scholarly journals Graves’ Disease Induced Severe Hypercalcemia

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A931-A931
Author(s):  
Zahira Marie Lugo Lopez ◽  
Laurianne El Musa Penna ◽  
Arnaldo Nieves Ortiz ◽  
Ivan Augusto Rivera ◽  
Andrea del Toro Diez ◽  
...  
Keyword(s):  
Isotonic Saline ◽  
Medical Attention ◽  
Graves Disease ◽  
Free T4 ◽  
Dihydroxyvitamin D ◽  
Patient Reports ◽  
Severe Hypercalcemia ◽  
Abdominopelvic Ct ◽  
Services Evaluation ◽  
25 Oh Vitamin D

Abstract Introduction: Hyperthyroidism is a well-known non-parathyroid hormone-mediated cause of hypercalcemia. Hypercalcemia associated with thyrotoxicosis is usually asymptomatic. Increased osteoclastogenesis is one of the mechanisms underlying this etiology. Hyperthyroidism is associated with mild to moderate levels of hypercalcemia in approximately 20% of patients, but severe hypercalcemia is rare. We report a case of a male with Grave’s disease-induced symptomatic severe hypercalcemia. Clinical Case: A 36-year-old male with type 2 diabetes mellitus and arterial hypertension who was transferred from another institution to our Emergency Department due to suspected primary hyperparathyroidism for Endocrinology Services evaluation. Family history is non-contributory. Patient reports palpitations, irritability, and unintentional weight loss of approximately fifty pounds in nine months. One month ago, he started with constipation, anxiety, depression, abdominal discomfort, nausea, and vomiting for which decided to seek medical attention. Physical examination was remarkable for tachycardia, dry mucous membranes, and goiter. Laboratory tests showed lipase 69 U/L (13-60U/L), albumin-corrected calcium 14.3 mg/dL (8.8-10.3mg/dL), phosphorus 3.30 mg/dL (2.4-4.2mg/dL), magnesium 1.58 mg/dL (1.8-2.2mg/dL), creatinine 1.38 mg/dL (0.90-1.30 mg/dL), alkaline phosphatase 77 IU/L (43-115IU/L), iPTH 4 pg/mL (11-67pg/mL), PTHrp <0.4 pmol/L (≤4.2pmol/L), 25-OH vitamin D 32.1 ng/mL (30-100ng/mL), 1,25-dihydroxyvitamin D <5.0 pg/mL(19.9-79.3pg/mL), hemoglobin 11.6 g/dL (14-18g/dL), negative serum and urine protein electrophoresis, TSH 0.003 uIU/mL (0.45-5.33 uIU/mL), free T4 2.80 ng/dL (0.71-1.85ng/dL), total T3 2.57 ng/mL (0.80-2.00ng/mL), TSI: 486% (<140%), urine calcium 24hr 525mg/day (100-300mg/day). Thoracic and abdominopelvic CT scan without contrast was unremarkable for masses, adenopathies, osseous lesions, or acute abdominal processes. Patient was treated with IV isotonic saline and methimazole 10mg oral daily with resolution of symptoms. Finally, diagnosed with Graves’ disease as the cause of hypercalcemia after ruling out other etiologies. He was discharged home with calcium levels 10.8 mg/dL, normal renal function, methimazole, and follow up with Endocrinology Services. Conclusion: This is a case of an atypical presentation of hyperthyroidism-induced symptomatic hypercalcemia. It is important to consider hyperthyroidism in the differential diagnoses of severe hypercalcemia. Prompt suspicion is essential due to the effective treatments available for Graves’ disease. Early treatment of hypercalcemia is important for quick resolution of symptoms and decreased associated mortality.

scholarly journals Rescue pre-operative treatment with Lugol’s solution in uncontrolled Graves’ disease

