Clinical Signs Of Hyperthyroidism Research Articles

FRI513 Pathological Bone Fracture In An Adolescent With Graves’ Disease

Abstract Disclosure: J. Hayes dorado: None. M. Calla Ayala: None. D. Vargas Sejas: None. E. Coca Tapia: None. G. Justiniano Vargas: None. F. Leon Arze: None. Graves’ disease is the most common pediatric cause of hyperthyroidism. Although hyperthyroidism has been reported to cause a decrease in bone mineral density (BMD), its association with bone fractures is rare. A 12-year-old female patient presented to emergency with left arm pain that started after collision with an electricity pole. Her medical history included fractured right femur one year previously. Her heart rate 128 beats/min, blood pressure 120/70 mm Hg, weight 44 kg, height 156 cm (75th percentile) and BMI 18 kg/m2(50th percentile). Family history was unremarkable. He had prominent thyromegaly with diffuse enlargement and soft consistency on palpation. X-ray revealed a fracture of left humerus. Demineralization of bone was detected. Blood Tests: calcium 8.9 mg/dL (8.5-10.5); phosphate 4.36 mg/dL (3.7-5.6); alkaline phosphatase 239 U/L (42-362); PTH 23 pg/mL (12-88); 25-OHD 22.8 ng/mL (20-80); TSH <0.01 μIU/mL (0.38-5.33); fT3 29 pg/mL (2.6-4.37); and fT4 5.13 ng/dL (0.61-1.2). Auto-antibodies were positive: thyroid peroxidase Abs 42 IU/mL (0-9), thyroglobulin Abs 21 IU/mL (0-4) and TSH Receptor Abs 7.33 IU/L (0-0.1). Complete blood count, liver, kidney function tests were normal. Thyroid ultrasonography showed a significant increase in thyroid gland volume and vascularization. A diagnosis of Graves’ disease was confirmed. Methimazole, propranolol, calcium and vitamin D therapies were started. Pre-treatment bone densitometry showed significantly low BMD: lumbar BMD (L1-L4) was 0.701 g/cm2 (Z-score - 2) and femoral BMD was 0.639 g/cm2 (Z-score -2). Euthyroidism was achieved after ten weeks of treatment and clinical signs of hyperthyroidism had improved. At six months follow up there were no clinical signs of hyperthyroidism and the patient remained euthyroid. Bone densitometry investigation one year after diagnosis showed marked improvement: lumbar BMD (L1-L4) was 0.898 g/cm2 (Z-score -0.5) and femoral BMD was 0.799 g/cm2 (Z-score -0.4). Untreated adolescents with Graves’ disease may present with fractures. It highlights the importance of considering hyperthyroidism as a possible diagnosis among the differential diagnoses of pathological bone fractures. Presentation: Friday, June 16, 2023

Influence of Thyroid Peroxidase Antibodies Serum Levels in Graves' Disease: A Retrospective Cohort Study.

Purpose Graves' disease (GD) is an autoimmune disorder caused by the presence of antibodies to the thyroid stimulating hormone (TSH) receptor (TRAbs), usually presenting with clinical signs of hyperthyroidism. Previous evidence suggests that higher serum levels of thyroid peroxidase antibodies (TPOAbs) may lead to more sustained remission of hyperthyroidism after treatment with antithyroid drugs (AT). However, doubts about the influence of TPOAbs in Graves' disease outcomes still remain. Methods A retrospective, unicenter cohort study was performed. All patients with GD (TRAbs > 1.58U/L), biochemical primary hyperthyroidism (TSH < 0.4µUI/mL), and TPOAbs measurement at diagnosis, treated with AT between January 2008 and January 2021, were included for analysis. Results One hundred and forty-two patients (113 women) with a mean age of 52 ± 15 years old were included. They were followed up for 65.4 ± 43.8months. TPOAbs positivity was present in 71.10% (n=101) of those patients. Patients were treated with AT for a median of 18 (IQR (12; 24)) months. Remission occurred in 47.2% of patients. Patients with remission presented with lower TRAbs and free thyroxine (FT4) levels at the diagnosis. (p-value <0.001, p-value 0.003, respectively). No association was found in the median TPOAbs serum levels of patients who remitted and those who maintained biochemical hyperthyroidism after the first course of AT. Relapse of hyperthyroidism occurred in 54 patients (57.4%). No difference was found in TPOAbs serum levelsregarding the patient's relapse. Moreover, a time-based analysis revealed no differences in the relapse rate after 18 months of AT therapy between patients with and without TPOAbs positivity at the diagnosis(p-value0.176). It was found a weak positive correlation (r=0.295; p-value <0.05) between TRAbs and TPOAbs titters at the moment of Graves' diagnosis. Conclusion In this study, a correlation between TRAbs measurements and TPOAbs titter was described, although no significant association was found between the presence of TPOAbs and the outcomes of patients with GD treated with AT. These results do not support the use of TPOAbs as a useful biomarker to predict remission or relapse of hyperthyroidism in GDpatients.

