Primary hypothyroidism followed by hyperthyroidism Five case reports

1984 ◽  
Vol 105 (2) ◽  
pp. 179-183 ◽  
Author(s):  
Ståle Skare ◽  
Harald M. M. Frey ◽  
Ragnvald Konow-Thorsen
Keyword(s):  
Case Reports ◽  
Primary Hypothyroidism ◽  
Graves Disease

Abstract. Five patients are described, who developed primary hypothyroidism between 25 and 57 years of age. They were all adequately treated with l-thyroxine. Graves' disease developed six months to 34 years later. Two had TSH binding inhibiting immunoglobulin (TBII) in their serum at this stage. All were treated with carbimazole, and 3 have experienced relapse upon withdrawal. Our patients are discussed in relation to the 16 cases previously reported. The pathogenesis of this condition is open to speculation.

scholarly journals Hyperthyroid Graves' Disease and Primary Hypothyroidism Caused by TSH Receptor Antibodies in Monozygotic Twins: Case Reports.

1998 ◽  
Vol 45 (1) ◽  
pp. 117-121 ◽  
Author(s):  
JUN-ICHI TANI ◽  
KATSUMI YOSHIDA ◽  
HIROSHI FUKAZAWA ◽  
YOSHINORI KISO ◽  
NORIYO SAYAMA ◽  
...  
Keyword(s):  
Case Reports ◽  
Monozygotic Twins ◽  
Primary Hypothyroidism ◽  
Tsh Receptor ◽  
Graves Disease ◽  
Receptor Antibodies ◽  
Tsh Receptor Antibodies

scholarly journals Antiphospholipid Antibody Syndrome Associated with Graves' Disease Presenting as Inferior Vena Cava Thrombosis with Bilateral Lower Limb DVT

2014 ◽  
Vol 7 ◽  
pp. CCRep.S15302 ◽  
Author(s):  
Ankur Jain
Keyword(s):  
Inferior Vena Cava ◽  
Lower Limb ◽  
Inferior Vena ◽  
Case Reports ◽  
Vena Cava ◽  
Antithyroid Drugs ◽  
Graves Disease ◽  
Antiphospholipid Antibody ◽  
Antiphospholipid Antibody Syndrome ◽  
Bilateral Lower Limb

We report a case of a 60-year-old lady who presented with bilateral lower limb swelling and a thyroid swelling with clinical features consistent with thyrotoxicosis. Investigations revealed the presence of a thrombus in bilateral external, internal iliac veins, and inferior vena cava extending up to its infrahepatic part. Hormone profile and radioiodine uptake scan confirmed the diagnosis of Graves' disease. Further workup revealed the presence of antiphospholipid antibodies (confirmed after a repeat test at 12 weeks). The patient was treated with antithyroid drugs and anticoagulants. The patient improved with normalization of thyroid function and partial recanalization of the infrahepatic part of inferior vena cava. Hyperthyroidism has been implicated as a potential hypercoagulable state; however, the association of Graves' disease with antiphospholipid antibody syndrome is limited to isolated case reports. This case highlights a new mechanism underlying hypercoagulability associated with Graves' disease.

scholarly journals Unmasking of Neurosarcoidosis

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A618-A618
Author(s):  
Sharini Venugopal ◽  
Binita Neupane ◽  
Mahesh Nepal ◽  
Luis F Chavez
Keyword(s):  
Diabetes Insipidus ◽  
Medical History ◽  
Case Reports ◽  
Rare Complication ◽  
Case Series ◽  
Primary Hypothyroidism ◽  
Past Medical History ◽  
Water Excretion ◽  
History Of ◽  
Glucocorticoid Deficiency