2017 ◽  
Vol 6 (4) ◽  
pp. 200-205 ◽  
Author(s):  
Jan Calissendorff ◽  
Henrik Falhammar
Keyword(s):  
Heart Rate ◽  
Thyroid Hormone ◽  
Side Effects ◽  
Definitive Treatment ◽  
Graves Disease ◽  
Free T4 ◽  
Hormone Levels ◽  
Free T3 ◽  
Adherence To Medication ◽  
Thyroid Hormone Levels

Background Graves’ disease is a common cause of hyperthyroidism. Three therapies have been used for decades: pharmacologic therapy, surgery and radioiodine. In case of adverse events, especially agranulocytosis or hepatotoxicity, pre-treatment with Lugol’s solution containing iodine/potassium iodide to induce euthyroidism before surgery could be advocated, but this has rarely been reported. Methods All patients hospitalised due to uncontrolled hyperthyroidism at the Karolinska University Hospital 2005–2015 and treated with Lugol’s solution were included. All electronic files were carefully reviewed manually, with focus on the cause of treatment and admission, demographic data, and effects of iodine on thyroid hormone levels and pulse frequency. Results Twenty-seven patients were included. Lugol’s solution had been chosen due to agranulocytosis in 9 (33%), hepatotoxicity in 2 (7%), other side effects in 11 (41%) and poor adherence to medication in 5 (19%). Levels of free T4, free T3 and heart rate decreased significantly after 5–9 days of iodine therapy (free T4 53–20 pmol/L, P = 0.0002; free T3 20–6.5 pmol/L, P = 0.04; heart rate 87–76 beats/min P = 0.0007), whereas TSH remained unchanged. Side effects were noted in 4 (15%) (rash n = 2, rash and vomiting n = 1, swelling of fingers n = 1). Thyroidectomy was performed in 26 patients (96%) and one was treated with radioiodine; all treatments were without serious complications. Conclusion Treatment of uncontrolled hyperthyroidism with Lugol’s solution before definitive treatment is safe and it decreases thyroid hormone levels and heart rate. Side effects were limited. Lugol’s solution could be recommended pre-operatively in Graves’ disease with failed medical treatment, especially if side effects to anti-thyroid drugs have occurred.

scholarly journals Determinants of Extraocular Muscle Volume in Patients with Graves' Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-4 ◽  
Author(s):  
Samer El-Kaissi ◽  
Jack R. Wall
Keyword(s):  
Extraocular Muscle ◽  
Tsh Receptor ◽  
Graves Disease ◽  
Thyroid Function Tests ◽  
Thyroid Scintigraphy ◽  
Free T4 ◽  
Receptor Antibody ◽  
Tsh Receptor Antibody ◽  
Antibody Positivity ◽  
Serum Tsh

Background. To examine factors contributing to extraocular muscle (EOM) volume enlargement in patients with Graves’ hyperthyroidism.Methods. EOM volumes were measured with orbital magnetic resonance imaging (MRI) in 39 patients with recently diagnosed Graves’ disease, and compared to EOM volumes of 13 normal volunteers. Thyroid function tests, uptake on thyroid scintigraphy, anti-TSH-receptor antibody positivity and other parameters were then evaluated in patients with EOM enlargement.Results. 31/39 patients had one or more enlarged EOM, of whom only 2 patients had clinical EOM dysfunction. Compared to Graves’ disease patients with normal EOM volumes, those with EOM enlargement had significantly higher mean serum TSH (0.020±0.005versus0.007±0.002mIU/L;Pvalue 0.012), free-T4 (52.9±3.3versus41.2±1.7 pmol/L;Pvalue 0.003) and technetium uptake on thyroid scintigraphy (13.51±1.7%versus8.55±1.6%;Pvalue 0.045). There were no differences between the 2 groups in anti-TSH-receptor antibody positivity, the proportion of males, tobacco smokers, or those with active ophthalmopathy.Conclusions. Patients with recently diagnosed Graves’ disease and EOM volume enlargement have higher serum TSH and more severe hyperthyroidism than patients with normal EOM volumes, with no difference in anti-TSH-receptor antibody positivity between the two groups.