Thyrotoxic periodic paralysis together with thyrotoxic heart disease in a Ghanaian man: case report and literature review

&lt;abstract&gt; &lt;p&gt;Thyrotoxic periodic paralysis (TPP) is an uncommon symmetrical paralysis usually affecting proximal muscles, which occurs in the hyperthyroid state with associated hypokalemia. It is more prevalent in East Asian males and extremely rare in blacks. Data on TPP is scarce in Africa and no report has been made in Ghana. We report a case of a middle-aged Ghanaian man who had three episodes of paralysis in all four limbs occurring at night with the second and third episodes requiring hospital visit. He had no clinical signs of hyperthyroidism during his first hospital visit but had developed clinical and biochemical evidence of hyperthyroidism on the second visit with serum potassium levels of 1.9 mmol/l; and he was eventually diagnosed with TPP. His paralysis resolved with correction of the hypokalemia. It is important to evaluate patients presenting with paralysis comprehensively. Less common differential diagnosis such as TPP may also be considered in such patients to ensure early diagnosis and treatment which can prevent complications.&lt;/p&gt; &lt;/abstract&gt;

Effect of iodine 131 in the treatment of Graves’ disease on thyroid mass and clinical signs of hyperthyroidism

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Effect of iodine 131 in the treatment of Graves’ disease on thyroid mass and clinical signs of hyperthyroidism

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Effect of iodine 131 in the treatment of Graves’ disease on thyroid mass and clinical signs of hyperthyroidism

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

A Case of Definitive Therapy in Persistent Congenital Hyperthyroidism Secondary to an Activating Variant of the TSHR Gene

Background: Sporadic congenital non-autoimmune hyperthyroidism (SCNAH) causes permanent hyperthyroidism secondary to activating mutations in the TSHR gene. SCNAH usually presents during infancy and can be difficult to treat with antithyroid drugs or subtotal thyroidectomy.1 When adequate therapy is delayed, irreversible sequela such as craniosynostosis, growth failure, and cognitive delays may develop. Definitive therapy for children with SCNAH is recommended with no consensus on timing or type of intervention. Our case highlights the importance of early total thyroidectomy to optimize clinical outcomes in patients with SCNAH.Clinical case: A now 3-year-old male was born small for gestational age (SGA) at 34 weeks gestation with biochemical and clinical signs of hyperthyroidism in the neonatal period. On day of life 6, his TSH was 0.02 mcU/mL (reference range 0.34-5.6 mcU/mL) and free thyroxine (T4) was 5.42 ng/dL (reference range 0.58-1.64 ng/dL). Methimazole (MMI) 0.3 mg/kg/day was started at that time, and the dose was titrated over 6 weeks of life to 0.8 mg/kg/day due to continued elevation of free T4 levels. Negative thyroid autoantibodies and normal maternal thyroid studies prompted genetic testing at 3 months of age. This testing revealed a heterozygous variant in the TSHR gene [c.842G->A (p.G116R)] that was determined to be pathologic. Despite frequent MMI dose changes and confirmation of medication adherence, high-dose MMI was not effective in consistently normalizing his TSH and free T4 levels in the first two years of life. Concerns for poor growth and hyperactive behavior were also present. A “block and replace” strategy was not feasible since the patient remained hyperthyroid even at MMI doses up to 0.8 mg/kg/day. Despite normal insulin-like growth factor 1 and insulin-like growth factor binding protein 3 levels, poor linear growth persisted with a height Z-score of -3.61 by age 3 years. While he was SGA at birth, his recurrent hyperthyroidism impeded catch-up growth potential, so treatment with growth hormone (rhGH) was initiated. His height Z-score improved to -2.39 after 9 months on rhGH dosed at 0.18 mg/kg/week. Due to the difficulty in consistently managing him medically with MMI, he underwent total thyroidectomy at age three.Conclusion: There is currently no consensus on the timing of definitive therapy for children with SCNAH. This case highlights the importance of considering total thyroidectomy at an early age to avoid long-term sequela of persistent hyperthyroidism.1. Gozu HI, Lublinghoff J, Bircan R, Paschke R. Genetics and phenomics of inherited and sporadic non-autoimmune hyperthyroidism. Mol Cell Endocrinol. 2010;322:125–34.

