of biomarkers to assess iodine intake, with an emphasis on the UIC and thyroglobulin.

An unsuspected complication with immune checkpoint blockade: a case report.

BACKGROUND: Immunotherapy treatment with immune-checkpoint blockade has become a new paradigm in cancer treatment. Despite its efficacy, it has also given rise to a new class of adverse events, immune-related adverse events, which may affect any organ, including the thyroid and the pituitary. CASE PRESENTATION: We present a case of a 77-year-old Caucasian man with metastatic renal cell carcinoma on immunotherapy treatment who was admitted to our hospital with a severe persistent headache of sudden onset. He had been on corticosteroid therapy for 10 days for suspected immune-related thyroiditis. The patient had tachycardia and mild diarrhea, and his thyroid function tests were compatible with subclinical hyperthyroidism with a suppressed thyroid-stimulating hormone level of 0.01 µIU/ml (0.4-4.5), a raised free T4 level of 2.17 ng/dl (0.7-1.9), and a free T3 level of 4.66 pg/ml (2.27-5). Computed tomography and magnetic resonance imaging revealed an enlargement of the pituitary gland compatible with macroadenoma. In the face of a probable immune-related hypophysitis, high-dose corticosteroid treatment was started. A posterior hormonal evaluation revealed secondary hypothyroidism with a suppressed thyroid-stimulating hormone level of 0.11 µIU/ml (0.4-4.5) and low thyroid hormones, a normal free T4 level of 1.02 ng/dl (0.7-1.9), and a low free T3 level of 1.53 pg/ml (2.27-5). These new findings suggested central hypothyroidism possibly due to pituitary apoplexy as a complication of the macroadenoma. Therefore, levothyroxine substitution was started along with the previously started corticosteroid therapy. The patient's headache and asthenia gradually resolved, and after a few days, he was released from the hospital with levothyroxine substitution and corticosteroid tapering. CONCLUSIONS: This case emphasizes the importance of the differential diagnosis when dealing with patients on immune checkpoint inhibitors because other non-immune-related events may present. Our patient was finally diagnosed with immune-related hyperthyroidism and a concurrent pituitary macroadenoma. This case also highlights the importance of a prompt start of corticosteroid therapy once immune-related adverse events such as hypophysitis are suspected, because otherwise the outcome would be fatal.

Effect of excess iodine intake on thyroid on human health.

The recommended daily intake of iodide, is 150 µg for adolescents and adults, 250 µg for pregnancy and lactation. Thyroid gland is an effective collector of iodine. The active iodine uptake along the basolateral membrane of thyroid cell is followed by its transport to the apical edge of the cell and then to the follicle lumen. TSH acts through cAMP and stimulates NIS gene expression and protein synthesis. The major proportion of iodine in the thyroid gland is bound to Thyroglobulin. The non-organic intrathyroidal iodine is usually low, but significantly greater compared to plasma. Large doses of iodine reduce both the uptake and the organification (Wolff-Chaikoff effect) and cause partial inhibition of Tg proteolysis. The thyroid gland has several protective mechanisms resulting on the maintenance of normal thyroid function despite wide fluctuations of the daily iodine intake. Ingestion of several commonly used drugs and food conservatives results in acute or chronic excessive iodine intake. Failure to escape from the iodine induced organification inhibition can cause hypothyroidism, which is temporary and subsides after iodine exposure ceases. Iodine excess may also establish a status of excessive thyroid hormone synthesis and release, thus inducing autonomic thyroid function in iodopenic areas or can contribute to the development of iodine-induced hyperthyroidism in iodine abundant areas. The anti-arrhythmic Amiodarone, is a benzofuranic product with a very high iodine content, is associated with either hypo- or hyperthyroidism development. In the presence of defective auto-protective mechanisms, excessive iodine ingestion can divert the normal thyroid function.

Effect of Selenium Supplementation on Recurrent Hyperthyroidism Caused by Graves' Disease: A Prospective Pilot Study.