Graves’ Hyperthyroidism-Induced Psychosis Treated With Aripiprazole—A Case Report

2012 ◽  
Vol 26 (1) ◽  
pp. 59-61 ◽  
Author(s):  
Livia R. Macedo ◽  
Jehan Marino ◽  
Brady Bradshaw ◽  
Joseph Henry
Keyword(s):  
Atrial Fibrillation ◽  
Psychiatric Symptoms ◽  
Thyroid Stimulating Hormone ◽  
Graves Disease ◽  
Long Term Effects ◽  
Free T4 ◽  
History Of ◽  
Antithyroid Peroxidase Antibody ◽  
First Time

Graves’ disease is an autoimmune syndrome with symptoms such as tachycardia, atrial fibrillation, and psychiatric symptoms. Limited evidence exists for the treatment of Graves’ hyperthyroidism-induced psychosis with atypical antipsychotics. A 47-year-old female with a psychiatric history of bipolar disorder presented for the first time to the psychiatric hospital. She was agitated and grossly psychotic with delusions. Electrocardiogram showed atrial fibrillation and tachycardia. Drug screen urinalysis was negative. Endocrine workup resulted in a diagnosis of Graves’ disease (thyroid-stimulating hormone [TSH]: 0.005 μIU/mL, triiodothyronine [T3]: 537 ng/dL, thyroxine [T4]: 24 mcg/dL, free T4: 4.5 ng/dL, positive antithyroid peroxidase antibody, and antinuclear antibody). Aripiprazole 10 mg daily was initiated and titrated to 15 mg daily on day 4. On day 16, her suspicious behavior, judgment, and insight improved. Other medications given included aspirin 325 mg daily, metoprolol 25 mg twice daily, titrated to 12.5 mg twice daily, and methimazole 30 mg daily, titrated to 20 mg twice daily, and discontinued on day 29. The patient received radioiodine I-131 treatment 1 week later. We report the first known case on the use of aripriprazole to treat Graves’ hyperthyroidism-induced psychosis. Further studies examining the long-term effects and appropriate dose and duration of aripiprazole in this patient population are needed.

Manifestation of Graves’ disease, resulting from radiosurgical treatment of acromegaly, in a patient with panhypopituitarism

2019 ◽  
Vol 65 (2) ◽  
pp. 101-106
Author(s):  
Ludmila I. Astafyeva ◽  
Pavel L. Kalinin ◽  
Tatyana A. Kienia ◽  
Valentin V. Fadeyev
Keyword(s):  
Radiation Therapy ◽  
Pituitary Adenoma ◽  
Thyroid Stimulating Hormone ◽  
Hormone Deficiency ◽  
Graves Disease ◽  
Free T4 ◽  
Disease Manifestation ◽  
Secondary Hypothyroidism ◽  
Residual Tissue ◽  
High Level

Cases of thyrotoxicosis associated with a previous case of secondary hypothyroidism are extremely rare. This article presents a rare clinical case of Graves disease manifestation in a patient with secondary hypothyroidism after radiosurgical treatment of acromegaly. A 38-year old woman presented with acromegaly and endo-supra-laterosellar pituitary adenoma. After non-radical removal of the pituitary adenoma, radiosurgical treatment of the of the residual tissue of the pituitary tumor in the cavernous sinus area was performed. After 14 months of radiation therapy, the acromegaly was in remission; after 24 months of radiation therapy, panhypopituitarism developed (secondary hypothyroidism, adrenal insufficiency, hypogonadism, and growth hormone deficiency). Furthermore, 1.5 years after the panhypopituitarism was diagnosed, the manifestation of Graves disease was also noted, requiring thyrostatic and radioactive iodine treatments. Diagnostic criteria for secondary hypothyroidism are low levels of the thyroid hormones free T4 and free T3, with a reduced, normal or slightly elevated level of thyroid stimulating hormone (TSH). The criterion for the development of thyrotoxicosis in the context of the secondary hypothyroidism was the persistent increase in the level of free T4 despite adequate drug therapy with levothyroxine. In the case report, the patients diagnosis of Graves disease was confirmed by the presence of a high level of antibodies to the TSH receptor.