Abstract Introduction: Central diabetes insipidus is a rare complication of neurosarcoidosis. In patients with concomitant adrenal insufficiency (AI), the symptoms of Diabetes Insipidus (DI) can be masked. Case: A 55-year-old female with past medical history of sarcoidosis presented to the hospital with hematemesis, nausea and dizziness. She has a past medical history of cardiac sarcoidosis that was revealed on a PET scan done before 10 years for which she was being treated with methotrexate and prednisone. She was off prednisone for a year prior to hospitalization. She underwent an upper endoscopy that showed diffusely erythematous gastric mucosa in the antrum. She was also hypotensive on admission, and she received packed red blood transfusions after which her sodium increased from 145mmol/L to 165mmol/L (Normal: 135-145mmol/L) in 48 hours. Further workup revealed persistent hypernatremia and urine osmolality was 75mOsm/kg H2O. (Normal: 50-1200mOsm/kg H2O). She was also hypoglycemic and hypotensive requiring multiple fluid boluses throughout her hospitalization. This prompted us to perform a random cortisol that came back at 2.1ug/dl (Normal: 3-23ug/dl) and 1.8ug/dl on two occasions. Cortisol Stimulation test was subsequently ordered, but was done only at 30 minutes, and Cortisol increased from 1.8ug/dl to 6.3ug/dl. Free thyroxine was 0.5 ng/dl (Normal: 0.9-1.8 ng/dl) and her TSH was 7.58uIU/ml (Normal: 0.55-4.78uIU/ml). MRI of the brain revealed extensive areas of extra-axial supra-sellar/infundibular nodular homogeneous intense enhancement that is most consistent with neuro-sarcoid. She was started on prednisone 40 mg daily, Desmopressin 0.05 mg twice daily, and levothyroxine as well. Her sodium level normalized and was 137mmol/L at discharge. She followed up later with outpatient Endocrinology and reported around 90lbs weight gain and no more episodes of nausea or vomiting or epistaxis or lightheadedness. Conclusion: The involvement of the hypothalamic-pituitary axis in sarcoidosis is extremely rare and attributes to < 1% of patients with a sellar mass. Small case series have shown that hypogonadism is the most common endocrine abnormality followed by DI. Our patient had a long-standing history of sarcoidosis with her pituitary dysfunction unmasked only on admission for other causes. She did not manifest any symptoms of DI or AI. There have been case reports where the symptoms of DI are masked due to underlying glucocorticoid deficiency. There have been theories that glucocorticoid deficiency impairs renal water excretion by both ADH (Anti-diuretic hormone) dependent and ADH independent pathways. Another notable feature in our case is that our patient presented with primary hypothyroidism. In fact, sarcoidosis has been commonly implicated in auto-immune polyglandular syndromes type 3, which can present with auto-immune thyroiditis more so in females.

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.

Anti-TSH antibodies in Graves' disease and their failure to interact with TSH receptor antibodies

1989 ◽  
Vol 120 (6) ◽  
pp. 773-777 ◽  
Author(s):  
Y. Ochi ◽  
T. Nagamune ◽  
Y. Nakajima ◽  
M. Ishida ◽  
Y. Kajita ◽  
...  
Keyword(s):  
Primary Hypothyroidism ◽  
Tsh Receptor ◽  
Graves Disease ◽  
Antibody Technique ◽  
Α Subunit ◽  
Occasional Occurrence ◽  
Assay Methods ◽  
Receptor Antibodies ◽  
Hyperthyroid Patients ◽  
Tsh Receptor Antibodies

Abstract. The occasional occurrence in sera of patients with Graves' disease of negative values in the assay for TSH receptor antibodies led to the discovery of endogenous antibodies to TSH. We examined the sera of approximately 2500 patients with Graves' disease. Eight positive sera were found. The IgG in all 8 sera showed higher binding with both bTSH and porcine TSH (pTSH) than with human TSH (hTSH). This means that autoantibodies to TSH in sera from patients with Graves' disease are rare and often directed towards heterologous bovine and porcine TSH. When hTSH levels were determined in sera of hyperthyroid patients with positive antibodies to hTSH, discrepancies in serum hTSH levels were observed when using different assay methods, i.e. hTSH levels were higher with the double-antibody technique, and lower with immunoradiometric assays. Antibodies in these sera showed higher binding to pTSH-α subunit than to -β subunit. The binding of the two pTSH subunits with antibodies could be displaced by intact bTSH. Neither stimulation in Graves' disease nor blocking in primary hypothyroidism of TSH receptor antibodies interfered with the binding of the anti-TSH antibodies to 125I-labelled pTSH, pTSH-α, and pTSH-β. Consequently, using this type of autoantibodies to TSH we were unable to obtain evidence that the TSH receptor antibodies of patients with Graves' disease was an anti-idiotype antibody against anti-TSH antibodies.

