scholarly journals Acute Drug-Induced Cholestatic Syndrome in Basedow Graves’ Disease

2020 ◽  
Vol 5 (2) ◽  
pp. 81-85 ◽  
Author(s):  
Robert Aurelian Tiucă ◽  
Alina Mioara Boeriu ◽  
Rareș Adrian Georgescu ◽  
Ionela Maria Pașcanu
Keyword(s):  
Liver Damage ◽  
Therapeutic Option ◽  
Autoimmune Disorder ◽  
Thyroid Stimulating Hormone ◽  
Antithyroid Drugs ◽  
Graves Disease ◽  
Drug Induced ◽  
Immune Mediated ◽  
Viral Hepatitis A ◽  
Cholestatic Syndrome

AbstractIntroduction: Graves’ disease (GD), an autoimmune disorder caused by high levels of auto-antibodies against the thyroid-stimulating hormone receptor, is considered the most common cause of thyrotoxicosis, characterized by features such as goiter, ophthalmopathy and dermopathy. In our country, the administration of antithyroid drugs (ATD) is the first line of treatment in this disease. Side effects are rare but some of them, such as agranulocytosis or liver damage, may become serious.Case presentation: We report the case of a 20-year-old female patient who was diagnosed with GD after being previously diagnosed with viral hepatitis A. Treatment was initiated with methimazole 30 mg/day, and three weeks later she developed intense hepatic cytolysis and cholestatic syndrome, therefore the ATD was stopped. A suspicion of autoimmune liver disease was raised, and a liver biopsy was performed in order to establish the diagnosis. The next therapeutic option for hyperthyroidism was radioactive iodine (RAI). Three months following RAI, the patient presented severe hypothyroidism, thereupon treatment with levothyroxine was initiated.Conclusions: Although severe acute liver injury is rare, mild liver dysfunction is quite common in patients with GD. The overproduction of thyroid hormones, or the treatment with ATD through immune mediated processes or drug reactions, represent possible mechanisms responsible for liver damage.

scholarly journals PANCYTOPENIA SECONDARY TO AUTOIMMUNE VITAMIN B12 DEFICIENCY IN GRAVES DISEASE

2020 ◽  
Vol 6 (6) ◽  
pp. e282-e285
Author(s):  
Vilmarie Rodriguez ◽  
Kristen M. Gonzales ◽  
Anoop Mohamed Iqbal ◽  
Natasha Arbelo-Ramos ◽  
Kirk D. Wyatt ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Biopsy ◽  
White Blood Cells ◽  
Vitamin B12 Deficiency ◽  
Thyroid Stimulating Hormone ◽  
Antithyroid Drugs ◽  
Graves Disease ◽  
Vitamin B ◽  
Thyroid Function Tests ◽  
Drug Induced

Objective: To describe a case of Graves disease (GD) and coexistent pancytopenia associated with autoimmune vitamin B12 deficiency. While thyrotoxicosis and antithyroid drugs can cause pancytopenia, other autoimmune conditions such as vitamin B12 deficiency can occur, leading to severe anemia and pancytopenia. Methods: A 19-year-old female with GD treated with methimazole presented with thyrotoxicosis and evidence of pancytopenia. Diagnostic studies included a complete blood cell count, peripheral blood smears, thyroid function tests, and a bone marrow biopsy. Results: White blood cells were 2.4 × 109 cells/L (reference range [RR] is 3.4 to 9.6 × 109 cells/L), hemoglobin was 7.9 g/dL (RR is 11.6 to 15.0 g/dL), neutrophil count was 1.2 × 109 cells/L, and platelets were 84 × 109 cells/L (RR is 157 to 371 × 109 cells/L). Thyroid-stimulating hormone was <0.01 mIU/L (RR is 0.50 to 4.30 mIU/L), free thyroxine was 3.7 ng/dL (RR is 1.0 to 1.6 ng/dL), and total triiodothyronine was 221 ng/dL (RR is 91 to 218 ng/dL). Due to suspicion for drug-induced pancytopenia, methimazole was discontinued. Three days later, she was hospitalized for a syncopal episode with a further decline in hemoglobin to 6.7 g/dL, neutrophils to 0.68 × 109 cells/L, and platelets to 69 × 109 cells/L. Bone marrow biopsy findings showing marrow hypercellularity and hypersegmented neutrophils suggested vitamin B12 deficiency. Vitamin B12 was <70 ng/L (RR is 180 to 914 ng/L). Intramuscular vitamin B12 injections were initiated, and pancytopenia resolved within 1 month. Conclusion: Although rarely described in the literature, autoimmune vitamin B12 deficiency can be missed as an underlying etiology for pancytopenia in patients with GD. The clinical picture can be further confounded when these patients are treated with antithyroid drugs known to cause bone marrow suppression.