Late and transient increases in free T4 after radioiodine treatment for Graves’ disease

1997 ◽  
Vol 20 (10) ◽  
pp. 580-584 ◽  
Author(s):  
A. D. Stensvold ◽  
R. Jorde ◽  
J. Sundsfjord
Keyword(s):  
Graves Disease ◽  
Radioiodine Treatment ◽  
Free T4

scholarly journals A rare case of tuberculosis-induced hypercalcemia

2020 ◽  
Vol 30 (3) ◽  
pp. 471-474
Author(s):  
Loris Wauthier ◽  
Xavier Theunssens ◽  
Patrick Durez ◽  
Catherine Fillée ◽  
Diane Maisin ◽  
...  
Keyword(s):  
Biochemical Parameters ◽  
Rare Case ◽  
Disease Modifying Antirheumatic Drugs ◽  
Antirheumatic Drugs ◽  
Atypical Case ◽  
Severe Hypercalcemia ◽  
Laboratory Investigations ◽  
Disease Modifying ◽  
25 Oh Vitamin D

Laboratory investigations of hypercalcemia involve testing of various biochemical parameters such as parathyroid hormone (PTH), 25-(OH) Vitamin D (25-(OH) VitD), 1,25-(OH)2 Vitamin D3 (calcitriol) and PTH related peptide (PTHrp). We herein present an atypical case of severe hypercalcemia in a patient with rheumatoid arthritis who has been treated for years by various biological disease-modifying antirheumatic drugs (DMARDs) and suddenly presented with general state alteration, oedema and ulceration of her right ankle. We illustrate how tuberculosis (TB) can cause high calcitriol concentration and subsequently lead to potentially severe hypercalcemia. Moreover, we highlight the importance of TB testing and follow-up in patients treated with biological DMARDs.

scholarly journals SUN-524 Patient with Pseudohypoparathyroidism Type 1B, Graves Disease, and False Positive HIV Screen- a Rare Presentation

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Viraj V Desai ◽  
Pratima V Kumar
Keyword(s):  
Western Blot ◽  
Autoimmune Diseases ◽  
False Positive ◽  
Thyroid Stimulating Hormone ◽  
Laboratory Evaluation ◽  
Graves Disease ◽  
Free T4 ◽  
Rare Presentation ◽  
Elisa Testing ◽  
History Of

Abstract Background: Pseudohypoparathyroidism 1B (PHP1B) is a disorder that can lead to thyroid stimulating hormone (TSH) resistance and hypothyroidism, although it is rarely associated with thyrotoxicosis. Clinical Case: A 25-year-old female with a history of PHP1B, seizures due to hypocalcemia, and family history of PHP1B in her three sisters and brother presented to our emergency room with a fever of 1030F and generalized malaise. Two months prior, she was seen at an outside hospital with palpitations and bulging of the left eye. There, she was diagnosed with hyperthyroidism, started on methimazole, and asked to continue levetiracetam and calcitriol upon discharge. On our exam, she had tachycardia of 120 beats per minute, left eye proptosis, positive Chvostek sign, and a large goiter with bruit. Reflexes were 3+. Laboratory evaluation revealed corrected serum calcium of 6.1 (8.5-10.5 mg/dL), TSH < 0.01 (0.34-5.60 mU/L), free T4 2.81 (0.60-1.60 ng/dL), free T3 13.0 (2.4-4.2 ng/dL), and iPTH 131 (12-88 pg/mL). ELISA testing for screening of HIV was positive. She was treated with IV calcium gluconate, methimazole, propranolol, and hydrocortisone. Her home doses of calcitriol and calcium were resumed. She was referred for total thyroidectomy as an outpatient once she became euthyroid. The confirmatory Western blot test for HIV was negative. It was determined that presence of thyroid stimulating immunoglobulin resulted in the false positive ELISA test. Discussion: Hyperthyroidism with Graves disease seen in PHP has only very rarely been reported. (1) It has been postulated that abnormal electrolytes and elevated parathyroid hormone from PHP may lead to stimulation of the thyroid gland and perpetuate Graves disease symptoms. (2) Furthermore, the presentation of thyrotoxicosis despite TSH resistance in PHP indicates that there may be other mechanisms for TSH receptor antibodies to take effect in these patients which have not yet been determined. (3) Lastly, autoimmune diseases, including Graves disease, can cause a false-positive HIV ELISA as seen in our patient. Conclusion: Although rare, thyrotoxicosis may present in patients with PHP1B. Additionally, it should be kept in mind that autoimmune diseases such as Graves disease can cause a false positive HIV ELISA, and follow-up Western blot testing should therefore be performed. References: (1) Gerhardt A, Hackenberg K. 2002. Pseudohypoparathyroidism and Graves’ disease: a rare combination of two endocrinological diseases. Exp Clin Endocrinol Diabetes. 110:245-247 (2) Morón-Díaz et al. 2019. A rare case of Graves’ disease in a patient with type 1B pseudohypoparathyroidism and associated TSH resistance. Endocrine Abstracts. 63:96 (3) Richard Prokesch. 2010. Navigating False Positive Testing. HIV Specialist (AAHIVS). 2:27