The effect of selenium supplementation on recurrent hyperthyroidism caused by Graves' disease is unclear. Our study aimed to assess the efficacy of selenium supplementation therapy on recurrent Graves' disease. Forty-one patients with recurrent Graves' disease were enrolled in this study. All patients received the routine treatment using methimazole (MMI), while patients allocated to the selenium group received additional selenium therapy for 6 months. The influence of selenium supplementation on the concentrations of thyroid stimulating hormone (TSH), anti-TSH-receptor antibodies (TRAb), free thyroxine (FT4), and free triiodothyronine (FT3) were assessed. The remission rate was also compared between 2 groups. There was no obvious difference in the demographic data and the levels of serum FT4, FT3, TSH, and TRAb between the 2 groups at baseline. Both FT4 and FT3 decreased more at 2 months in the selenium group than the controls, while the TSH level increased more in patients receiving selenium supplementation (p<0.05). The TRAb level was significantly lower in patients receiving selenium supplementation (2.4 IU/l vs. 5.6 IU/l, p=0.04). The percentages of patients with normal TRAb level at 6 months was also significantly higher in the selenium group (19.0 vs. 0%, p=0.016). Kaplan-Meier survival curve showed patients receiving selenium supplementation had a significantly higher rate of remission than controls (Log-rank test p=0.008). In conclusion, selenium supplementation can enhance the effect of antithyroid drugs in patients with recurrent Graves' disease. Randomized trials with large number of participants are needed to validate the finding above.

Role of Cholestyramine in Refractory Hyperthyroidism: A Case Report and Literature Review.

BACKGROUND: Hyperthyroidism is a common disease that usually responds to the conventional therapy of anti-thyroidal medications (methimazole or PTU) and beta-blocker. Refractory hyperthyroidism is a rare condition in which hyperthyroidism fails to respond to the above therapy. Cholestyramine has been shown to decrease thyroid hormone level when added to the ongoing anti-thyroidal medications. CASE REPORT: A 52-year-old woman with past medical history of enlarging goiter presented with obstructive symptoms of worsening shortness of breath and snoring. Admission thyroid function test showed mild hyperthyroidism (suppressed TSH, slightly high FT4, and high normal FT3) that worsened after she received a CT scan with contrast and failed to respond to a 3-week course of high-dose dexamethasone, high-dose carbimazole, and up-titrated propranolol. Five days after cholestyramine was added, her FT4 decreased by 30% and normalized after 12 days. The patient underwent total thyroidectomy as definitive treatment for the hyperthyroidism and for the obstructive symptoms. CONCLUSIONS: Cholestyramine is an effective additional treatment for hyperthyroidism and may be an effective treatment for refractory iodine-induced hyperthyroidism. The possibility of self-remission (natural course) is less likely given the dramatic and rapid response to cholestyramine.

A review of the iodine status of UK pregnant women and its implications for the offspring.

Iodine, as a component of the thyroid hormones, is crucial for brain development and is therefore especially important during pregnancy when the brain is developing most rapidly. While randomised controlled trials of pregnant women in regions of severe iodine deficiency have shown that prenatal iodine deficiency causes impaired cognition, less is known of the effects in regions of mild deficiency. This is relevant to the UK as the World Health Organisation now classifies the UK as mildly iodine deficient, based on a national study of 14-15 year old schoolgirls in 2011. We have previously published a study using samples and data from the UK-based Avon Longitudinal Study of Parents and Children (ALSPAC) that found an association between low iodine status in early pregnancy (urinary iodine-to-creatinine ratio <150 µg/g) and lower verbal IQ and reading scores in the offspring. Though the women in ALSPAC were recruited in the early 1990s, the results of the study are still relevant as their iodine status was similar to that reported in recent studies of UK pregnant women. This review discusses the evidence that mild-to-moderate iodine deficiency during pregnancy has deleterious effects on child neurodevelopment and relates that evidence to the data on iodine status in the UK. It has highlighted a need for nationwide data on iodine status of pregnant women and that a randomised controlled trial of iodine supplementation in pregnant women in a region of mild-to-moderate iodine deficiency with child outcomes as the primary endpoint is required.