Cardiothyreosis in Sub-Saharan Africa (Benin)

This is a retrospective study over a 5-year period from January 1, 2013 to December 31, 2018. The diagnosis of cardiothyreosis was retained before clinical signs of hyperthyroidism confirmed to biology by an elevation of T4 and a collapse of ultrasensitive TSH associated with at least one of the following heart failure: insufficiency heart disease, coronary heart failure, rhythm disorder. Sociodemographic, anthropometric, clinical and paraclinical data were analyzed from medical records. Follow-up was evaluated over a period of 6 months to one year after being put on synthetic antithyroids. Results: Of 72 patients seen with hyperthyroidism conditions during the period, we identified 10 cases of cardiothyresis at the departments of Endocrinology and Cardiology of the CNHU/HKM Teaching hospital of Cotonou, Benin. The frequency of cardiothyreosis among hyperthyroidsis was 13.88%. The mean-age for our patients was 50.9 years with bounds from 29 to 79 years. The predominance was female, 8 women for 2 men. A clinical background of high blood pressure is founded in 6/10 patients; 4/10 had a history of hyperthyroidism. All patients had heart failure associated with complete arrhythmia by atrial fibrillation in 6 patients. The multi-modular goiter was found in 5/10 of the patients, the vascular goiter 5/10. Synthetic antithyroids, hygienic-dietary measures and a specific treatment for heart failure were used. The average length of hospital’s stay was 7 days. Immediate development is satisfactory with euthyroidism in all patients and improved functional signs. Conclusion: Cardiothyreosis is infrequent in Cotonou. This is a serious complication of hyperthyroidism, which is expensive to manage. Hence the need for early diagnosis and effective treatment of hyperthyroidism.

Safety of orally administered, USP-compliant levothyroxine sodium tablets in dogs.

The safety of synthetic levothyroxine sodium tablets (Thyro-Tabs® Canine; LLOYD, Inc.) in dogs was evaluated in a randomized, sham-dose controlled, parallel-group study. Young, healthy, euthyroid Beagle dogs were randomized into four groups (four females and four males per group) and received single daily doses of 0×, 2× (0.044mg/kg), 6× (0.132mg/kg), or 10× (0.22mg/kg) the labeled starting dose of 0.022mgkg-1 day-1 for 182days. Every 2weeks, physical examinations, electrocardiology examinations, and sample collections for thyroid panel, hematology, serum biochemistry, coagulation panel, and urinalysis were performed. At the end of the study, the dogs were euthanized and full necropsies performed. The most overt finding was the expected dose-dependent increase in serum concentrations of total and free thyroxine with dose-dependent suppression of the hypothalamic-pituitary-thyroid axis as evidenced by decreased serum thyroid-stimulating hormone concentrations, decreased thyroid+parathyroid/body weight ratios, and a trend for decreased pituitary weight/brain weight ratios. Clinical signs of thyrotoxicosis (excitation, tachypnea, tachycardia) in the treated dogs were sporadic with no dose-response relationship. Other findings statistically associated with levothyroxine treatment were generally mild and not clinically important. In summary, doses of levothyroxine sodium up to 10× the labeled starting dose were well tolerated in healthy dogs.