scholarly journals Graves’ Disease

2021 ◽  
Author(s):  
Sanjay Saran
Keyword(s):  
Older Patients ◽  
Autoimmune Disorder ◽  
Organ System ◽  
Antithyroid Drugs ◽  
Graves Disease ◽  
Younger Patients ◽  
Skin Symptoms ◽  
Diffuse Goiter ◽  
Pretibial Myxedema ◽  
Symptoms And Signs

Graves’ disease (GD) is an autoimmune disorder characterized by presence of TSH receptor autoantibody. It is most common cause of hyperthyroidism worldwide. Though GD can occur any age but peak incidence is seen during adulthood in between 20 to 50 years of age. GD is more commonly seen in female. GD is primarily disease of thyroid gland but affects multi organ system i.e. heart, liver, muscle, eye and skin. Symptoms and signs are result from hyperthyroidism or a consequence of underlying autoimmunity. Weight loss, fatigue, heat intolerance, tremor, and palpitations are the most common symptoms. Diffuse goiter presents in most of younger patients with thyrotoxicosis but less common in older patients. Graves’ ophthalmopathy and pretibial myxedema are extrathyroidal manifestations of GD which results from action of TSHR autoantibodies on TSHR present onfibroblast, adipocyte and T cells in extrathyroidal tissue. Treatment of GD remains in between antithyroid drugs, radioiodine or surgery. In this review we discuss the diagnosis and management of GD.

scholarly journals The Role of the Microbiota in Graves’ Disease and Graves’ Orbitopathy

2021 ◽  
Vol 11 ◽  
Author(s):  
Jueyu Hou ◽  
Yunjing Tang ◽  
Yongjiang Chen ◽  
Danian Chen
Keyword(s):  
Gut Microbiota ◽  
Negative Impact ◽  
Bifidobacterium Longum ◽  
Autoimmune Disorder ◽  
Thyroid Stimulating Hormone ◽  
Clinical Syndrome ◽  
Graves Disease ◽  
Material Transfer ◽  
T Helper 17 ◽  
Graves Orbitopathy

Graves‘ disease (GD) is a clinical syndrome with an enlarged and overactive thyroid gland, an accelerated heart rate, Graves’ orbitopathy (GO), and pretibial myxedema (PTM). GO is the most common extrathyroidal complication of GD. GD/GO has a significant negative impact on the quality of life. GD is the most common systemic autoimmune disorder, mediated by autoantibodies to the thyroid-stimulating hormone receptor (TSHR). It is generally accepted that GD/GO results from complex interactions between genetic and environmental factors that lead to the loss of immune tolerance to thyroid antigens. However, the exact mechanism is still elusive. Systematic investigations into GD/GO animal models and clinical patients have provided important new insight into these disorders during the past 4 years. These studies suggested that gut microbiota may play an essential role in the pathogenesis of GD/GO. Antibiotic vancomycin can reduce disease severity, but fecal material transfer (FMT) from GD/GO patients exaggerates the disease in GD/GO mouse models. There are significant differences in microbiota composition between GD/GO patients and healthy controls. Lactobacillus, Prevotella, and Veillonella often increase in GD patients. The commonly used therapeutic agents for GD/GO can also affect the gut microbiota. Antigenic mimicry and the imbalance of T helper 17 cells (Th17)/regulatory T cells (Tregs) are the primary mechanisms proposed for dysbiosis in GD/GO. Interventions including antibiotics, probiotics, and diet modification that modulate the gut microbiota have been actively investigated in preclinical models and, to some extent, in clinical settings, such as probiotics (Bifidobacterium longum) and selenium supplements. Future studies will reveal molecular pathways linking gut and thyroid functions and how they impact orbital autoimmunity. Microbiota-targeting therapeutics will likely be an essential strategy in managing GD/GO in the coming years.