The importance of iodine in public health.

Iodine (I) deficiency has been known for more than a century and is known to cause cretinism at the extreme end of the spectrum but also, importantly, impaired development and neurocognition in areas of mild deficiency. The WHO has indicated that median urinary iodine of 100-199 µg/l in a population is regarded as indicative of an adequate iodine intake. The understanding of the spectrum of iodine deficiency disorders led to the formation of The International Council for the Control of Iodine Deficiency Disorders which has promulgated the use of household iodized salt and the use of such salt in food processing and manufacture. Iodine deficiency is particularly important in pregnancy as the fetus relies on maternal thyroxine (T4) exclusively during the first 14 weeks and also throughout gestation. As this hormone is critical to brain and nervous system maturation, low maternal T4 results in low child intelligence quotient. The recommendation for I intake in pregnancy is 250 µg/day to prevent fetal and child brain function impairment. During the past 25 years, the number of countries with I deficiency has reduced to 32; these still include many European developed countries. Sustainability of adequate iodine status must be achieved by continuous monitoring and where this has not been performed I deficiency has often recurred. More randomized controlled trials of iodine supplementation in pregnancy are required in mild iodine-deficient areas to inform public health strategy and subsequent government action on suitable provision of iodine to the population at risk.

Transient hypercortisolism and symptomatic hyperthyroidism associated to primary hyperparathyroidism in an elderly patient: case report and literature review.

BACKGROUND: Primary hyperparathyroidism (PHPT) is often found on routine blood tests, at a relatively asymptomatic stage. However many studies suggest different systemic effects related to PHPT, which could be enhanced by an abnormal cortisol release due to chronic stress of hyperparathyroidism. Being PHPT frequently found in the 6(th) to 7(th) decade of life, a careful and multifaceted approach should be taken. CASE PRESENTATION: We report the case of an elderly patient with symptomatic PHPT and incidental pulmonary embolism. He was treated with hydration, zoledronic acid, cinacalcet and high-dose unfractionated heparin. Parathyroid surgery was successfully performed, but patient's conditions suddenly worsened because of a transient thyrotoxicosis, probably induced by a previous exposure to iodine load and/or thyroid surgical manipulation. A short-term treatment with beta-blockers was introduced for symptomatic relief. The patient also presented a transient hypercortisolism with elevated ACTH, likely due to stress related not only to aging and hospitalization but also to PHPT, resolved only four months after parathyroid surgery. CONCLUSION: Chronic hyperparathyroidism has been linked with increased all-cause mortality. A functional chronic hypercortisolism could be established, enhancing PHPT related disorders. Only parathyroid surgery has been demonstrated to cure PHPT and complications related, showing similar outcome between older and younger patients. However, the management of post-operative period should be more careful in fragile patients. In particular, the early diagnosis and treatment of a transient post-operative thyrotoxicosis could improve recovery. Due to the increase in prevalence and the evidence of many related complications even in asymptomatic PHPT, expert opinion-based guidelines for surgical treatment of PHPT should be developed especially for elderly patients.

Iodine deficiency and thyroid disorders.

