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.

Thyrotropin-secreting pituitary adenoma in an 11-year-old boy with type 1 autoimmune polyglandular syndrome

2016 ◽  
Vol 29 (2) ◽  
Author(s):  
Nadia Mazerkina ◽  
Yuri Trunin ◽  
Sergey Gorelyshev ◽  
Andrey Golanov ◽  
Boris Kadashev ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Radiation Therapy ◽  
Pituitary Adenoma ◽  
Clinical Signs ◽  
Thyroid Stimulating Hormone ◽  
Hormone Deficiency ◽  
Endocrine Diseases ◽  
Autoimmune Polyglandular Syndrome ◽  
First Case

AbstractThyrotropinomas (TSHomas) are rare pituitary adenomas, particularly in childhood. We present here the case of an 11-year-old boy with type 1 autoimmune polyglandular syndrome (APS1) and TSHoma which was diagnosed by elevated thyroid – stimulating hormone and thyroid hormones levels without evident clinical signs of hyperthyroidism. He was underwent partial resection of the tumor via transsphenoidal approach and subsequently radiation therapy. Consequently, 1 year after radiotherapy, the patient developed growth hormone deficiency, three and half years after radiation became euthyroid, and five and half years after treatment – hypothyroid. This is the first case of the coexistence of these two rare endocrine diseases in one patient.

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.

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.

scholarly journals Hypothyroidism: current state of the problem

2020 ◽  
pp. 96-107
Author(s):  
E. V. Biryukova ◽  
D. V. Kileynikov ◽  
I. V. Solovyeva
Keyword(s):  
Kinase Inhibitors ◽  
Clinical Manifestations ◽  
Final Diagnosis ◽  
Thyroid Stimulating Hormone ◽  
Pathological Process ◽  
Primary Hypothyroidism ◽  
The Body ◽  
Hormone Deficiency ◽  
Side Reactions ◽  
Secondary Hypothyroidism

The article presents the issues of epidemiology, classification, and clinic of hypothyroidism. The frequency of hypothyroidism increases significantly with age. The most common form is primary hypothyroidism, caused by a pathological process in the thyroid gland itself. Secondary hypothyroidism or tertiary hypothyroidism is caused by insufficient secretion of thyroid- stimulating hormone (TSH), or thyrotropin-releasing hormone. The article deals with the main causes of primary and secondary hypothyroidism. The most common cause of primary hypothyroidism is autoimmune thyroiditis, which can develop both separately and simultaneously with other autoimmune diseases, as part of polyglandular syndrome. Special attention should be paid to the change of thyroid status as a result of adverse side reactions when using a range of drugs. The questions about the mechanisms of thyroid insufficiency development as a result of unfavorable side reactions when using a number of drugs (lithium preparations, iodine-containing compounds, tyrosine kinase inhibitors, etc.) have been raised. Undiagnosed hypothyroidism is a risk factor for the progression of already existing cardiovascular diseases. The severity of clinical manifestations is determined by the severity of thyroid hormone deficiency. There are no significant clinical differences between the pronounced forms of primary and secondary hypothyroidism. Depending on the degree of lesion, secondary hypothyroidism may be complicated by other manifestations of hypothalamic-pituitary disorders, as well as the latter may include a decrease in the secretion of antidiuretic hormone at a certain stage of their development. Diagnostic difficulties are discussed, as hypothyroidism disrupts the functioning of most organs and systems of the body (musculoskeletal, cardiovascular, urinary, gastrointestinal, central and peripheral nervous systems) and can be masked by various diseases. The final diagnosis of hypothyroidism is clarified by a number of laboratory and instrumental studies. Substitution therapy with levothyroxine is used to treat hypothyroidism of any etiology.

scholarly journals Considerations for Thyroidectomy as Treatment for Graves Disease