Voedselgerelateerde hyperthyroïdie bij een rottweiler

In deze casuïstiek wordt een geval van voedselafhankelijke hyperthyroïdie bij een hond beschreven. Een mannelijke, intacte rottweiler van elf maanden oud werd aangeboden omwille van hijgen, gewichtsverlies en een gestegen serum-thyroxineconcentratie. Uit de anamnese bleek dat de hond een “bone and raw food” dieet te eten kreeg. Dit maakte de diagnose van voedselafhankelijke hyperthyroïdie zeer waarschijnlijk. Andere mogelijke differentiaaldiagnosen werden uitgesloten door middel van een uitgebreide diagnostiek. Uiteindelijk verdwenen de symptomen en normaliseerden de schildklierwaarden na verandering naar een klassiek commercieel onderhoudsdieet. Bij elke hond met een gestegen serum-thyroxineconcentratie, met of zonder symptomen van hyperthyroïdie, is een complete voedingsanamnese noodzakelijk. Eigenaars moeten geïnformeerd worden over het feit dat diëten met rauw vlees vaak nutritionele tekortkomingen hebben, het risico van bacteriële contaminatie dragen en andere veiligheidsproblemen hebben. Daarom zouden dierenartsen dit soort voeding beter afraden.

Thyroid Storm-induced Multi-organ Failure in the Setting of Gestational Trophoblastic Disease

BackgroundThyroid storm is a potentially life-threatening complication of gestational trophoblastic disease (GTD), with varying clinical severity. It should be considered in patients with GTD, abnormal vital signs, and clinical signs of hyperthyroidism. Case ReportA 45-year-old non-English-speaking patient presented to a New York City hospital in November 2011 with an aborting molar pregnancy and severe hemorrhage. Initial presentation was concerning for GTD. Laboratory values were obtained that confirmed the diagnosis of GTD, which was also by thyroid storm and congestive heart failure. This was evidenced by laboratory values of free thyroxine of 4.9 and beta human chorionic gonadotropin of 1,488,021 IU/mL. Dilation and curettage with 16-mm suction catheter was performed until all products of conception were removed and bleeding was controlled. The patient was admitted to the surgical intensive care unit and proceeded to have multi-organ failure, and remained intubated and unresponsive to verbal/visual and tactile stimuli. On postoperative day 13 the patient suddenly became alert and self-extubated, began to communicate verbally, and resolution of her multi-organ failure became evident. The patient was discharged with Gynecologic Oncology follow-up. Why should an emergency care physician be aware of this? This case represents the dangers associated with poor prenatal care and late diagnosis of molar pregnancy. It also represents the need for immediate recognition of the condition and initiation of appropriate medical care. Although this patient’s clinical outcome was good, the event could have been prevented had she received reliable medical care.

Three cases of thyrotoxic periodic paralysis due to painless thyroiditis

We present three cases of thyrotoxic periodic paralysis (TPP) due to painless thyroiditis presenting as acute quadriparesis. All responded to potassium supplementation and propranolol. TPP may be due to thyrotoxicosis of any etiology, commonly Grave's disease. The absence of clinical signs of thyrotoxicosis can delay diagnosis and treatment. Thyroid function tests should be a routine evaluation in all cases of hypokalemic periodic paralysis.

Giant struma ovarii

Monodermal teratomas are most commonly differentiated as struma ovarii or carcinoid tumor. Struma ovarii is defined as ovarian teratoma composed predominantly ([50 %) of thyroid-type tissue [1], representing less than 3 % of all teratomas [2]. Benign ovarian teratomas contain thyroid tissue in less than 15 %, but with thyroid function or a malignant thyroid component are also categorized as struma ovarii [3]. Clinical signs of hyperthyroidism can occur in 5 % [4] to 8 % [5].