Iodine deficiency early in life impairs cognition and growth, but iodine status is also a key determinant of thyroid disorders in adults. Severe iodine deficiency causes goitre and hypothyroidism because, despite an increase in thyroid activity to maximise iodine uptake and recycling in this setting, iodine concentrations are still too low to enable production of thyroid hormone. In mild-to-moderate iodine deficiency, increased thyroid activity can compensate for low iodine intake and maintain euthyroidism in most individuals, but at a price: chronic thyroid stimulation results in an increase in the prevalence of toxic nodular goitre and hyperthyroidism in populations. This high prevalence of nodular autonomy usually results in a further increase in the prevalence of hyperthyroidism if iodine intake is subsequently increased by salt iodisation. However, this increase is transient because iodine sufficiency normalises thyroid activity which, in the long term, reduces nodular autonomy. Increased iodine intake in an iodine-deficient population is associated with a small increase in the prevalence of subclinical hypothyroidism and thyroid autoimmunity; whether these increases are also transient is unclear. Variations in population iodine intake do not affect risk for Graves' disease or thyroid cancer, but correction of iodine deficiency might shift thyroid cancer subtypes toward less malignant forms. Thus, optimisation of population iodine intake is an important component of preventive health care to reduce the prevalence of thyroid disorders.

Radiofrequency ablation of benign symptomatic thyroid nodules: prospective safety and efficacy study.

BACKGROUND: Radiofrequency ablation (RFA) is a relatively novel procedure in the management of benign nodular goiter. This study was conducted to evaluate the safety and efficacy of ultrasound (US)-guided percutaneous RFA for benign symptomatic thyroid nodules as an alternative to surgery. METHODS: The study involved patients for whom a fine needle aspiration biopsy had proved a diagnosis of benign nodular goiter and had nodule-related symptoms such as dysphagia, cosmetic problems, sensation of foreign body in the neck, hyperthyroidism due to autonomous nodules or fear of malignancy. Percutaneous RFA was performed as an outpatient procedure under local anesthesia. The primary outcome was an evaluation of the changes in symptom scores (0-10) for pain, dysphagia and foreign body sensation at the 1st, 3rd, and 6th months after the RFA procedure. Secondary outcomes were assessing volume changes in nodules, complication rates, and changes in thyroid function status. RESULTS: A total of 33 patients (24% female, 76% male) and a total of 65 nodules were included into the study. More than one nodule was treated in 63.6% of the patients. We found a statistically significant improvement from baseline to values at the 1st, 3rd, and 6th months, respectively, as follows: pain scores (2.9 ± 2.7, 2.3 ± 2.01, 1.8 ± 1.7, and 1.5 ± 1.2, p 0.005), dysphagia scores (3.9 ± 2.7, 2.6 ± 1.9; 1.7 ± 1.6, and 1.1 ± 0.3, p 0.032), and foreign body sensation scores 3.6 ± 3, 2.5 ± 2.2; 1.6 ± 1.5, and 1.1 ± 0.4, p 0.002).The mean pre-treatment nodule volume was 7.3 ± 8.3 mL. There was a statistically significant size reduction in the nodules at the 1st, 3rd, and 6th months after RFA (3.5 ± 3.8, 2.7 ± 3.4, and 1.2 ± 1.7 mL, p 0.002). The volume reduction was found to be 74% at 6th months following the RFA (p 0.005). 8 patients had autonomously functioning nodules in the pre-treatment period, 50% (n: 4) became euthyroid at the 6th month after RFA. There were no complaints other than pain (12%). CONCLUSION: RFA can be an alternative treatment modality in the management of benign symptomatic thyroid nodules. The results showed that it is a safe and effective procedure.

A critical review of food-associated factors proposed in the etiology of feline hyperthyroidism.

Since the first description of feline hyperthyroidism (HT) in 1979, several studies have been undertaken to define the etiology of the disease. Epidemiologic studies, after investigating non-food- and food-associated factors, suggest a multifactorial etiology. However, in the absence of prospective cohort studies that can confirm a cause-and-effect relationship between HT and associated risk factors, no causative factor for HT has been identified to date. Feline HT resembles toxic nodular goiter in humans, with autonomously functioning upregulated iodide uptake systems. Contribution of the diet to HT development remains controversial. The purpose of this paper is to review critically the reported food-associated risk factors for HT.

Thyroid dysfunction during severe ovarian hyperstimulation syndrome. A case report.