2019 ◽  
Vol 12 ◽  
pp. 117955141984452 ◽  
Author(s):  
Mary Smithson ◽  
Ammar Asban ◽  
Jason Miller ◽  
Herbert Chen
Keyword(s):  
Clinical Manifestations ◽  
Endocrine System ◽  
Thyroid Stimulating Hormone ◽  
Clinical State ◽  
Antithyroid Drugs ◽  
Graves Disease ◽  
Replacement Rate ◽  
Free T4 ◽  
Organ Systems ◽  
Toxic Multinodular Goiter

Hyperthyroidism is a clinical state that results from abnormally elevated thyroid hormones. Thyroid gland affects many organ systems; therefore, patients usually present with multiple clinical manifestations that involve many organ systems such as the nervous, cardiovascular, muscular, and endocrine system as well as skin manifestations. Hyperthyroidism is most commonly caused by Graves disease, which is caused by autoantibodies to the thyrotropin receptor (TRAb). Other causes of hyperthyroidism include toxic multinodular goiter, toxic single adenoma, and thyroiditis. Diagnosis of hyperthyroidism can be established by measurement of thyroid-stimulating hormone (TSH), which will be suppressed with either elevated free T4 and/or T3 (overt hyperthyroidism) or normal free T3 and T4 (subclinical hyperthyroidism). Hyperthyroidism can be treated with antithyroid drugs (ATDs), radioactive iodine (RAI), or thyroidectomy. ATDs have a higher replacement rate when compared with RAI or thyroidectomy. Recent evidence has shown that thyroidectomy is a very effective, safe treatment modality for hyperthyroidism and can be performed as an outpatient procedure. This review article provides some of the most recent evidence on diagnosing and treating patients with hyperthyroidism.

scholarly journals THYROID ACROPACHY: A RARE MANIFESTATION OF GRAVES DISEASE IN JOINTS

2019 ◽  
Vol 5 (6) ◽  
pp. e369-e371 ◽  
Author(s):  
Nicolas Perini ◽  
Roberto Bernardo Santos ◽  
João Hamilton Romaldini ◽  
Danilo Villagelin
Keyword(s):  
Elevated Serum ◽  
Clinical Signs ◽  
Thyroid Stimulating Hormone ◽  
Graves Disease ◽  
Free T4 ◽  
Tissue Edema ◽  
Rare Manifestation ◽  
Small Joint ◽  
History Of ◽  
Hands And Feet

Objective: The objective of this report was to describe a patient with Graves acropachy, a rare manifestation of Graves disease (GD) that is clinically defined by skin tightness, digital clubbing, small-joint pain, and soft tissue edema progressing over months or years with gradual curving and enlargement of the fingers. Methods: The patient was evaluated regarding thyroid function (serum free T4 [FT4] and thyroid-stimulating hormone [TSH] quantifications) and autoimmunity biomarkers (thyroid receptor antibody [TRAb]) as well as radiographic investigation of the extremities. Results: A 52-year-old man presented with a history of thyrotoxicosis and clinical signs of Graves orbitopathy. Laboratory tests showed suppressed TSH (0.01 UI/L; normal, 0.4 to 4.5 UI/L) and elevated serum FT4 (7.77 ng/dL; normal, 0.93 to 1.7 ng/dL), with high TRAb levels (40 UI/L; normal, <1.75 UI/L). A diagnosis of thyrotoxicosis due to GD was made and the patient was treated with methimazole. After the patient complained of swelling in hands and feet, X-ray evaluation was conducted and established the thyroid acropachy. Conclusion: We present a case of a patient with GD associated with worsening extrathyroid manifestations during orbitopathy, dermopathy, and developed acropachy in hands and feet.

scholarly journals Graves disease-induced thrombotic thrombocytopenic purpura: a case report

2019 ◽  
Vol 13 (1) ◽  
Author(s):  
Saira Chaughtai ◽  
Ijaz Khan ◽  
Varsha Gupta ◽  
Zeeshan Chaughtai ◽  
Raquel Ong ◽  
...  
Keyword(s):  
Thrombotic Thrombocytopenic Purpura ◽  
African American Woman ◽  
Case Reports ◽  
American Woman ◽  
Pulseless Electrical Activity ◽  
Thyroid Stimulating Hormone ◽  
Graves Disease ◽  
Free T4 ◽  
Thrombocytopenic Purpura ◽  
History Of