scholarly journals Graves Disease in Infancy

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A929-A930
Author(s):  
Kara A Beliard ◽  
Srinidhi Shyamkumarb ◽  
Mabel Yau ◽  
Cassie Mintz ◽  
Robert Rapaport
Keyword(s):  
Thyroid Gland ◽  
English Literature ◽  
Receptor Gene ◽  
Clinical Signs ◽  
Signs And Symptoms ◽  
Thyroid Stimulating Hormone ◽  
Graves Disease ◽  
Free T4 ◽  
Ocular Changes ◽  
Clinical Signs And Symptoms

Abstract Background: Graves disease (GD) is the most common cause of hyperthyroidism worldwide. The usual age of presentation is between 20-30 years, and it is more common in females. Transient hyperthyroidism does occur in infants born to mothers with GD, however, the novo GD in infants is extremely rare. We are aware of only four cases of GD in children under the age of 2 years old previously reported in the literature, with the youngest being of 18 months. Although rare, the complications can be devastating, so identifying and treating GD in infants is vital. We describe an infant who presented at 12 months of life with poor weight gain. Patient Findings: A 12-month old female patient presented with weight loss, tachycardia, diaphoresis and hypertension. She had a palpable thyroid gland without ocular changes. She was found to have an undetectable Thyroid Stimulating Hormone (TSH) with an elevated free T4 of 2.1 ng/dL (normal 0.80 - 1.50 ng/dL). She was stabilized in the intensive care unit with beta-blocker and methimazole. The diagnosis of GD was subsequently confirmed with an extremely elevated elevated Thyroid Stimulating Immunoglobulins (TSI) titer of 263 Iu/L (normal 0.00-0.55 IU/L), her TSH receptor gene was normal. At 34 months of age, her TSI titer is still elevated at 34 IU/L and she still requires methimazole to maintain a euthyroid state. She is growing and developing appropriately. Conclusion: To our knowledge, this report describes the youngest child to be diagnosed with GD in the English literature. Only four patients between the ages of 18 - 24 months have been described. Autoimmune diseases are rare in infants, the reason for which GD developed at such a young age remains unclear. Clinical signs and symptoms of hyperthyroidism in infants can be subtle and easily missed: increased growth velocity, failure to gain weight, autonomic changes, and irritability. Most patients have an enlarged thyroid gland, and some have ocular changes. The major long-term complications of undiagnosed hyperthyroidism include craniosynostosis and permanent neurocognitive damage. A high index of suspicion is needed for the recognition and prompt treatment of GD in infants, leading to better clinical outcome.

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