Thyroid disorders, both in women who wish to conceive and in gravidas, has become a topic of much interest to numerous researchers. Ovarian hyperstimulation syndrome (OHSS) is a potentially life-threatening condition among women undergoing controlled ovarian hyperstimulation (COH). We present a case of thyroid dysfunction in severe OHSS in a patient diagnosed with subclinical hypothyroidism before COH. The dose of L-thyroxine (L-T4) was increased before the procedure in order to reach TSH levels below 2.5 mU/L, and from day 1 of the stimulation the dose of L-T4 was increased by 33%. The patient remained clinically and biochemically euthyroid until day 8 after the embriotransfer (ET). Then, the woman developed severe OHSS, with fluid in the pleural and peritoneal cavity and laboratory evidence of severe OHSS. Laboratory thyroid function tests revealed overt hypothyroidism. L-T4 dose was not increased due to serious clinical condition of the patient. Iodine supplementation was initiated instead. After the symptoms subsided, a period of clinical and laboratory euthyroid state was observed, followed by gestational hyperthyroidism. The L-T4 dose was reduced and iodine supplementation was temporarily ceased. The thyroid function stabilized, while maintaining the L-T4 and iodine supplementation, at 20 weeks of gestation. The patient gave birth by a caesarean section at 37 weeks of gestation and returned to the pre-pregnancy dose of L-T4. To the best of our knowledge, this has been the first report about a patient with thyroid dysfunction in severe OHSS in the Polish literature. On the basis of the presented case and a review of the literature on thyroid dysfunction in women undergoing COH and OHSS, we conclude that clinical signs and biochemical parameters need to be taken into consideration while making therapeutic decision in women with thyroid dysfunction in the course of OHSS. Also, further studies are necessary to elucidate the matter.

Antenatal management of recurrent fetal goitrous hyperthyroidism associated with fetal cardiac failure in a pregnant woman with persistent high levels of thyroid-stimulating hormone receptor antibody after ablative therapy.

High titer of maternal thyroid-stimulating hormone receptor antibody (TRAb) in patients with Graves' disease could cause fetal hyperthyroidism during pregnancy. Clinical features of fetal hyperthyroidism include tachycardia, goiter, growth restriction, advanced bone maturation, cardiomegaly, and fetal death. The recognition and treatment of fetal hyperthyroidism are believed to be important to optimize growth and intellectual development in affected fetuses. We herein report a case of fetal treatment in two successive siblings showing in utero hyperthyroid status in a woman with a history of ablative treatment for Graves' disease. The fetuses were considered in hyperthyroid status based on high levels of maternal TRAb, a goiter, and persistent tachycardia. In particular, cardiac failure was observed in the second fetus. With intrauterine treatment using potassium iodine and propylthiouracil, fetal cardiac function improved. A high level of TRAb was detected in the both neonates. To the best of our knowledge, this is the first report on the changes of fetal cardiac function in response to fetal treatment in two siblings showing in utero hyperthyroid status. This case report illustrates the impact of prenatal medication via the maternal circulation for fetal hyperthyroidism and cardiac failure.

Treatment of pretibial myxedema with dexamethazone injected subcutaneously by mesotherapy needles.

Pretibial myxedema (PTM) is a rare extrathyroidal manifestation of Graves' disease that requires treatment when the clinical picture is markedly evident. In addition to topical treatment with steroid ointments, there have been previous reports of subcutaneous injections of steroids. This procedure may cause nodular degeneration of the skin due to fat atrophy when standard needles are used. In the present study, we have tried a novel modality of treatment of PTM by injecting a solution of dexamethasone in the subcutaneous tissue using needles employed for mesotherapy. These needles are ≤4 mm long and deliver the medication within the dermis or the first layer of the subcutaneous fat. We have treated five patients, four with diffuse and one with elephanthiasic PTM. We utilized multiple injections of a solution of dexamethasone, lidocaine, and saline in the PTM plaque and in the pretibial area, both in the PTM plaque and in the area surrounding the lesions, once a week for three consecutive weeks. Two patients with a more severe form of PTM underwent another two cycles four to six weeks after initial treatment. Patients were studied before and after treatment by clinical assessment and ultrasound of the pretibial skin. The treatment was well-tolerated, with only moderate pain upon injection of the solution. One month after treatment, all patients showed improvement of PTM at clinical assessment and a reduction of the thickness of the lesions at ultrasound of ∼15%, involving mostly the dermis. Moreover, all patients reported amelioration of the leg appearance. The present study, although preliminary, shows that intralesion steroid injection with mesotherapy needles in PTM is effective and well tolerated, and does not cause undesired long-term modifications of the skin. More studies are warranted to standardize such treatment in larger groups of patients.