Abstract Background Thrombotic thrombocytopenic purpura is an autoimmune disease that carries a high mortality. Very few case reports in the literature have described a relationship between Graves disease and thrombotic thrombocytopenic purpura. We present a case of a patient with Graves disease who was found to be biochemically and clinically hyperthyroid with concurrent thrombotic thrombocytopenic purpura. Case presentation Our patient was a 30-year-old African American woman with a history of hypertension and a family history of Graves disease who had recently been diagnosed with hyperthyroidism and placed on methimazole. She presented to our hospital with the complaints of progressive shortness of breath and dizziness. Her vital signs were stable. On further evaluation, she was diagnosed with thrombotic thrombocytopenic purpura, depending on clinical and laboratory results, and also was found to have highly elevated free T4 and suppressed thyroid-stimulating hormone. She received multiple sessions of plasmapheresis and ultimately had a total thyroidectomy. The patient’s hospital course was complicated by pneumonia and acute respiratory distress syndrome. Her platelets stabilized at approximately 50,000/μl, and her ADAMTS13 activity normalized despite multiple complications. The patient ultimately had a cardiac arrest with pulseless electrical activity and died despite multiple attempts at cardiopulmonary resuscitation. Conclusion Graves disease is an uncommon trigger for the development of thrombotic thrombocytopenic purpura, and very few cases have been reported thus far. Therefore, clinicians should be aware of this association in the appropriate clinical context to comprehensively monitor hyperthyroid patients during treatment.

Evaluation of Serum Ferritin and Anti-Thyroid Peroxidase Antibody Status in Newly Diagnosed Subclinical Cases of Hypothyroidism

2020 ◽  
Vol 20 ◽  
Author(s):  
Rajlaxmi Tiwari ◽  
Gautom Kumar Saharia ◽  
Manaswini Mangaraj
Keyword(s):  
Serum Ferritin ◽  
Multinomial Logistic Regression ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Peroxidase ◽  
Newly Diagnosed ◽  
Free T4 ◽  
Ferritin Concentration ◽  
Serum Ferritin Concentration ◽  
Significant Difference ◽  
High Level

Background:: Serum ferritin concentrations are altered in hypothyroidism, but there is no available literature regarding the status of serum ferritin in anti-thyroid peroxidase (anti-TPO) positive hypothyroidism. The objectives: of our study were to evaluate the titer of anti-TPO and serum ferritin in newly diagnosed hypothyroid patients and to find out any difference of serum ferritin concentration between antibody-positive and antibody-negative patients. Methods:: A total of 143 subjects above the age of 18 years were recruited, and serum Thyroid Stimulating Hormone (TSH), free T3, free T4, anti-TPO, and ferritin were assayed by chemiluminescence method. According to their serum analysis findings, three groups were made as Group 1 of 49 subjects with hypothyroidism and anti-TPO positive, Group 2 of 47 subjects with hypothyroidism and anti-TPO negative, and Group 3 of 47 euthyroid and anti-TPO negative controls. Results: : Kruskal Wallis H test was applied, and the difference in concentration of TSH, FT3, FT4, Ferritin, anti-TPO amongst the three groups was found to be significant. The relationship between anti-TPO levels and serum ferritin concentration was further studied by multinomial logistic regression. We have found that there is a significant difference between the concentrations of ferritin; hence, it is highly likely that those with a high level of anti-TPO antibody shall have a higher concentration of serum ferritin. Conclusion:: ferritin concentrations were decreased in anti-TPO negative hypothyroidism, but in case of anti-TPO positive hypothyroidism the ferritin concentrations are raised. Hence, hypothyroidism should not always be considered as an iron deficiency state.

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