99mTc-MDP uptake in thyroid nodule: Contribution of SPECT-CT and ultrasonography

Iodine kinetic studies were performed in seven patients with hot thyroid nodules, three diffuse toxic goiters and one normal control, using a double label technique (131I and 125I-thyroxine). The investigation was complemented by partial kinetic studies in 29 further subjects, including normal control subjects and euthyroid or hyperthyroid patients with diffuse or nodular goiter. Thyroid iodide uptake and hormonal secretion parameters were significantly increased, up to twice control values, in hot nodules without clinical signs of thyrotoxicosis. Values similar to those of Graves' disease were found in toxic nodular goiter. The exchangeable iodine pool was markedly reduced in those glands where the nodule was adenomatous and radioiodide uptake of normal parenchyma was completely suppressed. In two cases of nontoxic hot nodule with histologic diagnosis of multinodular goiter, and incomplete suppression of the “extranodular” thyroid, the exchangeable iodine pool was comparable to that of normals. The T4 disposal rate was increased, mainly due to a significantly higher metabolic deiodination which seemed to keep pace with the increased T4 production rate in nontoxic nodules. This could be the reason why the mean peripheral T4 pool of clinically nontoxic patients with hot nodules is comparable to that of normal persons, and there are no evident signs of hypermetabolism in spite of the greater thyroid hormone production. A significant “non-T4-iodine” release, probably mainly iodide, was found in every subject. The amount of iodine lost by the thyroid through this “iodide leak” did not relate to the T4 secretion rate but seems to be directly related to the thyroid exchangeable iodine pool size.

Recurrence of Graves' Disease in Thyroglossal Duct Remnants: Relapse After Total Thyroidectomy

Ectopic thyroid tissue can be found anywhere between the foramen cecum and the normal position of the thyroid gland, most commonly located in the anterior cervical area, the region of the thyroglossal duct. Although thyroid cancer has been described frequently in thyroglossal duct remnants, thyroid dysfunction related to this tissue is rare. We report a patient with recurrent Graves' disease arising in a thyroglossal duct remnant. A 40-year-old woman with a history of total thyroidectomy for Graves' disease, presented with a slowly enlarging midline neck mass in association with clinical signs of hyperthyroidism. Serum-free triiodothyronine (6.6 pg/mL) and serum-free thyroxine (2.2 ng/dL) were elevated (normal range, 2.3-4.2 pg/mL and 0.9-1.8 ng/dL, respectively), and thyroid-stimulating hormone was suppressed (<0.01 mIU/mL; normal range, 0.35-5.50 mIU/mL). Neck ultrasonography showed a solid mass, localized at the infrahyoid area; radionuclide scanning confirmed an increased uptake at the same level. A 4 cm solid mass was removed by the Sistrunk technique. Microscopic examination revealed marked follicular hyperplasia, with tall cells, small follicles, scant, and scalloped colloid, in association with patchy lymphocytic infiltrate consistent with Graves' disease. There appears to be no reason why thyroid cells within thyroglossal duct remnants should not be influenced by the thyroid-stimulating immunoglobulins of Graves' disease. Thyrotoxicosis resulting from this must be very rare, however, as were unable to find reports of patients with thyrotoxicosis due to Graves' disease in thyroglossal duct remnants. Although some thyroid tissue can be found within the thyroglossal duct in 1.6% to 40% of normal adults, the risk of thyroid dysfunction from this is far too low to justify new therapeutic approaches.

Clinical efficacy and safety of a once‐daily formulation of carbimazole in cats with hyperthyroidism

Evaluation of efficacy and safety of a novel controlled-release formulation of carbimazole in feline hyperthyroidism. A multicentre, self-controlled study in 44 client-owned cats with history and clinical signs of hyperthyroidism, and total thyroxine concentration greater than or equal to 50 nmol/l. Treatment was started at 15 mg once daily, response assessed after 10 days, and 3, 5, 8, 26 and 53 weeks and dose adjusted as required. The median dose of carbimazole was 10 mg (range 10 to 15 mg) and 15 mg (5 to 25 mg) once daily after 3 and 53 weeks, respectively. Median total thyroxine concentration dropped significantly from 118 nmol/l (50 to 320 nmol/l) at presentation to 33 nmol/l (n=40) after 10 days, 31 nmol/l (n=34) at 3 weeks and 21 nmol/l (n=18) at 53 weeks. Clinical signs improved or resolved in almost all cats within three weeks after starting treatment. Twenty-one adverse reactions possibly (20) or probably (1) related to treatment were reported. During treatment, increased blood urea nitrogen concentration was observed in 25 per cent of the cats, eosinophilia in 20 per cent and lymphopenia in 16 per cent, while liver enzymes tended to improve. Once daily administration of controlled-release carbimazole tablets was effective and had expected tolerance in hyperthyroid cats during short- and long-term treatment.