Development of Primary Hypothyroidism with the Appearance of Blocking-Type Antibody to Thyrotropin Receptor in Graves' Disease in Late Pregnancy

Thyroid ◽  
1999 ◽  
Vol 9 (2) ◽  
pp. 179-182 ◽  
Author(s):  
YOSHIHIKO UETA ◽  
HIROKO FUKUI ◽  
HIROSHI MURAKAMI ◽  
YUMI YAMANOUCHI ◽  
REI YAMAMOTO ◽  
...  
Keyword(s):  
Late Pregnancy ◽  
Primary Hypothyroidism ◽  
Graves Disease ◽  
Thyrotropin Receptor ◽  
Blocking Type

scholarly journals Emergence of Autoimmune Type 1 Diabetes and Acute Adrenal Crisis Following COVID-19

2021 ◽  
Author(s):  
Seda Hanife Oğuz ◽  
Alper Gürlek
Keyword(s):  
Type 1 Diabetes ◽  
Autoimmune Thyroiditis ◽  
Case Reports ◽  
Hormone Replacement ◽  
Autoimmune Disorders ◽  
Primary Hypothyroidism ◽  
Adrenal Crisis ◽  
Acth Stimulation ◽  
New Onset

Abstract Objective: Several case reports have indicated a possible link between Coronavirus Disease 2019 (COVID-19) and new-onset autoimmune disorders while co-precipitation of autoimmune type 1 diabetes and Addison’s disease has never been reported to date. Case Description: A 60-year-old male presented with extreme fatigue and weight loss three weeks after testing positive for COVID-19. The course of COVID-19 was mild, without pulmonary involvement. The patient showed symptoms and laboratory signs of new-onset diabetes without ketoacidosis and acute primary adrenal insufficiency, latter of which was confirmed with an ACTH stimulation test. GAD-65 antibody and antibodies to the adrenal cortex were positive in high titers, and the patient also had primary hypothyroidism associated with autoimmune thyroiditis. Previous medical records of the patient revealed no hyperglycemia or electrolyte abnormalities prior to current admission, but an earlier test result compatible with primary hypothyroidism. The patient was diagnosed with autoimmune polyglandular syndrome type II (APS II). Clinical and laboratory findings improved after starting appropriate hormone replacement therapies along with insulin. Conclusions: Evidence mostly obtained from case reports suggests that COVID-19 may induce a variety of autoimmune disorders in susceptible subjects. In our case, COVID-19 might have simply precipitated T1D and adrenal crisis in whom autoimmune thyroiditis may have been the first manifestation of an undiagnosed APS II. Or, COVID-19 may have triggered autoimmunity in the patient who was possibly predisposed to autoimmune disorders, and led to the development of APS II. Anyhow, more research is required to evaluate the possible link between COVID-19 and autoimmune disorders.

A Case Report on Methimazole Induced Anti-Thyroid Arthritis Syndrome: A Rare Drug Induced Migratory Polyarthritis

2021 ◽  
pp. 5483-5488
Author(s):  
Aiswarya Mohan ◽  
Aravind H ◽  
Chakravarthy S Maddipati ◽  
Roshni P R
Keyword(s):  
Adverse Effect ◽  
Case Reports ◽  
Antithyroid Drugs ◽  
Drug Discontinuation ◽  
Graves Disease ◽  
Drug Induced ◽  
Laboratory Findings ◽  
Diagnosis And Management ◽  
Life Threatening ◽  
Migratory Polyarthritis