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 Neurological manifestations of Graves’ disease: A case report and review of the literature

2016 ◽  
Vol 7 (01) ◽  
pp. 153-156 ◽  
Author(s):  
Swayamsidha Mangaraj ◽  
Arun Kumar Choudhury ◽  
Binoy Kumar Mohanty ◽  
Anoj Kumar Baliarsinha
Keyword(s):  
Similar Case ◽  
Clinical Manifestations ◽  
Autoimmune Disorder ◽  
Thyroid Stimulating Hormone ◽  
Graves Disease ◽  
Diagnostic Dilemma ◽  
Ocular Manifestations ◽  
Thyroid Associated Ophthalmopathy ◽  
Organ Specific ◽  
High Degree

ABSTRACTGraves’ disease (GD) is characterized by a hyperfunctioning thyroid gland due to stimulation of the thyroid-stimulating hormone receptor by autoantibodies directed against it. Apart from thyrotoxicosis, other clinical manifestations include ophthalmopathy, dermopathy, and rarely acropachy. GD is an organ-specific autoimmune disorder, and hence is associated with various other autoimmune disorders. Myasthenia gravis (MG) is one such disease, which is seen with patients of GD and vice versa. Though the association of GD and myasthenia is known, subtle manifestations of latter can be frequently missed in routine clinical practice. The coexistence of GD and ocular MG poses a significant diagnostic dilemma to treating physicians. The ocular manifestations of myasthenia can be easily missed in case of GD and falsely attributed to thyroid associated ophthalmopathy due to closely mimicking presentations of both. Hence, a high degree of the clinical vigil is necessary in such cases to appreciate their presence. We present a similar case which exemplifies the above said that the clinical challenge in diagnosing coexistent GD and ocular myasthenia.

Management of thyrotoxicosis in children and adolescents: 35 years’ experience in 304 patients

2018 ◽  
Vol 31 (2) ◽  
pp. 159-165 ◽  
Author(s):  
Fereidoun Azizi ◽  
Atieh Amouzegar
Keyword(s):  
Children And Adolescents ◽  
Treatment Modality ◽  
Radioiodine Therapy ◽  
Thyroid Stimulating Hormone ◽  
Antithyroid Drugs ◽  
Graves Disease ◽  
The Mean ◽  
Toxic Goiter ◽  
Original Treatment

Abstract Background: Diffuse toxic goiter accounts for about 15% of all childhood thyroid diseases. There is great controversy over the management of Graves’ disease in children and adolescents. This article reports our experience in 304 children and juvenile patients with Graves’ disease. Methods: Between 1981 and 2015, 304 patients aged 5–19 years with diffuse toxic goiter were studied, of whom 296 patients were treated with antithyroid drugs (ATD) for 18 months. Patients with persistent or relapsed hyperthyroidism who refused ablative therapy with surgery or radioiodine were managed with continuous methimazole (MMI) treatment. Results: In 304 patients (245 females and 59 males), the mean age was 15.6±2.6 years. After 18 months of ATD therapy, 37 remained in remission and of the 128 who relapsed, two, 29 and 97 patients chose surgery, continuous ATD and radioiodine therapy, respectively. Of the 136 patients who received radioiodine, 66.2% became hypothyroid. Twenty-nine patients received continuous ATD therapy for 5.7±2.4 years. The mean MMI dose was 4.6±12 mg daily, no serious complications occurred and all of them remained euthyroid during the follow-up. Less abnormal thyroid-stimulating hormone (TSH) values were observed in these patients, as compared to patients who were on a maintenance dose of levothyroxine after radioiodine induced hypothyroidism. Conclusions: Original treatment with ATD and subsequent radioiodine therapy remain the mainstay of treatment for juvenile hyperthyroidism. Continuous ATD administration may be considered as another treatment modality for hyperthyroidism.

scholarly journals A Case of Antithyroid Drug-Induced Agranulocytosis Pre-Covid 19 Era

2020 ◽  
pp. 1-4
Author(s):  
MosabNouraldein Mohammed Hamad
Keyword(s):  
Side Effects ◽  
Neutrophil Count ◽  
Antithyroid Drug ◽  
Drug Effects ◽  
Medical Advice ◽  
Antithyroid Drugs ◽  
Graves Disease ◽  
Drug Induced ◽  
Immunological Mechanisms ◽  
Noticeable Reduction