Effects and safety of iopanoic acid in cats administered levothyroxine.

The purpose of this study was to evaluate the safety and effect of iopanoic acid in 13 cats with hyperthyroidism induced by daily subcutaneous administration of 25microg/kg levothyroxine for a period of 42 days. On day 28 of levothyroxine administration, cats were randomly allocated to receive treatment twice daily with a placebo (control group; n=4), 50mg iopanoic acid (low dose group; n=5), or 100mg iopanoic acid (high dose group; n=4) for 14 days. Compared to the control group, T(3) concentrations were significantly decreased in both the low dose and high dose groups on days 35 and 42. T(3) concentrations in the low dose and high dose groups at days 35 and 42 were not different from day -8. The effect of iopanoic acid on clinical signs of hyperthyroidism was less apparent. Further clinical studies evaluating the long-term effect in cats with spontaneous hyperthyroidism are warranted.

Diagnostic Tests for Hyperthyroidism in Cats

The diagnosis of hyperthyroidism, one of the most common disorders affecting elderly cats, is usually straightforward and considered routine by most practitioners. Nowadays, however, most cats suffering from hyperthyroidism tend to be diagnosed earlier and at a milder stage of the disease than those cats diagnosed 10 to 25 years ago. There are, in fact, a growing number of cats with clinical signs of hyperthyroidism and palpably large thyroid glands whose baseline serum total thyroid hormone concentrations are within the normal or borderline range, making diagnosis problematic. This paper reviews the available tests used to confirm a diagnosis of hyperthyroidism in cats and discusses their overall usefulness.

Trastorno de pánico e hipertiroidismo: curso clínico en dos pacientes

In two females aged 27 and 32 years old, an aggravation of their panic disorder coincided with the appearance of clinical signs of hyperthyroidism. The clinical diagnosis was confirmed with the finding of raised thyroid hormone levels and undetectable TSH levels. These two cases highlight the importance of routine thyroid function assessment in patients with panic disorder, mainly in those with partial response to medications or when symptoms aggravate, despite an adequate treatment.

Asymptomatic thyroiditis; a few typical cases and the prevalence of this disease

Although asymptomatic thyroiditis (АГ) is well known by the present time, the prevalence of this disease is still disputed. We evaluated the incidence of A T at Thyroidology Department of Omori Hospital. Asymptomatic thyroiditis was detected in 61 out of 1113 patients (5.5%) during the period of July 1993 to June 1996. On admission, high levels of free thyroxin in the blood (hyperthyroxinemia) were detected in 306 patients. Asymptomatic thyroiditis was the cause of this condition in 38 (12.4%) patients. By the moment of examination of patients with A T, thyrotoxicosis was revealed in 38 patients, euthyroid status in 17, and hypothyrosis in 6 patients. Patients with euor hypothyrosis had complaints and presented with clinical signs of thyrotoxicosis 1-2 months before examination. Antibodies to thyroperoxidase and/or thyroglobulin were detected in 51 out of 61 (84%) patients with A T. Sometimes A T is regarded as diffuse toxic goiter (DTG), but a patient with this condition can develop A T. We should always remember about the possibility of AT but not DTG even in cases with pronounced thyrotoxicosis or with a history of DTG. Regular check-ups of thyroid function will help diagnose the condition without resorting to 1221. If a patient has symptoms of thyrotoxicosis, e. g. palpitation, thyroid function should be examined.&#x0D; Неге аге 4 typical cases with AT to illustrate this. Patient No. 1 is a classical case of Hashimoto’s thyroiditis. Previously she developed an euthyroid status, and later thyroid destruction and dysfunction (transitory thyrotoxicosis followed by hypothyrosis) developed spontaneously without pregnancies or deliveries. Patient No. 2 had transitory thyrotoxicosis which was not followed by hypothyrosis, but with a transitory slight increase in TTH. She might have had AT3years before. Patient No. 3 aged 63years complained of angina pectoris and arrhythmia; later she was prescribed substitute therapy with L thyroxin for pronounced hypothyrosis (TTH 90.9 microunits/ml). In patient No. 4 DTG was erroneously diagnosed and she was prescribed therapy for this condition. Thyroid dysfunction was transitory in all patients, and the function recovered later.