Antithyroid drugs (ATD’s) are widely used as the first line treatment option for the management of hyperthyroidism, especially for patients with Graves’ disease. They are classified into thionamide (Methimazole, Carbimazole and Propylthiouracil) and Non-thionamide (Iodine containing compounds) ATD’s. These drugs are associated with various types of adverse effects ranging from mild to potentially life threatening. Antithyroid arthritis syndome (AAS) is one of the major and uncommon side effects of ATD therapy requiring immediate drug discontinuation and hospitalization presents itself with myalgia, arthralgia and arthritis along with fever and rash of varying severity and non-specific laboratory findings, making its diagnosis and management clinically challenging. Here we report the case of 32 year old female with Graves’ disease who experienced severe migratory polyarthritis after the initiation of methimazole therapy. Her symptoms started to disappear after the prompt withdrawal of methimazole. We also concluded that this adverse effect of ATD’s might not be dose dependent by comparing our case with 6 other case reports of AAS. Here our objective is to raise awareness among the clinicians regarding the differential diagnosis and management of this major, uncommon and potentially life threatening adverse effect of ATD therapy.

Thyroid autoimmunity in hyperprolactinaemic disorders

1983 ◽  
Vol 104 (1) ◽  
pp. 35-41 ◽  
Author(s):  
C. Ferrari ◽  
M. Boghen ◽  
A. Paracchi ◽  
P. Rampini ◽  
F. Raiteri ◽  
...  
Keyword(s):  
Thyroid Function ◽  
Thyroid Autoimmunity ◽  
Empty Sella ◽  
Primary Hypothyroidism ◽  
Graves Disease ◽  
Toxic Adenoma ◽  
Central Hypothyroidism ◽  
Nodular Goitre ◽  
The One ◽  
Tsh Levels

Abstract. Circulating thyroglobulin antibodies (TgAb) and microsomal antibodies (MsAb) and thyroid function (total and free T4 and T3, TSH basal and after TRH) have been evaluated in 92 hyperprolactinaemic patients (82 females and 10 males; 9 with macroprolactinoma, 22 with microprolactinoma, 4 with acromegaly, 5 with organic lesions of the hypothalamus, 2 with empty sella, 2 with idiopathic hypopituitarism, 2 with primary hypothyroidism, and 46 with idiopathic hyperprolactinaemia). Thyroid function was normal in all cases except 3 with hypothalamic disease and central hypothyroidism, the 2 patients with primary hypothyroidism and 2 with thyrotoxicosis (one due to Graves' disease and one to autonomous thyroid adenoma). High titres of TgAb (≥1/1250) and/or MsAb (≥ 1/1600) were found in the subject with Graves' disease, in one acromegalic, in the 2 primary hypothyroids, and in 12 women with either adenomatous or idiopathic hyperprolactinaemia; low titres of one or both antibodies were found in 9 other euthyroid women and in the one with toxic adenoma. In a control population of 185 subjects studied with the same methods, the prevalence of TgAb and/or MsAb positive (low titres) was 3.3% in females and 2.5% in males. Diffuse thyroid hyperplasia was clinically detectable in 12 euthyroid women and in the one with Graves' disease; 3 others had been previously operated for nodular goitre with histological evidence of Hashimoto's thyroiditis (2 cases) or for a cold nodule; a single thyroid nodule was present in the woman with toxic adenoma and in one euthyroid woman. Most of these subjects also had circulating TgAb and/or MsAb, and a few had increased TSH secretion. No significant differences were found in mean thyroid hormone and TSH levels between euthyroid hyperprolactinaemic subjects and healthy controls, but TRH-stimulated TSH levels were significantly higher in thyroid antibodies positive than negative subjects. These data, in agreement with a few previous reports, suggest that autoimmune thyroid disorders (especially asymptomatic autoimmune thyroiditis) occur in hyperprolactinaemic women with a prevalence far exceeding that observed in many surveys in the general population.

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