Agranulocytosis is an infrequent and serious side effect of antithyroid drugs characterized by a noticeable reduction in granulocyte and neutrophil count, it usually occurs within the first 2-3 months of treatment. There is a variety of mechanisms by which ATD can induce agranulocytosis, direct drug effects, and immunological mechanisms. We present 33 years old female attended Atbara teaching hospital who has developed agranulocytosis 2 weeks after starting ATD to treat relapsed Graves' disease. What was unusual about this patient is that symptoms have occurred in a period less than 15 days of starting treatment and with a dose of 45 mg /day. The physician must educate the patient about the possibility of early onset of serious side effects of ATD and to seek medical advice as soon as possible.

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.

scholarly journals Graves’ Disease

2021 ◽  
Author(s):  
Vasudha Bakshi ◽  
Gollapalli Rajeev Kumar
Keyword(s):  
Thyroid Gland ◽  
Hormone Receptor ◽  
Treatment Options ◽  
Positive Family History ◽  
Current Treatment ◽  
Thyroid Stimulating Hormone ◽  
Antithyroid Drugs ◽  
Graves Disease ◽  
Autoimmune Thyroid ◽  
Stimulating Hormone

Graves’ disease (GD) is an autoimmune thyroid disorder where autoantibodies are produced against TSH (Thyroid Stimulating Hormone) receptor causing thyrotoxicosis. It is characterized by goiter, ophthalmopathy, and occasionally pretibial myxedema. The autoimmune mechanism causing disease is not well understood and it is complex. It involves multifactorial etiology involving environmental and genetic factors. Smoking and positive family history contributing to the development of GD. GD can be diagnosed based on the clinical manifestation and demonstrating low concentration of TSHs, high TRab (Thyroid Stimulating Hormone receptor autoantibodies), and high FT4 (Free thyroxine) concentration. Current treatment options aimed at stable restoration of euthyroidism by following different modalities of suppressing thyroid gland using antithyroid drugs, removing/ablating thyroid gland by surgery, and radioactive iodine treatment with iodine- 131.

scholarly journals Thyroid-stimulating hormone receptor (TSHR) fusion proteins in Graves’ disease

2020 ◽  
Vol 246 (2) ◽  
pp. 135-147
Author(s):  
Hans-Peter Holthoff ◽  
Kerstin Uhland ◽  
Gabor Laszlo Kovacs ◽  
Andreas Reimann ◽  
Kristin Adler ◽  
...  
Keyword(s):  
Mouse Model ◽  
Fusion Proteins ◽  
Recombinant Adenovirus ◽  
Disease Model ◽  
Autoimmune Disorder ◽  
Thyroid Stimulating Hormone ◽  
Graves Disease ◽  
Serum Samples

Graves’ disease is an autoimmune disorder, which is characterized by stimulatory antibodies targeting the human thyrotropin receptor (TSHR), resulting in hyperthyroidism and multiple organ damage. We systematically investigated monomeric and dimeric fusion proteins of the A subunit of TSHR for efficacy to bind to the monoclonal patient antibody M22, to interact with Graves’ patient serum samples, and to impact on anti-TSHR antibody titers, hyperthyroidism, tachycardia and other in vivo read-outs in a long-term mouse model of Graves’ disease induced by immunization with a recombinant adenovirus encoding TSHR A. Binding assays and functional measurements of TSHR-dependent cAMP formation showed binding of monomeric TSHR-His and dimeric TSHR-Fc to the anti-TSHR antibody M22 at low-effective concentrations (EC50 of 5.7 nmol/L and 8.6 nmol/L) and inhibition of the effects of this antibody at high efficiencies (IC50 values of 16–20 nmol/L). Both proteins also block the effects of polyclonal anti-TSHR antibodies occurring in Graves’ patient sera with somewhat lower average efficiencies (mean IC50 values of 29 nmol/L and 68 nmol/L). However, in vivo characterization of epicutaneous patch administrations of TSHR-Fc at doses of 0.3 and 0.6 mg/kg body weight in a murine Graves’ disease model did not result in any improvement of disease parameters. In conclusion, high affinity binding of TSHR-Fc to pathological anti-TSHR antibodies was not matched by efficacy to improve Graves’ disease parameter in a long-term mouse model.

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