Evaluation of oxidative status in patients with hyperthyroidism.

Data on the antioxidant levels enzyme in patients with hyperthyroidism are limited and conflicting. Therefore, the objective of this study was to evaluate the oxidative status using an automated method in patients with hyperthyroidism. Thirty-six subjects with hyperthyroidism and 30 healthy controls were enrolled in this study. Serum oxidative status was determined via measurement of total antioxidant capacity (TAC) and total oxidant status (TOS) and calculation of oxidative stress index (OSI). Serum TAC levels were significantly lower in patients with hyperthyroidism than controls (P=0.002), while serum TOS levels and OSI values were significantly higher (P=0.008, 0.004; respectively). Serum TAC levels were correlated with TSH levels (rho=0.223, P=0.032), FT3 levels (rho=-0.434, P=0.002) and FT4 levels (rho=-0.363, P=0.003) in patients. Further, TOS levels and OSI values were correlated with TSH levels (rho=-0.245, P=0.037; rho=-0.312, P=0.011, respectively), FT3 levels (rho=0.293, P=0.017, rho=0.505, P=0.002, respectively), and FT4 levels (rho=0.302, P=0.006, rho=0.321, P=0.008, respectively) in patients. Duration of disease was significantly correlated with OSI values in patients (rho=0.420, P=0.011), while no correlation with serum TAC levels and TOS levels (P>0.05). Oxidants are increased and antioxidants are decreased in patients with hyperthyroidism; as a result, the oxidative-antioxidative balance is shifted to the oxidative side. Increased oxidative stress may play a role in the pathogenesis of hyperthyroidism. It is believed that supplementation of antioxidant vitamins such as vitamins C and E may be helpful for these patients.

Periplogenin, isolated from Lagenaria siceraria, ameliorates L-T4-induced hyperthyroidism and associated cardiovascular problems.

The importance of glycoside in the regulation of thyroid dysfunction is not well understood. In the present investigation, effects of periplogenin-3- O-D-glucopyranosyl (1→6)(1→4)-D-cymaropyranoside, isolated from the vegetable, LAGENARIA SICERARIA, in L-thyroxine (L-T4)-induced hyperthyroidism and in related cardiovascular abnormalities have been revealed in Wistar albino rats. L-T4 (500 µg/kg, s. c./d) administration for 12 days significantly increased serum concentrations of thyroxine (T4), triidothyronine (T3), and hepatic 5'-deiodinase I (5'-DI) activity with a parallel increase in lipid peroxidation (LPO) in different organs such as heart, liver and kidney; serum glucose and insulin concentrations and a decrease in cardiac Na (+)-K (+)-ATPase activity as well as serum total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol and triglycerides. Most of these adverse effects were reversed following the administration of isolated periplogenin. However, out of its 3 different concentrations (5.0, 10, and 25 mg/kg), 5 mg/kg appeared to be the most effective one as it could nearly normalize the level of T3, glucose, insulin, Na (+)-K (+)-ATPase activity, tissue LPO and different serum lipids suggesting the protective role of periplogenin against thyrotoxicosis and associated cardiovascular problems. It appears that the periplogenin actions are mediated through its direct antithyroidal and/or LPO inhibiting properties.